Heart failure: Difference between revisions

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The definition of congestive '''heart failure''' has evolved.
In 2007, the [[National Library of Medicine]] defined heart failure as:
:"defective cardiac filling and/or impaired contraction and emptying, resulting in the heart's inability to pump a sufficient amount of blood to meet the needs of the body tissues or to be able to do so only with an elevated filling pressure".<ref>{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?field=uid&term=D006333 |title=Heart Failure, Congestive|author=National Library of Medicine |accessdate=2007-10-19 |format= |work=}}</ref>
In 2009, the [[National  Library of Medicine]]  defined heart failure as:
:"a heterogeneous condition in which the heart is unable to pump out  sufficient blood to meet the metabolic need of the body. Heart failure  can be caused by structural defects, functional abnormalities  ([[ventricular dysfunction]]), or a sudden overload beyond its capacity.<ref>{{MeSH}}</ref>


Congestive heart failure is defined as "defective cardiac filling and/or impaired contraction and emptying, resulting in the heart's inability to pump a sufficient amount of blood to meet the needs of the body tissues or to be able to do so only with an elevated filling pressure".<ref>{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?field=uid&term=D006333 |title=Heart Failure, Congestive|author=National Library of Medicine |accessdate=2007-10-19 |format= |work=}}</ref>
This, like some other terms in cardiology, can be confusing to laymen. "Heart failure" does not mean the heart has completely failed; if the heart were the fuel pump of an automobile, the diagnosis might be "pump slowdown." In like manner, "sudden cardiac death syndrome" does not mean the victim is dead; the automotive equivalent might be "running again after a jump start, but we need to know why the engine stalled."


==Classification==
==Classification==
===Systolic dysfunction===
===Systolic dysfunction===
{{main|Systolic heart failure}}
Systolic heart failure is "heart failure caused by abnormal myocardial contraction during [[systole]]  leading to defective cardiac emptying."<ref>{{MeSH|Systolic heart failure}}</ref>
===Diastolic dysfunction===
===Diastolic dysfunction===
{{main|Diastolic heart failure}}
Diastolic heart failure is "heart failure caused by abnormal myocardial relaxation during [[diastole]] leading to defective cardiac filling."<ref>{{MeSH|Diastolic heart  failure}}</ref>
==Etiology / cause==
Heart failure may be caused by [[coronary heart disease]], [[hypertension]], [[ethanol]], [[myocarditis]], [[connective tissue disease]] and others.<ref name="pmid10760308">{{cite journal| author=Felker GM, Thompson RE, Hare JM, Hruban RH, Clemetson DE, Howard DL et al.| title=Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy. | journal=N Engl J Med | year= 2000 | volume= 342 | issue= 15 | pages= 1077-84 | pmid=10760308
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=10760308 }} </ref>
* 50% are cases are idiopathic.<ref name="pmid10760308"/>
* 20% to 50% of idiopathic cardiomyopathy may be familial.<ref name="pmid15808750">{{cite journal| author=Burkett EL, Hershberger RE| title=Clinical and genetic issues in familial dilated cardiomyopathy. | journal=J Am Coll Cardiol | year= 2005 | volume= 45 | issue= 7 | pages= 969-81 | pmid=15808750 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=15808750 | doi=10.1016/j.jacc.2004.11.066 }} </ref><ref name="pmid16027452">{{cite journal| author=Mahon NG, Murphy RT, MacRae CA, Caforio AL, Elliott PM, McKenna WJ| title=Echocardiographic evaluation in asymptomatic relatives of patients with dilated cardiomyopathy reveals preclinical disease. | journal=Ann Intern Med | year= 2005 | volume= 143 | issue= 2 | pages= 108-15 | pmid=16027452
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=16027452 }} </ref>


==Diagnosis==
==Diagnosis==
===History and physical examination===
===History and physical examination===
The best findings for detecting increased filling pressure are jugular venous distention and radiographic redistribution. The best findings for detecting systolic dysfunction are abnormal apical impulse, radiographic cardiomegaly, and q waves or left bundle branch block on an electrocardiogram. <ref name="pmid9169900">{{cite journal |author=Badgett RG, Lucey CR, Mulrow CD |title=Can the clinical examination diagnose left-sided heart failure in adults? |journal=JAMA |volume=277 |issue=21 |pages=1712-9 |year=1997 |pmid=9169900 |doi=}}</ref>
{| class="wikitable" align="right"
{| class="wikitable" align="right"
|+ Hemodynamic Profiles
|+ Hemodynamic Profiles
! colspan="2" rowspan="2"| !! colspan="2" | Congestion†?<br>(jugular venous distention and <br>radiographic redistribution)<ref name="pmid9169900">{{cite journal |author=Badgett RG, Lucey CR, Mulrow CD |title=Can the clinical examination diagnose left-sided heart failure in adults? |journal=JAMA |volume=277 |issue=21 |pages=1712-9 |year=1997 |pmid=9169900 |doi=}}</ref>
! colspan="2" rowspan="2"| !! colspan="2" | Congestion†?<br>(jugular venous distention and <br>radiographic redistribution)<ref name="pmid9169900">{{cite journal |author=Badgett RG, Lucey CR, Mulrow CD |title=Can the clinical examination diagnose left-sided heart failure in adults? |journal=JAMA |volume=277 |issue=21 |pages=1712-9 |year=1997 |pmid=9169900 |doi=}}</ref>
|-
|-
|  No || Yes
|  '''No''' || '''Yes'''
|-
|-
| rowspan="2" | '''Hypoperfusion‡?'''<br>(proportional pulse pressure < 25%<ref name="pmid2913385">{{cite journal |author=Stevenson LW, Perloff JK |title=The limited reliability of physical signs for estimating hemodynamics in chronic heart failure |journal=JAMA |volume=261 |issue=6 |pages=884–8 |year=1989 |pmid=2913385 |doi=}}</ref><ref name="pmid11420761">{{cite journal |author=Shah MR, Hasselblad V, Stinnett SS, ''et al'' |title=Hemodynamic profiles of advanced heart failure: association with clinical characteristics and long-term outcomes |journal=J. Card. Fail. |volume=7 |issue=2 |pages=105–13 |year=2001 |pmid=11420761 |doi=10.1054/jcaf.2001.24131}}</ref>, <br>cool extremities<ref name="pmid11303155">{{cite journal |author=Kaplan LJ, McPartland K, Santora TA, Trooskin SZ |title=Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients |journal=The Journal of trauma |volume=50 |issue=4 |pages=620–7; discussion 627–8 |year=2001 |pmid=11303155 |doi=}}</ref>) || No || Warm and dry<br>(46% mortality at one year) || Warm and wet
| rowspan="2" | '''Hypoperfusion‡?'''<br>(proportional pulse pressure < 25%<ref name="pmid2913385">{{cite journal |author=Stevenson LW, Perloff JK |title=The limited reliability of physical signs for estimating hemodynamics in chronic heart failure |journal=JAMA |volume=261 |issue=6 |pages=884–8 |year=1989 |pmid=2913385 |doi=}}</ref><ref name="pmid11420761">{{cite journal |author=Shah MR, Hasselblad V, Stinnett SS, ''et al'' |title=Hemodynamic profiles of advanced heart failure: association with clinical characteristics and long-term outcomes |journal=J. Card. Fail. |volume=7 |issue=2 |pages=105–13 |year=2001 |pmid=11420761 |doi=10.1054/jcaf.2001.24131}}</ref>, <br>cool extremities<ref name="pmid11303155">{{cite journal |author=Kaplan LJ, McPartland K, Santora TA, Trooskin SZ |title=Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients |journal=The Journal of trauma |volume=50 |issue=4 |pages=620–7; discussion 627–8 |year=2001 |pmid=11303155 |doi=}}</ref><ref name="pmid19885995">{{cite journal| author=Grissom CK, Morris AH, Lanken PN, Ancukiewicz M, Orme JF, Schoenfeld DA et al.| title=Association of physical examination with pulmonary artery  catheter parameters in acute lung injury. | journal=Crit Care Med | year= 2009 | volume= 37 | issue= 10 | pages= 2720-6 | pmid=19885995
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=19885995 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref>) || '''No''' || Warm and dry<br/>(33% mortality at one year) || Warm and wet
|-
|-
| Yes|| Cold and dry || Cold and wet<br>(33% mortality at one year<ref name="pmid11420761"/>)
| '''Yes'''|| Cold and dry || Cold and wet<br/>(46% mortality at one year<ref name="pmid11420761"/>)
|-
|-
| colspan="4" | Notes:<br>
| colspan="4" | Notes:<br>
Adapted from Figure 1 of Nohria et al.<ref name="pmid11829703">{{cite journal |author=Nohria A, Lewis E, Stevenson LW |title=Medical management of advanced heart failure |journal=JAMA |volume=287 |issue=5 |pages=628–40 |year=2002 |pmid=11829703 |doi=}}</ref><br>
Adapted from Figure 1 of Nohria et al.<ref name="pmid11829703">{{cite journal |author=Nohria A, Lewis E, Stevenson LW |title=Medical management of advanced heart failure |journal=JAMA |volume=287 |issue=5 |pages=628–40 |year=2002 |pmid=11829703 |doi=}}</ref><br>
† Congestion is defined as [[pulmonary capillary wedge pressure]] of 20 mm Hg or more<ref name="pmid11420761"/><br>
† Congestion is defined as [[pulmonary capillary wedge pressure]] of 20 mm Hg or more<ref name="pmid11420761"/><br>
‡ Hypoperfusion is defined as [[cardiac index]] of 1.8 L/min/m<sup>2</sup>.<ref name="pmid11420761"/> This is associated with elevate lactate.<ref name="pmid11303155">{{cite journal |author=Kaplan LJ, McPartland K, Santora TA, Trooskin SZ |title=Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients |journal=The Journal of trauma |volume=50 |issue=4 |pages=620–7; discussion 627–8 |year=2001 |pmid=11303155 |doi=}}</ref>
‡ Hypoperfusion is defined as [[cardiac index]] of 1.8 L/min/m<sup>2</sup>.<ref name="pmid11420761"/> This is associated with elevate lactate.<ref name="pmid11303155">{{cite journal |author=Kaplan LJ, McPartland K, Santora TA, Trooskin SZ |title=Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients |journal=The Journal of trauma |volume=50 |issue=4 |pages=620–7; discussion 627–8 |year=2001 |pmid=11303155 |doi=}}</ref> Other measures are at [[Critical care#Tissue_perfusion]].
|}
|}


The history and physical examination can also be used for patients with advanced heart failure to place the patient into a hemodynamic profile to guide management.<ref name="pmid11829703">{{cite journal |author=Nohria A, Lewis E, Stevenson LW |title=Medical management of advanced heart failure |journal=JAMA |volume=287 |issue=5 |pages=628–40 |year=2002 |pmid=11829703 |doi=}}</ref><ref name="pmid11420761">{{cite journal |author=Shah MR, Hasselblad V, Stinnett SS, ''et al'' |title=Hemodynamic profiles of advanced heart failure: association with clinical characteristics and long-term outcomes |journal=J. Card. Fail. |volume=7 |issue=2 |pages=105–13 |year=2001 |pmid=11420761 |doi=10.1054/jcaf.2001.24131}}</ref><ref name="pmid11303155">{{cite journal |author=Kaplan LJ, McPartland K, Santora TA, Trooskin SZ |title=Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients |journal=The Journal of trauma |volume=50 |issue=4 |pages=620–7; discussion 627–8 |year=2001 |pmid=11303155 |doi=}}</ref> Patients in the "cold and wet" category may need to "warm up in order to dry out" by stopping [[beta-blockers]] and [[ACE inhibitors]].<ref name="pmid11829703"/>
The best findings for detecting increased filling pressure are [[central venous pressure|jugular venous distention]] and radiographic redistribution. The best findings for detecting systolic dysfunction are abnormal apical impulse, radiographic cardiomegaly, and q waves or left bundle branch block on an electrocardiogram. <ref name="pmid9169900">{{cite journal |author=Badgett RG, Lucey CR, Mulrow CD |title=Can the clinical examination diagnose left-sided heart failure in adults? |journal=JAMA |volume=277 |issue=21 |pages=1712-9 |year=1997 |pmid=9169900 |doi=}}</ref>


===Echocardiogram===
The history and physical examination can also be used for patients with advanced heart failure to place the patient into a hemodynamic profile to guide management.<ref name="pmid11829703">{{cite journal |author=Nohria A, Lewis E, Stevenson LW |title=Medical management of advanced heart failure |journal=JAMA |volume=287 |issue=5 |pages=628–40 |year=2002 |pmid=11829703 |doi=}}</ref><ref name="pmid11420761">{{cite journal |author=Shah MR, Hasselblad V, Stinnett SS, ''et al'' |title=Hemodynamic profiles of advanced heart failure: association with clinical characteristics and long-term outcomes |journal=J. Card. Fail. |volume=7 |issue=2 |pages=105–13 |year=2001 |pmid=11420761 |doi=10.1054/jcaf.2001.24131}}</ref><ref name="pmid11303155">{{cite journal |author=Kaplan LJ, McPartland K, Santora TA, Trooskin SZ |title=Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients |journal=The Journal of trauma |volume=50 |issue=4 |pages=620–7; discussion 627–8 |year=2001 |pmid=11303155 |doi=}}</ref> Patients in the "cold and wet" category may need to "warm up in order to dry out" by stopping [[adrenergic beta-receptor blockader]]s (beta-blockers) and [[angiotensin-converting enzyme inhibitor]]s (ACE inhibitors).<ref name="pmid11829703"/>
The fractional shortening can estimate the left ventricular ejection fraction.<ref name="pmid6627386">{{cite journal |author=Tortoledo FA, Fernandez GC, Quinones MA |title=An accurate and simplified method to calculate angiographic left ventricular ejection fraction |journal=Catheterization and cardiovascular diagnosis |volume=9 |issue=4 |pages=357-62 |year=1983 |pmid=6627386 |doi=}}</ref><ref name="pmid7273375">{{cite journal |author=Quinones MA, Waggoner AD, Reduto LA, ''et al'' |title=A new, simplified and accurate method for determining ejection fraction with two-dimensional echocardiography |journal=Circulation |volume=64 |issue=4 |pages=744-53 |year=1981 |pmid=7273375 |doi=}}</ref><ref name="pmid6745290">{{cite journal |author=Erbel R, Schweizer P, Krebs W, Meyer J, Effert S |title=Sensitivity and specificity of two-dimensional echocardiography in detection of impaired left ventricular function |journal=Eur. Heart J. |volume=5 |issue=6 |pages=477-89 |year=1984 |pmid=6745290 |doi=}}</ref>
 
===Brain natriuretic peptide===
{{main|Brain natriuretic peptide}}
The role of the [[brain natriuretic peptide]] is limited when experienced physicians evaluate patients.<ref name="pmid19293069">{{cite journal| author=Schneider HG, Lam L, Lokuge A, Krum H, Naughton MT, De Villiers Smit P et al.| title=B-type natriuretic peptide testing, clinical outcomes, and health services use in emergency department patients with dyspnea: a randomized trial. | journal=Ann Intern Med | year= 2009 | volume= 150 | issue= 6 | pages= 365-71 | pmid=19293069
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=19293069 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref>
 
[[Clinical practice guideline]]s state regarding the BNP and NT-proBNP:<ref name="pmid19324966">{{cite journal| author=Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG et al.| title=2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. | journal=Circulation | year= 2009 | volume= 119 | issue= 14 | pages= e391-479 | pmid=19324966
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=19324966 | doi=10.1161/CIRCULATIONAHA.109.192065 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref>
:"Measurement of natriuretic peptides (BNP and NT-proBNP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of HF is uncertain. Measurement of natriuretic peptides (BNP and NT-proBNP) can be helpful in risk stratification."
 
===Chest radiograph===
The accuracy of the chest radiograph is below.<ref name="pmid8945695">{{cite journal| author=Badgett RG, Mulrow CD, Otto PM, Ramírez G| title=How well can the chest radiograph diagnose left ventricular dysfunction? | journal=J Gen Intern Med | year= 1996 | volume= 11 | issue= 10 | pages= 625-34 | pmid=8945695
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8945695 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref>
For diagnosing decreased ejection fraction with:
Cardiomegaly
* [[sensitivity (tests)|sensitivity]] = 51%
* [[specificity (tests)|specificity]] = 79%
Redistribution:
* [[sensitivity (tests)|sensitivity]] = 37%
* [[specificity (tests)|specificity]] = 85%
 
For diagnosing increased preload with:
Redistribution
* [[sensitivity (tests)|sensitivity]] = 65%
* [[specificity (tests)|specificity]] = 67%
 
Various definitions have been proposed for determining redistribution; definitions with absolute measurements probably best apply to 72 inch erect, postero-anterior radiograph:<ref name="pmid8945695"/>
* Pulonary veins in the upper lobes are larger than the lower lobe vein. Distinguishing pulmonary veins from arteries is not important as pulmonary veins are larger than pulmonary arteries.
* Upper lobe veins 3 mm or larger in the first anterior interspace
* Upper lobe veins 7 mm or larger at the level of the pulmonary artery
 
===Echocardiography===
[[Echocardiography]] measures the fractional shortening of the ventricle which can estimate the left ventricular ejection fraction.<ref name="pmid6627386">{{cite journal |author=Tortoledo FA, Fernandez GC, Quinones MA |title=An accurate and simplified method to calculate angiographic left ventricular ejection fraction |journal=Catheterization and cardiovascular diagnosis |volume=9 |issue=4 |pages=357-62 |year=1983 |pmid=6627386 |doi=}}</ref><ref name="pmid7273375">{{cite journal |author=Quinones MA, Waggoner AD, Reduto LA, ''et al'' |title=A new, simplified and accurate method for determining ejection fraction with two-dimensional echocardiography |journal=Circulation |volume=64 |issue=4 |pages=744-53 |year=1981 |pmid=7273375 |doi=}}</ref><ref name="pmid6745290">{{cite journal |author=Erbel R, Schweizer P, Krebs W, Meyer J, Effert S |title=Sensitivity and specificity of two-dimensional echocardiography in detection of impaired left ventricular function |journal=Eur. Heart J. |volume=5 |issue=6 |pages=477-89 |year=1984 |pmid=6745290 |doi=}}</ref>
 
Various parameters on echocardiogram can estimate left ventricular end diastolic pressure.<ref name="pmid20849482">{{cite journal| author=Dokainish H, Nguyen J, Sengupta R, Pillai M, Alam M, Bobek J et al.| title=New, simple echocardiographic indexes for the estimation of filling pressure in patients with cardiac disease and preserved left ventricular ejection fraction. | journal=Echocardiography | year= 2010 | volume= 27 | issue= 8 | pages= 946-53 | pmid=20849482 | doi=10.1111/j.1540-8175.2010.01177.x | pmc= | url= }} </ref>
 
===Clinical score===
====Framingham score====
The [[Framingham congestive-heart-failure score]] can be used  (two major or one major and two minor criteria).<ref name="pmid8376698">{{cite journal| author=Ho KK, Pinsky JL, Kannel WB, Levy D| title=The epidemiology of heart failure: the Framingham Study. | journal=J Am Coll Cardiol | year= 1993 | volume= 22 | issue= 4 Suppl A | pages= 6A-13A | pmid=8376698
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=8376698 }} </ref>
 
====National Health and Nutrition Examination Survey score====
The National Health and Nutrition Examination Survey (NHANES) congestive heart failure score (scores of 3 or more) can be used


==Treatment==
==Treatment==
[[Clinical practice guideline]]s address management.<ref name="pmid21844551">{{cite journal| author=Mant J, Al-Mohammad A, Swain S, Laramée P, Guideline Development Group| title=Management of chronic heart failure in adults: synopsis of the National Institute For Health and clinical excellence guideline. | journal=Ann Intern Med | year= 2011 | volume= 155 | issue= 4 | pages= 252-9 | pmid=21844551 | doi=10.1059/0003-4819-155-4-201108160-00009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21844551  }} </ref><ref name="pmid23741058">{{cite journal| author=WRITING COMMITTEE MEMBERS. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE et al.| title=2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. | journal=Circulation | year= 2013 | volume= 128 | issue= 16 | pages= e240-327 | pmid=23741058 | doi=10.1161/CIR.0b013e31829e8776 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23741058  }} </ref>
===Treatment goals===
Treating based on [[brain natriuretic peptide]] (BNP) might improve care according to a [[meta-analysis]] of [[randomized controlled trial]]s conducted through 2013<ref name="pmid24603309">{{cite journal| author=Troughton RW, Frampton CM, Brunner-La Rocca HP, Pfisterer M, Eurlings LW, Erntell H et al.| title=Effect of B-type natriuretic peptide-guided treatment of chronic heart failure on total mortality and hospitalization: an individual patient meta-analysis. | journal=Eur Heart J | year= 2014 | volume= 35 | issue= 23 | pages= 1559-67 | pmid=24603309 | doi=10.1093/eurheartj/ehu090 | pmc=PMC4057643 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24603309  }} </ref> and 2008<ref name="pmid20308637">{{cite journal| author=Porapakkham P, Porapakkham P, Zimmet H, Billah B, Krum H| title=B-Type Natriuretic Peptide-Guided Heart Failure Therapy: A Meta-analysis. | journal=Arch Intern Med | year= 2010 | volume= 170 | issue= 6 | pages= 507-14 | pmid=20308637 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=20308637 | doi=10.1001/archinternmed.2010.35 }}</ref>. In one trial included in the meta-analysis, there was no improvement by treating for a goal of [[brain natriuretic peptide]] less than 400 pg/mL in patients younger than 75 years and less than 800 pg/mL in patients aged 75 years or older.<ref name="pmid19176440">{{cite journal |author=Pfisterer M, Buser P, Rickli H, ''et al'' |title=BNP-guided vs symptom-guided heart failure therapy: the Trial of Intensified vs Standard Medical Therapy in Elderly Patients With Congestive Heart Failure (TIME-CHF) randomized trial |journal=JAMA |volume=301 |issue=4 |pages=383–92 |year=2009 |month=January |pmid=19176440 |doi=10.1001/jama.2009.2 |url=http://openurl.ebscohost.com/linksvc/linking.aspx?genre=article&sid=PubMed&issn=0098-7484&title=JAMA&volume=301&issue=4&spage=383&atitle=BNP-guided%20vs%20symptom-guided%20heart%20failure%20therapy:%20the%20Trial%20of%20Intensified%20vs%20Standard%20Medical%20Therapy%20in%20Elderly%20Patients%20With%20Congestive%20Heart%20Failure%20(TIME-CHF)%20randomized%20trial.&aulast=Pfisterer&date=2009 |issn=}}</ref>
Subsequent [[randomized controlled trial]]s report:
* Uncertain benefit from targeting NT-proBNP level < 150 pmol/l.<ref name="pmid20117364">{{cite journal| author=Lainchbury JG, Troughton RW, Strangman KM, Frampton CM, Pilbrow A, Yandle TG et al.| title=N-terminal pro-B-type natriuretic peptide-guided treatment for chronic heart failure: results from the BATTLESCARRED (NT-proBNP-Assisted Treatment To Lessen Serial Cardiac Readmissions and Death) trial. | journal=J Am Coll Cardiol | year= 2009 | volume= 55 | issue= 1 | pages= 53-60 | pmid=20117364
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=20117364 | doi=10.1016/j.jacc.2009.02.095 }}</ref>
* An individualized goal BNP may be best.<ref name="pmid21144969">{{cite journal| author=Eurlings LW, van Pol PE, Kok WE, van Wijk S, Lodewijks-van der Bolt C, Balk AH et al.| title=Management of chronic heart failure guided by individual N-terminal pro-B-type natriuretic peptide targets: results of the PRIMA (Can PRo-brain-natriuretic peptide guided therapy of chronic heart failure IMprove heart fAilure morbidity and mortality?) study. | journal=J Am Coll Cardiol | year= 2010 | volume= 56 | issue= 25 | pages= 2090-100 | pmid=21144969 | doi=10.1016/j.jacc.2010.07.030 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21144969  }} </ref> In this study of patients recently discharged after [[hospitalization]] for heart failure, the goal BNP was defined as "lowest level at discharge or 2 weeks thereafter."<ref name="pmid21144969"/>
* "Heart failure therapy guided by N-terminal BNP did not improve overall clinical outcomes or quality of life compared with symptom-guided treatment." Symptoms were measured with the [[New York Heart Association Functional Classification]].<ref name="pmid19176440"/>
* Targeting a clinical score to a score of 2 or less based on the [[Framingham congestive-heart-failure score]] with the following findings may<ref  name="pmid20117364"/> or may<ref name="pmid10791374">{{cite journal| author=Troughton RW, Frampton CM, Yandle TG, Espiner EA, Nicholls MG, Richards AM| title=Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide (N-BNP) concentrations. | journal=Lancet | year= 2000 | volume= 355 | issue= 9210 | pages= 1126-30 | pmid=10791374
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=10791374 }} </ref> not be similar to targeting BNP level.
===Medications===
===Medications===
====Angiotensin-converting enzyme inhibitors====
 
[[Angiotensin-converting enzyme inhibitors]] (ACE inhibitors) should not be used if:<ref name="pmid16160202">{{cite journal |author=Hunt SA, Abraham WT, Chin MH, ''et al'' |title=ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society |journal=Circulation |volume=112 |issue=12 |pages=e154–235 |year=2005 |pmid=16160202 |doi=10.1161/CIRCULATIONAHA.105.167586}} [http://www.ngc.gov/summary/summary.aspx?ss=15&doc_id=7664 National Guidelines Clearinghouse]</ref>
{| class="wikitable" border="1" align="right"
|+ Reduction in mortality from selected medications for heart failure.<ref name="pmid19454044">{{cite journal| author=McKelvie RS| title=Heart failure. | journal=Clin Evid (Online) | year= 2007 | volume= 2007 | issue=  | pages=  | pmid=19454044 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19454044  }} </ref>
! Medication!! Evidence!! Benefit
|-
| [[Angiotensin-converting enzyme inhibitor|ACE inhibitors]]||  [[Systematic review]] (individual patient):<ref name="pmid10821360">{{cite journal| author=Flather MD, Yusuf S, Køber L, Pfeffer M, Hall A, Murray G et al.| title=Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients. ACE-Inhibitor Myocardial Infarction Collaborative Group. | journal=Lancet | year= 2000 | volume= 355 | issue= 9215 | pages= 1575-81 | pmid=10821360 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10821360  }} </ref><br/>&bull;&nbsp;12,763 patients<br/>&bull;&nbsp;5 [[randomized controlled trial|RCTs]]|| OR = 0.80 ([[Confidence interval|95% CI]]:0.74-0.87)
|-
| [[Adrenergic beta-antagonist|Beta-blockers]]||  [[Systematic review]]:<ref name="pmid19487713">{{cite journal| author=McAlister FA, Wiebe N, Ezekowitz JA, Leung AA, Armstrong PW| title=Meta-analysis: beta-blocker dose, heart rate reduction, and death in patients with heart failure. | journal=Ann Intern Med | year= 2009 | volume= 150 | issue= 11 | pages= 784-94 | pmid=19487713 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19487713  }} </ref><br/>&bull;&nbsp;19 ,209 patients<br/>&bull;&nbsp;23[[randomized controlled trial|RCTs]]|| RR = 0.76
|-
| [[Digoxin]]||  [[Systematic review]]:<ref name="pmid15106182">{{cite journal| author=Hood WB, Dans AL, Guyatt GH, Jaeschke R, McMurray JJ| title=Digitalis for treatment of congestive heart failure in patients in sinus rhythm. | journal=Cochrane Database Syst Rev | year= 2004 | volume=  | issue= 2 | pages= CD002901 | pmid=15106182 | doi=10.1002/14651858.CD002901.pub2 | pmc= | url= }} </ref><br/>&bull;&nbsp;3872 patients<br/>&bull;&nbsp;8 [[randomized controlled trial|RCTs]]||OR = 0.98 ([[Confidence interval|95% CI]]: 0.89-1.09)
|-
| [[Aldosterone antagonist]]s|| [[Systematic review]]:<ref name="pmid19066207">{{cite journal| author=Ezekowitz JA, McAlister FA| title=Aldosterone blockade and left ventricular dysfunction: a systematic review of randomized clinical trials. | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 4 | pages= 469-77 | pmid=19066207 | doi=10.1093/eurheartj/ehn543 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19066207  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19687483 Review in: Ann Intern Med. 2009 Aug 18;151(4):JC2-9] </ref><br/>&bull;&nbsp;10,807 patients<br/>&bull;&nbsp;19 [[randomized controlled trial|RCTs]]||RR = 0.76
|}
 
The medications for heart failure have been reviewed.<ref>Anonymous. (2009) [http://www.medicalletter.org/restrictedtg/t83.html Drugs for Treatment of Chronic Heart Failure]. The Medical Letter. 2009;7 (83)</ref>
 
====Angiotensin-converting enzyme inhibitors (ACEi)====
Angiotensin-converting enzyme inhibitor can reduce morbidity from heart failure according to a [[systematic review]]<ref name="pmid7654275">{{cite journal |author=Garg R, Yusuf S |title=Overview of randomized trials of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials |journal=JAMA |volume=273 |issue=18 |pages=1450–6 |year=1995 |month=May |pmid=7654275 |doi= |url= |issn=}}</ref> of studies such as the Consensus trial<ref name="pmid2883575">{{cite journal| author=| title=Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). The CONSENSUS Trial Study Group. | journal=N Engl J Med | year= 1987 | volume= 316 | issue= 23 | pages= 1429-35 | pmid=2883575 | doi=10.1056/NEJM198706043162301 | pmc= | url= }} </ref>.
 
[[Angiotensin-converting enzyme inhibitor]]s (ACE inhibitors) should not be used if:<ref name="pmid16160202">{{cite journal |author=Hunt SA, Abraham WT, Chin MH, ''et al'' |title=ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society |journal=Circulation |volume=112 |issue=12 |pages=e154–235 |year=2005 |pmid=16160202 |doi=10.1161/CIRCULATIONAHA.105.167586}} [http://www.ngc.gov/summary/summary.aspx?ss=15&doc_id=7664 National Guidelines Clearinghouse]</ref>
* Baseline serum potassium is < 5.5 mmol per liter.
* Baseline serum potassium is < 5.5 mmol per liter.
* No prior life-threatening adverse reactions (angioedema or anuric renal failure) during previous exposure to the drug
* No prior life-threatening adverse reactions (angioedema or anuric renal failure) during previous exposure to the drug
Line 43: Line 133:
* Bilateral renal artery stenosis is not present
* Bilateral renal artery stenosis is not present


====Angiotensin-converting enzyme inhibitors combined with angiotensin-receptor blockers====
There is conflicting evidence whether [[ACE inhibitor]]s are as effective in African-American patients as in Anglo patients.<ref name="pmid12742294">{{cite journal |author=Shekelle PG, Rich MW, Morton SC, ''et al'' |title=Efficacy of angiotensin-converting enzyme inhibitors and beta-blockers in the management of left ventricular systolic dysfunction according to race, gender, and diabetic status: a meta-analysis of major clinical trials |journal=J. Am. Coll. Cardiol. |volume=41 |issue=9 |pages=1529–38 |year=2003 |pmid=12742294 |doi=}}</ref><ref name="pmid11333991">{{cite journal |author=Exner DV, Dries DL, Domanski MJ, Cohn JN |title=Lesser response to angiotensin-converting-enzyme inhibitor therapy in black as compared with white patients with left ventricular dysfunction |journal=N. Engl. J. Med. |volume=344 |issue=18 |pages=1351–7 |year=2001 |pmid=11333991 |doi=}}</ref>
This combination should be avoided due to increased azotemia, hyperkalemia, and symptomatic hypotension.<ref name="pmid17923591">{{cite journal |author=Phillips CO, Kashani A, Ko DK, Francis G, Krumholz HM |title=Adverse effects of combination angiotensin II receptor blockers plus angiotensin-converting enzyme inhibitors for left ventricular dysfunction: a quantitative review of data from randomized clinical trials |journal=Arch. Intern. Med. |volume=167 |issue=18 |pages=1930–6 |year=2007 |pmid=17923591 |doi=10.1001/archinte.167.18.1930}}</ref>
 
====ACEi combined with angiotensin-receptor blockers====
The addition of a[[ngiotensin II receptor antagonist]]s to [[angiotensin-converting enzyme inhibitor]]s is controversial. [[Clinical practice guideline]]s state:
* 2011 The National Institute for Health and Clinical Excellence<ref name="pmid18799522">{{cite journal|  author=Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ,  Ponikowski P, Poole-Wilson PA et al.| title=ESC Guidelines for the  diagnosis and treatment of acute and chronic heart failure 2008: the  Task Force for the Diagnosis and Treatment of Acute and Chronic Heart  Failure 2008 of the European Society of Cardiology. Developed in  collaboration with the Heart Failure Association of the ESC (HFA) and  endorsed by the European Society of Intensive Care Medicine (ESICM). |  journal=Eur Heart J | year= 2008 | volume= 29 | issue= 19 | pages=  2388-442 | pmid=18799522 | doi=10.1093/eurheartj/ehn309 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18799522  }} </ref>
** Consider adding an ARB, but the guideline lists the option of adding an aldosterone antagonist first
* 2008 European Society of Cardiology:<ref name="pmid18799522">{{cite journal|  author=Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ,  Ponikowski P, Poole-Wilson PA et al.| title=ESC Guidelines for the  diagnosis and treatment of acute and chronic heart failure 2008: the  Task Force for the Diagnosis and Treatment of Acute and Chronic Heart  Failure 2008 of the European Society of Cardiology. Developed in  collaboration with the Heart Failure Association of the ESC (HFA) and  endorsed by the European Society of Intensive Care Medicine (ESICM). |  journal=Eur Heart J | year= 2008 | volume= 29 | issue= 19 | pages=  2388-442 | pmid=18799522 | doi=10.1093/eurheartj/ehn309 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18799522  }} </ref>
**  "Unless contraindicated or not tolerated, an ARB is recommended in  patients with HF and an LVEF ≤40% who remain symptomatic despite optimal treatment with an ACEI and β-blocker, unless also taking an aldosterone  antagonist."
* 2009 update of ACC/AHA guidelines:<ref name="pmid19358937">{{cite journal|  author=Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats  TG  et al.| title=2009 Focused update incorporated into the ACC/AHA  2005  Guidelines for the Diagnosis and Management of Heart Failure in  Adults A  Report of the American College of Cardiology  Foundation/American Heart  Association Task Force on Practice Guidelines  Developed in Collaboration  With the International Society for Heart  and Lung Transplantation. |  journal=J Am Coll Cardiol | year= 2009 |  volume= 53 | issue= 15 | pages=  e1-e90 | pmid=19358937 |  doi=10.1016/j.jacc.2008.11.013 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19358937  }} </ref>
**  "Addition of an aldosterone antagonist is recommended in selected  patients with moderately severe to severe symptoms of HF and reduced  LVEF who can be carefully monitored for preserved renal function and  normal potassium concentration. Creatinine should be 2.5 mg per dL or  less in men or 2.0 mg per dL or less in women and potassium should be less than 5.0 mEq per liter."
** "potassium should be reassessed within 1 to 2 weeks after initiation and followed closely after changes in dose"
 
[[Drug toxicity]] includes azotemia, hyperkalemia, and symptomatic hypotension.<ref name="pmid17923591">{{cite journal |author=Phillips CO, Kashani A, Ko DK, Francis G, Krumholz HM |title=Adverse effects of combination angiotensin II receptor blockers plus angiotensin-converting enzyme inhibitors for left ventricular dysfunction: a quantitative review of data from randomized clinical trials |journal=Arch. Intern. Med. |volume=167 |issue=18 |pages=1930–6 |year=2007 |pmid=17923591 |doi=10.1001/archinte.167.18.1930}}</ref>
 
====Beta-blockers====
Two [[cohort study|cohort studies]] suggest that the [[beta-blocker]]s [[atenolol]] and [[carvedilol]] may be more effect than [[metoprolol]] for the treatment of heart failure.<ref name="pmid19064824">{{cite journal |author=Kramer JM, Curtis LH, Dupree CS, ''et al'' |title=Comparative effectiveness of beta-blockers in elderly patients with heart failure |journal=Arch. Intern. Med. |volume=168 |issue=22 |pages=2422–8; discussion 2428–32 |year=2008 |month=December |pmid=19064824 |doi=10.1001/archinternmed.2008.511 |url=http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=19064824 |issn=}}</ref><ref name="pmid19064823">{{cite journal |author=Go AS, Yang J, Gurwitz JH, Hsu J, Lane K, Platt R |title=Comparative effectiveness of different beta-adrenergic antagonists on mortality among adults with heart failure in clinical practice |journal=Arch. Intern. Med. |volume=168 |issue=22 |pages=2415–21 |year=2008 |month=December |pmid=19064823 |doi=10.1001/archinternmed.2008.506 |url=http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=19064823 |issn=}}</ref>
 
Drugs with intrinsic sympathomimetic activity may have less benefit<ref name="pmid10381708">{{cite journal |author=Freemantle N, Cleland J, Young P, Mason J, Harrison J |title=beta Blockade after myocardial infarction: systematic review and meta regression analysis |journal=BMJ |volume=318 |issue=7200 |pages=1730–7 |year=1999 |month=June |pmid=10381708 |pmc=31101 |doi= |url=http://bmj.com/cgi/pmidlookup?view=long&pmid=10381708 |issn=}}</ref> A [[systematic review]] of [[randomized controlled trial]]s concluded "metoprolol, carvedilol, and bisoprolol all exhibited statistically significant mortality rate reductions compared with placebo, the data were inconclusive for nebivolol or atenolol" and "for every heart rate reduction of 5 beats/min with β-blocker treatment, a commensurate 18% reduction in the risk for death occurred."<ref name="pmid19487713"/>
 
There is conflicting evidence whether [[beta-blocker]]s are as effective in African-American patients as in Anglo patients.<ref name="pmid12742294">{{cite journal |author=Shekelle PG, Rich MW, Morton SC, ''et al'' |title=Efficacy of angiotensin-converting enzyme inhibitors and beta-blockers in the management of left ventricular systolic dysfunction according to race, gender, and diabetic status: a meta-analysis of major clinical trials |journal=J. Am. Coll. Cardiol. |volume=41 |issue=9 |pages=1529–38 |year=2003 |pmid=12742294 |doi=}}</ref> This may be due to a polymorphism in African-American patients of the G protein–coupled [[cell surface receptor]] kinase (GRK5) ([http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600870 OMIM]) that confers a natural "genetic beta-blockade".<ref name="doi10.1038/nm1750">Liggett, Stephen B et al. 2008. A GRK5 polymorphism that inhibits [beta]-adrenergic receptor signaling is protective in heart failure. Nat Med advanced online publication. http://dx.doi.org/10.1038/nm1750 (Accessed April 29, 2008).</ref>
 
====Loop diuretics====
Loop [[diuretic]]s help decompensated heart failure with similar effect from low dose (a single dose equal to a patient's total daily dose) or high dose or twice a day bolus versus continuous [[intravenous infusion]].<ref name="pmid21366472">{{cite journal| author=Felker GM, Lee KL, Bull DA, Redfield MM, Stevenson LW, Goldsmith SR et al.| title=Diuretic strategies in patients with acute decompensated heart failure. | journal=N Engl J Med | year= 2011 | volume= 364 | issue= 9 | pages= 797-805 | pmid=21366472 | doi=10.1056/NEJMoa1005419 | pmc= | url= }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21768571 Review in: Ann Intern Med. 2011 Jul 19;155(2):JC1-5] </ref>
 
A [[meta-analysis]] concluded that "administering [[furosemide]] as a continuous infusion for greater diuresis and reduction in total body weight in patients hospitalized with ADHF". <ref name="pmid22125127">{{cite journal| author=Amer M, Adomaityte J, Qayyum R| title=Continuous infusion versus intermittent bolus furosemide in ADHF: an updated meta-analysis of randomized control trials. | journal=J Hosp Med | year= 2012 | volume= 7 | issue= 3 | pages= 270-5 | pmid=22125127 | doi=10.1002/jhm.991 | pmc= | url= }} </ref>


====Aldosterone antagonists====
====Aldosterone antagonists====
Aldosterone antagonists, initial dose of [[spironolactone]] 12.5 mg or [[eplerenone]] 25 mg, may be used as long as:<ref name="pmid16160202"/>
[[Aldosterone]] antagonists, initial dose of [[spironolactone]] 12.5 mg or [[eplerenone]] 25 mg may be used if the estimated [[glomerular filtration rate]] is >30 mL/min/1.73m2 and potassium levels are <5 mEq/dL. According to [[clinical practice guideline]]s by the American College of Cardiology, the risk of [[hyperkalemia]] is reduced by:<ref name="pmid23741058">{{cite journal| author=WRITING COMMITTEE MEMBERS. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE et al.| title=2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. | journal=Circulation | year= 2013 | volume= 128 | issue= 16 | pages= e240-327 | pmid=23741058 | doi=10.1161/CIR.0b013e31829e8776 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23741058  }} </ref>
 
# "Impaired renal function is a risk factor for hyperkalemia during treatment with aldosterone antagonists. The risk of hyperkalemia increases progressively when serum creatinine exceeds 1.6 mg/dL.* In elderly patients or others with low muscle mass in whom serum creatinine does not accurately reflect glomerular filtration rate, determination that glomerular filtration rate or creatinine clearance exceeds 30 ml per minute is recommended."
# "Aldosterone antagonists should not be administered to patients with baseline serum potassium in excess of 5.0 mEq per liter."
# "An initial dose of spironolactone of 12.5 mg or eplerenone 25 mg is recommended, following which the dose may be increased to spironolactone 25 mg or eplerenone 50 mg if appropriate."
# "The risk of hyperkalemia is increased with concomitant use of higher doses of ACEIs (captopril greater than or equal to 75 mg daily; enalapril or lisinopril greater than or equal to 10 mg daily."
# "Non-steroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors should be avoided."
# "Potassium supplements should be discontinued or reduced."
# "Close monitoring of serum potassium is required; potassium levels and renal function should be checked in 3 days and at 1 week after initiating therapy and at least monthly for the first 3 months."
# "Diarrhea or other causes of dehydration should be addressed emergently."
 
=====Spironolactone=====
[[Spironolactone]] can help patients who have New York Heart Association (NYHA) class IV heart failure and had a left ventricular ejection fraction of no more than 35%.<ref name="pmid10471456">{{cite journal| author=Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A et al.| title=The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. | journal=N Engl J Med | year= 1999 | volume= 341 | issue= 10 | pages= 709-17 | pmid=10471456
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10471456 }}</ref>, although it is both used incorrectly<ref name="pmid15295047">{{cite journal| author=Juurlink DN, Mamdani MM, Lee DS, Kopp A, Austin PC, Laupacis A et al.| title=Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study. | journal=N Engl J Med | year= 2004 | volume= 351 | issue= 6 | pages= 543-51 | pmid=15295047
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15295047 | doi=10.1056/NEJMoa040135 }}></ref> and at the same time is underutilized<ref name="pmid19843900">{{cite journal| author=Albert NM, Yancy CW, Liang L, Zhao X, Hernandez AF, Peterson ED et al.| title=Use of aldosterone antagonists in heart failure. | journal=JAMA | year= 2009 | volume= 302 | issue= 15 | pages= 1658-65 | pmid=19843900
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=19843900 | doi=10.1001/jama.2009.1493 }}</ref>. They may be used as long as:<ref name="pmid16160202"/>
* Serum creatinine 1.6 mg per dL or less and [[glomerular filtration rate]] or creatinine clearance exceeds 30 mL per minute.
* Serum creatinine 1.6 mg per dL or less and [[glomerular filtration rate]] or creatinine clearance exceeds 30 mL per minute.
* Baseline serum potassium is < 5.0 mEq per liter
* Baseline serum potassium is < 5.0 mEq per liter
Line 61: Line 189:
* Potassium levels and renal function should be checked monthly for the first 3 months.
* Potassium levels and renal function should be checked monthly for the first 3 months.
* Diarrhea or other causes of dehydration should be addressed emergently
* Diarrhea or other causes of dehydration should be addressed emergently
=====Eplerenone=====
[[Eplerenone]] is a selective aldosterone antagonist. In the EMPHASIS-HF [[randomized controlled trial]], reduced death and hospitalization among patients who were "an age of at least 55 years, NYHA functional class II symptoms, an ejection fraction of no more than 30% (or, if >30 to 35%, a QRS duration of >130 msec on electrocardiography), and treatment with an angiotensin-converting–enzyme (ACE) inhibitor, an angiotensin-receptor blocker (ARB), or both and a beta-blocker (unless contraindicated) at the recommended dose or maximal tolerated dose" and without "NYHA class III or IV heart failure, a serum potassium level exceeding 5.0 mmol per liter, an estimated glomerular filtration rate (GFR) of less than 30 ml per minute per 1.73 m2 of body-surface area, a need for a potassium-sparing diuretic".<ref name="pmid21073363">{{cite journal| author=Zannad F, McMurray JJ, Krum H, van Veldhuisen DJ, Swedberg K, Shi H et al.| title=Eplerenone in Patients with Systolic Heart Failure and Mild Symptoms. | journal=N Engl J Med | year= 2010 | volume=  | issue=  | pages=  | pmid=21073363 | doi=10.1056/NEJMoa1009492 | pmc= | url= }} </ref> However, less that 15% of the patients also received device therapy.
To avoid hyperkalemia, the following protocol was used by EPHESUS:
Starting dose of eplerenone:
* If the estimated GFR was 50  ml per minute per 1.73 m<sup>2</sup> or more: started at 25 mg once daily and was increased after 4 weeks to 50 mg once daily
* If the estimated GFR was less than 50  ml per minute per 1.73 m<sup>2</sup>: started at 25 mg on alternate days, and increased to 25 mg daily
Thereafter, investigators evaluated patients every 4 months and were instructed to decrease the dose of the study drug if the serum potassium level was 5.5 to 5.9 mmol per liter and to withhold the study drug if the serum potassium level was 6.0 mmol per liter or more. Potassium was to be remeasured within 72 hours after the dose reduction or study-drug withdrawal, and the study drug was to be restarted only if the level was below 5.0 mmol per liter.
Monitoring of serum potassium:
* At baseline, then after week 1, week 4, then every 4 months.
====Isosorbide dinitrate and hydralazine combination treatment====
<!-- Start of race-based therapeutics text box -->
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|
<span style="font-weight:bold;font-size:larger;">Race-based therapeutics?</span><br>
The controversial approval<ref name="pmid17200222">{{cite journal |author=Bibbins-Domingo K, Fernandez A |title=BiDil for heart failure in black patients: implications of the U.S. Food and Drug Administration approval |journal=Ann. Intern. Med. |volume=146 |issue=1 |pages=52–6 |year=2007 |pmid=17200222 |doi=|url=http://www.annals.org/cgi/content/full/146/1/52}}</ref> by the U.S. Food and Drug Administration of the drug NitroMed has led to the concept of race-based therapeutics.<ref name="pmid15533852">{{cite journal |author=Bloche MG |title=Race-based therapeutics |journal=N. Engl. J. Med. |volume=351 |issue=20 |pages=2035–7 |year=2004 |pmid=15533852 |doi=10.1056/NEJMp048271|url=http://content.nejm.org/cgi/content/full/351/20/2035}}</ref> Presumably, [[pharmacogenomics]] will lead to individualized drug treatment; until then the use of race may be a proxy of pharmacogenomic variations.<br>
'''Angiotensin-converting enzyme inhibitors'''<br>
There is conflicting evidence whether [[ACE inhibitor]]s are as effective in African-American patients as in Anglo patients.<ref name="pmid12742294">{{cite journal |author=Shekelle PG, Rich MW, Morton SC, ''et al'' |title=Efficacy of angiotensin-converting enzyme inhibitors and beta-blockers in the management of left ventricular systolic dysfunction according to race, gender, and diabetic status: a meta-analysis of major clinical trials |journal=J. Am. Coll. Cardiol. |volume=41 |issue=9 |pages=1529–38 |year=2003 |pmid=12742294 |doi=}}</ref><ref name="pmid11333991">{{cite journal |author=Exner DV, Dries DL, Domanski MJ, Cohn JN |title=Lesser response to angiotensin-converting-enzyme inhibitor therapy in black as compared with white patients with left ventricular dysfunction |journal=N. Engl. J. Med. |volume=344 |issue=18 |pages=1351–7 |year=2001 |pmid=11333991 |doi=}}</ref><br>
'''Beta-blockers'''<br>
There is conflicting evidence whether [[beta-blocker]]s are as effective in African-American patients as in Anglo patients.<ref name="pmid12742294">{{cite journal |author=Shekelle PG, Rich MW, Morton SC, ''et al'' |title=Efficacy of angiotensin-converting enzyme inhibitors and beta-blockers in the management of left ventricular systolic dysfunction according to race, gender, and diabetic status: a meta-analysis of major clinical trials |journal=J. Am. Coll. Cardiol. |volume=41 |issue=9 |pages=1529–38 |year=2003 |pmid=12742294 |doi=}}</ref><br>
'''Isosorbide dinitrate and hydralazine combination'''<br>
Isosorbide dinitrate and hydralazine combination treatment reduces mortality in African-American patients with [[New York Heart Association Functional Classification|functional class]] III or IV heart failure.<ref name="pmid15533851">{{cite journal |author=Taylor AL, Ziesche S, Yancy C, ''et al'' |title=Combination of isosorbide dinitrate and hydralazine in blacks with heart failure |journal=N. Engl. J. Med. |volume=351 |issue=20 |pages=2049–57 |year=2004 |pmid=15533851|url=http://content.nejm.org/cgi/content/full/351/20/2049 |doi=10.1056/NEJMoa042934}}</ref> Whether this benefit is more than occurs for Anglo patients is unclear, but is suggested by two controversial<ref name="pmid17679712b">{{cite journal |author=Temple R, Stockbridge NL |title=BiDil for heart failure in black patients |journal=Ann. Intern. Med. |volume=147 |issue=3 |pages=215–6 |year=2007 |pmid= |doi=|url=http://www.annals.org/cgi/content/full/147/3/215-a}}</ref><ref name="pmid17679712">{{cite journal |author=Bibbins-Domingo K, Fernandez A |title=BiDil for heart failure in black patients |journal=Ann. Intern. Med. |volume=147 |issue=3 |pages=214–5 |year=2007 |pmid=17679712 |doi=|url=http://www.annals.org/cgi/content/full/147/3/214}}</ref> post-hoc analyses<ref name="pmid10496190">{{cite journal |author=Carson P, Ziesche S, Johnson G, Cohn JN |title=Racial differences in response to therapy for heart failure: analysis of the vasodilator-heart failure trials. Vasodilator-Heart Failure Trial Study Group |journal=J. Card. Fail. |volume=5 |issue=3 |pages=178–87 |year=1999 |pmid=10496190 |doi=10.1016/S1071-9164(99)90001-5}}</ref> of subgroups in the earlier  V-HeFT-1<ref name="pmid3520315">{{cite journal |author=Cohn JN, Archibald DG, Ziesche S, ''et al'' |title=Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study |journal=N. Engl. J. Med. |volume=314 |issue=24 |pages=1547–52 |year=1986 |pmid=3520315 |doi=}}</ref> and V-HeFT-2<ref name="pmid2057035">{{cite journal |author=Cohn JN, Johnson G, Ziesche S, ''et al'' |title=A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure |journal=N. Engl. J. Med. |volume=325 |issue=5 |pages=303–10 |year=1991 |pmid=2057035 |doi=}}</ref> [[randomized controlled trial]]s (''see [[randomized controlled trial]]s for details about post-hoc and subgroup analyses'').
|}
<!-- End of race-based therapeutics text box -->
According to [[clinical practice guideline]]s:."<ref name="pmid16160202"/>
* "The addition of a combination of hydralazine and a nitrate is reasonable for patients with reduced LVEF who are already taking an [[angiotensin-converting enzyme inhibitor|ACEI]] and [[beta-blocker]] for symptomatic HF and who have persistent symptoms."
* "A combination of hydralazine and a nitrate might be reasonable in patients with current or prior symptoms of HF and reduced LVEF who cannot be given an [[angiotensin-converting enzyme inhibitor|ACEI]] or [[Angiotensin II receptor antagonist|ARB]] because of drug intolerance, hypotension, or renal insufficiency."
* "The addition of isosorbide dinitrate and hydralazine to a standard medical regimen for HF, including ACEIs and beta-blockers, is reasonable and can be effective in blacks with NYHA functional class III or IV HF."
"Treatment with either type of drug should not be initiated in patients who have systolic blood pressures less than 80 mm Hg."<ref name="pmid16160202"/>
Isosorbide dinitrate and hydralazine combination treatment reduces mortality in African-American patients with [[New York Heart Association Functional Classification|functional class]] III or IV heart failure according to the A-HeFT [[randomized controlled trial]].<ref name="pmid15533851">{{cite journal |author=Taylor AL, Ziesche S, Yancy C, ''et al'' |title=Combination of isosorbide dinitrate and hydralazine in blacks with heart failure |journal=N. Engl. J. Med. |volume=351 |issue=20 |pages=2049–57 |year=2004 |pmid=15533851|url=http://content.nejm.org/cgi/content/full/351/20/2049 |doi=10.1056/NEJMoa042934}}</ref> The [[number needed to treat]] is 26.<ref name="pmid15739984">{{cite journal |author=Massie BM |title=Isosorbide dinitrate plus hydralazine was effective for advanced heart failure in black patients |journal=ACP J. Club |volume=142 |issue=2 |pages=37 |year=2005 |pmid=15739984 |doi=|url=http://www.acpjc.org/Content/142/2/issue/ACPJC-2005-142-2-037.htm}}</ref> The U.S. Food and Drug Administration has approved the drug BiDil for African Americans<ref name="pmid17200223">{{cite journal |author=Temple R, Stockbridge NL |title=BiDil for heart failure in black patients: The U.S. Food and Drug Administration perspective |journal=Ann. Intern. Med. |volume=146 |issue=1 |pages=57–62 |year=2007 |pmid=17200223 |doi=|url=http://www.annals.org/cgi/content/full/146/1/57}}</ref> which has created controversy<ref name="pmid17200222">{{cite journal |author=Bibbins-Domingo K, Fernandez A |title=BiDil for heart failure in black patients: implications of the U.S. Food and Drug Administration approval |journal=Ann. Intern. Med. |volume=146 |issue=1 |pages=52–6 |year=2007 |pmid=17200222 |doi=|url=http://www.annals.org/cgi/content/full/146/1/52}}</ref> for reasons including the approval helped the manufacturer, NitroMed, add a second race-related patent that extended protection for BiDil for 13 years<ref name="pmid17679713">{{cite journal |author=Kahn JD |title=BiDil for heart failure in black patients |journal=Ann. Intern. Med. |volume=147 |issue=3 |pages=215; author reply 215–6 |year=2007 |pmid=17679713 |doi=|url=http://www.annals.org/cgi/content/full/147/3/215}}</ref>.
Whether the benefit to African-Americans is more than occurs for Anglo patients is unclear, but is suggested by two controversial<ref name="pmid17679712b"/><ref name="pmid17679712"/> post-hoc analyses<ref name="pmid10496190">{{cite journal |author=Carson P, Ziesche S, Johnson G, Cohn JN |title=Racial differences in response to therapy for heart failure: analysis of the vasodilator-heart failure trials. Vasodilator-Heart Failure Trial Study Group |journal=J. Card. Fail. |volume=5 |issue=3 |pages=178–87 |year=1999 |pmid=10496190 |doi=10.1016/S1071-9164(99)90001-5}}</ref> of subgroups in the earlier  V-HeFT-1<ref name="pmid3520315">{{cite journal |author=Cohn JN, Archibald DG, Ziesche S, ''et al'' |title=Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study |journal=N. Engl. J. Med. |volume=314 |issue=24 |pages=1547–52 |year=1986 |pmid=3520315 |doi=}}</ref> and V-HeFT-2<ref name="pmid2057035">{{cite journal |author=Cohn JN, Johnson G, Ziesche S, ''et al'' |title=A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure |journal=N. Engl. J. Med. |volume=325 |issue=5 |pages=303–10 |year=1991 |pmid=2057035 |doi=}}</ref>
In response to the results of the A-HeFT study, the [[American Heart Association]] [[clinical practice guideline]]s state "the effect of this combination of isosorbide dinitrate and hydralazine in other patients with HF who are undergoing standard therapy is not known because the population studied was limited to blacks, but there is no reason to believe that this benefit is limited to blacks."<ref name="pmid16160202"/>
====Digitalis glycosides====
Digitalis preparations are among the oldest drugs known to medicine. Due to the variability in preparations from the foxglove plant, synthetic digoxin is most commonly used.  Digoxin was the agent used in the Digitalis Investigation Group trial, the only randomized clinical trial of digitalis in chronic HF.<ref name=Ahmed>{{citation  | title = An Update on the Role of Digoxin in Older Adults with Chronic Heart Failure  | first = Ali | last = Ahmed  | journal = Geriatrics Aging  | year = 2008  | volume = 11(1)  | pages = 37-41  | url = http://www.medscape.com/viewarticle/573855_print }}</ref> The principal motivation for use of these drugs in HF is their positive inotropic property, increasing the contractile ability of the heart.
An additional property relevant to HF, appears to be due to  neurohormonal suppressing properties. Digoxin is approved by both the U.S. Food and Drug Administration and the Canadian Cardiovascular Society for HF treatment.
====Brain (B-type) natriuretic peptide====
[[Nesiritide]], a brain (B-type) natriuretic peptide, may help patients with decompensated congestive heart failure according to a [[randomized controlled trial]].<ref name="pmid10911006">Colucci WS, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. Nesiritide Study Group. N Engl J Med. 2000 Jul 27;343(4):246-53. Erratum in: N Engl J Med 2000 Nov 16;343(20):1504. N Engl J Med 2000;343:896. PMID 10911006</ref> Natriuretic peptide causes diuresis, vasodilitation, and suppression of the [[renin-angiotensin system]] and [[sympathetic nervous system]].<ref name="pmid10911006"/>
====Vasopressin receptor inhibition====
Tolvaptan, a [[vasopressin]] antagonist, may be beneficial according to a [[randomized controlled trial]].<ref>Gheorghiade M et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: the EVEREST Clinical Status Trials. JAMA 2007;297:1332-43. Epub 2007 Mar 25. PMID 17384438</ref><ref>Konstam MA et al. Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial. JAMA 2007;297:1319-31. Epub 2007 Mar 25. PMID 17384437</ref>  Tolvaptan is a selective [[cell surface receptor]]s V2 antagonist in the distal nephron which causes loss of free water.<ref>Goldsmith SR, Gheorghiade M. Vasopressin antagonism in heart failure. J Am Coll Cardiol. 2005;46:1785-91. PMID 16286160</ref>  Other [[vasopressin]] antagonists act mainly on V1a [[cell surface receptor]]s.
====Statins====
[[Hydroxymethylglutaryl-coenzyme A reductase inhibitor]]s (statins) do not help according to [[randomized controlled trial]]s.<ref name="pmid18757089">{{cite journal| author=Gissi-HF Investigators. Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG et al.| title=Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. | journal=Lancet | year= 2008 | volume= 372 | issue= 9645 | pages= 1231-9 | pmid=18757089 | doi=10.1016/S0140-6736(08)61240-4 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18757089  }} </ref><ref name="pmid17984166">{{cite journal| author=Kjekshus J, Apetrei E, Barrios V, Böhm M, Cleland JG, Cornel JH et al.| title=Rosuvastatin in older patients with systolic heart failure. | journal=N Engl J Med | year= 2007 | volume= 357 | issue= 22 | pages= 2248-61 | pmid=17984166 | doi=10.1056/NEJMoa0706201 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17984166  }} </ref>
===Noninvasive positive pressure ventilation===
Noninvasive positive pressure ventilation (NPP) can help treat acute cardiac pulmonary edema according to a [[meta-analysis|meta-analyses]] of [[randomized controlled trial]]s.<ref name="pmid16616558">{{cite journal |author=Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD |title=Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis |journal=Lancet |volume=367 |issue=9517 |pages=1155–63 |year=2006 |pmid=16616558 |doi=10.1016/S0140-6736(06)68506-1}}</ref><ref name="pmid16380593">{{cite journal |author=Masip J, Roque M, Sánchez B, Fernández R, Subirana M, Expósito JA |title=Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis |journal=JAMA |volume=294 |issue=24 |pages=3124–30 |year=2005 |pmid=16380593 |doi=10.1001/jama.294.24.3124}}</ref> Among the different modes of NPPV, CPAP may be slightly better than BiPAP.<ref name="pmid16380593"/> It is not clear that NPPV helps patients with normal partial pressures of carbon dioxide.<ref name="pmid12958051">{{cite journal |author=Nava S, Carbone G, DiBattista N, ''et al'' |title=Noninvasive ventilation in cardiogenic pulmonary edema: a multicenter randomized trial |journal=Am. J. Respir. Crit. Care Med. |volume=168 |issue=12 |pages=1432–7 |year=2003 |pmid=12958051 |doi=10.1164/rccm.200211-1270OC}}</ref>


===Implantable devices===
===Implantable devices===
Several implantable devices may help; however, it is not clear that implantable cardioverter-defibrillators (ICD) add benefit over cardiac resynchronisation therapy (CRT).<ref name="pmid17932160">{{cite journal |author=Lam SK, Owen A |title=Combined resynchronisation and implantable defibrillator therapy in left ventricular dysfunction: Bayesian network meta-analysis of randomised controlled trials |journal=BMJ |volume=335 |issue=7626 |pages=925 |year=2007 |pmid=17932160 |doi=10.1136/bmj.39343.511389.BE}}</ref>
Several implantable devices may help long term treatment. Both [[cardiac resynchronization therapy]] and [[implantable cardioverter-defibrillator]]s should be combined in selected patients: those with [[New York Heart Association Functional Classification]] class II or III, left ventricular [[ejection fraction]] of 30% or less, and an intrinsic QRS duration of 120 msec.<ref name="pmid21073365">{{cite journal| author=Tang AS, Wells GA, Talajic M, Arnold MO, Sheldon R, Connolly S et al.| title=Cardiac-resynchronization therapy for mild-to-moderate heart failure. | journal=N Engl J Med | year= 2010 | volume= 363 | issue= 25 | pages= 2385-95 | pmid=21073365 | doi=10.1056/NEJMoa1009540 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21073365  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21436182 Review in: Evid Based Med. 2011 Oct;16(5):138-9] </ref> The result of this trial contradicted an earlier meta-analysis that was based on limited studies available.<ref name="pmid17932160">{{cite journal |author=Lam SK, Owen A |title=Combined resynchronisation and implantable defibrillator therapy in left ventricular dysfunction: Bayesian network meta-analysis of randomised controlled trials |journal=BMJ |volume=335 |issue=7626 |pages=925 |year=2007 |pmid=17932160 |doi=10.1136/bmj.39343.511389.BE}}</ref>


====Cardiac resynchronization therapy====
====Cardiac resynchronization therapy====
[[Clinical practice guideline]]s by the [[American Heart Association]] address [[cardiac resynchronization therapy]] (CRT).<ref name="pmid22975230">{{cite journal| author=Tracy CM, Epstein AE, Darbar D, Dimarco JP, Dunbar SB, Estes NA et al.| title=2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2012 | volume= 60 | issue= 14 | pages= 1297-313 | pmid=22975230 | doi=10.1016/j.jacc.2012.07.009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22975230  }} [http://cardiology.jwatch.org/cgi/content/full/2012/1003/2 Summary in Journal Watch]</ref>
According to a [[systematic review]], [[cardiac resynchronization therapy]] (CRT), which is biventricular pacing, can reduce morbiity and mortality if the ejection fraction is less than 35%.<ref name="pmid17565085">{{cite journal |author=McAlister FA, Ezekowitz J, Hooton N, ''et al'' |title=Cardiac resynchronization therapy for patients with left ventricular systolic dysfunction: a systematic review |journal=JAMA |volume=297 |issue=22 |pages=2502–14 |year=2007 |pmid=17565085 |doi=10.1001/jama.297.22.2502}} [http://www.acpjc.org/Content/147/3/issue/ACPJC-2007-147-3-058.htm ACPJC summary]</ref> 30 patients must be treated to avoid one death ([[number needed to treat]] is 30). Cardiac resynchronization should only be used for patients with a QRS duration of at least 120 msec.<ref name="pmid17986493">{{cite journal |author=Beshai JF, Grimm RA, Nagueh SF, ''et al'' |title=Cardiac-Resynchronization Therapy in Heart Failure with Narrow QRS Complexes |journal= |volume= |issue= |pages= |year=2007 |pmid=17986493 |doi=10.1056/NEJMoa0706695}}</ref>
According to a [[systematic review]], [[cardiac resynchronization therapy]] (CRT), which is biventricular pacing, can reduce morbiity and mortality if the ejection fraction is less than 35%.<ref name="pmid17565085">{{cite journal |author=McAlister FA, Ezekowitz J, Hooton N, ''et al'' |title=Cardiac resynchronization therapy for patients with left ventricular systolic dysfunction: a systematic review |journal=JAMA |volume=297 |issue=22 |pages=2502–14 |year=2007 |pmid=17565085 |doi=10.1001/jama.297.22.2502}} [http://www.acpjc.org/Content/147/3/issue/ACPJC-2007-147-3-058.htm ACPJC summary]</ref> 30 patients must be treated to avoid one death ([[number needed to treat]] is 30). Cardiac resynchronization should only be used for patients with a QRS duration of at least 120 msec.<ref name="pmid17986493">{{cite journal |author=Beshai JF, Grimm RA, Nagueh SF, ''et al'' |title=Cardiac-Resynchronization Therapy in Heart Failure with Narrow QRS Complexes |journal= |volume= |issue= |pages= |year=2007 |pmid=17986493 |doi=10.1056/NEJMoa0706695}}</ref>


====Implantable cardioverter-defibrillator====
====Implantable cardioverter-defibrillator====
Implantable cardioverter-defibrillators (ICD) can reduce mortality in patients who have an ejection fraction of less than 35%.<ref name="pmid15659722">{{cite journal |author=Bardy GH, Lee KL, Mark DB, ''et al'' |title=Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure |journal=N. Engl. J. Med. |volume=352 |issue=3 |pages=225–37 |year=2005 |pmid=15659722 |doi=10.1056/NEJMoa043399}}</ref>
[[Implantable cardioverter-defibrillator]]s (ICD) can reduce mortality in patients who have an ejection fraction of less than 35%.<ref name="pmid15659722">{{cite journal |author=Bardy GH, Lee KL, Mark DB, ''et al'' |title=Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure |journal=N. Engl. J. Med. |volume=352 |issue=3 |pages=225–37 |year=2005 |pmid=15659722 |doi=10.1056/NEJMoa043399}}</ref>


====Left ventricular assist devices====
====Left ventricular assist devices====
Left ventricular assist devices (LVADs) may be an option for patients with end stage heart failure.<ref name="pmid17723934">{{cite journal |author=Delgado RM, Radovancevic B |title=Symptomatic relief: left ventricular assist devices versus resynchronization therapy |journal=Heart failure clinics |volume=3 |issue=3 |pages=259–65 |year=2007 |pmid=17723934 |doi=10.1016/j.hfc.2007.05.004}}</ref>
Left ventricular assist devices (LVADs) may be an option for patients with end stage heart failure.<ref name="pmid17723934">{{cite journal |author=Delgado RM, Radovancevic B |title=Symptomatic relief: left ventricular assist devices versus resynchronization therapy |journal=Heart failure clinics |volume=3 |issue=3 |pages=259–65 |year=2007 |pmid=17723934 |doi=10.1016/j.hfc.2007.05.004}}</ref>
===Disease management===
[[Disease management]] may reduce hospitalizations.<ref name="pmid11286953">{{cite journal| author=McAlister FA, Lawson FM, Teo KK, Armstrong PW| title=A systematic review of randomized trials of disease management programs in heart failure. | journal=Am J Med | year= 2001 | volume= 110 | issue= 5 | pages= 378-84 | pmid=11286953
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=11286953 }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=11915796 Review in: Evid Based Nurs. 2002 Jan;5(1):18] </ref><ref name="pmid15312864">{{cite journal| author=McAlister FA, Stewart S, Ferrua S, McMurray JJ| title=Multidisciplinary strategies for the management of heart failure patients at high risk for admission: a systematic review of randomized trials. | journal=J Am Coll Cardiol | year= 2004 | volume= 44 | issue= 4 | pages= 810-9 | pmid=15312864
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=15312864 | doi=10.1016/j.jacc.2004.05.055 }} </ref><ref name="pmid17116767">{{cite journal| author=Inglis SC, Pearson S, Treen S, Gallasch T, Horowitz JD, Stewart S| title=Extending the horizon in chronic heart failure: effects of multidisciplinary, home-based intervention relative to usual care. | journal=Circulation | year= 2006 | volume= 114 | issue= 23 | pages= 2466-73 | pmid=17116767
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=17116767 | doi=10.1161/CIRCULATIONAHA.106.638122 }} </ref><ref name="pmid10509499">{{cite journal| author=Stewart S, Marley JE, Horowitz JD| title=Effects of a multidisciplinary, home-based intervention on unplanned readmissions and survival among patients with chronic congestive heart failure: a randomised controlled study. | journal=Lancet | year= 1999 | volume= 354 | issue= 9184 | pages= 1077-83 | pmid=10509499
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=10509499 }} </ref><ref name="pmid9605777">{{cite journal| author=Stewart S, Pearson S, Horowitz JD| title=Effects of a home-based intervention among patients with congestive heart failure discharged from acute hospital care. | journal=Arch Intern Med | year= 1998 | volume= 158 | issue= 10 | pages= 1067-72 | pmid=9605777
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=9605777 }} </ref> This includes contacting health care provider for weight gain of more than 2 poiunsd in one day or 4 pounds in one week.
===Ultrafiltration===
Ultrafiltration might help patients with cardiorenal syndrome.<ref name="pmid19215834">{{cite journal |author=Jessup M, Costanzo MR |title=The cardiorenal syndrome: do we need a change of strategy or a change of tactics? |journal=J. Am. Coll. Cardiol. |volume=53 |issue=7 |pages=597–9 |year=2009 |month=February |pmid=19215834 |doi=10.1016/j.jacc.2008.11.012 |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(08)03801-1 |issn=}}</ref>
===Treatment of iron deficiency===
Treating iron deficiency, even in the absence of [[iron deficiency anemia]], may be beneficial according to a short [[randomized controlled trial]].<ref name="pmid19920054">{{cite journal| author=Anker SD, Comin Colet J, Filippatos G, Willenheimer R, Dickstein K, Drexler H et al.| title=Ferric carboxymaltose in patients with heart failure and iron deficiency. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 25 | pages= 2436-48 | pmid=19920054
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=19920054 | doi=10.1056/NEJMoa0908355 }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=20404374 Review in: Ann Intern Med. 2010 Apr 20;152(8):JC4-5] </ref>
===Exercise===
[[Exercise]] may improve self-reported health status<ref name="pmid19351942">{{cite journal| author=Flynn KE, Piña IL, Whellan DJ, Lin L, Blumenthal JA, Ellis SJ et al.| title=Effects of exercise training on health status in patients with chronic heart failure: HF-ACTION randomized controlled trial. | journal=JAMA | year= 2009 | volume= 301 | issue= 14 | pages= 1451-9 | pmid=19351942
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=19351942 | doi=10.1001/jama.2009.457 | pmc=PMC2690699 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref> and possibly combined mortality and hospitalization<ref name="pmid19351941">{{cite journal| author=O'Connor CM, Whellan DJ, Lee KL, Keteyian SJ, Cooper LS, Ellis SJ et al.| title=Efficacy and safety of exercise training in patients with chronic heart failure: HF-ACTION randomized controlled trial. | journal=JAMA | year= 2009 | volume= 301 | issue= 14 | pages= 1439-50 | pmid=19351941
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=19351941 | doi=10.1001/jama.2009.454 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref> according to the HF-ACTION [[randomized controlled trial]]. Home based and center based cardiac rehabilitation may be equally effective.<ref name="pmid20085991">{{cite journal| author=Dalal HM, Zawada A, Jolly K, Moxham T, Taylor RS| title=Home based versus centre based cardiac rehabilitation: Cochrane systematic review and meta-analysis. | journal=BMJ | year= 2010 | volume= 340 | issue=  | pages= b5631 | pmid=20085991
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=20085991 | pmc=PMC2808470 | doi=10.1136/bmj.b5631 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref><ref name="pmid20091618">{{cite journal| author=Taylor RS, Dalal H, Jolly K, Moxham T, Zawada A| title=Home-based versus centre-based cardiac rehabilitation. | journal=Cochrane Database Syst Rev | year= 2010 | volume=  | issue= 1 | pages= CD007130 | pmid=20091618
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=20091618 | doi=10.1002/14651858.CD007130.pub2 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref>
==Prognosis==
Mortality can be predicted with the The Seattle Heart Failure Model<ref name="pmid16534009">{{cite journal |author=Levy WC, Mozaffarian D, Linker DT, ''et al'' |title=The Seattle Heart Failure Model: prediction of survival in heart failure |journal=Circulation |volume=113 |issue=11 |pages=1424–33 |year=2006 |pmid=16534009 |doi=10.1161/CIRCULATIONAHA.105.584102 |issn=}}</ref>, which has been independently validated<ref name="pmid18523222">{{cite journal |author=Allen LA, Yager JE, Funk MJ, ''et al.'' |title=Discordance between patient-predicted and model-predicted life expectancy among ambulatory patients with heart failure |journal=JAMA |volume=299 |issue=21 |pages=2533–42 |year=2008 |month=June |pmid=18523222 |doi=10.1001/jama.299.21.2533 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18523222 |issn=}}</ref>. The model can show the affect of interventions on prognosis. The model is available online at http://depts.washington.edu/shfm/. Patients, especially younger patients, tend to overestimate their life expectancy.<ref>Allen LA et al. Discordance between patient-predicted and model-predicted life expectancy among ambulatory patients with heart failure.
JAMA. 2008;299:2533-42. PMID 18523222</ref>
A simpler four-item clinical prediction rule is available with similar area under the [[receiver operating characteristic curve]]:<ref name="pmid18482294">{{cite journal| author=Huynh BC, Rovner A, Rich MW| title=Identification of older patients with heart failure who may be candidates for hospice care: development of a simple four-item risk score. | journal=J Am Geriatr Soc | year= 2008 | volume= 56 | issue= 6 | pages= 1111-5 | pmid=18482294 | doi=10.1111/j.1532-5415.2008.01756.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18482294  }} </ref>
*Risk factors for death
** BUN > 30 mg/dl
** SBP < 120
** Peripheral arterial disease
**  Sodium < 135 mEq/L
*Number of risks factors and mortality at 6 months
** 1 = 4%
** 2 = 16%
** 3 = 41%
** 4 = 67%
===Other risk factors===
A reduced ejection fraction is independently associated with reduced survival according to an individual patient data [[meta-analysis]].<ref name="pmid21821849">{{cite journal| author=Meta-analysis Global Group in Chronic Heart Failure (MAGGIC)| title=The survival of patients with heart failure with preserved or reduced left ventricular ejection fraction: an individual patient data meta-analysis. | journal=Eur Heart J | year= 2011 | volume=  | issue=  | pages=  | pmid=21821849 | doi=10.1093/eurheartj/ehr254 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21821849  }} </ref>
A prolonged QRS duration of 120 ms or more is associated with reduced survival.<ref name="pmid18544725">{{cite journal |author=Wang NC, Maggioni AP, Konstam MA, ''et al'' |title=Clinical implications of QRS duration in patients hospitalized with worsening heart failure and reduced left ventricular ejection fraction |journal=JAMA |volume=299 |issue=22 |pages=2656–66 |year=2008 |month=June |pmid=18544725 |doi=10.1001/jama.299.22.2656 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18544725 |issn=}}</ref>
Blood urea nitrogen adds a small, but significant amount to the Seattle Heart Failure Model.<ref name="pmid19185637">{{cite journal |author=Giamouzis G, Kalogeropoulos AP, Georgiopoulou VV, ''et al.'' |title=Incremental value of renal function in risk prediction with the Seattle Heart Failure Model |journal=Am. Heart J. |volume=157 |issue=2 |pages=299–305 |year=2009 |month=February |pmid=19185637 |doi=10.1016/j.ahj.2008.10.007 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-8703(08)00888-0 |issn=}}</ref>


==References==
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[[Category:Suggestion Bot Tag]]

Latest revision as of 11:32, 11 October 2024

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The definition of congestive heart failure has evolved. In 2007, the National Library of Medicine defined heart failure as:

"defective cardiac filling and/or impaired contraction and emptying, resulting in the heart's inability to pump a sufficient amount of blood to meet the needs of the body tissues or to be able to do so only with an elevated filling pressure".[1]

In 2009, the National Library of Medicine defined heart failure as:

"a heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (ventricular dysfunction), or a sudden overload beyond its capacity.[2]

This, like some other terms in cardiology, can be confusing to laymen. "Heart failure" does not mean the heart has completely failed; if the heart were the fuel pump of an automobile, the diagnosis might be "pump slowdown." In like manner, "sudden cardiac death syndrome" does not mean the victim is dead; the automotive equivalent might be "running again after a jump start, but we need to know why the engine stalled."

Classification

Systolic dysfunction

For more information, see: Systolic heart failure.

Systolic heart failure is "heart failure caused by abnormal myocardial contraction during systole leading to defective cardiac emptying."[3]

Diastolic dysfunction

For more information, see: Diastolic heart failure.

Diastolic heart failure is "heart failure caused by abnormal myocardial relaxation during diastole leading to defective cardiac filling."[4]

Etiology / cause

Heart failure may be caused by coronary heart disease, hypertension, ethanol, myocarditis, connective tissue disease and others.[5]

  • 50% are cases are idiopathic.[5]
  • 20% to 50% of idiopathic cardiomyopathy may be familial.[6][7]

Diagnosis

History and physical examination

Hemodynamic Profiles
Congestion†?
(jugular venous distention and
radiographic redistribution)[8]
No Yes
Hypoperfusion‡?
(proportional pulse pressure < 25%[9][10],
cool extremities[11][12])		 No Warm and dry
(33% mortality at one year)		 Warm and wet
Yes Cold and dry Cold and wet
(46% mortality at one year[10])
Notes:

Adapted from Figure 1 of Nohria et al.[13]
† Congestion is defined as pulmonary capillary wedge pressure of 20 mm Hg or more[10]
‡ Hypoperfusion is defined as cardiac index of 1.8 L/min/m2.[10] This is associated with elevate lactate.[11] Other measures are at Critical care#Tissue_perfusion.

The best findings for detecting increased filling pressure are jugular venous distention and radiographic redistribution. The best findings for detecting systolic dysfunction are abnormal apical impulse, radiographic cardiomegaly, and q waves or left bundle branch block on an electrocardiogram. [8]

The history and physical examination can also be used for patients with advanced heart failure to place the patient into a hemodynamic profile to guide management.[13][10][11] Patients in the "cold and wet" category may need to "warm up in order to dry out" by stopping adrenergic beta-receptor blockaders (beta-blockers) and angiotensin-converting enzyme inhibitors (ACE inhibitors).[13]

Brain natriuretic peptide

For more information, see: Brain natriuretic peptide.

The role of the brain natriuretic peptide is limited when experienced physicians evaluate patients.[14]

Clinical practice guidelines state regarding the BNP and NT-proBNP:[15]

"Measurement of natriuretic peptides (BNP and NT-proBNP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of HF is uncertain. Measurement of natriuretic peptides (BNP and NT-proBNP) can be helpful in risk stratification."

Chest radiograph

The accuracy of the chest radiograph is below.[16] For diagnosing decreased ejection fraction with: Cardiomegaly

Redistribution:

For diagnosing increased preload with: Redistribution

Various definitions have been proposed for determining redistribution; definitions with absolute measurements probably best apply to 72 inch erect, postero-anterior radiograph:[16]

  • Pulonary veins in the upper lobes are larger than the lower lobe vein. Distinguishing pulmonary veins from arteries is not important as pulmonary veins are larger than pulmonary arteries.
  • Upper lobe veins 3 mm or larger in the first anterior interspace
  • Upper lobe veins 7 mm or larger at the level of the pulmonary artery

Echocardiography

Echocardiography measures the fractional shortening of the ventricle which can estimate the left ventricular ejection fraction.[17][18][19]

Various parameters on echocardiogram can estimate left ventricular end diastolic pressure.[20]

Clinical score

Framingham score

The Framingham congestive-heart-failure score can be used (two major or one major and two minor criteria).[21]

National Health and Nutrition Examination Survey score

The National Health and Nutrition Examination Survey (NHANES) congestive heart failure score (scores of 3 or more) can be used

Treatment

Clinical practice guidelines address management.[22][23]

Treatment goals

Treating based on brain natriuretic peptide (BNP) might improve care according to a meta-analysis of randomized controlled trials conducted through 2013[24] and 2008[25]. In one trial included in the meta-analysis, there was no improvement by treating for a goal of brain natriuretic peptide less than 400 pg/mL in patients younger than 75 years and less than 800 pg/mL in patients aged 75 years or older.[26]

Subsequent randomized controlled trials report:

  • Uncertain benefit from targeting NT-proBNP level < 150 pmol/l.[27]
  • An individualized goal BNP may be best.[28] In this study of patients recently discharged after hospitalization for heart failure, the goal BNP was defined as "lowest level at discharge or 2 weeks thereafter."[28]
  • "Heart failure therapy guided by N-terminal BNP did not improve overall clinical outcomes or quality of life compared with symptom-guided treatment." Symptoms were measured with the New York Heart Association Functional Classification.[26]
  • Targeting a clinical score to a score of 2 or less based on the Framingham congestive-heart-failure score with the following findings may[27] or may[29] not be similar to targeting BNP level.

Medications

Reduction in mortality from selected medications for heart failure.[30]
Medication Evidence Benefit
ACE inhibitors Systematic review (individual patient):[31]
• 12,763 patients
• 5 RCTs		 OR = 0.80 (95% CI:0.74-0.87)
Beta-blockers Systematic review:[32]
• 19 ,209 patients
• 23RCTs		 RR = 0.76
Digoxin Systematic review:[33]
• 3872 patients
• 8 RCTs		 OR = 0.98 (95% CI: 0.89-1.09)
Aldosterone antagonists Systematic review:[34]
• 10,807 patients
• 19 RCTs		 RR = 0.76

The medications for heart failure have been reviewed.[35]

Angiotensin-converting enzyme inhibitors (ACEi)

Angiotensin-converting enzyme inhibitor can reduce morbidity from heart failure according to a systematic review[36] of studies such as the Consensus trial[37].

Angiotensin-converting enzyme inhibitors (ACE inhibitors) should not be used if:[38]

  • Baseline serum potassium is < 5.5 mmol per liter.
  • No prior life-threatening adverse reactions (angioedema or anuric renal failure) during previous exposure to the drug
  • They are not pregnant
  • Systolic blood pressure less than 80 mm Hg
  • Serum levels of creatinine greater than 3 mg per dL
  • Bilateral renal artery stenosis is not present

There is conflicting evidence whether ACE inhibitors are as effective in African-American patients as in Anglo patients.[39][40]

ACEi combined with angiotensin-receptor blockers

The addition of angiotensin II receptor antagonists to angiotensin-converting enzyme inhibitors is controversial. Clinical practice guidelines state:

  • 2011 The National Institute for Health and Clinical Excellence[41]
    • Consider adding an ARB, but the guideline lists the option of adding an aldosterone antagonist first
  • 2008 European Society of Cardiology:[41]
    • "Unless contraindicated or not tolerated, an ARB is recommended in patients with HF and an LVEF ≤40% who remain symptomatic despite optimal treatment with an ACEI and β-blocker, unless also taking an aldosterone antagonist."
  • 2009 update of ACC/AHA guidelines:[42]
    • "Addition of an aldosterone antagonist is recommended in selected patients with moderately severe to severe symptoms of HF and reduced LVEF who can be carefully monitored for preserved renal function and normal potassium concentration. Creatinine should be 2.5 mg per dL or less in men or 2.0 mg per dL or less in women and potassium should be less than 5.0 mEq per liter."
    • "potassium should be reassessed within 1 to 2 weeks after initiation and followed closely after changes in dose"

Drug toxicity includes azotemia, hyperkalemia, and symptomatic hypotension.[43]

Beta-blockers

Two cohort studies suggest that the beta-blockers atenolol and carvedilol may be more effect than metoprolol for the treatment of heart failure.[44][45]

Drugs with intrinsic sympathomimetic activity may have less benefit[46] A systematic review of randomized controlled trials concluded "metoprolol, carvedilol, and bisoprolol all exhibited statistically significant mortality rate reductions compared with placebo, the data were inconclusive for nebivolol or atenolol" and "for every heart rate reduction of 5 beats/min with β-blocker treatment, a commensurate 18% reduction in the risk for death occurred."[32]

There is conflicting evidence whether beta-blockers are as effective in African-American patients as in Anglo patients.[39] This may be due to a polymorphism in African-American patients of the G protein–coupled cell surface receptor kinase (GRK5) (OMIM) that confers a natural "genetic beta-blockade".[47]

Loop diuretics

Loop diuretics help decompensated heart failure with similar effect from low dose (a single dose equal to a patient's total daily dose) or high dose or twice a day bolus versus continuous intravenous infusion.[48]

A meta-analysis concluded that "administering furosemide as a continuous infusion for greater diuresis and reduction in total body weight in patients hospitalized with ADHF". [49]

Aldosterone antagonists

Aldosterone antagonists, initial dose of spironolactone 12.5 mg or eplerenone 25 mg may be used if the estimated glomerular filtration rate is >30 mL/min/1.73m2 and potassium levels are <5 mEq/dL. According to clinical practice guidelines by the American College of Cardiology, the risk of hyperkalemia is reduced by:[23]

  1. "Impaired renal function is a risk factor for hyperkalemia during treatment with aldosterone antagonists. The risk of hyperkalemia increases progressively when serum creatinine exceeds 1.6 mg/dL.* In elderly patients or others with low muscle mass in whom serum creatinine does not accurately reflect glomerular filtration rate, determination that glomerular filtration rate or creatinine clearance exceeds 30 ml per minute is recommended."
  2. "Aldosterone antagonists should not be administered to patients with baseline serum potassium in excess of 5.0 mEq per liter."
  3. "An initial dose of spironolactone of 12.5 mg or eplerenone 25 mg is recommended, following which the dose may be increased to spironolactone 25 mg or eplerenone 50 mg if appropriate."
  4. "The risk of hyperkalemia is increased with concomitant use of higher doses of ACEIs (captopril greater than or equal to 75 mg daily; enalapril or lisinopril greater than or equal to 10 mg daily."
  5. "Non-steroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors should be avoided."
  6. "Potassium supplements should be discontinued or reduced."
  7. "Close monitoring of serum potassium is required; potassium levels and renal function should be checked in 3 days and at 1 week after initiating therapy and at least monthly for the first 3 months."
  8. "Diarrhea or other causes of dehydration should be addressed emergently."
Spironolactone

Spironolactone can help patients who have New York Heart Association (NYHA) class IV heart failure and had a left ventricular ejection fraction of no more than 35%.[50], although it is both used incorrectly[51] and at the same time is underutilized[52]. They may be used as long as:[38]

  • Serum creatinine 1.6 mg per dL or less and glomerular filtration rate or creatinine clearance exceeds 30 mL per minute.
  • Baseline serum potassium is < 5.0 mEq per liter

Risk of hyperkalemia is increased if the following drugs are used:[38]

  • Higher doses of ACE inhibitors (captopril greater than or equal to 75 mg daily; enalapril or lisinopril greater than or equal to 10 mg daily).
  • Nonsteroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors
  • Potassium supplements

After starting aldosterone antagonists:[38]

  • Potassium levels and renal function should be checked in 3 days
  • Potassium levels and renal function should be checked at 1 week
  • Potassium levels and renal function should be checked monthly for the first 3 months.
  • Diarrhea or other causes of dehydration should be addressed emergently
Eplerenone

Eplerenone is a selective aldosterone antagonist. In the EMPHASIS-HF randomized controlled trial, reduced death and hospitalization among patients who were "an age of at least 55 years, NYHA functional class II symptoms, an ejection fraction of no more than 30% (or, if >30 to 35%, a QRS duration of >130 msec on electrocardiography), and treatment with an angiotensin-converting–enzyme (ACE) inhibitor, an angiotensin-receptor blocker (ARB), or both and a beta-blocker (unless contraindicated) at the recommended dose or maximal tolerated dose" and without "NYHA class III or IV heart failure, a serum potassium level exceeding 5.0 mmol per liter, an estimated glomerular filtration rate (GFR) of less than 30 ml per minute per 1.73 m2 of body-surface area, a need for a potassium-sparing diuretic".[53] However, less that 15% of the patients also received device therapy.

To avoid hyperkalemia, the following protocol was used by EPHESUS:

Starting dose of eplerenone:

  • If the estimated GFR was 50 ml per minute per 1.73 m2 or more: started at 25 mg once daily and was increased after 4 weeks to 50 mg once daily
  • If the estimated GFR was less than 50 ml per minute per 1.73 m2: started at 25 mg on alternate days, and increased to 25 mg daily

Thereafter, investigators evaluated patients every 4 months and were instructed to decrease the dose of the study drug if the serum potassium level was 5.5 to 5.9 mmol per liter and to withhold the study drug if the serum potassium level was 6.0 mmol per liter or more. Potassium was to be remeasured within 72 hours after the dose reduction or study-drug withdrawal, and the study drug was to be restarted only if the level was below 5.0 mmol per liter.

Monitoring of serum potassium:

  • At baseline, then after week 1, week 4, then every 4 months.

Isosorbide dinitrate and hydralazine combination treatment

Race-based therapeutics?
The controversial approval[54] by the U.S. Food and Drug Administration of the drug NitroMed has led to the concept of race-based therapeutics.[55] Presumably, pharmacogenomics will lead to individualized drug treatment; until then the use of race may be a proxy of pharmacogenomic variations.
Angiotensin-converting enzyme inhibitors
There is conflicting evidence whether ACE inhibitors are as effective in African-American patients as in Anglo patients.[39][40]
Beta-blockers
There is conflicting evidence whether beta-blockers are as effective in African-American patients as in Anglo patients.[39]
Isosorbide dinitrate and hydralazine combination
Isosorbide dinitrate and hydralazine combination treatment reduces mortality in African-American patients with functional class III or IV heart failure.[56] Whether this benefit is more than occurs for Anglo patients is unclear, but is suggested by two controversial[57][58] post-hoc analyses[59] of subgroups in the earlier V-HeFT-1[60] and V-HeFT-2[61] randomized controlled trials (see randomized controlled trials for details about post-hoc and subgroup analyses).

According to clinical practice guidelines:."[38]

  • "The addition of a combination of hydralazine and a nitrate is reasonable for patients with reduced LVEF who are already taking an ACEI and beta-blocker for symptomatic HF and who have persistent symptoms."
  • "A combination of hydralazine and a nitrate might be reasonable in patients with current or prior symptoms of HF and reduced LVEF who cannot be given an ACEI or ARB because of drug intolerance, hypotension, or renal insufficiency."
  • "The addition of isosorbide dinitrate and hydralazine to a standard medical regimen for HF, including ACEIs and beta-blockers, is reasonable and can be effective in blacks with NYHA functional class III or IV HF."

"Treatment with either type of drug should not be initiated in patients who have systolic blood pressures less than 80 mm Hg."[38]

Isosorbide dinitrate and hydralazine combination treatment reduces mortality in African-American patients with functional class III or IV heart failure according to the A-HeFT randomized controlled trial.[56] The number needed to treat is 26.[62] The U.S. Food and Drug Administration has approved the drug BiDil for African Americans[63] which has created controversy[54] for reasons including the approval helped the manufacturer, NitroMed, add a second race-related patent that extended protection for BiDil for 13 years[64].

Whether the benefit to African-Americans is more than occurs for Anglo patients is unclear, but is suggested by two controversial[57][58] post-hoc analyses[59] of subgroups in the earlier V-HeFT-1[60] and V-HeFT-2[61]

In response to the results of the A-HeFT study, the American Heart Association clinical practice guidelines state "the effect of this combination of isosorbide dinitrate and hydralazine in other patients with HF who are undergoing standard therapy is not known because the population studied was limited to blacks, but there is no reason to believe that this benefit is limited to blacks."[38]

Digitalis glycosides

Digitalis preparations are among the oldest drugs known to medicine. Due to the variability in preparations from the foxglove plant, synthetic digoxin is most commonly used. Digoxin was the agent used in the Digitalis Investigation Group trial, the only randomized clinical trial of digitalis in chronic HF.[65] The principal motivation for use of these drugs in HF is their positive inotropic property, increasing the contractile ability of the heart.

An additional property relevant to HF, appears to be due to neurohormonal suppressing properties. Digoxin is approved by both the U.S. Food and Drug Administration and the Canadian Cardiovascular Society for HF treatment.

Brain (B-type) natriuretic peptide

Nesiritide, a brain (B-type) natriuretic peptide, may help patients with decompensated congestive heart failure according to a randomized controlled trial.[66] Natriuretic peptide causes diuresis, vasodilitation, and suppression of the renin-angiotensin system and sympathetic nervous system.[66]

Vasopressin receptor inhibition

Tolvaptan, a vasopressin antagonist, may be beneficial according to a randomized controlled trial.[67][68] Tolvaptan is a selective cell surface receptors V2 antagonist in the distal nephron which causes loss of free water.[69] Other vasopressin antagonists act mainly on V1a cell surface receptors.

Statins

Hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) do not help according to randomized controlled trials.[70][71]

Noninvasive positive pressure ventilation

Noninvasive positive pressure ventilation (NPP) can help treat acute cardiac pulmonary edema according to a meta-analyses of randomized controlled trials.[72][73] Among the different modes of NPPV, CPAP may be slightly better than BiPAP.[73] It is not clear that NPPV helps patients with normal partial pressures of carbon dioxide.[74]

Implantable devices

Several implantable devices may help long term treatment. Both cardiac resynchronization therapy and implantable cardioverter-defibrillators should be combined in selected patients: those with New York Heart Association Functional Classification class II or III, left ventricular ejection fraction of 30% or less, and an intrinsic QRS duration of 120 msec.[75] The result of this trial contradicted an earlier meta-analysis that was based on limited studies available.[76]

Cardiac resynchronization therapy

Clinical practice guidelines by the American Heart Association address cardiac resynchronization therapy (CRT).[77]

According to a systematic review, cardiac resynchronization therapy (CRT), which is biventricular pacing, can reduce morbiity and mortality if the ejection fraction is less than 35%.[78] 30 patients must be treated to avoid one death (number needed to treat is 30). Cardiac resynchronization should only be used for patients with a QRS duration of at least 120 msec.[79]

Implantable cardioverter-defibrillator

Implantable cardioverter-defibrillators (ICD) can reduce mortality in patients who have an ejection fraction of less than 35%.[80]

Left ventricular assist devices

Left ventricular assist devices (LVADs) may be an option for patients with end stage heart failure.[81]

Disease management

Disease management may reduce hospitalizations.[82][83][84][85][86] This includes contacting health care provider for weight gain of more than 2 poiunsd in one day or 4 pounds in one week.

Ultrafiltration

Ultrafiltration might help patients with cardiorenal syndrome.[87]

Treatment of iron deficiency

Treating iron deficiency, even in the absence of iron deficiency anemia, may be beneficial according to a short randomized controlled trial.[88]

Exercise

Exercise may improve self-reported health status[89] and possibly combined mortality and hospitalization[90] according to the HF-ACTION randomized controlled trial. Home based and center based cardiac rehabilitation may be equally effective.[91][92]

Prognosis

Mortality can be predicted with the The Seattle Heart Failure Model[93], which has been independently validated[94]. The model can show the affect of interventions on prognosis. The model is available online at http://depts.washington.edu/shfm/. Patients, especially younger patients, tend to overestimate their life expectancy.[95]

A simpler four-item clinical prediction rule is available with similar area under the receiver operating characteristic curve:[96]

  • Risk factors for death
    • BUN > 30 mg/dl
    • SBP < 120
    • Peripheral arterial disease
    • Sodium < 135 mEq/L
  • Number of risks factors and mortality at 6 months
    • 1 = 4%
    • 2 = 16%
    • 3 = 41%
    • 4 = 67%

Other risk factors

A reduced ejection fraction is independently associated with reduced survival according to an individual patient data meta-analysis.[97]

A prolonged QRS duration of 120 ms or more is associated with reduced survival.[98]

Blood urea nitrogen adds a small, but significant amount to the Seattle Heart Failure Model.[99]

References

  1. ↑ National Library of Medicine. Heart Failure, Congestive. Retrieved on 2007-10-19.
  2. ↑ Anonymous (2024), Heart failure (English). Medical Subject Headings. U.S. National Library of Medicine.
  3. ↑ Anonymous (2024), Systolic heart failure (English). Medical Subject Headings. U.S. National Library of Medicine.
  4. ↑ Anonymous (2024), Diastolic heart failure (English). Medical Subject Headings. U.S. National Library of Medicine.
  5. ↑ 5.0 5.1 Felker GM, Thompson RE, Hare JM, Hruban RH, Clemetson DE, Howard DL et al. (2000). "Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy.". N Engl J Med 342 (15): 1077-84. PMID 10760308.
  6. ↑ Burkett EL, Hershberger RE (2005). "Clinical and genetic issues in familial dilated cardiomyopathy.". J Am Coll Cardiol 45 (7): 969-81. DOI:10.1016/j.jacc.2004.11.066. PMID 15808750. Research Blogging.
  7. ↑ Mahon NG, Murphy RT, MacRae CA, Caforio AL, Elliott PM, McKenna WJ (2005). "Echocardiographic evaluation in asymptomatic relatives of patients with dilated cardiomyopathy reveals preclinical disease.". Ann Intern Med 143 (2): 108-15. PMID 16027452.
  8. ↑ 8.0 8.1 Badgett RG, Lucey CR, Mulrow CD (1997). "Can the clinical examination diagnose left-sided heart failure in adults?". JAMA 277 (21): 1712-9. PMID 9169900. [e]
  9. ↑ Stevenson LW, Perloff JK (1989). "The limited reliability of physical signs for estimating hemodynamics in chronic heart failure". JAMA 261 (6): 884–8. PMID 2913385. [e]
  10. ↑ 10.0 10.1 10.2 10.3 10.4 Shah MR, Hasselblad V, Stinnett SS, et al (2001). "Hemodynamic profiles of advanced heart failure: association with clinical characteristics and long-term outcomes". J. Card. Fail. 7 (2): 105–13. DOI:10.1054/jcaf.2001.24131. PMID 11420761. Research Blogging.
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  26. ↑ 26.0 26.1 Pfisterer M, Buser P, Rickli H, et al (January 2009). "BNP-guided vs symptom-guided heart failure therapy: the Trial of Intensified vs Standard Medical Therapy in Elderly Patients With Congestive Heart Failure (TIME-CHF) randomized trial". JAMA 301 (4): 383–92. DOI:10.1001/jama.2009.2. PMID 19176440. Research Blogging.
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  28. ↑ 28.0 28.1 Eurlings LW, van Pol PE, Kok WE, van Wijk S, Lodewijks-van der Bolt C, Balk AH et al. (2010). "Management of chronic heart failure guided by individual N-terminal pro-B-type natriuretic peptide targets: results of the PRIMA (Can PRo-brain-natriuretic peptide guided therapy of chronic heart failure IMprove heart fAilure morbidity and mortality?) study.". J Am Coll Cardiol 56 (25): 2090-100. DOI:10.1016/j.jacc.2010.07.030. PMID 21144969. Research Blogging.
  29. ↑ Troughton RW, Frampton CM, Yandle TG, Espiner EA, Nicholls MG, Richards AM (2000). "Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide (N-BNP) concentrations.". Lancet 355 (9210): 1126-30. PMID 10791374.
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  34. ↑ Ezekowitz JA, McAlister FA (2009). "Aldosterone blockade and left ventricular dysfunction: a systematic review of randomized clinical trials.". Eur Heart J 30 (4): 469-77. DOI:10.1093/eurheartj/ehn543. PMID 19066207. Research Blogging. Review in: Ann Intern Med. 2009 Aug 18;151(4):JC2-9
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  36. ↑ Garg R, Yusuf S (May 1995). "Overview of randomized trials of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials". JAMA 273 (18): 1450–6. PMID 7654275. [e]
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  40. ↑ 40.0 40.1 Exner DV, Dries DL, Domanski MJ, Cohn JN (2001). "Lesser response to angiotensin-converting-enzyme inhibitor therapy in black as compared with white patients with left ventricular dysfunction". N. Engl. J. Med. 344 (18): 1351–7. PMID 11333991. [e]
  41. ↑ 41.0 41.1 Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole-Wilson PA et al. (2008). "ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM).". Eur Heart J 29 (19): 2388-442. DOI:10.1093/eurheartj/ehn309. PMID 18799522. Research Blogging.
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  51. ↑ Juurlink DN, Mamdani MM, Lee DS, Kopp A, Austin PC, Laupacis A et al. (2004). "Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study.". N Engl J Med 351 (6): 543-51. DOI:10.1056/NEJMoa040135. PMID 15295047. Research Blogging. >
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