Heart failure: Difference between revisions

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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>
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>


==Classification==
==Classification==

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The definition of congestive heart failurehas 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]

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]

Diagnosis

History and physical examination

Hemodynamic Profiles
Congestion†?
(jugular venous distention and
radiographic redistribution)[5]
No Yes
Hypoperfusion‡?
(proportional pulse pressure < 25%[6][7],
cool extremities[8][9])		 No Warm and dry
(33% mortality at one year)		 Warm and wet
Yes Cold and dry Cold and wet
(46% mortality at one year[7])
Notes:

Adapted from Figure 1 of Nohria et al.[10]
† Congestion is defined as pulmonary capillary wedge pressure of 20 mm Hg or more[7]
‡ Hypoperfusion is defined as cardiac index of 1.8 L/min/m2.[7] This is associated with elevate lactate.[8] 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. [5]

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.[10][7][8] 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).[10]

Brain natriuretic peptide

For more information, see: Brain natriuretic peptide.

The role of the brain natriuretic peptide is limited when experienced physicians evaluate patients.[11]

Clinical practice guidelines state regarding the BNP and NT-proBNP:[12]

"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.[13] 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:[13]

  • 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

Echocardiogram

The fractional shortening can estimate the left ventricular ejection fraction.[14][15][16]

Treatment

Goals

Treating based on BPN might improve care according to a meta-analysis.[17] 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.[18] A second trial found uncertain benefit from targeting NT-proBNP level < 150 pmol/l.[19]

Targeting a clinical score to a score of 2 or less based on the Framingham diagnosis of heart failure with the following findings may[19] or may[20] not be similar to targeting BNP level:

  • Major findings (1 point each)
  • Minor findings (0.5 point each)
    • Orthopnea
    • Reduction in exercise tolerance
    • Resting heart rate > 100 bpm
    • Hepatomegaly
    • Peripheral edema

Medications

Race-based therapeutics?
The controversial approval[21] by the U.S. Food and Drug Administration of the drug NitroMed has led to the concept of race-based therapeutics.[22] 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.[23][24]
Beta-blockers
There is conflicting evidence whether beta-blockers are as effective in African-American patients as in Anglo patients.[23]
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.[25] Whether this benefit is more than occurs for Anglo patients is unclear, but is suggested by two controversial[26][27] post-hoc analyses[28] of subgroups in the earlier V-HeFT-1[29] and V-HeFT-2[30] randomized controlled trials (see randomized controlled trials for details about post-hoc and subgroup analyses).

The medications for heart failure have been reviewed.[31]

Angiotensin-converting enzyme inhibitors (ACEi)

Angiotensin-converting enzyme inhibitor can reduce morbidity from heart failure.[32]

Angiotensin-converting enzyme inhibitors (ACE inhibitors) should not be used if:[33]

  • 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.[23][24]

ACEi combined with angiotensin-receptor blockers

This combination should be avoided due to increased azotemia, hyperkalemia, and symptomatic hypotension.[34]

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.[35][36]

Drugs with intrinsic sympathomimetic activity may have less benefit[37] 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."[38]

There is conflicting evidence whether beta-blockers are as effective in African-American patients as in Anglo patients.[23] 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".[39]

Aldosterone antagonists

Aldosterone antagonists, initial dose of spironolactone 12.5 mg or eplerenone 25 mg may be used. 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%.[40], although it is both used incorrectly[41] and at the same time is underutilized[42]. They may be used as long as:[33]

  • 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:[33]

  • 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:[33]

  • 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

Isosorbide dinitrate and hydralazine combination treatment

According to clinical practice guidelines:."[33]

  • "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."[33]

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.[25] The number needed to treat is 26.[43] The U.S. Food and Drug Administration has approved the drug BiDil for African Americans[44] which has created controversy[21] for reasons including the approval helped the manufacturer, NitroMed, add a second race-related patent that extended protection for BiDil for 13 years[45].

Whether the benefit to African-Americans is more than occurs for Anglo patients is unclear, but is suggested by two controversial[26][27] post-hoc analyses[28] of subgroups in the earlier V-HeFT-1[29] and V-HeFT-2[30]

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."[33]

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.[46] 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.[47] Natriuretic peptide causes diuresis, vasodilitation, and suppression of the renin-angiotensin system and sympathetic nervous system.[47]

Vasopressin receptor inhibition

Tolvaptan, a vasopressin antagonist, may be beneficial according to a randomized controlled trial.[48][49] Tolvaptan is a selective cell surface receptors V2 antagonist in the distal nephron which causes loss of free water.[50] Other vasopressin antagonists act mainly on V1a cell surface receptors.

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.[51][52] Among the different modes of NPPV, CPAP may be slightly better than BiPAP.[52] It is not clear that NPPV helps patients with normal partial pressures of carbon dioxide.[53]

Implantable devices

Several implantable devices may help long term treatment; however, it is not clear that implantable cardioverter-defibrillators (ICD) add benefit over cardiac resynchronisation therapy (CRT).[54]

Cardiac resynchronization therapy

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%.[55] 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.[56]

Implantable cardioverter-defibrillator

Implantable cardioverter-defibrillators (ICD) can reduce mortality in patients who have an ejection fraction of less than 35%.[57]

Left ventricular assist devices

Left ventricular assist devices (LVADs) may be an option for patients with end stage heart failure.[58]

Ultrafiltration

Ultrafiltration might help patients with cardiorenal syndrome.[59]

Treatment of iron deficiency

Treating iron deficiency, even in the absence of anemia, may be beneficial according to a short randomized controlled trial.[60]

Exercise

Exercise may improve self-reported health status[61] and possibly combined mortality and hospitalization[62] according to the HF-ACTION randomized controlled trial. Home based and center based cardiac rehabilitation may be equally effective.[63][64]

Prognosis

Mortality can be predicted with the The Seattle Heart Failure Model[65], which has been independently validated[66]. 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.[67]

Other risk factors

A prolonged QRS duration of 120 ms or more is associated with reduced survival.[68]

Blood urea nitrogen adds a small, but significant amount to the Seattle Heart Failure Model.[69]

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 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]
  6. ↑ 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]
  7. ↑ 7.0 7.1 7.2 7.3 7.4 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.
  8. ↑ 8.0 8.1 8.2 Kaplan LJ, McPartland K, Santora TA, Trooskin SZ (2001). "Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients". The Journal of trauma 50 (4): 620–7; discussion 627–8. PMID 11303155. [e]
  9. ↑ Grissom CK, Morris AH, Lanken PN, Ancukiewicz M, Orme JF, Schoenfeld DA et al. (2009). "Association of physical examination with pulmonary artery catheter parameters in acute lung injury.". Crit Care Med 37 (10): 2720-6. PMID 19885995.
  10. ↑ 10.0 10.1 10.2 Nohria A, Lewis E, Stevenson LW (2002). "Medical management of advanced heart failure". JAMA 287 (5): 628–40. PMID 11829703. [e]
  11. ↑ Schneider HG, Lam L, Lokuge A, Krum H, Naughton MT, De Villiers Smit P et al. (2009). "B-type natriuretic peptide testing, clinical outcomes, and health services use in emergency department patients with dyspnea: a randomized trial.". Ann Intern Med 150 (6): 365-71. PMID 19293069.
  12. ↑ Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG et al. (2009). "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.". Circulation 119 (14): e391-479. DOI:10.1161/CIRCULATIONAHA.109.192065. PMID 19324966. Research Blogging.
  13. ↑ 13.0 13.1 Badgett RG, Mulrow CD, Otto PM, Ramírez G (1996). "How well can the chest radiograph diagnose left ventricular dysfunction?". J Gen Intern Med 11 (10): 625-34. PMID 8945695.
  14. ↑ Tortoledo FA, Fernandez GC, Quinones MA (1983). "An accurate and simplified method to calculate angiographic left ventricular ejection fraction". Catheterization and cardiovascular diagnosis 9 (4): 357-62. PMID 6627386. [e]
  15. ↑ Quinones MA, Waggoner AD, Reduto LA, et al (1981). "A new, simplified and accurate method for determining ejection fraction with two-dimensional echocardiography". Circulation 64 (4): 744-53. PMID 7273375. [e]
  16. ↑ Erbel R, Schweizer P, Krebs W, Meyer J, Effert S (1984). "Sensitivity and specificity of two-dimensional echocardiography in detection of impaired left ventricular function". Eur. Heart J. 5 (6): 477-89. PMID 6745290. [e]
  17. ↑ Porapakkham P, Porapakkham P, Zimmet H, Billah B, Krum H (2010). "B-Type Natriuretic Peptide-Guided Heart Failure Therapy: A Meta-analysis.". Arch Intern Med 170 (6): 507-14. DOI:10.1001/archinternmed.2010.35. PMID 20308637. Research Blogging.
  18. ↑ 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.
  19. ↑ 19.0 19.1 Lainchbury JG, Troughton RW, Strangman KM, Frampton CM, Pilbrow A, Yandle TG et al. (2009). "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.". J Am Coll Cardiol 55 (1): 53-60. DOI:10.1016/j.jacc.2009.02.095. PMID 20117364. Research Blogging. Cite error: Invalid <ref> tag; name "pmid20117364" defined multiple times with different content
  20. ↑ 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.
  21. ↑ 21.0 21.1 Bibbins-Domingo K, Fernandez A (2007). "BiDil for heart failure in black patients: implications of the U.S. Food and Drug Administration approval". Ann. Intern. Med. 146 (1): 52–6. PMID 17200222. [e]
  22. ↑ Bloche MG (2004). "Race-based therapeutics". N. Engl. J. Med. 351 (20): 2035–7. DOI:10.1056/NEJMp048271. PMID 15533852. Research Blogging.
  23. ↑ 23.0 23.1 23.2 23.3 Shekelle PG, Rich MW, Morton SC, et al (2003). "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". J. Am. Coll. Cardiol. 41 (9): 1529–38. PMID 12742294. [e]
  24. ↑ 24.0 24.1 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]
  25. ↑ 25.0 25.1 Taylor AL, Ziesche S, Yancy C, et al (2004). "Combination of isosorbide dinitrate and hydralazine in blacks with heart failure". N. Engl. J. Med. 351 (20): 2049–57. DOI:10.1056/NEJMoa042934. PMID 15533851. Research Blogging.
  26. ↑ 26.0 26.1 Temple R, Stockbridge NL (2007). "BiDil for heart failure in black patients". Ann. Intern. Med. 147 (3): 215–6. [e] Cite error: Invalid <ref> tag; name "pmid17679712b" defined multiple times with different content
  27. ↑ 27.0 27.1 Bibbins-Domingo K, Fernandez A (2007). "BiDil for heart failure in black patients". Ann. Intern. Med. 147 (3): 214–5. PMID 17679712. [e] Cite error: Invalid <ref> tag; name "pmid17679712" defined multiple times with different content
  28. ↑ 28.0 28.1 Carson P, Ziesche S, Johnson G, Cohn JN (1999). "Racial differences in response to therapy for heart failure: analysis of the vasodilator-heart failure trials. Vasodilator-Heart Failure Trial Study Group". J. Card. Fail. 5 (3): 178–87. DOI:10.1016/S1071-9164(99)90001-5. PMID 10496190. Research Blogging.
  29. ↑ 29.0 29.1 Cohn JN, Archibald DG, Ziesche S, et al (1986). "Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study". N. Engl. J. Med. 314 (24): 1547–52. PMID 3520315. [e]
  30. ↑ 30.0 30.1 Cohn JN, Johnson G, Ziesche S, et al (1991). "A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure". N. Engl. J. Med. 325 (5): 303–10. PMID 2057035. [e]
  31. ↑ Anonymous. (2009) Drugs for Treatment of Chronic Heart Failure. The Medical Letter. 2009;7 (83)
  32. ↑ 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]
  33. ↑ 33.0 33.1 33.2 33.3 33.4 33.5 33.6 Hunt SA, Abraham WT, Chin MH, et al (2005). "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". Circulation 112 (12): e154–235. DOI:10.1161/CIRCULATIONAHA.105.167586. PMID 16160202. Research Blogging. National Guidelines Clearinghouse
  34. ↑ Phillips CO, Kashani A, Ko DK, Francis G, Krumholz HM (2007). "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". Arch. Intern. Med. 167 (18): 1930–6. DOI:10.1001/archinte.167.18.1930. PMID 17923591. Research Blogging.
  35. ↑ Kramer JM, Curtis LH, Dupree CS, et al (December 2008). "Comparative effectiveness of beta-blockers in elderly patients with heart failure". Arch. Intern. Med. 168 (22): 2422–8; discussion 2428–32. DOI:10.1001/archinternmed.2008.511. PMID 19064824. Research Blogging.
  36. ↑ Go AS, Yang J, Gurwitz JH, Hsu J, Lane K, Platt R (December 2008). "Comparative effectiveness of different beta-adrenergic antagonists on mortality among adults with heart failure in clinical practice". Arch. Intern. Med. 168 (22): 2415–21. DOI:10.1001/archinternmed.2008.506. PMID 19064823. Research Blogging.
  37. ↑ Freemantle N, Cleland J, Young P, Mason J, Harrison J (June 1999). "beta Blockade after myocardial infarction: systematic review and meta regression analysis". BMJ 318 (7200): 1730–7. PMID 10381708. PMC 31101. [e]
  38. ↑ McAlister FA, Wiebe N, Ezekowitz JA, Leung AA, Armstrong PW (June 2009). "Meta-analysis: beta-blocker dose, heart rate reduction, and death in patients with heart failure". Ann. Intern. Med. 150 (11): 784–94. PMID 19487713. [e]
  39. ↑ 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).
  40. ↑ Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A et al. (1999). "The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators.". N Engl J Med 341 (10): 709-17. PMID 10471456.
  41. ↑ 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.
  42. ↑ Albert NM, Yancy CW, Liang L, Zhao X, Hernandez AF, Peterson ED et al. (2009). "Use of aldosterone antagonists in heart failure.". JAMA 302 (15): 1658-65. DOI:10.1001/jama.2009.1493. PMID 19843900. Research Blogging.
  43. ↑ Massie BM (2005). "Isosorbide dinitrate plus hydralazine was effective for advanced heart failure in black patients". ACP J. Club 142 (2): 37. PMID 15739984. [e]
  44. ↑ Temple R, Stockbridge NL (2007). "BiDil for heart failure in black patients: The U.S. Food and Drug Administration perspective". Ann. Intern. Med. 146 (1): 57–62. PMID 17200223. [e]
  45. ↑ Kahn JD (2007). "BiDil for heart failure in black patients". Ann. Intern. Med. 147 (3): 215; author reply 215–6. PMID 17679713. [e]
  46. ↑ Ahmed, Ali (2008), "An Update on the Role of Digoxin in Older Adults with Chronic Heart Failure", Geriatrics Aging 11(1): 37-41
  47. ↑ 47.0 47.1 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
  48. ↑ 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
  49. ↑ 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
  50. ↑ Goldsmith SR, Gheorghiade M. Vasopressin antagonism in heart failure. J Am Coll Cardiol. 2005;46:1785-91. PMID 16286160
  51. ↑ Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD (2006). "Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis". Lancet 367 (9517): 1155–63. DOI:10.1016/S0140-6736(06)68506-1. PMID 16616558. Research Blogging.
  52. ↑ 52.0 52.1 Masip J, Roque M, Sánchez B, Fernández R, Subirana M, Expósito JA (2005). "Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis". JAMA 294 (24): 3124–30. DOI:10.1001/jama.294.24.3124. PMID 16380593. Research Blogging.
  53. ↑ Nava S, Carbone G, DiBattista N, et al (2003). "Noninvasive ventilation in cardiogenic pulmonary edema: a multicenter randomized trial". Am. J. Respir. Crit. Care Med. 168 (12): 1432–7. DOI:10.1164/rccm.200211-1270OC. PMID 12958051. Research Blogging.
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  57. ↑ Bardy GH, Lee KL, Mark DB, et al (2005). "Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure". N. Engl. J. Med. 352 (3): 225–37. DOI:10.1056/NEJMoa043399. PMID 15659722. Research Blogging.
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  61. ↑ Flynn KE, Piña IL, Whellan DJ, Lin L, Blumenthal JA, Ellis SJ et al. (2009). "Effects of exercise training on health status in patients with chronic heart failure: HF-ACTION randomized controlled trial.". JAMA 301 (14): 1451-9. DOI:10.1001/jama.2009.457. PMID 19351942. PMC PMC2690699. Research Blogging.
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  69. ↑ Giamouzis G, Kalogeropoulos AP, Georgiopoulou VV, et al. (February 2009). "Incremental value of renal function in risk prediction with the Seattle Heart Failure Model". Am. Heart J. 157 (2): 299–305. DOI:10.1016/j.ahj.2008.10.007. PMID 19185637. Research Blogging.
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