Electronic letters to:

Review:
Larry A. Allen and Christopher M. O'Connor
Management of acute decompensated heart failure
CMAJ 2007; 176: 797-805 [Abstract] [Full text] [PDF]
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Electronic letters published:

[Read eLetter] IN response to "Management of acute decompensated heart failure"
Joe Nemeth   (16 April 2007)
[Read eLetter] Dosing of Nitroglycerin for Acute Decompensated Heart Failure
Howard A Smithline   (12 April 2007)
[Read eLetter] Diagnostic and Prognostic Utility of B-type Natriuretic Peptide in Acute Heart Failure
John R. Kapoor   (5 April 2007)

IN response to "Management of acute decompensated heart failure" 16 April 2007
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Joe Nemeth
McGill UNiversity

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Re: IN response to "Management of acute decompensated heart failure"

joe.nemeth{at}mcgill.ca Joe Nemeth

Although Allen and O’Connor’s review of the management of acute decompensated heart failure (ADHF) was generally well written, I do however have certain reservations about their interpretation of evidence regarding the role of loop diuretics-specifically furosemide-and consequent recommendations regarding its place in the treatment armamentarium of ADHF.

First of all, I disagree with their implication that “congestion” infers volume overload and as such their suggestion that clinicians consequently “rely heavily on diuretic therapy”. These statements are inappropriate and further help to perpetuate the misuse of furosemide in ADHF. In fact it is well known that up to 50% of patients with acute cardiogenic pulmonary edema are euvolemic and subsequently treatment should emphasize fluid redistribution rather than fluid removal.

Second, although the use of diuretics has been weakly shown (see quoted odds ratio and wide 95% CI) Faris et al Int J Cardiol 2002 to improve mortality, its use-if relied on exclusively-in the in-hospital, acute setting has shown the opposite.

Third, in ADHF caused by high afterload (eg. hypertensive emergency), renal perfusion can actually drop by as much as 80% and as such furosemide will exhibit a delayed diuretic effect of 30-120 minutes after administration.

And lastly, there is very little evidence for any beneficial hemodynamic effect of furosemide. In fact many studies (Nelson et al- Eur H Jour 1983, Francis et al-Ann Int Med 1985, Kraus et al-Chest 1990) have shown that furosemide is responsible for adverse hemodynamic effects in patients with ADHF by causing an initial catecholamine release and activation of the renin-angiotensin system.

In conclusion I disagree with the authors’ summary that loop diuretics “currently forms the foundation” of treatment of ADHF despite good evidence that its use should be reserved as a third line agent behind preload and afterload reduction (eg. nitroglycerine and ACE inhibition) in in-hospital ADHF.

Dr. Joe Nemeth Assistant Professor Emergency Medicine Montreal General Hospital Montreal Children’s Hospital McGill University Health Centre Montreal

Conflict of Interest:

None declared
Dosing of Nitroglycerin for Acute Decompensated Heart Failure 12 April 2007
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Howard A Smithline
Baystate Medical Center

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Re: Dosing of Nitroglycerin for Acute Decompensated Heart Failure

howard.smithline{at}bhs.org Howard A Smithline

I read with interest the review article, Management of Acute Decompensated Heart Failure by Larry A. Allen and Christopher M. O’Connor. (1) The authors commented that nitroglycerin use in acute decompensated heart failure is probably underutilized. Yet when converting from sublingual to IV nitroglycerin, the dose they recommend for initiating the IV nitroglycerin seems low. A sublingual regimen of 0.4 mg very 5 minutes (the typical dose at my institution) is mathematically equivalent to 80 mcg/min.

One quoted figure for the bioavailability of sublingual nitroglycerin is 38%. (2) However, this can be highly variable. (3) In many patients the tablets appear to be absorbed quickly and completely. Not infrequently, one finds an undissolved tablet after 5 minutes. Perhaps in these patients a lower dose, such as what you recommend, would be suitable. However, in the patient with marked hypertension not responding to completely dissolved sublingual nitroglycerin, a higher starting dose may be more appropriate.

1. Allen LA, O'Connor CM. Management of acute decompensated heart failure. CMAJ. 2007 Mar 13;176(6):797-805.

2. Kirsten R, Nelson K, Kirsten D, Heintz B. Clinical pharmacokinetics of vasodilators. Part II. Clin Pharmacokinet. 1998 Jul;35(1):9-36.

3. Noonan PK, Benet LZ. Incomplete and delayed bioavailability of sublingual nitroglycerin. Am J Cardiol. 1985 Jan 1;55(1):184-7.

Conflict of Interest:

None declared
Diagnostic and Prognostic Utility of B-type Natriuretic Peptide in Acute Heart Failure 5 April 2007
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John R. Kapoor
Division of Cardiology, Stanford University

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Re: Diagnostic and Prognostic Utility of B-type Natriuretic Peptide in Acute Heart Failure

jkapoor{at}stanford.edu John R. Kapoor

I read with interest Allen and O’Conner’s review on acute decompensated heart failure (ADHF)(1). Though a discussion of the use of B-type natriuretic peptides (BNP) in the diagnosis of ADHF was included, there was no mention of the very important limitations to its use or its prognostic significance. Caveats to the use of BNP should be kept in mind by the practicing clinician. Elevated levels of BNP may occur in noncardiac conditions, including acute pulmonary embolism, chronic kidney disease and pulmonary hypertension (2). Higher levels are also seen in women, with older age and certain drugs (3). Substantial interassay and intraindividual variation in levels also exist, such that only serial measurements revealing a 100% change are considered significant (4).

BNP should thus be used in the context of other data. The rapid BNP assay in conjunction with clinical assessment reduces the number of hospital admissions, decreases length of stay, and reduces costs (5). Levels also predict risk for future cardiovascular events, whereas decreases in levels during hospitalization are associated with lower rates of death and 30-day readmissions. In fact, BNP levels at discharge are predictive of survival (6).

REFERENCES

1. Allen LA and O’Connor CM. Management of acute decompensated heart failure. CMAJ. 2007 Mar 13;176(6):797-805.

2. Maisel AS, Krishnaswamy P, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161-167.

3. Lainchbury JG, Campbell E, et al. Brain natriuretic peptide and n -terminal brain natriuretic peptide in the diagnosis of heart failure in patients with acute shortness of breath. J Am Coll Cardiol. 2003;42:728- 735.

4. Wu AH, Smith A. Biological variation of the natriuretic peptides and their role in monitoring patients with heart failure. Eur J Heart Fail. 2004;6:355-358.

5. Mueller C, Scholer A, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med. 2004;350:647 -654.

6. Cheng V, Kazanagra R, et al. A rapid bedside test for B-type peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study. J Am Coll Cardiol. 2001;37:386-391.

Conflict of Interest:

None declared