Several groups of drugs can induce or exacerbate chronic heart failure (CHF), notably those which increase preload or afterload and/or have negative inotropic properties (Table I). The most susceptible patients are those with preexisting left ventricular dysfunction who are already at risk of heart failure.
Table I. Drugs that induce or exacerbate chronic heart failure (CHF).
The following drugs should be combined with caution, or avoided, with any form of heart failure treatment.
Nonsteroidal anti-inflammatory drugs.
NSAIDs are associated with fluid retention and the induction of CHF, primarily because they interfer with prostaglandin biosynthesis by inhibiting the function of the enzyme cyclooxygenase.
In patients with impaired left ventricular function, renal perfusion is maintained by prostaglandins, which reduce afferent arteriolar resistance, and by angiotensin II, which increases efferent arteriolar resistance. Angiotensin-converting enzyme (ACE) inhibition may reduce this effect of angiotensin II.
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NSAIDs can offset the significant contribution of prostaglandins to the preservation of adequate renal function in heart failure. Thus, impaired renal function is more frequent in elderly patients using NSAIDs with a long half-life or combined with diuretics or ACE inhibitors. Ongoing NSAID use doubles the risk of hospitalization for CHF. The risk is dose-dependent, higher with NSAIDs having a long half-life, and higher in the first month of therapy.
All NSAIDs, including aspirin, can be nephrotoxic (though rarely), causing interstitial nephritis, nephrotic syndrome, and reversible renal failure, while exacerbating hypertension. The risk can increase in elderly patients with a history of renal disease. This prompted the introduction of self-styled renal-sparing NSAIDs, eg, sulindac, nabumetone, and meloxicam. However, comprehensive data on the renal and cardiovascular effects of these agents in patients with left ventricular dysfunction are not yet available.
Aspirin and ACE inhibitors are often used concomitantly, especially in patients with both CHF and ischemic heart disease (the most common underlying cause of CHF). The safety of this combination has been questioned because the drugs have contrary effects on prostaglandin synthesis. Some ACE inhibitor benefits might be due to the reduced degradation of bradykinin (a compound which enhances prostaglandin synthesis), while aspirin, which inhibits cyclooxygenase, inhibits prostaglandin synthesis. However, pooled analyses have not shown any clinically significant deterioration when aspirin was combined with ACE inhibitors.
Class I antiarrhythmics.
These drugs should be avoided as they have arrhyth-mogenic effects on the ventricle and adverse hemodynamic and prognostic effects in heart failure. Clinical trials have shown that they increase the risk of sudden death, particularly if ventricular dysfunction is severe. The only exception is the treatment of immediately life-threatening ventricular arrhythmias that are refractory to treatment.