There is a wealth of data to show that mineralocorticoid antagonists (MRAs) reduce morbidity and mortality in patients with heart failure when LVEF is reduced and perhaps also when LVEF… Click to show full abstract
There is a wealth of data to show that mineralocorticoid antagonists (MRAs) reduce morbidity and mortality in patients with heart failure when LVEF is reduced and perhaps also when LVEF is fairly well preserved.1–5 Chin et al. investigated whether the benefits of MRAs were reduced amongst patients prescribed aspirin.6 They concluded that no important interaction could be observed. If true, this is good news, but still does not justify prescription of aspirin for patients with heart failure and CAD. The evidence that chronic aspirin therapy is safe or effective, regardless of LVEF, for any cardiovascular condition is not robust.7–10 Admittedly, there is good evidence that aspirin reduces coronary events and mortality when given for 4–12 weeks after an acute vascular event, but any suggestion of a long-term effect owes more to the fertile imagination of cardiologists rather than to clinical trial data. In this era, which we pretend is one of evidence-based medicine, it is not to the credit of the medical community that aspirin enjoys such widespread abuse. Many patients with heart failure have CAD as a cause of cardiac dysfunction and heart failure, and it may be an important co-morbidity in others. There is a widespread belief that these patients should receive an antiplatelet agent, usually aspirin, in order to reduce the risk of vascular events and prolong life. Unfortunately, there is no evidence to support such a view. Adequate randomized controlled trials comparing aspirin with placebo in patients with heart failure are lacking, but the few data that exist are not reassuring.10,11 There are concerns that aspirin might detract from the therapeutic benefits of agents that are known to improve outcome in heart failure, including ACE inhibitors and beta-blockers, possibly by blocking prostaglandin production, resulting in impaired vasodilatation, renal dysfunction, sodium and water retention, and hyponatraemia.7 Aspirin will also increase gastrointestinal blood loss and may be at the root of the current epidemic of iron deficiency in the heart failure population.12 A key attribute of MRAs is that they increase sodium excretion, which may be attenuated by aspirin;13 a key problem with MRAs is a fall
               
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