To whatever extent the improvement in symptoms and survival rendered by treatment with ACE inhibitors is attributable to their effects on the circulation and the kidneys, this benefit can be rescinded by concomitant administration of aspirin. Although some useful prostaglandin-independent actions may persist, shutting down the entire prostaglandin system and trading off a substantial portion of the potential risk reduction with forfeit of salutary hemodynamic and renal effects is a high price to pay just to suppress production of TXA2. In patients requiring treatment for heart failure, if possible, aspirin should be avoided and the integrity of prostaglandin metabolism respected; the severer the heart failure the more compelling. There are other ways to inhibit platelet aggregation, some equally effective or even better than aspirin. Orally active platelet glycoprotein IIb/IIIa receptor antagonists, which may be more efficient than aspirin, have been developed and are now in clinical testing. Ticlopidine and clopidogrel, although more expensive than aspirin, are as easy to use and at least as effective as aspirin. Finally, because patients with severer heart failure are likely to be those with very low ejection fractions, these patients are good candidates for oral anticoagulation even though this treatment requires additional monitoring.