Jgf. Cleland et al., Does aspirin attenuate the effect of angiotensin-converting enzyme inhibitors in hypertension or heart failure?, CURR OP NEP, 10(5), 2001, pp. 625-631
There is a wealth of data that suggests an important interaction between as
pirin and angiotensin-converting enzyme inhibitors in patients with chronic
stable cardiovascular disease. The interaction is less obvious in the post
infarction setting, possibly reflecting the fact that many patients stop th
eir aspirin therapy within a few months of such an event. An interaction is
biologically plausible, because there is considerable evidence that angiot
ensin-converting enzyme inhibitors exert important effects through increasi
ng the production of vasodilator prostaglandins, whereas aspirin blocks the
ir production through inhibition of cyclooxygenase, even at low doses. Ther
e is some evidence that low-dose aspirin may raise systolic and diastolic b
lood pressure. There is also considerable evidence that aspirin may entirel
y neutralize the clinical benefits of angiotensin-converting enzyme inhibit
ors in patients with heart failure. In addition, aspirin may have an advers
e effect on outcome in patients with heart failure that is independent of a
ny interaction with angiotensin-converting enzyme inhibitors, possibly by b
locking endogenous vasodilator prostaglandin production and enhancing the v
asoconstrictor potential of endothelin. The evidence is not sufficient to j
ustify advising long-term aspirin therapy for patients with cardiovascular
disease in general, and for those with heart failure in particular. Thus, t
he lack of evidence of benefit with aspirin in patients with heart failure
and coronary disease, along with growing evidence that aspirin is directly
harmful in patients with heart failure and that aspirin may negate the bene
fits of angiotensin-converting enzyme inhibitors suggest that, unless there
is an opportunity to randomize the patient into a study of antithrombotic
strategies, then aspirin should be withdrawn or possibly substituted with a
n anticoagulant or an antiplatelet agent that does not block cyclooxygenase
. In contrast, there is fairly robust evidence for a benefit of both aspiri
n and angiotensin-converting enzyme inhibitors during the first 5 weeks aft
er a myocardial infarction, with little evidence of an interaction. The com
bination of aspirin and angiotensin-converting enzyme inhibitors is warrant
ed during this period, after which discontinuation or substitution of aspir
in with another agent should be considered. Curr Opin Nephrol Hypertens 10:
62--631, (C) 2001 Lippincott Williams & Wilkins.