Effect of combined aspirin and angiotensin-converting enzyme inhibitor therapy versus angiotensin-converting enzyme inhibitor therapy alone on readmission rates in heart failure

Harjai, Kishore J.; Núñez, Eduardo; Turgut, Tansel; Newman, Jeff

doi:10.1016/s0002-9149(00)01412-0

Cited by 27 publications

(24 citation statements)

References 13 publications

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“…The increased risk related to digoxin use in the present observational study probably reflects those attributes and suggests that the authors' multivariable analysis did not adequately control for all important confounders, a limitation that is not rectified by having a large sample size. It is also important to note that other, albeit smaller, observational studies 16,17 have reached a conclusion different from that of McAlister et al…”

Section: Article P 2572mentioning

confidence: 64%

Does Aspirin Reduce the Benefit of an Angiotensin-Converting Enzyme Inhibitor?

Jhund

McMurray

2006

Circulation

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F ourteen years ago, Hall and colleagues 1 reported observations that initiated a vigorous debate about a possible interaction between aspirin and angiotensinconverting enzyme (ACE) inhibitors that continues to this day. That debate centers on whether the apparent pharmacological interaction between aspirin and ACE inhibitors might influence clinical outcomes and has been heightened greatly by the provocative suggestion that long-term aspirin use might not be beneficial in patients with chronic coronary heart disease, including those with heart failure. 2 The arguments used in the debate and the studies on which they are based highlight the strengths and weaknesses of many of the main strands of modern cardiovascular therapeutic research and illustrate many useful lessons about the interpretation of these different types of study. Article p 2572Hall et al 1 carried out what might be called a "mechanistic" study, demonstrating that the short-term hemodynamic effects of an ACE inhibitor in patients with severe heart failure were attenuated by aspirin. Many but not all subsequent studies have supported this finding. [3][4][5][6] Although interesting, the clinical importance of this observation is uncertain. First, whether the effect of aspirin persists in the longer term is unknown. Second, we do not know how an ACE inhibitor exerts its beneficial effect and therefore how important its hemodynamic or other actions are. Third, experience has taught us that however plausible a pharmacological mechanism may seem, it may not lead to the expected effect on clinical outcome. Consequently, studies on the actions of drugs on potentially important biological mechanisms can only be hypothesis generating with respect to clinical outcomes and often have been misleading. 7,8 Despite these limitations, such studies remain the foundation of therapeutic drug development.The report by McAlister and colleagues 9 represents a completely different approach in contemporary cardiovascular research, one that is becoming increasingly common with the availability of relatively inexpensive and powerful statistical software and the growing number of large administrative data sets created as a result of the explosion in information technology in healthcare systems. McAlister et al looked for a potential interaction between ACE inhibitors and aspirin in a large observational study of patients discharged from hospital in Ontario with a primary diagnosis of heart failure, recording death and readmission for heart failure over the subsequent year. 9 The authors did not find evidence of an interaction between the 2 treatments. Can we be reassured by this? The reader should have both specific and general reservations about the study by McAlister and colleagues. Specifically, the proportion of patients with nonischemic heart failure (44%) was unusually high, even assuming that the recorded origin was reliable, and because it is not indicated in nonischemic heart failure, it is unclear why some of these patients were treated with aspirin. Aspirin is ...

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Section: Article P 2572mentioning

confidence: 64%

Does Aspirin Reduce the Benefit of an Angiotensin-Converting Enzyme Inhibitor?

Jhund

McMurray

2006

Circulation

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“…10,57 Finally, three studies evaluated the aspirin-ACE-I interaction using clinical endpoints (Table 3). [58][59][60] One was…”

Section: Interaction Between Low-and Intermediate-dose Aspirin Raas mentioning

confidence: 99%

“…59 The third study demonstrated an increase in hospitalisations for heart failure with aspirin compared with placebo or warfarin, according to a prospective, blinded protocol. 60 Collectively, these data support the existence of a possible deleterious effect and/or a counteraction of part of ACE-I efficacy by aspirin.…”

mentioning

confidence: 99%

Interaction between cyclooxygenase and the renin-angiotensin-aldosterone system: rationale and clinical relevance

Meune

Mourad

Bergmann

et al. 2003

J Renin Angiotensin Aldosterone Syst

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Increased understanding of pathophysiological mechanisms of cardiovascular diseases has shown that the renin-angiotensin-aldosterone system (RAAS) is activated in this setting and suggests a central role for the angiotensin-converting enzyme (ACE). ACE transforms angiotensin I (Ang I) to angiotensin II (Ang II), and also promotes the degradation of bradykinin into inactive metabolites. These bradykinins stimulate nitric oxide synthesis and vasodilatator prostaglandin synthesis via a cyclooxygenase (COX)

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“…Even the SAVE and AIRE trials showed a trend toward less benefit with captopril and ramipril, respectively, among users of aspirin [21,22]. In a study of 514 patients with heart failure [23], aspirin combined with an ACE inhibitor resulted in a significantly higher rate of readmission compared to ACE inhibitor therapy alone (adjusted odds ratio = 2.6; 95% CI = 1.2-4.9; p = 0.03).…”

Section: Clinical Evidence Supporting Aspirin-ace Inhibitor Interactionmentioning

confidence: 99%

Aspirin and ACE Inhibitors in Patients with Heart Failure: WATCHing for a Potential Interaction

Moore¹,

Steinhubl²

2001

Heart Drug

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Coronary artery disease is the leading cause of chronic heart failure and consequently a large proportion of patients with left ventricular (LV) dysfunction are treated with aspirin. Angiotensin-converting enzyme (ACE) inhibitors have emerged as the standard therapy for patients with both symptomatic and asymptomatic LV dysfunction. When the respective actions of these two agents with regard to prostaglandin synthesis are considered, the potential for an antagonistic interaction is evident. In a bradykinin-dependent mechanism, ACE inhibitors stimulate the synthesis of the vasodilator prostacyclin. Aspirin, a cyclooxygenase inhibitor, inhibits the production of prostaglandins. There is evidence that in patients with LV dysfunction, the favorable effects of ACE inhibitors on hemodynamic measures of systemic vascular resistance, cardiac output and LV filling pressures are significantly attenuated by the coadministration of aspirin. There is an accumulating body of retrospective clinical trial data suggesting that these hemodynamic influences translate into a reduction in the mortali- ty benefit seen in ACE inhibitor-treated patients not receiving aspirin. This review will address the mechanism of this potential interaction, as well as the hemodynamic and clinical trial data suggesting the relevance of this interaction. The Warfarin Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial, an ongoing study designed to address the issue of the appropriate antithrombotic therapy for patients with chronic heart failure will be discussed.

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Effect of combined aspirin and angiotensin-converting enzyme inhibitor therapy versus angiotensin-converting enzyme inhibitor therapy alone on readmission rates in heart failure

Cited by 27 publications

References 13 publications

Does Aspirin Reduce the Benefit of an Angiotensin-Converting Enzyme Inhibitor?

Does Aspirin Reduce the Benefit of an Angiotensin-Converting Enzyme Inhibitor?

Interaction between cyclooxygenase and the renin-angiotensin-aldosterone system: rationale and clinical relevance

Aspirin and ACE Inhibitors in Patients with Heart Failure: WATCHing for a Potential Interaction

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