Aspirin Inhibits the Acute Arterial and Venous Vasodilator Response to Captopril in Patients with Chronic Heart Failure

MacIntrye, Iain M.; Jhund, Pardeep S.; McMurray, John J.V.

doi:10.1007/s10557-005-3309-3

Cited by 12 publications

(5 citation statements)

References 27 publications

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“…Thus the alteration in arterial function was dose‐mediated [25]. However, using venous occlusion plethysmography, even 75 mg aspirin was shown to inhibit the acute arterial and venous vasodilator response to the ACE‐inhibitor captopril in patients with chronic heart failure [26].…”

Section: Discussionmentioning

confidence: 99%

Renal effects of aspirin are clearly dose‐dependent and are of clinical importance from a dose of 160 mg

Juhlin

Jönsson

Höglund

2008

European J of Heart Fail

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Background: High doses of aspirin counteract the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors. It is not known how low-dose aspirin, with concomitant ACE-inhibitor treatment, affects renal function. Aim: To study renal effects of different doses of aspirin in elderly healthy volunteers who had an activated renin-angiotensin system. Methods: Sixteen subjects each received two different doses of aspirin (0 and160 mg or 80 and 320 mg) after pre-treatment with bendroflumethiazide and enalapril, in a randomised double-blind, cross-over fashion. Results: Least square means of the observations 30 to 180 min after dosing, showed that urine flow, GFR, excretion rates of sodium, osmolality clearance and free water clearance were significantly decreased in a dose-dependent manner. Urine flow, sodium excretion rate and free water clearance were significantly lower with 320 mg aspirin vs. 0 mg and 80 mg, and GFR was significantly lower with 320 mg vs. 80 mg. Urine flow, sodium excretion rate, free water and osmolality clearance was significantly lower with aspirin 160 mg vs. 0 mg. Conclusion: The dose-dependent renal effects of aspirin are of clinical importance from a dose of 160 mg. The adverse influence of aspirin doses higher than 80 mg should be taken into consideration in patients with heart failure.

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Section: Discussionmentioning

confidence: 99%

Renal effects of aspirin are clearly dose‐dependent and are of clinical importance from a dose of 160 mg

Juhlin

Jönsson

Höglund

2008

European J of Heart Fail

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“…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.…”

Section: Article P 2572mentioning

confidence: 98%

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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“…4 Generally, it acts as a vasodilator. 5 In 2006, the Food and Drug Administration (FDA) reported that ibuprofen can interfere with the anti-platelet effects of low-dose aspirin (81 mg daily). In this context, the work of Van Westrhenen et al 6 provided evidence that ibuprofen reduced the preventative effect of aspirin against cardiovascular disease, and also, Hong et al 7 provided a summary on the inhibition, induced by aspirin and ibuprofen, of platelet aggregation in healthy subjects.…”

Section: Introductionmentioning

confidence: 99%

Competitive binding of small molecules with biopolymers: a fluorescence spectroscopy and chemometrics study of the interaction of aspirin and ibuprofen with BSA

Zhu

Kokot

2011

Analyst

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The interaction of aspirin and ibuprofen with bovine serum albumin (BSA) was studied by spectrofluorimetry under simulated physiological conditions. Both aspirin and ibuprofen quenched the intrinsic fluorescence of BSA and the binding ratios obtained were 2 : 1 for aspirin-BSA and 3 : 1 for ibuprofen-BSA interactions, respectively. The thermodynamic parameters (ΔH, ΔS and ΔG) obtained from the fluorescence spectroscopy data showed that the binding of aspirin to BSA involved van der Waals interactions and hydrogen bonds. Competitive experiments using warfarin and diazepam as site markers indicated that aspirin was mainly located in the hydrophobic pocket of site II of the protein as well as to a small extent in site I. Furthermore, the competitive interaction of the aspirin and ibuprofen with BSA, which was studied with the use of the three-way excitation-emission fluorescence spectra and a parallel factor analysis (PARAFAC) chemometrics method, showed that the competitive effect of ibuprofen was stronger than that of aspirin, i.e. the former molecule replaced the aspirin from the aspirin-BSA complex.

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Aspirin Inhibits the Acute Arterial and Venous Vasodilator Response to Captopril in Patients with Chronic Heart Failure

Abstract: In patients with chronic heart failure even low dose aspirin inhibits both the acute arterial and venous dilator responses to captopril. This action of aspirin may reduce the long-term clinical benefits of ACE inhibitors.

Cited by 12 publications

References 27 publications

Renal effects of aspirin are clearly dose‐dependent and are of clinical importance from a dose of 160 mg

Renal effects of aspirin are clearly dose‐dependent and are of clinical importance from a dose of 160 mg

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

Competitive binding of small molecules with biopolymers: a fluorescence spectroscopy and chemometrics study of the interaction of aspirin and ibuprofen with BSA

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