EFFECTS OF ACETYLSALICYLIC-ACID ON PERIPHERAL HEMODYNAMICS IN PATIENTS WITH CHRONIC HEART-FAILURE TREATED WITH ANGIOTENSIN-CONVERTING ENZYME-INHIBITORS

Citation
J. Vanwijngaarden et al., EFFECTS OF ACETYLSALICYLIC-ACID ON PERIPHERAL HEMODYNAMICS IN PATIENTS WITH CHRONIC HEART-FAILURE TREATED WITH ANGIOTENSIN-CONVERTING ENZYME-INHIBITORS, Journal of cardiovascular pharmacology, 23(2), 1994, pp. 240-245
Citations number
12
Categorie Soggetti
Cardiac & Cardiovascular System","Respiratory System","Pharmacology & Pharmacy
ISSN journal
01602446
Volume
23
Issue
2
Year of publication
1994
Pages
240 - 245
Database
ISI
SICI code
0160-2446(1994)23:2<240:EOAOPH>2.0.ZU;2-6
Abstract
Cyclooxygenase inhibitors may affect the hemodynamic status of patient s with heart failure adversely and may also block the vasodilatory eff ects of angiotensin-converting enzyme (ACE) inhibitors in such patient s. Relatively low doses of the cyclooxygenase inhibitor acetylsalicyli c acid (ASA) are now used routinely in ischemic heart disease, the mos t important cause of heart failure. Therefore, we investigated the hem odynamic interaction between ASA and captopril in heart failure. In a randomized, cross-over study, 13 patients with congestive heart failur e (CHF) who were already receiving maintenance treatment with an ACE i nhibitor received a single dose of 25 mg captopril combined with 236 m g ASA or placebo. Peripheral blood flow was studied noninvasively by v enous occlusion plethysmography of the calves. Liver blood flow was es timated from indocyanine green (ICG) clearance. Administration of capt opril alone significantly decreased blood pressure (BP), and ICG clear ance. Calf blood flow remained unchanged. However, after arterial occl usion, hyperemic calf blood flow persisted for longer. Captopril alone did not significantly change the plasma levels of the vasodilating pr ostaglandins PGI(2) and PGE(2) or the vasoconstricting thromboxane A(2 ) (TXA(2)). In contrast, captopril combined with ASA reduced the plasm a levels of these vasoactive substances, with significant decreases in PGE(2) and TXA(2) as compared with captopril alone, yet the hemodynam ic alterations after captopril plus ASA were similar to those observed after captopril alone. A single antithrombotic dose of ASA (236 mg) i n 13 patients with CHF [New York Heart Association (NYHA) class II-IV] undergoing chronic treatment with ACE inhibitors had no discernible e ffect on hemodynamic status. These results cannot be extrapolated to c hronic ASA administration and must be interpreted with caution with re gard to patients in NYHA stage IV of the disease.