title: Effects of acetylsalicylic acid on peripheral hemodynamics in patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors.
abstract: Cyclooxygenase inhibitors may affect the hemodynamic status of patients with heart failure adversely and may also block the vasodilatory effects of angiotensin-converting enzyme (ACE) inhibitors in such patients. Relatively low doses of the cyclooxygenase inhibitor acetylsalicylic acid (ASA) are now used routinely in ischemic heart disease, the most important cause of heart failure. Therefore, we investigated the hemodynamic interaction between ASA and captopril in heart failure. In a randomized, cross-over study, 13 patients with congestive heart failure (CHF) who were already receiving maintenance treatment with an ACE inhibitor received a single dose of 25 mg captopril combined with 236 mg ASA or placebo. Peripheral blood flow was studied noninvasively by venous occlusion plethysmography of the calves. Liver blood flow was estimated from indocyanine green (ICG) clearance. Administration of captopril alone significantly decreased blood pressure (BP), and ICG clearance. Calf blood flow remained unchanged. However, after arterial occlusion, hyperemic calf blood flow persisted for longer. Captopril alone did not significantly change the plasma levels of the vasodilating prostaglandins PGI2 and PGE2 or the vasoconstricting thromboxane A2 (TXA2). In contrast, captopril combined with ASA reduced the plasma levels of these vasoactive substances, with significant decreases in PGE2 and TXA2 as compared with captopril alone, yet the hemodynamic alterations after captopril plus ASA were similar to those observed after captopril alone. A single antithrombotic dose of ASA (236 mg) in 13 patients with CHF [New York Heart Association (NYHA) class II-IV] undergoing chronic treatment with ACE inhibitors had no discernible effect on hemodynamic status.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pharmacology/Clinical Pharmacology, University of Groningen, The Netherlands.
authors.forename: J
authors.initials: J
authors.lastname: van Wijngaarden
authors.forename: A J
authors.initials: AJ
authors.lastname: Smit
authors.forename: P A
authors.initials: PA
authors.lastname: de Graeff
authors.forename: W H
authors.initials: WH
authors.lastname: van Gilst
authors.forename: S A
authors.initials: SA
authors.lastname: van der Broek
authors.forename: D J
authors.initials: DJ
authors.lastname: van Veldhuisen
authors.forename: K I
authors.initials: KI
authors.lastname: Lie
authors.forename: H
authors.initials: H
authors.lastname: Wesseling
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001132:Arm / Q000098:blood supply; D001241:Aspirin / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000627:therapeutic use; D002908:Chronic Disease; D004311:Double-Blind Method; D004347:Drug Interactions; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007208:Indocyanine Green; D007866:Leg / Q000098:blood supply; D008297:Male; D008875:Middle Aged; D011453:Prostaglandins / Q000097:blood; D012039:Regional Blood Flow / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D011453:Prostaglandins; D002216:Captopril; D007208:Indocyanine Green; D001241:Aspirin