title: Correlation of flow mediated dilation with inflammatory markers in patients with impaired cardiac function. Beneficial effects of inhibition of ACE.
abstract: Impaired cardiac function is frequently accompanied by peripheral vascular dysfunction and a pro-inflammatory condition, which may be associated with elevated levels of angiotensin II. We hypothesized that the magnitude of flow mediated dilatation (FMD) of the brachial artery of post myocardial infarction patients will correlate with serum levels of tumor necrosis factor alpha (TNFalpha) and C-reactive protein (CRP), and that treatment with angiotensin converting enzyme inhibitors (ACEI) will increase FMD by reducing TNFalpha and CRP. Patients were treated with low dose (10 mg/day) quinapril (Q) or enalapril (E) and their effects on FMD and inflammatory markers were evaluated after 8 and 12 weeks. Before treatment, in both groups FMD showed a low value (Q: 2.95+0.42% and E: 3.3+/-0.33%), whereas TNF-alpha (Q: 31.65+/-8.23 pg/ml and E: 29.5+/-5.9 pg/ml) and CRP (Q: 7.28+/-2.96 mg/ml and E: 7.08+/-3.02 mg/ml) were elevated. In the Q group, but not in the E group FMD increased significantly, (to 5.96+1.10%), whereas TNF-alpha (19.0+/-12.21 pg/ml) and CRP (to 3.91+/-1.82 mg/L) significantly decreased after 8 and 12 weeks of Q treatment. Moreover, the magnitude of FMD showed a strong inverse correlation with serum levels of TNF-alpha and CRP after Q treatment. Thus, in post myocardial infarction patients endothelial dysfunction assessed by FMD correlates with elevated levels of plasma inflammatory markers, and low dose quinapril improves endothelial function, likely by reducing vascular inflammation.
authors.affiliation: Markusovszky Hospital, Endothelium study group, H-9700, Szombathely, Hungary.
authors.forename: Imre
authors.initials: I
authors.lastname: Kovacs
authors.forename: Janos
authors.initials: J
authors.lastname: Toth
authors.forename: Jeno
authors.initials: J
authors.lastname: Tarjan
authors.forename: Akos
authors.initials: A
authors.lastname: Koller
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000032:analysis; D004656:Enalapril / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D000077583:Quinapril; D012039:Regional Blood Flow / Q000187:drug effects; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D044005:Tetrahydroisoquinolines / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D018608:Ultrasonography, Doppler; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D044005:Tetrahydroisoquinolines; D014409:Tumor Necrosis Factor-alpha; D004656:Enalapril; D002097:C-Reactive Protein; D000077583:Quinapril