© 2005 European Society of Cardiology
Correlation of flow mediated dilation with inflammatory markers in patients with impaired cardiac function. Beneficial effects of inhibition of ACE
a Markusovszky Hospital, Endothelium study group H-9700, Szombathely, Hungary
b Department of Pathophysiology, Semmelweis University H-1445, Budapest, Hungary
c Department of Physiology, New York Medical College Valhalla NY 10595, USA
* Corresponding author. Department of Physiology, New York Medical College, Valhalla, NY 10595, USA. Tel.: +1 914 594 4085; fax: +1 914 594 4018. Email address: koller{at}nymc.edu
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Abstract |
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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 (TNF
) and C-reactive protein (CRP), and that treatment with angiotensin converting enzyme inhibitors (ACEI) will increase FMD by reducing TNF 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- (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- (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- 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.
Key Words: Endothelial function • Tissue renin–angiotensin system • Flow mediated dilatation • Vascular inflammation • Angiotensin converting enzyme inhibitor
Received January 27, 2005; Revised July 30, 2005; Accepted October 17, 2005
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