Time course of microvascular resistance of the infarct and noninfarct coronary artery following an anterior wall acute myocardial infarction

被引:49
作者
Bax, M
de Winter, RJ
Koch, KT
Schotborgh, CE
Tijssen, JGP
机构
[1] Univ Amsterdam, Acad Med Ctr, Dept Cardiol, NL-1105 AZ Amsterdam, Netherlands
[2] Haga Teaching Hosp, Dept Cardiol, The Hague, Netherlands
关键词
D O I
10.1016/j.amjcard.2005.11.026
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Previous studies have suggested that coronary flow velocity reserve (CFVR) in the early phase of acute myocardial infarction (AMI) is abnormal in infarcted and remote regions. This study determined the coronary microvascular resistance of infarct-related arteries (IRAs) and non-IRAs during AMI and at follow-up in patients who were treated with primary percutaneous intervention. In 73 patients with a first anterior wall AMI, baseline and minimal microvascular resistance in IRAs and non-IRAs immediately after reperfusion and at 1-week and 6-month follow-up were calculated as the ratio of mean transvascular pressure gradient to mean baseline and to adenosine-induced hyperemic blood flow velocity, respectively. CFVR in IRAs increased from 1.6 +/- 0.4 after reperfusion to 1.9 +/- 0.5 at 1 week and to 3.0 +/- 0.8 at 6 months (p < 0.0001) and in non-IRAs from 2.4 +/- 0.5 to 2.7 +/- 0.6 at 1 week to 3.3 +/- 0.6 at 6 months (p < 0.0001). Minimal microvascular resistance in IRAs and non-IRAs (3.2 +/- 1.7 and 2.2 +/- 0.6 mm Hg/second/cm, respectively) decreased significantly at follow-up (2.0 +/- 0.6 and 1.7 +/- 0.6 mm Hg/second/cm at 1 week and 1.8 +/- 0.6 and 1.8 +/- 0.7 mm Hg/second/cm at 6 months, respectively). After correction for rate-pressure product, baseline microvascular resistance after reperfusion and at 6 months did not significantly differ between IRAs and non-IRAs. In conclusion, minimal microvascular resistance is higher in infarcted and noninfarcted regions during AMI than at follow-up. The low CFVR in remote regions during AMI is probably due more to disturbed autoregulation than to increased myocardial workload. (c) 2006 Elsevier Inc. All rights reserved.
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收藏
页码:1131 / 1136
页数:6
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