Page 49 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Microvascular resistance of infarct and noninfarct coronary arteries
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 3 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.
The objective of reperfusion therapy in acute myocardial infarction (AMI) is salvage of myocardial tissue by reestablishing blood flow to the jeopardized microcirculation to preserve left ventricular function and decrease mortality.1 Despite restoration of epicardial blood flow, microvascular integrity and function of the infarct-related artery (IRA) may be decreased,2, 3 which represents microvascular obstruction, a phenomenon also known as the “no- reflow” phenomenon.4 Recent studies have demonstrated that intracoronary measured coronary flow velocity reserve (CFVR) in the IRA improves during the early phase of AMI but fails to reach normal levels at long-term follow- up.5, 6 Some clinical7, 8 and experimental9, 10 studies have suggested a disturbed CFVR in the non-IRA in the acute phase of AMI. It has been postulated that neurohumoral activation contributes to this phenomenon. This is of clinical relevance because of the compensatory hyperkinesis of remote vascular territories in the setting of AMI. However, the change over time of coronary
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