Page 108 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Chapter 6
compensatory vasodilation of the coronary resistance vessels to maintain stable resting coronary blood flow to the distal myocardium. This mechanism is capable of maintaining resting blood flow until the epicardial artery becomes narrowed by >85% of the lumen diameter, after which basal flow starts to decrease.19 In the setting of stable CAD, prolonged compensatory vasodilation of the coronary resistance vessels because of chronic deprivation of perfusion pressure in the presence of progressive epicardial artery narrowing may impair the autoregulatory mechanism of the coronary microvasculature. An abrupt restoration of perfusion pressure by percutaneous intervention may then fail to induce appropriate adaptation of the microvasculature, resulting in an increased flow velocity at rest.15,17 However, after percutaneous coronary intervention, this change in baseline flow velocity in response to coronary intervention was found to be transient, normalizing toward reference values at ≈6-month follow-up.15,17
In contrast to the previous investigations after percutaneous intervention, we assessed CFVR in vessels without flow-limiting coronary stenoses. Furthermore, we performed the intracoronary measurements at the start of the procedure before revascularization of the target lesions. The combination of an increased baseline flow velocity in the presence of decreased microvascular resistance in the present study, therefore, implies pre-existent disturbance of the coronary autoregulatory mechanism in adequately perfused myocardium. Furthermore, the same alterations were present in the target vessel, indicating that disturbance of the autoregulatory mechanism is present throughout the myocardium and implicating a systemic origin of such microvascular dysfunction. Apparently, in patients with impaired reference vessel CFVR, coronary autoregulation fails to adapt distal vascular tone appropriately to regulate coronary flow, resulting in an increase in baseline flow velocity and impairing the achievable CFVR, which apparently puts these patients at high risk for future events. In contrast, the microvascular response to a potent vasodilator remains intact and, therefore, does not provide an explanation for the adverse outcome observed in these patients.
The combination of findings in the present study allocates the cause of the impaired flow reserve to the coronary autoregulatory mechanism. Preclinical studies suggest a role of hypertension-associated left ventricular
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