Page 107 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Coronary autoregulation and fatal events in stable CAD
resistance. In contrast, hyperemic microvascular resistance and hyperemic APV did not differ between abnormal and normal reference vessel CFVR groups. Furthermore, similar alterations in baseline flow velocity and microvascular resistance were also present in the target vessel.
Reference Coronary Flow Velocity and Microvascular Function
In the absence of a significant coronary stenosis, the vasodilator response of
the coronary circulation is determined by the resistance vessels of the coronary microcirculation.3 In response to a potent vasodilatory stimulus, such as adenosine, this CFVR in a reference vessel may increase >4-fold in healthy young volunteers.10,13 In adult patients with chest pain syndromes and risk factors for
CAD, reference vessel CFVR is expected to increase >2.7-fold.10,13,14 As CFVR is determined as the ratio of hyperemic to basal coronary blood flow velocity, impairment of reference vessel CFVR may follow from either a decrease in hyperemic or an increase in basal coronary blood flow. While the former may
be ascribed to impaired vasodilatory function of the coronary microvasculature 6 and is usually associated with a high hyperemic microvascular resistance, the
latter may be ascribed to disturbed coronary autoregulation and is usually associated with low microvascular resistance under baseline conditions.15 The discrimination between these 2 entities, which can only be made by selective evaluation of the relative contributions of baseline and hyperemic components of CFVR, may provide essential insights into the pathophysiological origin of the impaired vasodilator reserve.
Interpretation of Impaired Reference Vessel CFVR in the Present Study
An increased baseline flow velocity in the presence of decreased baseline microvascular resistance has previously been described in patients with stable CAD after angioplasty and coronary stenting, contributing to the impaired flow velocity reserve frequently found in this setting.15–17 This increase in baseline flow velocity was repeatedly ascribed to disturbed coronary autoregulation.15,17 Under physiological circumstances, coronary autoregulation regulates vasodilation and vasoconstriction of the coronary resistance vessels to maintain stable coronary blood flow to the distal myocardium within a physiological range of perfusion pressures.18 In response to a loss of perfusion pressure to the distal myocardium as a result of progressive epicardial coronary narrowing, autoregulation facilitates
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