Page 110 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Chapter 6
Interpretation
In part, our conclusions are consistent with these previous reports, because we found a similar important prognostic value of microvascular function determined by CFVR in reference vessels for long-term clinical outcome in patients with stable CAD. However, the present study is the first to indicate a significant association between reference vessel vasodilator reserve and long-term fatal events. In the previous evaluations of the prognostic value of reference vessel CFVR for long-term adverse events, nonfatal adverse events were included in the composite end points, such as stroke and revascularization of de novo coronary artery lesions, of which a direct relationship with pre- existent coronary microvascular functional alterations documented during the index procedure may be questionable.
The most important difference between our findings and the conclusions from Pepine et al2and Britten et al5 is the origin of the impaired reference vessel CFVR. Both reports conclude that microvascular reactivity to a potent vasodilator was impaired in patients with an abnormal reference vessel CFVR. However, the relative influence of baseline and hyperemic flow velocity and microvascular resistance was not reported to support this conclusion, even though such discrimination seems important because an impaired vasodilator response to a potent vasodilator is most likely because of different pathophysiology than disturbed autoregulation under basal conditions. Therefore, identification of the exact origin of reference vessel CFVR impairment may alter the potential target for risk stratification or evaluation of preventive therapeutic strategies.2
According to the combination of observations in the present study, we postulate that impaired reference vessel CFVR does not originate from an impaired hyperemic vasodilator response of the coronary microvasculature as reported previously, but from pre-existent disturbed coronary autoregulation under baseline conditions that is present throughout the myocardium. The disturbed autoregulation results in an increased baseline flow velocity, and thereby in depletion of the vasodilator reserve throughout the myocardium. Further elucidation of factors underlying this disturbed autoregulation in patients with stable CAD may identify appropriate targets for risk stratification or evaluation of preventive treatment strategies.
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