Page 88 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax
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Chapter 5
Coronary Flow Velocity Reserve and Long-term Fatal Cardiac Events
In our study, in which we focused on cardiac mortality only, we found an unequivocal relationship between impaired microvascular function in a reference coronary artery and long-term fatal cardiac events, independent of left ventricular function. CFVR, the presence of SRF, or rapid DDT in the infarct-related artery did not identify individual patients at high risk for cardiac mortality at long-term follow-up. However, CFVR in the infarct-related artery was associated with a high risk for early cardiac mortality, which dissipated over time. In bivariate analysis with reference vessel CFVR, the marginal association of infarct-related artery CFVR with long-term cardiac mortality was eclipsed by the hazard inherited by impairment of reference vessel CFVR. Intuitively, the physiological alterations in the myocardium because of the acute ischemic event are more pronounced in the infarct-related artery, than in regions more remote from the infarction. The information on the microvascular status derived from CFVR in the infarct-related artery is obscured by the impact of acute and continuous ischemia, and the possible detrimental effects of reperfusion on myocardial tissue. In contrast, reference vessel CFVR provides information on the general functional status of the microvasculature after the acute ischemic event. Reference vessel CFVR may therefore be considered a more selective marker of microvascular function, which apparently plays a pivotal role in long- term outcome after STEMI.
Cause of Impaired Reference Vessel Coronary Flow Velocity Reserve After STEMI
During acute regional ischemia, several factors have been shown to impair CFVR in regions remote from the infarction. First, the regional dysfunction of the ischemic myocardium leads to a compensatory hyperkinesis of remote nonischemic myocardium.32,33 This was reported to result in an impaired reference vessel CFVR because of a predominant increase in baseline flow velocity.28,32,34 Second, apart from the systolic mechanical interaction between the myocardium and the coronary microvasculature, cardiac mechanics exert their effect also during diastole.35 A restriction in myocardial capacitance, which may result from either an increase in left ventricular end-diastolic pressure (LVEDP), or stiffening of the myocardium because of hypoxic perfusion in the absence of an increased LVEDP,36 limits coronary flow during late diastole. This is expresses as an isolated decrease in hyperemic APV in the infarct-related artery
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