Invasive evaluation of patients after reperfused STEMI: One-stop-shop for anatomy and physiology

Despite micro-remobilization and reperfusion injury associated with reperfusion therapy, the initial goal of therapy in patients with ST elevation myocardial infarction (STEMI) is to halt the ongoing ischemic insult to the myocardium by achieving myocardial reperfusion. Reperfusion can rarely occur spontaneously, and is facilitated by anti-platelet and anti-thrombotic therapy, but optimally requires percutaneous coronary intervention (PCI), fibrinolytic therapy, or combination pharmaco-invasive therapy. Patients who initially receive fibrinolytic but fail pharmacologic reperfusion are referred for emergent rescue PCI. Those patients who undergo successful primary or rescue PCI have the advantage of not only achieving myocardial reperfusion by recanalization of the obstructed vessel, but also revascularization of any residual epicardial stenosis such that any residual viable peri-infarct myocardium will not remain ischemic. However, as there are only a limited number of centers that can perform emergency mechanical reperfusion by primary PCI, the majority of STEMI patients who have access to contemporary medical therapy undergo pharmacologic reperfusion. Once epicardial and microvascular reperfusion are achieved and the patient stabilized, the next priority is to identify residual hemodynamically significant lesions in the infarct and other myocardial beds that would require revascularization. Therefore, pharmacologically reperfused STEMI patients either undergo non-invasive testing or coronary angiography to identify residual ischemia in the infarct bed and the remaining myocardium. Among patients who undergo non-invasive risk stratification, those with preserved ventricular function and no evidence of ischemia are managed medically and patients with reduced ventricular function and/or with inducible ischemia are referred for angiography. In the cardiac catheterization laboratory, in addition to anatomical assessment of lesion severity by angiography, physiologic evaluation of epicardial and microvascular beds can be performed using angioplastytype guide wires with pressure and velocity sensors. The epicardial lesion can be assessed by measuring fractional flow reserve (FFR) or hyperemic stenosis resistance (HSR), the microcirculation by measuring the index of microcirculatory resistance (IMR) or the hyperemic myocardial resistance index (HMR), and both epicardial and microcirculatory beds by measuring coronary flow reserve (CFR). So what tools in the cardiac catheterization laboratory are best suited to assess lesion severity in the post-infarct bed? Because FFR has been extensively validated in patient’s normal ventricles and is now gaining traction with interventional cardiologists as a simple and robust physiologic index of lesion severity, if validated in this setting, it would be the ideal tool to assess lesion severity in reperfused STEMI patients. Fractional flow reserve is defined as the ratio of the hyperemic flow distal to a stenosis to hyperemic normal flow. As flow is equal to pressure divided by resistance and resistance can be cancelled from both the numerator (stenotic flow) and the denominator (normal or aortic flow) when it is minimal and constant during hyperemia, then FFR can simply be calculated as the ratio of distal to aortic pressure during hyperemia. However, theoretically, when the microcirculatory resistance is elevated, such as after STEMI, pressure-derived FFR might underestimate the physiologic significance of a stenosis. In other words, the calculated FFR value would be higher in a post-infarct bed than for an identical lesion subtending a normal myocardial bed. However, proponents of FFR have argued that although microvascular resistance is elevated in the infarcted bed, it is nevertheless minimal and constant during hyperemia and therefore it can be cancelled from the numerator and the denominator without significant error in the FFR From the Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA. Dr. Samady has received research grants from Volcano Therapeutics. Reprint requests: Habib Samady, MD, FACC, Division of Cardiology, Department of Medicine, Emory University School of Medicine, Suite F606, 1365, Clifton Road, Atlanta, GA; hsamady@emory.edu. J Nucl Cardiol 2010;17:775–7. 1071-3581/$34.00 Copyright 2010 American Society of Nuclear Cardiology. doi:10.1007/s12350-010-9283-6