Mechanism of Increased Fractional Flow
Reserve and Increased Ischemia Threshold
Following Myocardial Infarction

Schwammenthal E 1, Shaviv H 2, Rosenfeld M 3
1Sheba Medical Center, and Sackler School of Medicine, Tel-Aviv University
2Fluid Mechanics Department, Faculty of Engineering, Tel-Aviv University
Fractional flow reserve (FFR) measured following myocardial infarction (MI) has been observed to be higher in patients with more extensive infarction and less residual ischemia for comparable luminal diameters of the culprit stenosis. This may be due to damage to the microvasculature with loss of capillaries blunting the hyperemic response and reducing the transstenotic pressure gradient. The purpose of the project was to test the hypothesis that the increase in FFR may not only reflect a shrinked vascular bed, but also an absolute increase in hyperemic myocardial blood flow to the residual myocardium. We used a finite element coronary flow model employing FLUENTŪ, a software which solves the Navier-Stokes equations for laminar Newtonian flow in a two-dimensional model. The model was divided into four different segments: Main coronary artery with or without stenosis (Figure 1), subendocardial and subepicardial coronary artery resistance, and capillary bed. The ability of the resistance vessels to change their diameter (flow reserve) was simulated by modeling them as porous media with a variable porous factor. We also took into account that the total amount of cross sectional vessel area increases as their diameter decreases, according to the growth function: G=[ds/dm]2+[dl/dm]2; where G is the cross sectional vessel area at each bifurcation, ds and dl are the diameters of the daughter branches, and dm is the diameter of the mother branch. We simulated coronary blood flow to a myocardial region perfused with a driving pressure of 90 mm Hg at a flow rate of 60 ml/min The diameter of the proximal coronary segment, where different degrees of stenosis were created, was assumed to be 4 mm. Loss of myocardium was simulated by loss of a proportional amount of the vascular bed. Increasing degrees of stenosis resulted in a decrease in coronary flow reserve (CFR), as expected. For progressive loss of myocardium (vascular bed) the decline in perfusion resulted in a decrease in transstenotic gradient. This resulted not only in an increase in FFR, but - because of the increased poststenotic perfusion pressure - in a decrease in the need for baseline vasodilatation and, consequently, in an increase in CFR. The model suggests that the increase in FFR post MI may not only reflect a decrease in perfused mass, but also an increase in CFR within the residual viable myocardium. We also developed an pig model allowing to measure FFR and CFR in the two branches of a coronary bifurcation subtended by a proximal stenosis. The aim was, similar to the numerical model, to attempt to assess the impact of myocardial cell loss on FFR and CFR. So far, the model was not stable enough to allow valid data collection. Attempts to improve the model will be made during the subsequent months.