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Myocardial fractional flow reserve (FFR), an important index of coronary stenosis, is measured by a pressure sensor guidewire. The determination of FFR, only based on the dimensions (lumen diameters and length) of stenosis and hyperaemic coronary flow with no other ad hoc parameters, is currently not possible. We propose an analytical model derived from conservation of energy, which considers various energy losses along the length of a stenosis, i.e. convective and diffusive energy losses as well as energy loss due to sudden constriction and expansion in lumen area. In vitro (constrictions were created in isolated arteries using symmetric and asymmetric tubes as well as an inflatable occluder cuff) and in vivo (constrictions were induced in coronary arteries of eight swine by an occluder cuff) experiments were used to validate the proposed analytical model. The proposed model agreed well with the experimental measurements. A least-squares fit showed a linear relation as (Δp or FFR)(experiment) = a(Δp or FFR)(theory) + b, where a and b were 1.08 and -1.15 mmHg (r(2) = 0.99) for in vitro Δp, 0.96 and 1.79 mmHg (r(2) = 0.75) for in vivo Δp, and 0.85 and 0.1 (r(2) = 0.7) for FFR. Flow pulsatility and stenosis shape (e.g. eccentricity, exit angle divergence, etc.) had a negligible effect on myocardial FFR, while the entrance effect in a coronary stenosis was found to contribute significantly to the pressure drop. We present a physics-based experimentally validated analytical model of coronary stenosis, which allows prediction of FFR based on stenosis dimensions and hyperaemic coronary flow with no empirical parameters.

Since the right and left ventricles (RV and LV) function under different loading conditions, it is not surprising that they differ in their mechanics (intramyocardial pressure), structure, and metabolism; such differences may also contribute to differences in the coronary vessel wall. Our hypothesis is that intima-media thickness (IMT), IMT-to-radius (IMT-to-R) ratio, and vessel wall stress vary transmurally in the LV, much more than in the RV. Five normal Yorkshire swine were used in this study. The major coronary arteries were cannulated through the aorta and perfusion fixed with 6.25% glutaraldehyde and casted with a catalyzed silicone-elastomer solution. Arterial and venous vessels were obtained from different transmural locations of the RV and LV, processed for histological analysis, and measured with an imaging software. A larger transmural gradient was found for IMT, IMT-to-R ratio, and diastolic circumferential stress in vessels from the LV than the nearly zero transmural slope in the RV. The IMT of arterial vessels in the LV showed a slope of 0.7 +/- 0.5 compared with 0.3 +/- 0.3 of arterial vessels in the RV (P

There is no doubt that scaling relations exist between myocardial mass and morphometry of coronary vasculature. The purpose of this study is to quantify several morphological (diameter, length, and volume) and functional (flow) parameters of the coronary arterial tree in relation to myocardial mass. Eight normal porcine hearts of 117-244 g (mean of 177.5 +/- 32.7) were used in this study. Various coronary subtrees of the left anterior descending, right coronary, and left circumflex arteries were perfused at pressure of 100 mmHg with different colors of a polymer (Microfil) to obtain rubber casts of arterial trees corresponding to different regions of myocardial mass. Volume, diameter, and cumulative length of coronary arteries were reconstructed from casts to analyze their relationship to the perfused myocardial mass. Volumetric flow was measured in relationship with perfused myocardial mass. Our results show that arterial volume is linearly related to regional myocardial mass, whereas the sum of coronary arterial branch lengths, vessel diameters, and volumetric flow show an approximately 3/4, 3/8, and 3/4 power-law relationship, respectively, in relation to myocardial mass. These scaling laws suggest fundamental design principles underlying the structure-function relationship of the coronary arterial tree that may facilitate diagnosis and management of diffuse coronary artery disease.

The potential of the coronary veins for revascularization has been evaluated by many investigators for more than a century. The major hurdle has been the damage of veins during sudden exposure to arterial pressure. The solution to this problem has typically involved the use of intricate and complicated apparatus and devices, which has prevented routine clinical utility in the catheterization laboratory. This review examines this old concept from a new perspective and proposes a novel hypothesis to address previous shortcomings. We speculate on an approach that may serve to eliminate the edema and hemorrhage that result during venous retroperfusion as the pressure is suddenly increased to arterial values. We propose the rationale to increase the venous pressure to arterial values more gradually to allow prearterializations of the veins before full exposure of arterial pressure. Finally, we discuss various possible indications for this selective autoretroperfusion strategy to combat myocardial ischemia in cardiogenic shock patients, ST-elevation myocardial infarct patients, no-option patients, and beyond. [ABSTRACT FROM AUTHOR]