Coronary flow patterns in normal and ischemic hearts: transmyocardial and artery to vein distribution.
The dynamics of the transmyocardial coronary flow patterns during normal and ischemic conditions are complex and relatively inaccessible to measurements. Therefore, theoretical analyses are needed to help in understanding these phenomena. The proposed model employs compartmental division to three layers, each with four vessel-size compartments which are characterized by resistance and compliance. These compartments are subjected to the extravascular compressive pressure (ECP) generated by cardiac contraction, which by modifying the transmural pressure causes changes in cross-sectional area of the vessels in each compartment continuously determining the resistance and capacitance values. Autoregulation and collaterals are also included in order to simulate the flow patterns during regional ischemia. Using these features, the model predicts the typical out of phase arterial and venous flow patterns. Systolic collapse of the large intramyocardial veins during the normal cycle, as well as systolic arteriolar collapse during ischemia are predicted. The transmural flow during ischemia is characterized by alternating flows between the layers. The ECP is considered here is two ways: (a) as a function of left ventricle (LV) pressure, decreasing linearly from endocardium to epicardium and (b) as the interstitial fluid pressure, employing a multilayer muscle-collagen model of the LV. While both of these approaches can describe the dynamics of coronary flow under normal conditions, only the second approach predicts the large compressive effects due to high ECP obtained at very low cavity pressure, resulting from significant muscle shortening and radial collagen stretch. This approach, combining a detailed description of transmural coronary circulation interacting with the contracting myocardium agrees with many observations on the dynamics of coronary flow and suggests that the type of LV mechanical model is important for that interaction.
Beyar
R
R
Julius Silver Institute, Department of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa.
Caminker
R
R
Manor
D
D
Sideman
S
S
D000818:Animals; D001696:Biomechanical Phenomena; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology*; D005069:Evaluation Studies as Topic; D006439:Hemodynamics; D006706:Homeostasis; D008433:Mathematics; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology*; D051381:Rats; D012680:Sensitivity and Specificity