A computational study of the interaction between coronary blood flow and myocardial mechanics.
An anatomically based computational model of coronary blood flow, coupled to cardiac mechanics, is verified with experimental data and used to investigate the mechanisms by which myocardial contraction inhibits coronary blood flow. From finite deformation mechanics solutions the regional variation in intramyocardial pressure (IMP) exerted on coronary vessels embedded in the ventricular wall is calculated. This pressure is then coupled to a haemodymanic model of vascular blood flow to predict the spatial-temporal characteristics of perfusion throughout the myocardium. The calculated IMP is shown to vary approximately linearly between ventricular pressure at the endocardium and atmospheric pressure at the epicardium through the diastolic loading and isovolumic contraction phases. During the ejection and isovolumic relaxation phases IMP values rise slightly above ventricular pressure. The average radius of small arterial vessels embedded in the myocardium decreases during isovolumic contraction (18% at left ventricular endocardium) before increasing during ejection (10% at left ventricular endocardium) due to a rise in inflow pressure. Embedded venous vessels show a reduction in radius through both phases of contraction (35% at left ventricular endocardium). Calculated blood flows in both the large epicardial and small myocardial vessels show a 180 degrees phase difference between arterial and venous velocity patterns with arterial flow occurring predominantly during diastole and venous flow occurring predominantly during systole. These results indicate that the transmission of ventricular cavity pressure through the myocardium is the dominant mechanism by which coronary blood flow is reduced during the isovolumic phase of contraction. In the ejection phase of contraction myocardial stiffening plays a more significant role in inhibiting blood flow.
Smith
Nicolas P
NP
Bioengineering Institute, University of Auckland, Auckland 1020, New Zealand. np.smith@auckland.ac.nz
D001696:Biomechanical Phenomena; D003331:Coronary Vessels / Q000502:physiology*; D005544:Forecasting; D006321:Heart / Q000502:physiology*; D006439:Hemodynamics; D006801:Humans; D008953:Models, Anatomic; D009200:Myocardial Contraction / Q000502:physiology*; D011312:Pressure; D012039:Regional Blood Flow; D016277:Ventricular Function, Left