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Journal ArticleDOI

Modeling pressure-flow relations in cardiac muscle in diastole and systole.

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TLDR
Modeling cardiac contraction on the basis of the time-varying elastic properties of the myocardial tissue can explain coronary flow impediment and that contractions, with or without shortening, have a larger effect on coronary flow than changes in muscle length.
Abstract
Pressure-flow relations were calculated for a symmetrical, maximally dilated, crystalloid-perfused coronary vascular network embedded in cardiac muscle in (static) diastole and (static) systole at two muscle lengths: slack length and 90% of maximal muscle length (Lmax). The calculations are based on the "time-varying elastance concept." That is, the calculations include the mechanical properties of the vascular wall and the (varying) mechanical properties of the myocardial tissue (in cross-fiber direction). We found that, at any given perfusion pressure, coronary flow is smaller in systole than in diastole. Relative reduction in vascular cross-sectional area, which forms the basis of flow impediment, was largest for the smallest arterioles. At a constant perfusion pressure of 62.5 mmHg, the transition from (static) diastole to (static) systole at constant muscle length ("isometric contraction") was calculated to reduce flow by 74% (from 18.9 to 5.0 ml x min(-1) x g(-1)) and by 64% (from 12.6 to 4.6 ml x min(-1) x g(-1)) for the muscle fixed at slack length and 90% of Lmax, respectively. At this perfusion pressure, contraction with 14% shortening (from 90% of Lmax in diastole to slack length in systole) was calculated to reduce flow by 61% (from 12.6 to 5.0 ml x min(-1) x g(-1)). Increasing muscle length from slack length to 90% of Lmax decreases coronary flow by 34% in diastole and by 8% in systole. We conclude that modeling cardiac contraction on the basis of the time-varying elastic properties of the myocardial tissue can explain coronary flow impediment and that contractions, with or without shortening, have a larger effect on coronary flow than changes in muscle length.

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Journal ArticleDOI

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

TL;DR: The cardiac muscle and the coronary vasculature are in close proximity to each other, and a two-way interaction, called cross-talk, exists, and here the authors focus on the mechanical aspects of cross- talk including the role of the extracellular matrix.
Journal ArticleDOI

Dependence of Intramyocardial Pressure and Coronary Flow on Ventricular Loading and Contractility: A Model Study

TL;DR: A parameter sensitivity analysis shows that the normalized amplitude of coronary inflow is mainly determined by contractility, reflected in ventricular pressure and, at low ventricular volumes, radial wall stress, which is less sensitive to myocardial coronary compliance and resistance.
Journal ArticleDOI

Large-Scale 3-D Geometric Reconstruction of the Porcine Coronary Arterial Vasculature Based on Detailed Anatomical Data

TL;DR: The present model constitutes the first most extensive reconstruction of the entire coronary arterial system which will serve as a geometric foundation for future studies of flow in an anatomically accurate 3-D coronary vascular model.
Journal ArticleDOI

Mechanisms of myocardium-coronary vessel interaction

TL;DR: The results show that none of the three basic mechanisms alone can account for the measured data, and only the combined effect of the cavity-induced extracellular pressure and the shortening-induced intramyocyte pressure provides good agreement with the majority of measurements.
Journal ArticleDOI

A computational study of the interaction between coronary blood flow and myocardial mechanics.

TL;DR: The 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.
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