Effects Of Myocardial Contraction Research Articles

Is arterial wall-strain stiffening an additional process responsible for atherosclerosis in coronary bifurcations?: an in vivo study based on dynamic CT and MRI

Coronary bifurcations represent specific regions of the arterial tree that are susceptible to atherosclerotic lesions. While the effects of vessel compliance, curvature, pulsatile blood flow, and cardiac motion on coronary endothelial shear stress have been widely explored, the effects of myocardial contraction on arterial wall stress/strain (WS/S) and vessel stiffness distributions remain unclear. Local increase of vessel stiffness resulting from wall-strain stiffening phenomenon (a local process due to the nonlinear mechanical properties of the arterial wall) may be critical in the development of atherosclerotic lesions. Therefore, the aim of this study was to quantify WS/S and stiffness in coronary bifurcations and to investigate correlations with plaque sites. Anatomic coronary geometry and cardiac motion were generated based on both computed tomography and MRI examinations of eight patients with minimal coronary disease. Computational structural analyses using the finite element method were subsequently performed, and spatial luminal arterial wall stretch (LW(Stretch)) and stiffness (LW(Stiff)) distributions in the left main coronary bifurcations were calculated. Our results show that all plaque sites were concomitantly subject to high LW(Stretch) and high LW(Stiff), with mean amplitudes of 34.7 ± 1.6% and 442.4 ± 113.0 kPa, respectively. The mean LW(Stiff) amplitude was found slightly greater at the plaque sites on the left main coronary artery (mean value: 482.2 ± 88.1 kPa) compared with those computed on the left anterior descending and left circumflex coronary arteries (416.3 ± 61.5 and 428.7 ± 181.8 kPa, respectively). These findings suggest that local wall stiffness plays a role in the initiation of atherosclerotic lesions.

Modeling of the Coronary Circulatory System

The dynamics of the coronary system is complicated by its dependence on the mechanical properties of the coronary vessels, the anatomical distribution of the vasculature, the biochemical and neurohormonal regulation, and the effect of myocardial contraction. Several types of coronary system models were proposed, focusing on different aspects of coronary system behavior and supported by different animal experiment methodologies. The lumped models were based on well-controlled coronary pressure–flow measurement and simplified assumptions. They are probably most useful for interpreting hemodynamic data measured in modern catheterizaton labs. Anatomical models, with the advancement in morphometric research, coronary angiography, and video densitometry, provided branching pattern, geometric distribution, and distensibility of coronary vessels. Mathematical description based on vascular waterfall theory, intramyocardial pump model, and time varying elastance concept provided some explanation of the interaction between the coronary system and myocardial contraction. More accurate models would include intramyocardial pressure, microcirculatory hemodynamics, coronary flow regulation, and myocardial oxygen supply and consumption. The combination of different models, may lead to a more comprehensive understanding of the coronary system.

Echocardiographic assessment of diastolic function

Echocardiographic assessment of diastolic function

Effects of myocardial contraction on coronary blood flow: an integrated model.

The effects of myocardial contraction on the coronary flow are studied by means of an integrated structural model of left ventricular (LV) mechanics, coronary flow, and fluid and mass transport. This model relates global LV performance, and in particular coronary flow dynamics, to myocardial composition and structure and contractile sarcomere activity. Extravascular pressure is identified with hydrostatic tissue pressure, i.e., intramyocardial pressure (IMP), and is determined by the dynamics of myocardial contraction and fluid transport. Consistent with available experimental data, changes in myocardial function and contractile state are simulated by changing the sarcomere contractile properties or changing the LV loading conditions. The model's predictions are successfully compared with a wide range of experimental studies; all but one were performed at a constant coronary perfusion pressure and maximal vasodilation. The results indicate a dominant effect of the myocardial contractile state on coronary flow and a dissociation between coronary compression and LV cavity pressure (LVP) when the pressure is controlled by load changes. However, when active sarcomere contraction is regionally impaired by lidocaine, LVP plays an important role in the coronary flow characteristics. The model adequately predicts observations on the effect of cardiac contraction on systolic and diastolic coronary flows, as well as the role of LVP at different loading and contractile conditions. The analysis supports the hypothesis that coronary compression, as mediated through IMP, is independent of LV loading conditions and depends on myocardial contractility and coronary perfusion pressure.

Effect of myocardial contraction on systolic coronary resistance in conscious dogs

We studied the effect of cardiac contraction on systolic coronary resistance under the conditions of maximally dilated coronary resistance vessels in six conscious dogs. Subendocardial segment length in areas supplied by the left circumflex coronary artery, left ventricular pressure and left circumflex coronary artery flow were simultaneously measured. At 5 sec after release of the first 2 min of left circumflex coronary artery occlusion, diastolic coronary blood flow revealed its peak value in association with markedly depressed regional contractile function. With collateral development induced by repeated 2 min left circumflex coronary artery occlusions, segmental dysfunction during occlusion and early reperfusion was progressively attenuated. Before and after collateral development, diastolic coronary resistance at 5 sec of reperfusion remained unchanged, but systolic coronary resistance increased by 41% secondary to restoration of regional myocardial shortening. In each animal, normalized regional shortening correlated well with changes in systolic coronary resistance. The fraction of systolic coronary resistance due to active regional myocardial contraction was 52%. These studies demonstrate that when coronary vasomotor tone is abolished, regional myocardial contraction impedes the coronary systolic flow in proportion to the extent of shortening.

Effects of myocardial contraction on ultrasonic backscatter before and after ischemia

To determine whether contraction and relaxation influence quantitative myocardial ultrasonic backscatter we measured systolic and diastolic integrated backscatter separately in 10 pentobarbital-anesthetized dogs with defined, paced heart rates, before and after coronary occlusion. Data were acquired from intramural sites by coupling a broadband 5-MHz transducer to the left ventricular epicardium. Integrated backscatter was obtained from seven sequential ECG gated intervals throughout the cardiac cycle over the frequencies of 2.5-7.5 MHz and referenced to values obtained with a steel reflector. Before coronary occlusion myocardium in all dogs exhibited a decrease in integrated backscatter from end diastole to end systole (P less than 0.05) in control zones and in zones destined to become ischemic (P less than 0.05). Thirty minutes after occlusion integrated backscatter did not change in control zones but was elevated in ischemic zones with blunting of the diastolic-to-systolic variation. Thus myocardium undergoing contraction exhibits a decrease in integrated backscatter, and measurement of integrated backscatter at end systole differentiates ischemic from normal myocardium.