T S Feit | PubMed Health

PubMed1983

AV pacing and LV performance.

Five patients with impaired left ventricular function (LV) and implanted AV sequential pacemakers underwent serial radionuclide angiograms. The goal was a non-invasive evaluation of the rapid changes in left ventricular performance elicited by rate, pacing mode and AV interval manipulation. End diastolic volume, end systolic volume, stroke volume and cardiac output were increased by AV sequential pacing in comparison with ventricular pacing at 70 beats per minute. No significant change in ejection fraction and blood pressure were noted with changing AV sequential pacing rates at usual pacing rates. Our data suggest that a short AV interval (150 ms) improved LV performance more than a long AV interval (250 ms). A non-invasive technique to optimize left ventricular performance on an acute basis by varying heart rate, AV interval and pacing mode with the implanted AV sequential pacemaker is feasible and may be useful in selective clinical situations.

Aged↗

PubMed1979

Diastolic pressure-volume relations and distribution of pressure and fiber extension across the wall of a model left ventricle.

A model for left ventricular diastolic mechanics is formulated that takes into account noneligible wall thickness, incompressibility, finite deformation, nonlinear elastic effects, and the known fiber architecture of the ventricular wall. The model consists of a hollow cylindrical mass of muscle bound between two plates of negligible mass. The wall contains fiber elements that follow a helical course and carry only axial tension. The fiber angle (i.e., helical pitch) is constant along the length of each fiber but varies through the wall in accordance with the known distribution of fiber orientations in the canine left ventricle. To simplify the analysis and reduce the number of degrees of freedom, the anatomic distribution of fiber orientations is divided into a clockwise and counterclockwise system. The reference configuration for the model corresponds to a state in which, by hypothesis, the transmural pressure gradient is zero, the tension is zero for all fibers across the wall, and all fibers are assumed to have a sarcomere length of 1.9 micrometer. This choice of reference configuration is based on the empirical evidence that canine ventricles, fixed in a state of zero transmural pressure gradient and dissected, demonstrate sarcomere lengths between 1.9 and 2.0 micrometer in inner, middle, and outer wall layers, while isolated ventricular muscle bundles are observed to have zero resting tension when the sarcomere length ranges from 1.9 to 2.0 micrometer. An equation representing the global condition for equilibrium is derived and solved numerically. It is found that the model's pressure-volume relation is representative of diastolic filling in vivo over a wide range of filling pressures, and the calculated midwall sarcomere lengths in the model compare favorably with published experimental data. Subendocardial fibers are stretched beyond Lmax even at low filling pressures, i.e., 5 mm Hg, while fibers located between 60-80% of wall thickness extend minimally between 5 and 12 mm Hg. The hydrostatic pressure field within the wall is highly nonlinear. The pressure rises steeply in the subendocardial layers so that the net gain in pressure in the inner third of the wall is 85% of the filling pressure. It is demonstrated that these results are independent of heart size for a family of heart models that are scale models of each other. They are, however, critically dependent on the existence of longitudinally oriented fibers in the endocardial and epicardial regions of heart wall.

Animals↗

PubMed1977

Numerical study of the behavior of an activation parameter in a sliding filament cat papillary muscle model.

A previously existing model of cross-bridge kinetics is modified to make it applicable to cardiac muscle and incorporated into a macroscopic model of isolated heart muscle. Equations are formulated which describe the responses of this model during simulated isometric and isotonic contractions. These equations allow one to calculate the time variation of the activation parameter in the model when given the contraction time history, i.e. the time course of length and tension changes. The activation parameter is defined as the instantaneous rate constant for cross bridge attachment. We calculate the time course of the activation parameter with the model's responses set equal to the measured responses of isolated cat papillary muscle and the model parameters chosen appropriately for cat papillary muscle. It is found that in order for the model and muscle response to match, the degree of activation of the muscle model must first increase and then decrease with shortening. The behavior of the activation parameter in the muscle model is consistent with physiological investigations which suggest that shortening in cardiac muscle is associated with both activation and deactivation.

Animals↗