Cardiac cycle

About: Cardiac cycle is a research topic. Over the lifetime, 3290 publications have been published within this topic receiving 96159 citations.

Stop-action cardiac computed tomography.

Abstract: Computed tomographic (CT) cardiac imaging in vivo has been hampered by motion of the heart during its cardiac cycle A technique of post data-acquisition correlation of the angular projection data using the electrocardiogram as a reference signal is described This method produced seven "stop action" images of the heart and resulted in delineating morphological detail not recognizable on the conventional CT scan

Tri-modal regulation of cardiac muscle relaxation; intracellular calcium decline, thin filament deactivation, and cross-bridge cycling kinetics.

Abstract: Cardiac muscle relaxation is an essential step in the cardiac cycle. Even when the contraction of the heart is normal and forceful, a relaxation phase that is too slow will limit proper filling of the ventricles. Relaxation is too often thought of as a mere passive process that follows contraction. However, many decades of advancements in our understanding of cardiac muscle relaxation have shown it is a highly complex and well-regulated process. In this review, we will discuss three distinct events that can limit the rate of cardiac muscle relaxation: the rate of intracellular calcium decline, the rate of thin-filament de-activation, and the rate of cross-bridge cycling. Each of these processes are directly impacted by a plethora of molecular events. In addition, these three processes interact with each other, further complicating our understanding of relaxation. Each of these processes is continuously modulated by the need to couple bodily oxygen demand to cardiac output by the major cardiac physiological regulators. Length-dependent activation, frequency-dependent activation, and beta-adrenergic regulation all directly and indirectly modulate calcium decline, thin-filament deactivation, and cross-bridge kinetics. We hope to convey our conclusion that cardiac muscle relaxation is a process of intricate checks and balances, and should not be thought of as a single rate-limiting step that is regulated at a single protein level. Cardiac muscle relaxation is a system level property that requires fundamental integration of three governing systems: intracellular calcium decline, thin filament deactivation, and cross-bridge cycling kinetics.

Mechanical determinants of myocardial perfusion.

Abstract: Both, the phasic patterns of coronary arterial and venous flow and the time averaged coronary blood flow are strongly influenced by cardiac contraction. The effect is most pronounced at the subendocardium. The time varying stress in the ventricular wall seems to be the most important factor for these effects. However, left ventricular pressure is transmitted into the myocardial wall but its effect is strongest when the wall stresses are low. Left ventricular pressure may be a very important factor when by coronary artery disease a part of myocardium is underperfused. There left ventricular pressure may contribute considerably to the impeding effect. The interactions between arterial pressure as perfusion pressure and force of contraction as impeding pressure are best described by intramyocardial pump models. Although much work in this direction has been done a satisfactory model for the description of mechanical determinants of coronary flow is still lacking.

Apparatus and method for simultaneously displaying relative displacements of a fluctuating biological object

Abstract: X-ray apparatus and method for producing discrete images of a human organ in fluctuating motion, e.g., the heart and related vessels. Each image is derived at a selected time related to the cardiac cycle. The images are independently presented on respective discrete areas within a common image plane. A source of X-rays irradiates the organ. A physiological synchronizer produces timing signals within the cardiac cycle for controlling the periods of transmission of the X-ray beam through the organ during, for example, end diastole and end systole. An antiscattering, masking frame has alternate parallel slits and bars at equal intervals exposing substantially half the area of presentation of an X-ray sensitive film in alternate, equally spaced area strips during, e.g., diastole. The frame is repositioned in response to a signal from the synchronizer for actuating it relative to the film such that the bars then cover the sensitized areas of the film and expose substantially the remaining half of the film during systole. The image elements are interdigitally juxtaposed to present the diastolic and systolic images in an interlaced pattern. Relative displacements of the organ during a cardiac cycle may be determined from the juxtaposed image elements.

Physiological and pathophysiological implications of ventricular/vascular coupling.

Abstract: The purpose of this paper is to consider “ideal” ventricular/vascular coupling, and how this may be manifest in the time domain and in the frequency domain. The paper will also consider how such “ideal” coupling is achieved, and how it might be disturbed. The arterial system plays a crucial role in ventricular/vascular coupling since it separates the smallest vessels where flow is almost perfectly continuous from the ventricle, whose output is intermittent. Ventricular/vascular coupling can be assessed from measurements of pressure and flow in the ascending aorta (AA) (for left ventricle/systemic circulation), and in the main, pulmonary artery (MPA) (for right ventricle/pulmonary circulation). Ideal coupling is manifest as low pressure fluctuation in AA and MPA. Low pressure fluctuation results in pressure during systole being only slightly greater than pressure throughout the whole cardiac cycle, and pressure during diastole being only slightly less. This is desirable because pressure during systole determines ventricular output (when inotropic state and ventricular filling are constant), and ventricular metabolic requirement, while pressure during diastole in AA is a major determinant of coronary blood flow. In the frequency domain, “ideal” coupling is manifest as a correspondence between minimal values of impedance modulus in AA and MPA with maximal values of flow harmonics in AA and MPA, respectively. Factors responsible for “ideal” coupling have been identified as high distensibility of proximal arteries (with decreasing distensibility in peripheral arteries), wave reflection at arterial terminations, and a “match” between heart rate on the one hand and arterial length and wave velocity on the orther. This favourable “match” results in the heart operating for both systemic and pulmonary circulations close to a node of pressure and antinode of flow; this match is improved under conditions which simulate flight and fight. While ventricular/vascular coupling appears to be close to ideal in most large mammals, it appears to be less than ideal in adult humans and some small mammals including guinea pigs, rats, and mice. The cause for mismatch in small mammals is unclear. In humans however, finding are attributable to progressive arterial degeneration which is known to commence in childhood and is apparent in the elderly as dilated tortuous arteries, high pulse pressure, and high likelihood of developing ventricular failure.