Cardiac cycle

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

Cardiac Imaging Using Gated Magnetic Resonance

Abstract: To overcome the limitations of magnetic resonance (MR) cardiac imaging using nongated data acquisition, three methods for acquiring a gating signal, which could be applied in the presence of a magnetic field, were tested: an air-filled plethysmograph, a laser-Doppler capillary perfusion flowmeter, and an electrocardiographic gating device. The gating signal was used for timing of MR imaging sequences (IS). Application of each gating method yielded significant improvements in structural MR image resolution of the beating heart, although with both plethysmography and laser-Doppler velocimetry it was difficult to obtain cardiac images from the early portion of the cardiac cycle due to an intrinsic delay between the ECG R wave and peripheral detection of the gating signal. Variations in the temporal relationship between the R wave and plethysmographic and laser-Doppler signals produced inconsistencies in the timing of IS. Since the ECG signal is virtually free of these problems, the preferable gating technique is IS synchronization with an electrocardiogram. The gated images acquired with this method provide sharp definition of internal cardiac morphology and can be temporarily referenced to end diastole and end systole or intermediate points.

Velocity of Blood Flow in Normal Human Venae Cavae

Abstract: The velocity of flow and pressure in the venae cavae of four normal conscious subjects was studied. Velocity was measured with a catheter-tip electromagnetic transducer. The effects of respiration, Valsalva and Muller maneuvers, coughing, and exercise were studied. Caval blood velocities during breath holding showed marked cardiac pulsations, being maximal at the time of ventricular systole and minimal or reversed at atrial systole. Peak velocities during ventricular systole ranged from 30 to 45 cm/sec in the inferior, and from 10 to 35 cm/sec in the superior, vena cava. A second diastolic forward flow velocity ranged from 36 to 76% of the systolic peak. During inspiration, velocity transiently increased. Reduction of flow velocity in abdominal breathing and the Muller maneuver is consistent with the formation of a local area of inferior vena caval collapse at the diaphragm. During the Valsalva maneuver, abrupt reduction in caval flow was seen that persisted throughout the strain. There was immediate overshoot when the strain was released. Coughing produced a reduction of flow velocity with backflow in the superior vena cava. In leg exercise, inferior caval flow velocity rose immediately, and it remained high during recovery. Marked respiratory velocity variations with inspiratory increases occurred during and after exercise.

Regional ventricular wall thickening reflects changes in cardiac fiber and sheet structure during contraction: quantification with diffusion tensor MRI.

Abstract: Dynamic changes of myocardial fiber and sheet structure are key determinants of regional ventricular function. However, quantitative characterization of the contraction-related changes in fiber and sheet structure has not been reported. The objective of this study was to quantify cardiac fiber and sheet structure at selected phases of the cardiac cycle. Diffusion tensor MRI was performed on isolated, perfused Sprague-Dawley rat hearts arrested or fixed in three states as follows: 1) potassium arrested (PA), which represents end diastole; 2) barium-induced contracture with volume (BV+), which represents isovolumic contraction or early systole; and 3) barium-induced contracture without volume (BV-), which represents end systole. Myocardial fiber orientations at the base, midventricle, and apex were determined from the primary eigenvectors of the diffusion tensor. Sheet structure was determined from the secondary and tertiary eigenvectors at the same locations. We observed that the transmural distribution of the myofiber helix angle remained unchanged as contraction proceeded from PA to BV+, but endocardial and epicardial fibers became more longitudinally orientated in the BV- group. Although sheet structure exhibited significant regional variations, changes in sheet structure during myocardial contraction were relatively uniform across regions. The magnitude of the sheet angle, which is an index of local sheet slope, decreased by 23 and 44% in BV+ and BV- groups, respectively, which suggests more radial orientation of the sheet. In summary, we have shown for the first time that geometric changes in both sheet and fiber orientation provide a substantial mechanism for radial wall thickening independent of active components due to myofiber shortening. Our results provide direct evidence that sheet reorientation is a primary determinant of myocardial wall thickening.

Left atrial function: pathophysiology, echocardiographic assessment, and clinical applications

Abstract: This article describes the pathophysiology of left atrial mechanical function and discusses both conventional and new echocardiographic parameters used to evaluate left atrial function. The evidence regarding the clinical usefulness of left atrial function assessment is also presented. Atrial function, in a close interdependence with left ventricular (LV) function, plays a key role in maintaining an optimal cardiac performance. The left atrium (LA) modulates LV filling through its reservoir, conduit, and booster pump function, whereas LV function influences LA function throughout the cardiac cycle. The LA can act to increase LA pressure (in significant atrial disease) and can react to increased LV filling pressure (in significant ventricular disease). LA remodelling is related to LV remodellingw1 and LA function has a central role in maintaining optimal cardiac output despite impaired LV relaxation and reduced LV compliance.1 Understanding how each component of LA function is influenced by LV performance, and how each LA phasic function contributes to maintain an optimal stroke volume in normal and diseased hearts, is important for interpreting data derived from quantification of LA function. During LV systole and isovolumic relaxation, the LA functions as a reservoir, receiving blood from the pulmonary veins and storing energy in the form of pressure. This atrial function is modulated by LV contraction, through the descent of the LV base during systole, by right ventricular systolic pressure transmitted through the pulmonary circulation, and by LA properties (ie, relaxation and chamber stiffness).w2 During early …