Cardiac cycle

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

Transcutaneous measurement of frequency dispersion in the regional pulse wave velocity

Abstract: The pulse wave velocity (PWV) is the propagation speed of the pulsation along the artery due to the heartbeat; its measurement is being reported to estimate the elasticity of the arterial wall for noninvasive diagnosis of arteriosclerosis It is important for advanced diagnosis, to determine the PWV for each frequency and for each instance in time during the cardiac cycle Using a phased tracking method developed, the movement of the arterial wall is accurately tracked and small velocity signals at multiple points in the human carotid artery along a linear-type probe are all simultaneously measured with sub-micrometer accuracy By applying a spatial autoregressive modeling to the measured signals after using the Hilbert transform, the regional PWV of each frequency component was determined at the beginning of the ejection period, T/sub E/, and at the beginning of the ventricular diastole, T/sub D/ The novel detection of the PWV offers potential for quantitative diagnosis of atherosclerosis

Investigating the Role of Interventricular Interdependence in Development of Right Heart Dysfunction During LVAD Support: A Patient-Specific Methods-Based Approach.

Abstract: Predictive computation models offer the potential to uncover the mechanisms of treatments whose actions cannot be easily determined by experimental or imaging techniques. This is particularly relevant for investigating left ventricular mechanical assistance, a therapy for end-stage heart failure, which is increasingly used as more than just a bridge-to-transplant therapy. The high incidence of right ventricular failure following left ventricular assistance reflects an undesired consequence of treatment, which has been hypothesized to be related to the mechanical interdependence between the two ventricles. To investigate the implication of this interdependence specifically in the setting of LVAD support, we introduce a patient-specific finite-element model of dilated chronic heart failure. The model geometry and material parameters were calibrated using patient-specific clinical data, producing a mechanical surrogate of the failing in vivo heart that models its dynamic strain and stress throughout the cardiac cycle. The model of the heart was coupled to lumped-parameter circulatory systems to simulate realistic ventricular loading conditions. Finally, the impact of ventricular assistance was investigated by incorporating a pump with pressure-flow characteristics of an LVAD (HeartMate II™ operating between 8k–12k RPM) in parallel to the left ventricle. This allowed us to investigate the mechanical impact of acute left ventricular assistance at multiple operating-speeds on right ventricular mechanics and septal wall motion. Our findings show that left ventricular assistance reduces myofiber stress in the left ventricle and, to a lesser extent, right ventricle free wall, while increasing leftward septal-shift with increased operating-speeds. These effects were achieved with secondary, potentially negative effects on the interventricular septum which showed that support from left ventricular assistance devices introduces unnatural bending of the septum and with it, increased localized stress regions. Left ventricular assistance unloads the left ventricle significantly and shifts the right ventricular pressure-volume-loop toward larger volumes and higher pressures; a consequence of left-to-right ventricular interactions and a leftward septal shift. The methods and results described in the present study are a meaningful advancement of computational efforts to investigate heart-failure therapies in silico and illustrate the potential of computational models to aid understanding of complex mechanical and hemodynamic effects of new therapies.

The hemodynamic manifestation of normal myocardial relaxation. A framework for experimental and clinical evaluation.

Abstract: Myocardial relaxation clinically manifests itself as left ventricular pressure (LVP) fall. The transition from contraction to relaxation is the precise moment at which 81-84% of peak isometric force has developed or the equivalent timing early during ejection. Defining the completion of relaxation and distinguishing relaxation from diastole appears merely semantic. Diastole is not a passive phase of the cardiac cycle. During diastole mechanical left ventricular properties still change due to incomplete relaxation, due to creep and stress relaxation, and due to autoregulation by preload and by nitric oxide. Description of timing and rate of LVP fall may provide useful information on underlying cardiac diseases such as ischaemia and hypertrophy. This information will however only be reliable if systolic cardiac function and systolic load are normal, and in the absence of a significant degree of nonuniformity, such as induced by conduction disturbances or by regional myocardial ischemia. The various effects of load and of nonuniformity on myocardial relaxation in the normal heart are reviewed. Coupling of timing and rate of LVP fall are explained in terms of cross-bridge mechanics. Specific effects of systolic pressure on LVP fall and their relation to systolic cardiac function are emphasized. These data constitute a conceptual framework for the analysis of myocardial relaxation in cardiovascular research and in the cardiac patient. Comparison of clinical and experimental data during manipulation of afterload should lead to an improved understanding of clinical relaxation disturbances and to a therapeutic approach, which is relevant from the physiopathological point of view. LVP fall may provide useful and quantitative information on systolic LV function if measurements are performed under different conditions of systolic load. This information is similar to systolic pressure-volume relations, but can be performed with the sole use of a micromanometer in the LV cavity.

Cardiac cycle time effects on selection efficiency in vision.

Abstract: The effect of cardiac cycle time on attentional selection was investigated in an experiment in which participants classified target letters in a visual selection task. Stimulus onsets were aligned to the R wave of the electrocardiogram and stimuli presented either during the ventricular systole or diastole. Selection efficiency was operationalized as difference in target selection performance under conditions of homogeneous and heterogeneous distractors. Differences in performance (i.e., the impact selection difficulty had on the ability to select the target) were attenuated for stimuli presented during the ventricular systole compared to the diastole. Increased baroafferent signal transmission during the systole appears to reduce interference of highly distracting stimuli on visual selection efficiency.

Signal detection and the "cardiac arousal cycle".

Abstract: The hypothesis was tested that different phases of the cardiac cycle would be associated with differences in either sensory capacity or response bias, as estimated by signal detection analyses. Each of 10 subjects was given 800 signal (SN) and 800 non-signal (N) trials randomly distributed throughout the cardiac cycle. The signal was a 35 msec duration, 1000 Hz tone, which was preceded by a 1 sec warning light. Electrocardiograph (EKG) cycles were subsequently divided into four phases, and the phase during which the SN or N trial fell was determined. Signal detection analyses performed on auditory sensitivity (d.) and estimate of response bias (Criterion Location) showed no measurable effect of EKG phase on either parameter. Results are discussed in terms of recent neurophysiological findings of cardiac rhythmic input to the nucleus tractus solitarius (which can inhibit cortical arousal), but little cardiac rhythm in the observed output. These considerations imply that “cardiac cycle arousal effects” are likely to be minute or nonexistent.