Cardiac cycle

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

Abnormal Mitral Valve Motion in Patients with Elevated Left Ventricular Diastolic Pressures

Abstract: In order to see whether or not the echocardiographically recorded mitral valve could reflect alterations in left ventricular pressure, simultaneous mitral valve echograms and left ventricular pressures were obtained on patients undergoing diagnostic cardiac catheterization. Attention was given to the left ventricular initial diastolic pressure (LVIDP), left ventricular end-diastolic pressure (LVEDP), and the atrial component of the left ventricular pressure (LVa). The echocardiographic measurements included the opening velocity of the mitral valve in early diastole (D-E slope) and the interval between the A point, which is the onset of closure of the mitral valve following atrial systole, and the C point, which represents closure of the mitral valve as indicated by the meeting of the anterior and posterior mitral leaflets. In order to compensate for variations in atrioventricular conduction, the A-C interval was subtracted from the electrocardiographic P-R interval. In 19 patients, the LVIDP was less than...

Cardiac conduction is required to preserve cardiac chamber morphology

Abstract: Electrical cardiac forces have been previously hypothesized to play a significant role in cardiac morphogenesis and remodeling. In response to electrical forces, cultured cardiomyocytes rearrange their cytoskeletal structure and modify their gene expression profile. To translate such in vitro data to the intact heart, we used a collection of zebrafish cardiac mutants and transgenics to investigate whether cardiac conduction could influence in vivo cardiac morphogenesis independent of contractile forces. We show that the cardiac mutant dcos226 develops heart failure and interrupted cardiac morphogenesis following uncoordinated ventricular contraction. Using in vivo optical mapping/calcium imaging, we determined that the dco cardiac phenotype was primarily due to aberrant ventricular conduction. Because cardiac contraction and intracardiac hemodynamic forces can also influence cardiac development, we further analyzed the dco phenotype in noncontractile hearts and observed that disorganized ventricular conduction could affect cardiomyocyte morphology and subsequent heart morphogenesis in the absence of contraction or flow. By positional cloning, we found that dco encodes Gja3/Cx46, a gap junction protein not previously implicated in heart formation or function. Detailed analysis of the mouse Cx46 mutant revealed the presence of cardiac conduction defects frequently associated with human heart failure. Overall, these in vivo studies indicate that cardiac electrical forces are required to preserve cardiac chamber morphology and may act as a key epigenetic factor in cardiac remodeling.

Non-invasive method and device to monitor cardiac parameters

Abstract: A method of and a device for non-invasively measuring the hemodynamic state of a subject or a human patient involve steps and units of non-invasively measuring cardiac cycle period, electrical-mechanical interval, mean arterial pressure, and ejection interval and converting the measured electrical-mechanical interval, mean arterial pressure and ejection interval into the cardiac parameters such as Preload, Afterload and Contractility, which are the common cardiac parameters used by an anesthesiologist. The converted hemodynamic state of a patient is displayed on a screen as a three-dimensional vector with each of its three coordinates respectively representing Preload, Afterload and Contractility. Therefore, a medical practitioner looks at the screen and quickly obtains the important and necessary information.

Method and device for enhancement of cardiac contractility

Abstract: An apparatus for ultrasonic irradiation of the heart either when the chest is open after surgery or through the chest wall. It may also be used in conjunction with electrical defibrillation equipment or alone. The apparatus includes an EKG for detecting the heart beat, an ultrasonic generator and timing and pulsing circuits for providing timed pulses of ultrasound to coincide with selected events in the cardiac cycle.

Enzyme replacement therapy with agalsidase β improves cardiac involvement in Fabry's disease

Abstract: Fabry's disease is an X-linked lysosomal storage disease caused by a deficiency of alpha-galactosidase that results in an accumulation of neutral glycosphingolipids throughout the body, including the cardiovascular system. Fabry cardiomyopathy, characterized by progressive severe concentric left ventricular (LV) hypertrophy, is very frequent and is the most important cause of death in affected patients. Enzyme replacement therapy (ERT) allows a specific treatment for this disease, however, there are very few data on the effectiveness of therapy on cardiac involvement. Nine patients with Fabry cardiac disease were studied on basal condition and after 6 and 12 months of treatment with algasidase beta (Fabrazyme). A complete clinical, electrocardiographic and echocardiographic evaluation was performed in all patients. Interpretable Doppler recordings of transmitral flow and pulmonary flow velocity curves were also acquired. At baseline, the patients with Fabry's disease had increased LV septum and posterior wall thickness, normal LV fractional shortening, LV ejection fraction, normal Doppler parameters of mitral inflow but a duration of pulmonary vein flow velocity wave exceeding that of the mitral wave at atrial systole. ERT did not affect heart rate and arterial pressure. LV internal diameters did not change, there was a slight but not significant decrease in the LV posterior wall thickening and a progressive decrease in the interventricular septum thickening (p < 0.025) and in LV mass (p < 0.001) The difference in duration between pulmonary vein flow velocity wave and mitral wave at atrial systole significantly decreased (p < 0.001). These results suggest that ERT in patients with Fabry cardiomyopathy is able to reduce the LV mass and ameliorate the LV stiffness.