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Ventricular Chamber (ventricular + chamber)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Left Ventricular Non Compaction in Children

CONGENITAL HEART DISEASE, Issue 5 2010
Sara H. Weisz MD
ABSTRACT Left ventricular non compaction (LVNC) is a myocardial disease characterized by a hypertrabeculated myocardium. The hypertrabeculations in the left ventricular wall define deep recesses communicating with the left ventricular chamber where blood penetrates with increased risk of blood clots in the meshwork of the prominent trabeculations. The left ventricular apex and the free wall are particularly affected. During in utero ventriculogenesis, myocardial blood supply is initially linked to the presence of sinusoids, in which blood penetrates and diffuses nutriments and oxygen to myocardial cells. Progressively, with the development of the heart and the increase of cells demand of blood, coronary arteries system develops. This step is associated with myocardial modification that leads to compaction of hypertrabeculated myocardial net. Probably, the premature interruption of this process leads to ventricular noncompaction. Many studies have been conducted in adults with hypertrabeculated myocardium. To date, data regarding childhood LVNC are sparse. The aim of this review is to summarize the clinical and preclinical knowledge about LVNC in children. [source]

A New Pulsatile Volumetric Device With Biomorphic Valves for the In Vitro Study of the Cardiovascular System

ARTIFICIAL ORGANS, Issue 12 2009
Ettore Lanzarone
Abstract A pulsatile mock loop system was designed and tested. This prototype represents a versatile, adjustable, and controllable experimental apparatus for in vitro studies of devices meant to interface with the human circulatory system. The pumping system consisted of a ventricular chamber featuring two biomorphic silicone valves as the inlet and outlet valves. The chamber volume is forced by a piston pump moved by a computer-controlled, low-inertia motor. Fluid dynamic tests with the device were performed to simulate physiological conditions in terms of cardiac output (mean flow of 5 and 6 L/min, with beat rates from 60 to 80 bpm), of rheological properties of the processed fluid, and of systemic circulation impedance. The pulsating actuator performed a good replication of the physiological ventricular behavior and was able to guarantee easy control of the waveform parameters. Experimental pressure and flow tracings reliably simulated the physiological profiles, and no hemolytic subatmospheric pressures were revealed. The performance of the prototype valves was also studied in terms of dynamic and static backflow, effective orifice area, and pressure loss, resulting in their applicability for this device. Mechanical reliability was also tested over 8 h. The device proved to be a reliable lab apparatus for in vitro tests; the pumping system also represents a first step toward a possible future application of pulsating perfusion in the clinic arena, such as in short-term cardiac assist and pulsatile cardiopulmonary bypass. [source]

Defibrillation Causes Immediate Cardiac Dilation in Humans

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003
Erin Sylvester B.S.
Introduction: Prior studies in isolated heart tissue have shown both excitation and deexcitation to be the primary mechanism of defibrillation. This article presents the first evidence in man of deexcitation immediately following defibrillation by tracking the heart's mechanical response. Methods and Results: The geometric changes of the ventricular chambers were measured before and after defibrillation in seven human subjects receiving an implantable cardioverter defibrillator (ICD). The ICD was used to produce approximately three episodes of ventricular fibrillation and defibrillation in each subject. Twenty-two two-dimensional echocardiographic images of the right ventricle (RV) and 11 images of the left ventricle (LV) were recorded and analyzed at 30 frames per second. Just over 2 seconds of each episode were digitized, beginning half a second before the defibrillation shock. Individual frames were analyzed to yield cross-sectional, ventricular chamber area as a function of time. Immediately following defibrillation, ventricular chambers dilated with significant fractional area increase (RV: 1.58 ± 0.25, LV: 1.10 ± 0.06), with peak dilation at 194 ± 114 msec. Conclusion: Defibrillation causes a rapid increase in ventricular chamber area due to relaxation of the myocardium, suggesting that defibrillation synchronizes the cardiac cells to the deexcited state in man. (J Cardiovasc Electrophysiol, Vol. 14, pp. 832-836, August 2003) [source]

Aortic and ventricular dilation and myocardial reduction in gestation day 17 ICR mouse fetuses of diabetic mothers

BIRTH DEFECTS RESEARCH, Issue 6 2007
J. Claudio Gutierrez
Abstract BACKGROUND: Maternal diabetes mellitus is associated with increased fetal teratogenesis, including cardiovascular defects. Information regarding cardiovascular changes in late-gestation fetal mice, related to maternal hyperglycemia, is not present in the literature. METHODS: Late-gestation fetal heart and great vessel morphology were analyzed in fetuses from control and diabetic mice. Female ICR mice were injected with streptozocin (200 mg/kg IP) prior to mating to induce diabetes (n = 8). Nonhyperglycemic females were used as controls (n = 8). At day 17 of gestation, females were euthanized and one fetus was arbitrarily selected per litter to analyze the heart and great vessels. Six additional fetuses from different litters, showing external malformations (spina bifida and/or exencephaly), were also evaluated from the diabetic group. Fetal thoraxes were processed using routine histopathologic techniques, and 7-,m transversal sections were stained with hematoxylin-eosin. Digital images of sections were made and analyzed using NIH Image J software to compare regional cardiac development. Student's t tests for means were performed to determine differences between groups (p < .05). RESULTS: Maternal hyperglycemia caused a dilation of late-gestation fetal ventricular chambers, a reduction of total ventricular myocardial area, and an increase in transversal ascending thoracic aortic area. Three of six fetuses that displayed external malformations showed an overt cardiac defect, beyond the ventricular and myocardial changes. CONCLUSIONS: Maternal hyperglycemia altered morphology of the late-gestation fetal mouse heart. Postnatal persistence or consequences of late-gestation heart chamber dilation and myocardial reduction are not yet known. Birth Defects Research (Part A) 2007. © 2007 Wiley-Liss, [source]