Topic
Cardiac cycle
About: Cardiac cycle is a(n) research topic. Over the lifetime, 3290 publication(s) have been published within this topic receiving 96159 citation(s).
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TL;DR: Specified regions of the myocardium can be labeled in magnetic resonance (MR) imaging to serve as markers during contraction, thus permitting sampling of the entire contractile phase of the cardiac cycle.
Abstract: Specified regions of the myocardium can be labeled in magnetic resonance (MR) imaging to serve as markers during contraction. The technique is based on locally perturbing the magnetization of the myocardium with selective radio-frequency (RF) saturation of multiple, thin tag planes during diastole followed by conventional, orthogonal-plane imaging during systole. The technique was implemented on a 0.38-T imager and tested on phantoms and volunteers. In humans, tags could be seen 60-450 msec after RF saturation, thus permitting sampling of the entire contractile phase of the cardiac cycle. Tagged regions appear as hypointense stripes, and their patterns of displacement reflect intervening cardiac motion. In addition to simple translation and rotation, complex motions such as cardiac twist can be demonstrated. The effects of RF pulse angle, relaxation times, and heart rate on depiction of the tagged region are discussed.
1,479 citations
TL;DR: The heartbeat is a sign of life, and not surprisingly it has attracted much interest and curiosity since the early stages of scientific investigation, but a search for the basis of spontaneous cardiac activity could only be undertaken several centuries after primitive observations with the development of techniques that allowed the study of the electrical properties of excitable tissues.
Abstract: The heartbeat is a sign of life, and not surprisingly it has attracted much interest and curiosity since the early stages of scientific investigation. Even Leonardo da Vinci, in his anatomical studies, realized that rhythmic, restless activity was an intrinsic property of cardiac muscle (92), "As to the heart: it moves itself, and doth never stop, except it be for eternity." In fact, a search for the basis of spontaneous cardiac activity could only be undertaken several centuries after these primitive observations with the development of techniques that allowed the study of the electrical properties of excitable tissues and particularly of cardiac muscle (18, 71,77,23). Cardiac pacemaker activity originates in specialized myocytes located in restricted areas of the heart that are characterized by the ability to beat spontaneously even when separated from the rest of the cardiac muscle (24, 106, 103, 11, 81). Voltage-clamp investigation of pacemaker tissue opened the way to a better understanding of the ionic mechanisms promoting rhythmicity in pacemaker tissue (64, 6). In pacemaker cells of the mammalian sino-atrial (SA) node, spontaneous activity results from a typical phase of their action potential, the slow diastolic depolarization. The concept that a slow depolarization is an inherent property of spontaneously active myocar dium is an old one that has been actively investigated since the first recordings of cardiac electrical activity revealed the existence of a slow depolarizing phase preceding the action potential onset in beating tissue (for a review, see 105). During this phase, corresponding to diastole of the cardiac contraction cycle, the membrane slowly depolarizes following termination of an action potential, until threshold for a new action potential is reached. Thus, the
815 citations
TL;DR: The changes in ion channel and transporter properties associated with three important clinical and experimental paradigms: congestive heart failure, myocardial infarction, and atrial fibrillation are reviewed and important opportunities for improved therapeutic approaches are highlighted.
Abstract: Rhythmic and effective cardiac contraction depends on appropriately timed generation and spread of cardiac electrical activity. The basic cellular unit of such activity is the action potential, whi...
719 citations
Book•
01 Jan 1991
TL;DR: Overview of the Cardiovascular System: Excitation, Contraction and Relaxation Control of Blood Vessels, Specialization in Individual Circulations, Coordinated Cardiovascular Responses in Pathological Situations.
Abstract: Overview of the Cardiovascular System The Cardiac Cycle The Cardiac Myocyte: Excitation and Contraction Initiation and Nervous Control of Heartbeat Electrocardiography and Arrhythmias Control of Stroke Volume and Cardiac Output Assessment of Cardiac Output and Peripheral Pulse Haemodynamics: Flow, Pressure and Resistance The Endothelial Cell The Microcirculation and Solute Exchange Circulation of Fluid Between Plasma, Interstitium and Lymph Vascular Smooth Muscle: Excitation, Contraction and Relaxation Control Of Blood Vessels: I Intrinsic Control Control Of Blood Vessels: II Extrinsic Control by Nerves and Hormones Specialization in Individual Circulations Cardiovascular Receptors, Reflexes and Central Control Coordinated Cardiovascular Responses Cardiovascular Responses in Pathological Situations
617 citations
TL;DR: PRFR is determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index ofleft ventricular diastolic function.
Abstract: Peak rapid filling rate (PRFR) is often used clinically as an index of left ventricular relaxation, i.e., of early diastolic function. This study tests the hypothesis that early filling rate is a function of the atrioventricular pressure difference and hence is influenced by the left atrial pressure as well as by the rate of left ventricular relaxation. As indexes, we chose the left atrial pressure at the atrioventricular pressure crossover (PCO), and the time constant (T) of an assumed exponential decline in left ventricular pressure. We accurately determined the magnitude and timing of filling parameters in conscious dogs by direct measurement of phasic mitral flow (electromagnetically) and high-fidelity chamber pressures. To obtain a diverse hemodynamic data base, loading conditions were changed by infusions of volume and angiotensin II. The latter was administered to produce a change in left ventricular pressure of less than 35% (A-1) or a change in peak left ventricular pressure of greater than 35% (A-2). PRFR increased with volume loading, was unchanged with A-1, and was decreased with A-2; T and PCO increased in all three groups (p less than .005 for all changes). PRFR correlated strongly with the diastolic atrioventricular pressure difference at the time of PRFR (r = .899, p less than .001) and weakly with both T (r = .369, p less than .01) and PCO (r = .601, p less than .001). The correlation improved significantly when T and PCO were both included in the multivariate regression (r = .797, p less than .0001). PRFR is thus determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index of left ventricular diastolic function.
607 citations