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Cardiac cycle

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


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TL;DR: This issue of the JCI, Grant and colleagues investigate the manifestations of phenotypically opposite and overlapping cardiac arrhythmogenic syndromes that surprisingly stem from the same mutation.
Abstract: Normal cardiac excitation and relaxation involves a delicate balance of complex dynamic interactions between ionic currents passing through a variety of membrane channels and the cellular environment. Genetic defects, polymorphisms, therapeutic intervention or structural abnormalities can disrupt this balance and underlie severe arrhythmogenic phenotypes that lead to sudden cardiac death. Inheritable gene defects give rise to phenotypic variation and an unpredictable manifestation of syndromes, ranging from silent gene carriers to profoundly symptomatic individuals, even within single families (1–7). As such, realizing the relationship between genetic mutations and clinical syndromes is becoming increasingly complex. In this issue of the JCI, Grant and colleagues (3) investigate the manifestations of phenotypically opposite and overlapping cardiac arrhythmogenic syndromes that surprisingly stem from the same mutation (1–4). Cardiac excitation reflects membrane depolarization of cardiac myocytes, primarily due to the activation of fast voltage-dependent Na+ channels that underlie the action potential upstroke. Activation is followed by a long depolarized plateau phase that permits Ca2+-induced Ca2+ release from the sarcoplasmic reticulum, binding of Ca2+ to contractile proteins on the sarcomeres, and coordinated contraction. Repolarization follows due to the time- and voltage-dependent activation of repolarizing potassium currents. Relaxation of contraction is coupled to the electrical repolarization phase, which allows filling of the ventricles prior to the next excitation. Each of these electrical processes can be detected on the body surface electrocardiogram (ECG) as a signal average of the temporal and spatial gradients generated during each phase (8–11) (Figure ​(Figure1a).1a). Electrical excitation gradients in the atria (atrial depolarization) manifest on the ECG as P waves, while gradients of ventricular depolarization are seen as the QRS complex. Gradients in ventricular repolarization are reflected in the T wave (Figure ​(Figure11). Figure 1 Electrical gradients in the myocardium can be detected on the body surface ECG. (a) An illustrative example of a single cardiac cycle detected as spatial and temporal electrical gradients on the ECG. The P wave is generated by the spread of excitation ... A recently described example of a multi-syndrome genetic defect in the SCN5A gene, encoding the cardiac Na+ channel (Figure ​(Figure2),2), is the insertion of an aspartic acid, 1795insD, in the C-terminus of the cardiac Na+ channel that underlies both Brugada (BrS) and Long-QT (LQTs) cardiac arrhythmic syndromes (1, 2). Figure 2 The predicted transmembrane topology of domains I–IV of the cardiac Na+ channel α subunit encoded by SCN5A showing the location and nature of the mutations inducing LQTs, BrS, and isolated cardiac conduction disease. Grant and colleagues investigate an even more complex mutation (3). The deletion of lysine, ΔK1500, in the III–IV linker of SCN5A (Figure ​(Figure2)2) is associated with BrS, LQTs, and isolated cardiac conduction disease (ICCD). LQTs is typically associated with a gain of Na+ channel function that stems from mutation induced destabilization of channel inactivation, leading to a persistent inward Na+ current (INa) during the action potential (AP) plateau and prolonged repolarization (12, 13). Paradoxically, BrS and ICCD are linked to a loss of Na+ channel function and a resulting reduction in macroscopic current (3, 6, 7, 14, 15). How can multiple and seemingly contradictory arrhythmic syndromes arise from a mutation at a single locus?

62 citations

Journal ArticleDOI
TL;DR: The combined dynamic and imaging data show the developing structural capacity to accommodate increasing flow and the mechanotransducing networks that organize to effectively facilitate formation of the trabeculated four-chambered heart.
Abstract: Analyses of form-function relationships during heart looping are directly related to technological advances. Recent advances in four-dimensional optical coherence tomography (OCT) permit observations of cardiac dynamics at high-speed acquisition rates and high resolution. Real-time observation of the avian stage 13 looping heart reveals that interactions between the endocardial and myocardial compartments are more complex than previously depicted. Here we applied four-dimensional OCT to elucidate the relationships of the endocardium, myocardium, and cardiac jelly compartments in a single cardiac cycle during looping. Six cardiac levels along the longitudinal heart tube were each analyzed at 15 time points from diastole to systole. Using image analyses, the organization of mechanotransducing molecules, fibronectin, tenascin C, α-tubulin, and nonmuscle myosin II was correlated with specific cardiac regions defined by OCT data. Optical coherence microscopy helped to visualize details of cardiac architectural development in the embryonic mouse heart. Throughout the cardiac cycle, the endocardium was consistently oriented between the midline of the ventral floor of the foregut and the outer curvature of the myocardial wall, with multiple endocardial folds allowing high-volume capacities during filling. The cardiac area fractional shortening is much higher than previously published. The in vivo profile captured by OCT revealed an interaction of the looping heart with the extra-embryonic splanchnopleural membrane providing outside-in information. In summary, the combined dynamic and imaging data show the developing structural capacity to accommodate increasing flow and the mechanotransducing networks that organize to effectively facilitate formation of the trabeculated four-chambered heart.

62 citations

Journal ArticleDOI
TL;DR: Recent advances in the clinical use of applied potential tomography (APT), or electrical impedance imaging, showed that the APT system gives a good soft-tissue contrast and has good sensitivity to resistivity changes, and it is concluded that the origin of thoracic impedance changes related to cardiac activity can be deduced from APT images.
Abstract: The existence of variations of normal human thoracic impedance, during the cardiac cycle to high frequency electrical current is well known. Since the impedance variations within the thorax are synchronous with the electrocardiogram (ECG), they are attributed to cardiac activity. They can arise from the change of either the rate of blood flow or the blood volume in the heart chambers, the great blood vessels and the lungs. However, their relative contribution is not known. Many investigators have worked on the non-invasive determination of some cardiac parameters using surface electrode impedance measurements on the thorax. Since the relationships between the measurement results and the pulsatile circulation of blood in various organs inside the chest are not well known, the information determined by surface impedance measurements is not as accurate as the results of invasive techniques. Recent advances in the clinical use of applied potential tomography (APT), or electrical impedance imaging, showed that the APT system gives a good soft-tissue contrast and has good sensitivity to resistivity changes. It is therefore concluded that the origin of thoracic impedance changes related to cardiac activity can be deduced from APT images. Our initial studies of ECG gated dynamic APT images of the thorax show that cardiac related thoracic impedance variations originating from different organs can be separated. Sequential APT images of the thorax during the cardiac cycle are presented. The movement of blood from the ventricles to the lungs and vascular system and back to the ventricles is observable in these images.(ABSTRACT TRUNCATED AT 250 WORDS)

62 citations

Journal ArticleDOI
TL;DR: PV motion during systole may be instantaneously determined by PA flow change and the PA-RV pressure gradient during the cardiac cycle in experimental pulmonary hypertension.
Abstract: To clarify the determinants of pulmonary valve (PV) motion in pulmonary hypertension, we examined the correlations among PV echo patterns, the pulmonary artery (PA) flow curve just above the PA orifice and the pulmonary artery-right ventricle (PA-RV) pressure gradient. By constricting the PA, we could produce a variety of PV echo patterns, including midsystolic semiclosure in open-chest dogs. Throughout the experiments, the PV echo pattern and PA flow curve were similar in pattern and timing. When the PV echo showed midsystolic semiclosure with reopening. The PA flow curve showed a transient decrease followed by a transient increase during midsystole. The PA-RV pressure gradient became transiently positive (PA pressure greater than RV pressure) and then negative in midsystole only when the PV echo showed midsystolic semiclosure with reopening. In conclusion, PV motion during systole may be instantaneously determined by PA flow change and the PA-RV pressure gradient during the cardiac cycle in experimental pulmonary hypertension.

62 citations

Journal Article
TL;DR: In this paper, a finite element (FE) mechanical model of the left ventricle (LV) was used to simulate both normal and abnormal cardiac motions in the 4D NURBS-based Cardiac Torso (NCAT) phantom.
Abstract: The 4D NURBS-based Cardiac-Torso (NCAT) phantom, which provides a realistic model of the normal human anatomy and cardiac and respiratory motions, is used in medical imaging research to evaluate and improve imaging devices and techniques, especially dynamic cardiac applications. One limitation of the phantom is that it lacks the ability to accurately simulate altered functions of the heart that result from cardiac pathologies such as coronary artery disease (CAD). The goal of this work was to enhance the 4D NCAT phantom by incorporating a physiologically based, finite-element (FE) mechanical model of the left ventricle (LV) to simulate both normal and abnormal cardiac motions. The geometry of the FE mechanical model was based on gated high-resolution x-ray multi-slice computed tomography (MSCT) data of a healthy male subject. The myocardial wall was represented as transversely isotropic hyperelastic material, with the fiber angle varying from -90 degrees at the epicardial surface, through 0 degrees at the mid-wall, to 90 degrees at the endocardial surface. A time varying elastance model was used to simulate fiber contraction, and physiological intraventricular systolic pressure-time curves were applied to simulate the cardiac motion over the entire cardiac cycle. To demonstrate the ability of the FE mechanical model to accurately simulate the normal cardiac motion as well abnormal motions indicative of CAD, a normal case and two pathologic cases were simulated and analyzed. In the first pathologic model, a subendocardial anterior ischemic region was defined. A second model was created with a transmural ischemic region defined in the same location. The FE based deformations were incorporated into the 4D NCAT cardiac model through the control points that define the cardiac structures in the phantom which were set to move according to the predictions of the mechanical model. A simulation study was performed using the FE-NCAT combination to investigate how the differences in contractile function between the subendocardial and transmural infarcts manifest themselves in myocardial SPECT images. The normal FE model produced strain distributions that were consistent with those reported in the literature and a motion consistent with that defined in the normal 4D NCAT beating heart model based on tagged MRI data. The addition of a subendocardial ischemic region changed the average transmural circumferential strain from a contractile value of 0.19 to a tensile value of 0.03. The addition of a transmural ischemic region changed average circumferential strain to a value of 0.16, which is consistent with data reported in the literature. Model results demonstrated differences in contractile function between subendocardial and transmural infarcts and how these differences in function are documented in simulated myocardial SPECT images produced using the 4D NCAT phantom. In comparison to the original NCAT beating heart model, the FE mechanical model produced a more accurate simulation for the cardiac motion abnormalities. Such a model, when incorporated into the 4D NCAT phantom, has great potential for use in cardiac imaging research. With its enhanced physiologically-based cardiac model, the 4D NCAT phantom can be used to simulate realistic, predictive imaging data of a patient population with varying whole-body anatomy and with varying healthy and diseased states of the heart that will provide a known truth from which to evaluate and improve existing and emerging 4D imaging techniques used in the diagnosis of cardiac disease.

61 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202377
2022178
202169
202068
201979
201876