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Arrhythmias in acute coronary syndrome
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Phase I VT/VF occurs early when myocardial injury is still reversible and is associated with either ischaemia of large areas of the myocardium or with reperfusion injury where myocardial reperfusion results in cellular oedema and endothelial dysfunction. In contrast, phase II VT/VF occurs during the stage of infarct evolution. The damaged Purkinje fibre cells develop increased automaticity, resulting in re-entrant circuits within the ventricular myocardium [9].
Renal, Cardiovascular, and Pulmonary Functions of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The cardiovascular system is composed of the heart and the circulatory system. The heart, composed of ventricles and atria, works as a pump that pushes blood to organs, tissues, and cells. The blood delivers oxygen and nutrients to every cell in the body and removes the carbon dioxide and waste products made by those cells. The muscle mass of the heart, the myocardium, shares structural and functional characteristics of both smooth and skeletal muscle. The cardiomyocytes are rather small cells that form the highly branched network of the functional syncytium, which acts together mechanically and electrically. The atrial and ventricular muscle tissue are structurally similar but differ in their electrical properties. In addition to these, the heart has conducting tissue (Purkinje fibers) which is adapted for rapid and efficient conduction of action potential as well as sinoatrial and atrioventricular nodes that are involved in the initiation and conduction of the heartbeat.
Catheter Ablation of Ventricular Fibrillation and Polymorphic Ventricular Tachycardia
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Amin Al-Ahmad, Carola Gianni, Andrea Natale
VF poses a risk in both in the setting of acute myocardial infarction (AMI) and in the natural history of chronic ischemic heart disease, after scar formation. Once again, the Purkinje fibers and their ability to survive transmural myocardial infarction play an important role.24
De Winter electrocardiographic pattern in a young patient with acute myocardial infarction
Published in Baylor University Medical Center Proceedings, 2023
De Winter et al suggested different explanations for this ECG pattern. The presence of an anatomical variant of the Purkinje fibers, with endocardial conduction delay, could be a mechanism. Alternatively, ischemic ATP depletion may lead to lack of activation of sarcolemmal ATP-sensitive potassium channels, which can explain the lack of ST segment elevation, as has been shown in KATP knockout animal models of acute ischemia.3 Verouden et al suggested that the area of transmural ischemia might be so large that the injury current is directed toward lead aVR and away from the precordial leads.4 Some patients exhibiting the de Winter’s pattern who are not immediately reperfused may go on to develop overt ST elevation as well as Q waves.5–7 Many patients show a static pattern until the time of reperfusion despite ongoing ischemia for prolonged periods of time. This suggests that this pattern may lie somewhere along the continuum of ischemic ECG changes between subendocardial ischemia and the transmural infarction associated with ST elevation.7
Predicting the cardiac toxicity of drugs using a novel multiscale exposure–response simulator
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2018
Francisco Sahli Costabal, Jiang Yao, Ellen Kuhl
the L-type calcium current 1, right, illustrates the single-cell action potential for human Purkinje cells. Figure 2 shows the distribution of the Purkinje fiber network across the endocardial wall.
Histopathology of the Conduction System in Long QT Syndrome
Published in Fetal and Pediatric Pathology, 2022
Alexandra Rogers, Rachel Taylor, Janet Poulik, Bahig M. Shehata
The examination of the conduction system follows a specific protocol at our institution. Following IRB approval for this study, we used this standard procedure to examine section(s) from the SA node, AV node, and internodal tracts from the superior aspect to inferior aspect. We evaluated the bundle of His and Purkinje fibers from routine sections obtained from the right and left ventricles. All sections were stained with H&E and Masson Trichrome. The matched controls with comparable age, sex, and ethnic background who died of extracardiac causes were evaluated using the same methods. Depending on the size of a heart, between one to two blocks of the SA node can normally be evaluated. Here, we were able to section one block of the SA node which contained two to three fragments of tissue. Two blocks from the AV node containing three to four pieces of tissue were also evaluated. The thickness and amount of fibrosis of the conduction system fibers from the LQTS patients were compared to controls. Fibrosis was quantified by pathologist visualization of increased Trichrome distribution in the three LQTS patients compared to controls. Comparison of fiber size (atrophy) was performed with an eyepiece containing a microscale. Four measurements were taken from each photographed section of cardiac tissue. The number four was selected due to limitation of the amount of cardiac fibers in the internodal tracts. One-sided student’s t-tests were performed to determine statistical significance of fiber size in our LQTS patients against control patients. With degrees of freedom = 3, statistical significance with a p-value of 0.05 is proven with a t-test value less (more negative) than −3.182.