Clinical Electrophysiological Mechanisms of Tachycardias Arising from the Atrioventricular Junction

Author(s):  
Demosthenes G. Katritsis ◽  
A. John Camm
Author(s):  
Lian-Yu Lin ◽  
Ting-Tse Lin ◽  
Jien-Jiun Chen ◽  
Jiunn-Lee Lin ◽  
Shoei K. Stephen Huang

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Lubna Bakr ◽  
Hussam AlKhalaf ◽  
Ahmad Takriti

Abstract Background Primary cardiac tumours are extremely rare. Most of them are benign. Sarcomas account for 95% of the malignant tumours. Prognosis of primary cardiac angiosarcoma remains poor. Complete surgical resection is oftentimes hampered when there is extensive tumour involvement into important cardiac apparatus. We report a case of cardiac angiosarcoma of the right atrium and ventricle, infiltrating the right atrioventricular junction and tricuspid valve. Case presentation Initially, a 22-year-old man presented with dyspnoea. One year later, he had recurrent pericardial effusion. Afterwards, echocardiography revealed a large mass in the right atrium, expanding from the roof of the right atrium to the tricuspid valve. The mass was causing compression on the tricuspid valve, and another mass was seen in the right ventricle. Complete resection of the tumour was impossible. The mass was resected with the biggest possible margins. The right atrium was reconstructed using heterologous pericardium. The patient’s postoperative course was uneventful. Postoperative echocardiography showed a small mass remaining in the right side of the heart. Histopathology and immunohistochemistry confirmed the diagnosis of angiosarcoma. The patient underwent adjuvant chemotherapy and radiotherapy later on. He survived for 1 year and 5 days after the surgery. After a diagnosis of lung and brain metastases, he ended up on mechanical ventilation for 48 h and died. Conclusions Surgical resection combined with postoperative chemotherapy and radiotherapy is feasible even in patients with an advanced stage of cardiac angiosarcoma when it is impossible to perform complete surgical resection.


1985 ◽  
Vol 55 (1) ◽  
pp. 194-198 ◽  
Author(s):  
Melvin M. Scheinman ◽  
Saroja Bharati ◽  
Yin-Shi Wang ◽  
William A. Shapiro ◽  
Maurice Lev

Author(s):  
Shan Ling ◽  
Michael W Jenkins ◽  
Michiko Watanabe ◽  
Stephanie M Ford ◽  
Andrew M Rollins

The etiology of ethanol-related congenital heart defects has been the focus of much study, but most research has concentrated on cellular and molecular mechanisms. We have shown with optical coherence tomography (OCT) that ethanol exposure led to increased retrograde flow and smaller atrioventricular (AV) cushions compared to controls. Since AV cushions play a role in patterning the conduction delay at the atrioventricular junction (AVJ), this study aims to investigate whether ethanol exposure alters the AVJ conduction in early looping hearts and whether this alteration is related to the decreased cushion size. Quail embryos were exposed to a single dose of ethanol at gastrulation, and Hamburger-Hamilton stage 19 - 20 hearts were dissected for imaging. Cardiac conduction was measured using an optical mapping microscope and we imaged the endocardial cushions using OCT. Our results showed that, compared with controls, ethanol-exposed embryos exhibited abnormally fast AVJ conduction and reduced cushion size. However, this increased conduction velocity (CV) did not strictly correlate with decreased cushion volume and thickness. By matching the CV map to the cushion size map, we found that the slowest conduction location was consistently at the atrial side of the AVJ, which had the thinner cushions, not at the thickest cushion location at the ventricular side as expected. Our findings reveal regional differences in the AVJ myocardium even at this early stage in heart development. These findings reveal the early steps leading to the heterogeneity and complexity of conduction at the mature AVJ, a site where arrhythmias can be initiated.


1977 ◽  
Vol 233 (5) ◽  
pp. H535-H540
Author(s):  
L. S. D'Agrosa

The effects of ventrolateral and ventromedial cardiac nerve (left sympathetics) stimulation on cardiac force, on rate, and on arrhythmogenic responses were characterized and quantitated. The stimulation of left sympathetic nerves produced augmentation in cardiac contraction in 45% of the experiments, an augmentation of both a cardiac rate and force in 47%, and in cardioacceleration alone in 8%. Two characteristic patterns of arrhythmogenic responses were elicited from stimulations of 100 sympathetic nerves. The two types of neurally induced arrhythmias were atrioventricular junctional or ventricular in origin. The onset and duration of the arrhythmias were quantitated. Both types of neurally induced arrhythmias were prevented either by blocking the beta receptors with propranolol or by preventing the neural release of norepinephrine with bretylium tosylate. The neurally induced arrhythmias were probably the result of enhanced automaticity in the atrioventricular junction area and in the ventricles produced by stimulating the sympathetic nerve fibers. This report thus implicates the ventromedial cardiac nerve in the genesis of cardiac arrhythmias.


Sign in / Sign up

Export Citation Format

Share Document