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The heart
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
The specialized excitation and electrical conduction system in the heart consists of: Sinoatrial nodeInteratrial pathwayInternodal pathwayAtrioventricular nodeBundle of HisBundle branchesPurkinje fibers
Correlation between HCN4 gene polymorphisms and lone atrial fibrillation risk
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Xiao-Hong Li, Ya-Min Hu, Guang-Li Yin, Ping Wu
Relevant studies have indicated that atrial remodelling is the main pathogenesis for AF. Atrial remodelling includes atrial electrical remodelling (AER), systolic function reconstruction and atrial structural remodelling. Close association is observed between AF and AER [9]. A part of researches show that AER is caused by AF [10,11], while, other studies suggest that AER is the reason for AF onset [12,13]. Another view regards that AF develops secondary to sustaining atrial structural and electrical remodelling which is induced by AF itself [9]. Multiple theories have been proposed to explain the pathogenesis of AF. Sinoatrial node (SA node) of the heart generates the impulse, thereby, could regulate the electrical conduction system of the heart. Potential changes of SA node cells might lead to the abnormal impulse, finally result in arrhythmia including AF.
Cardiac manifestations in Finnish gelsolin amyloidosis patients
Published in Amyloid, 2021
Tuuli Mustonen, Arttu Holkeri, Miia Holmström, Sari Atula, Sami Pakarinen, Lauri Lehmonen, Sari Kiuru-Enari, Aapo L. Aro
CMR is a useful test for diagnosing cardiac amyloidosis, with 86% sensitivity and 92% specificity in AL and ATTR amyloidosis [20]. However, in this cohort of AGel amyloidosis patients, CMR findings have been shown to differ from those of typical cardiac amyloid disease. Local LGE was common (noted in 75% of the patients), but it concentrated mainly on the ventricular septum and inferiorly [6], rather than globally and subendocardially as in AL amyloidosis, or transmurally like in ATTR amyloidosis [21]. The septal pathology could possibly represent the underlying cause of the high prevalence of conduction disease among AGel amyloidosis patients, as the ventricular septum comprises an important part of the electrical conduction system of the heart. In these patients, there was a noteworthy association between LGE and conduction abnormalities. Nearly half of the patients with LGE had a first-degree AV-block or prolonged QRS duration, compared to less than 10% of those without LGE. The underlying cause of LGE in AGel amyloidosis requires histological verification, as it could be due to any process expanding the interstitial space, for example interstitially accumulating amyloid protein or fibrosis. In a previous histopathological autopsy study, AGel amyloid deposits in the heart were demonstrated in all study subjects, but only in minor amounts and co-localized with excess fibrosis in every case [5]. So far, the pathophysiology behind conduction alterations in cardiac amyloidosis remains unclear. Results from previous studies are conflicting, some favouring amyloid infiltration of the conduction system [22,23] and others suggesting fibrosis and atrophy [24] or cardiac sympathetic denervation to be the cause [12].