scholarly journals Conduction System Disease and Atrioventricular Block in Victims of COVID-19 in Iran

2021 ◽  
Author(s):  
Mohammad Hossein Nikoo ◽  
Alireza Sadeghi ◽  
Niloofar Dehdari Ebrahimi ◽  
Alireza Estedlal ◽  
Amirhossein Maktabi ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Medical Condition ◽  
Conduction System ◽  
P Value ◽  
Medical Sciences ◽  
Disease Manifestation ◽  
Fragmented Qrs ◽  
System Disease ◽  
Stratification Method ◽  
Conduction System Disease

Abstract Background More recently, a growing body of literature on COVID-19 has investigated the electrophysiological issues presetting as a disease manifestation of COVID-19 and highlight the spectrum of arrhythmias observed in patients with COVID-19 infection. This Study discuss the prevalence of arrhythmias and conduction system disease in patients with COVID-19. Method electrocardiographic data and comorbidity data of 432 expired COVID-19 patients admitted to Faghihi Hospital of Shiraz University of Medical Sciences from August 1st until December 1st were reviewed. Results AVB was found in 40(9.3%) patients. 28(6.5%) of the patients suffered from 1st degree AVB, and 12(2.8%) suffered from CHB. Changes in ST-T wave compatible with myocardial infarction or localized myocarditis appeared in 189(59.0%) patients. Findings compatible with myocardial injury such as fragmented QRS, and prolonged QTc were assessed with prevalence of 21.1% (91 patients), 6.5% (28 patients). In victims of COVID-19, conduction disease was not related to any underlying medical condition. Fragmented QRS, axis deviation, presence of S1Q3T3 and poor R wave progression were significantly related to conduction system disease in victims of COVID-19 (P value > 0.05, Table 3) Conclusion Our findings can serve in future studies that aim to develop a risk stratification method for susceptible COVID-19 patients. Myocardial injury appears to role significantly in COVID-19 morbidity and mortality. Consequently, we recommend health policymakers to consider separate catheterization laboratories that provide service only to COVID-19 patients.

Novel lamin A/C mutations in two families with dilated cardiomyopathy and conduction system disease

2001 ◽  
Vol 7 (3) ◽  
pp. 249-256 ◽  
Author(s):  
Petra M. Jakobs ◽  
Emily L. Hanson ◽  
Kathy A. Crispell ◽  
Warren Toy ◽  
Hugh Keegan ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Conduction System ◽  
Lamin A ◽  
System Disease ◽  
Conduction System Disease

scholarly journals Temporal Relationship of Conduction System Disease and Ventricular Dysfunction in LMNA Cardiomyopathy

2013 ◽  
Vol 19 (4) ◽  
pp. 233-239 ◽  
Author(s):  
Chad Brodt ◽  
Jill D. Siegfried ◽  
Mark Hofmeyer ◽  
Jose Martel ◽  
Evadnie Rampersaud ◽  
...  
Keyword(s):  
Temporal Relationship ◽  
Ventricular Dysfunction ◽  
Conduction System ◽  
System Disease ◽  
Conduction System Disease ◽  
Relationship Of

Sodium channel kinetic changes that produce Brugada syndrome or progressive cardiac conduction system disease

2007 ◽  
Vol 292 (1) ◽  
pp. H399-H407 ◽  
Author(s):  
Zhu-Shan Zhang ◽  
Joseph Tranquillo ◽  
Valentina Neplioueva ◽  
Nenad Bursac ◽  
Augustus O. Grant
Keyword(s):  
Action Potential ◽  
Sodium Channel ◽  
Brugada Syndrome ◽  
Sodium Current ◽  
Conduction System ◽  
Cardiac Conduction ◽  
Cardiac Conduction System ◽  
Wild Type ◽  
System Disease ◽  
Conduction System Disease

Some mutations of the sodium channel gene NaV1.5 are multifunctional, causing combinations of LQTS, Brugada syndrome and progressive cardiac conduction system disease (PCCD). The combination of Brugada syndrome and PCCD is uncommon, although they both result from a reduction in the sodium current. We hypothesize that slow conduction is sufficient to cause S-T segment elevation and undertook a combined experimental and theoretical study to determine whether conduction slowing alone can produce the Brugada phenotype. Deletion of lysine 1479 in one of two positively charged clusters in the III/IV inter-domain linker causes both syndromes. We have examined the functional effects of this mutation using heterologous expression of the wild-type and mutant sodium channel in HEK-293-EBNA cells. We show that ΔK1479 shifts the potential of half-activation, V1/2m, to more positive potentials ( V1/2m = −36.8 ± 0.8 and −24.5 ± 1.3 mV for the wild-type and ΔK1479 mutant respectively, n = 11, 10). The depolarizing shift increases the extent of depolarization required for activation. The potential of half-inactivation, V1/2h, is also shifted to more positive potentials ( V1/2h = −85 ± 1.1 and −79.4 ± 1.2 mV for wild-type and ΔK1479 mutant respectively), increasing the fraction of channels available for activation. These shifts are quantitatively the same as a mutation that produces PCCD only, G514C. We incorporated experimentally derived parameters into a model of the cardiac action potential and its propagation in a one dimensional cable (simulating endo-, mid-myocardial and epicardial regions). The simulations show that action potential and ECG changes consistent with Brugada syndrome may result from conduction slowing alone; marked repolarization heterogeneity is not required. The findings also suggest how Brugada syndrome and PCCD which both result from loss of sodium channel function are sometimes present alone and at other times in combination.

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