The sodium channel gene SCN5A and potassium channel genes KCNQ1 and KCNH2 have been widely reported to be genetic risk factors for arrhythmia including Brugada syndrome and long QT syndrome (LQTS).
In this study, we analyzed the genetic variants of KCNQ1, KCNH2, and SCN5A in patients from seven cohorts (total N = 11945, including patients clinically suspected to have inherited arrhythmia [n = 122], other cardiovascular diseases [n = 1045], epilepsy [n = 4797], or other diseases [n = 5841], and healthy controls [n = 140]) who had undergone genetic testing.
The sodium channel gene SCN5A and potassium channel genes KCNQ1 and KCNH2 have been widely reported to be genetic risk factors for arrhythmia including Brugada syndrome and long QT syndrome (LQTS).
In this study, we analyzed the genetic variants of KCNQ1, KCNH2, and SCN5A in patients from seven cohorts (total N = 11945, including patients clinically suspected to have inherited arrhythmia [n = 122], other cardiovascular diseases [n = 1045], epilepsy [n = 4797], or other diseases [n = 5841], and healthy controls [n = 140]) who had undergone genetic testing.
The sodium channel gene SCN5A and potassium channel genes KCNQ1 and KCNH2 have been widely reported to be genetic risk factors for arrhythmia including Brugada syndrome and long QT syndrome (LQTS).
In this study, we analyzed the genetic variants of KCNQ1, KCNH2, and SCN5A in patients from seven cohorts (total N = 11945, including patients clinically suspected to have inherited arrhythmia [n = 122], other cardiovascular diseases [n = 1045], epilepsy [n = 4797], or other diseases [n = 5841], and healthy controls [n = 140]) who had undergone genetic testing.
Atrial myocyte electrophysiology, Ca<sup>2+</sup> handling, and arrhythmia susceptibility were studied in wild-type and Scn5a knock-in mice expressing phosphomimetic (S571E) or phosphoresistant (S571A) Na<sub>V</sub>1.5 at Ser571.
2011, while indexes of parasympathetic (i.e., respiratory sinus arrhythmia [RSA]) and sympathetic (i.e., pre-ejection period [PEP] and electrodermal activity [EDA]) reactivity were obtained.
We hypothesized that CAB/CAR would more reliably index post-traumatic stress (PTS) responses compared to measuring the parasympathetic (i.e., respiratory sinus arrhythmia; RSA) and sympathetic (i.e., pre-ejection period; PEP) nervous systems in isolation.
Aberrant Ca<sup>2+</sup> release from cardiac ryanodine receptors (RyR2) has been shown to be one of the most important causes of lethal arrhythmia in various types of failing hearts.
We hypothesized that CAB/CAR would more reliably index post-traumatic stress (PTS) responses compared to measuring the parasympathetic (i.e., respiratory sinus arrhythmia; RSA) and sympathetic (i.e., pre-ejection period; PEP) nervous systems in isolation.
2011, while indexes of parasympathetic (i.e., respiratory sinus arrhythmia [RSA]) and sympathetic (i.e., pre-ejection period [PEP] and electrodermal activity [EDA]) reactivity were obtained.
We hypothesized that CAB/CAR would more reliably index post-traumatic stress (PTS) responses compared to measuring the parasympathetic (i.e., respiratory sinus arrhythmia; RSA) and sympathetic (i.e., pre-ejection period; PEP) nervous systems in isolation.
2011, while indexes of parasympathetic (i.e., respiratory sinus arrhythmia [RSA]) and sympathetic (i.e., pre-ejection period [PEP] and electrodermal activity [EDA]) reactivity were obtained.
In this review, recent progress in the biological studies of BIN1-related cardiomyocytes and the effect of cardiac dysfunction and malignant arrhythmia will be discussed.
The purpose of this study was to characterize the pathogenetic mechanism underlying a case of severe pediatric malignant arrhythmia associated with a defect in the TRDN gene.
2011, while indexes of parasympathetic (i.e., respiratory sinus arrhythmia [RSA]) and sympathetic (i.e., pre-ejection period [PEP] and electrodermal activity [EDA]) reactivity were obtained.
The reduction in hypothermia and ischaemia-induced reperfusion arrhythmias by the addition of sevoflurane to HTK solution may be related to the phosphorylation of Cx43 at serine 368.
However, enhanced phosphorylation of Cx43 at serine368 in hypothyroid SHRs might be associated with preservation of intercellular coupling and alleviation of the propensity of the heart to malignant arrhythmias.