Background-We have shown that the calmodulin inhibitor W-7 suppresses torsade de pointes (TdP) without shortening the QT interval, which is consistent with other findings that QT prolongation, per se, is insufficient to generate TdP. ECGs were analyzed from a well-characterized animal model of TdP to identify more reliable predictors of this life-threatening ventricular arrhythmia. Methods and Results-TdP was induced using methoxamine and clofilium in 12 of 14 rabbits pretreated with vehicle control, whereas pretreatment with W-7 (50 mol/kg), an inhibitor of the intracellular Ca 2ϩ -binding protein calmodulin, significantly suppressed TdP induction (1 of 11 rabbits with TdP, PϽ0.001). W-7 did not affect heart rate, increases in QT intervals, or dispersion compared with measurements in vehicle-treated control animals. However, a progressive and significant increase in the ratio of U-wave to T-wave amplitude (UTA) occurred before TdP onset in control animals, and this was prevented by W-7. Conclusions-Selective suppression of TdP inducibility by W-7, without shortening the duration of cardiac repolarization, allowed identification of the UTA ratio as a new electrocardiographic index for predicting TdP onset. These findings are consistent with the idea that prolonged repolarization is not the proximate cause of arrhythmia initiation, and they suggest that an increased UTA ratio reflects activation of intracellular Ca 2ϩ /calmodulin-dependent processes that are required for triggering TdP in this model.

Black Africans, Chinese, and Japanese had lower incidence of AF compared to Europeans. In the case of black Africans, this is despite an increased prevalence of AF risk factors.

Background: Cardiovasculareventshavebeenreportedinthesettingofcoronavirus disease-19(COVID-19).Ithasbeenhypothesizedthatsystemicinflammationmayaggravate arrhythmias or trigger new-onset conduction abnormalities. However, the specifictypeanddistributionofelectrocardiographicdisturbancesinCOVID-19as wellastheirinfluenceonmortalityremaintobefullycharacterized. Methods: Electrocardiograms (ECGs) were obtained from 186 COVID-19-positive patientsatalargetertiarycarehospitalinNorthernNevada.Thefollowingarrhythmiaswereidentifiedbycardiologists:sinusbradycardia,sinustachycardia,atrialfibrillation (A-Fib), atrial flutter, multifocal atrial tachycardia (MAT), premature atrial contraction (PAC), premature ventricular contraction (PVC), atrioventricular block (AVB),andrightbundlebranchblock(RBBB).ThemeanPRinterval,QRSduration, andcorrectedQTintervalweredocumented.Fisher'sexacttestwasusedtocompare the ECG features of patients who died during the hospitalization with those who survived.TheinfluenceofECGfeaturesonmortalitywasassessedwithmultivariable logistic regression analysis.Results: A-Fib,atrialflutter,andST-segmentdepressionwerepredictiveofmortality.In addition,themeanventricularratewashigheramongpatientswhodiedascompared to those who survived. The use of therapeutic anticoagulation was associated with reducedoddsofdeath;however,thisassociationdidnotreachstatisticalsignificance. Conclusion:The underlying pathogenesis of COVID-19-associated arrhythmias remains to be established, but we postulate that systemic inflammation and/or hypoxiamayinducepotentiallylethalconductionabnormalitiesinaffectedindividuals.ThisisanopenaccessarticleunderthetermsoftheCreativeCommonsAttribution-NonCommercial-NoDerivsLicense,whichpermitsuseanddistributionin anymedium,providedtheoriginalworkisproperlycited,theuseisnon-commercialandnomodificationsoradaptationsaremade. ©2021TheAuthors.Annals of Noninvasive ElectrocardiologypublishedbyWileyPeriodicalsLLC.

Despite some common risk factors for AF being more prevalent amongst blacks, AfricanAmericans are increasingly being reported with lower prevalence and incidence of atrial fibrillation (AF) compared to Caucasians or whites. Contemporary studies have not provided a complete explanation for this apparent AF paradox in African Americans. Although many traditional and novel risk factors for AF have been identified, the role of ethnic-specific risk factors has not been examined. Whereas hypertension has been the most common risk factor associated with AF, coronary artery disease (CAD) also plays an important role in AF pathophysiology in whites. Thereby, elucidating the role of ethnic-specific risk factors for AF may provide important insight into why African Americans are protected from AF or why whites are more prone to develop the arrhythmia. The link between AF susceptibility and genetic processes has only been recently uncovered. Polymorphisms in renin-angiotensin system genes have been characterized as predisposing to AF under certain environmental conditions. A number of ion channel genes, signaling molecules and several genetic loci have been linked with AF. Thereby, studies investigating genetic variants contributing to the differential AF risk in individuals of African American versus European ancestry may also provide important insight into the etiology of the AF paradox in blacks.