Background— Recent studies have demonstrated spatiotemporal organization in atrial fibrillation (AF), with a left-to-right atrial frequency gradient during AF in isolated sheep hearts. We hypothesized that human AF would also manifest a left-to-right atrial frequency gradient. Methods and Results— Thirty-one patients aged 56.7±10.5 years with a history of paroxysmal or persistent (>1 month) AF were included. Recordings were made at each pulmonary vein (PV) ostium and simultaneously from the coronary sinus (CS) and posterior right atrium (RA) during AF. Sequential fast Fourier transforms (FFTs) were performed. FFT profiles were analyzed to determine the dominant frequency (DF). There were 18 patients with paroxysmal AF and 13 with persistent AF. In the paroxysmal group, there was a significant left-to-right atrial DF gradient, with DF highest at the PV/left atrial (LA) junction, intermediate at the CS, and lowest in the RA (6.2±0.8, 5.5±0.7, and 5.1±0.6 Hz, respectively; P <0.001). There were no patients in whom DF was greater at the RA than the PV/LA junction. In the persistent group, there was no significant difference between DF recorded from the LA/PV junction, CS, and RA (6.1±0.7, 5.8±0.6, and 5.8±0.6 Hz, respectively; P =NS). Conclusions— In humans with paroxysmal AF, DFs are highest at the PV/LA junction, intermediate in the CS, and slowest in the posterior RA. These findings agree with animal models that suggest that the posterior LA may play an important role in maintaining paroxysmal AF. The role of the posterior LA in persistent AF requires further study.

More than 2,000,000 individuals worldwide have had coronavirus 2019 disease infection , yet there is no effective medical therapy. Multiple off-label and investigational drugs, such as chloroquine and hydroxychloroquine, have gained broad interest due to positive pre-clinical data and are currently used for treatment of COVID-19. However, some of these medications have potential cardiac adverse effects. This is important because up to one-third of patients with COVID-19 have cardiac injury, which can further increase the risk of cardiomyopathy and arrhythmias. Adverse effects of chloroquine and hydroxychloroquine on cardiac function and conduction are broad and can be fatal. Both drugs have an anti-arrhythmic property and are proarrhythmic. The American Heart Association has listed chloroquine and hydroxychloroquine as agents which can cause direct myocardial toxicity. Similarly, other investigational drugs such as favipiravir and lopinavir/ritonavir can prolong QT interval and cause Torsade de Pointes. Many antibiotics commonly used for the treatment of patients with COVID-19, for instance azithromycin, can also prolong QT interval. This review summarizes evidenced-based data regarding potential cardiac adverse effects due to off-label and investigational drugs including chloroquine and hydroxychloroquine, antiviral therapy, monoclonal antibodies, as well as common antibiotics used for the treatment of COVID-19. The article focuses on practical points and offers a point-of-care protocol for providers who are taking care of patients with COVID-19 in an inpatient and outpatient setting. The proposed protocol is taking into consideration that resources during the pandemic are limited.

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Key Points Question What is the association of family history with the pathogenesis of early-onset atrial fibrillation in patients of African, European, and Hispanic descent? Findings In this cohort study of 664 patients, probands with early-onset atrial fibrillation were significantly more likely to have a family history of arrhythmia in first-degree relatives than patients with non–early-onset atrial fibrillation. Compared with European American probands, African American and Hispanic/Latino probands with early-onset atrial fibrillation were more likely to have a first-degree relative with arrhythmia. Meaning These findings support genetic predisposition to early-onset atrial fibrillation across individuals of European, African, and Hispanic/Latino descent and have important implications for identifying family members at risk for atrial fibrillation and sequencing candidate genes.