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.

No abstract

This retrospective study unexpectedly observed no association between serum magnesium levels and QTc interval or sudden cardiac death. However, serum magnesium ≥2.4 mg/dL was an independent predictor of increased hospital morality among CCU patients.

Introduction Bileaflet mitral valve prolapse (MVP) can be associated with malignant ventricular arrhythmias. It is unknown whether surgical correction alone of this mitral valve pathology leads to a reduction in ventricular dysrhythmias. Methods We retrospectively analyzed 4,477 patients who underwent mitral valve surgery from 1993-2013 at the Mayo Clinic in Rochester, MN. Among these, eight patients with bileaflet MVP who had an internal cardioverter defibrillator (ICD) in place both pre and post-surgery were identified. ICD interrogation records were evaluated for episodes of ventricular tachycardia (VT), ventricular fibrillation (VF), and appropriate ICD shock therapy. Results Of these eight patients, five had malignant ventricular arrhythmia prior to surgery. Data was available 4.6 ± 2.9 years before versus 6.6 ± 4.2 years following surgical intervention. Among these patients, there was a reduction in VF (0.6 versus 0.14 events per-person-year pre- and post-surgery, respectively), VT (0.4 versus 0.05 events per-person-year pre- and post-surgery, respectively), and ICD shocks (0.95 versus 0.19 events per-person-year pre- and post-surgery) following mitral valve surgery. Conclusions We report a series of cases where surgical correction of bileaflet MVP alone was associated with a reduction in malignant arrhythmia and appropriate shocks. These early observations merit further investigation involving larger cohorts to further evaluate the association between abnormal mechanical forces in degenerative mitral valve disease and ventricular dysrhythmias.