Chronic Stress, Exercise and Cardiovascular Disease: Placing the Benefits and Risks of Physical Activity into Perspective.

Chronic stress, which has been exacerbated worldwide by the lingering COVID pandemic, has been strongly linked to cardiovascular disease (CVD). In addition, autonomic dysregulation via sustained sympathetic activity has been shown to increase the risk of arrhythmias, platelet aggregation, acute coronary syndromes and heart failure. Fortunately, effective coping strategies have been shown to attenuate the magnitude of hyperarousal associated with the stress response, including moderate-to-vigorous lifestyle activity and/or structured exercise. A good-to-excellent level of cardiorespiratory fitness also appears to be highly cardioprotective. These beneficial effects have been substantiated by numerous studies that have evaluated the levels of stress reactivity and stress recovery in physically active individuals versus matched sedentary controls, as well as before and after exercise interventions. On the other hand, unaccustomed strenuous exercise in habitually sedentary persons with underlying CVD is associated with a disproportionate incidence of acute cardiac events. Moreover, extreme exercise regimens appear to increase coronary calcification and the likelihood of developing atrial fibrillation. This review summarizes these relations and more, with specific reference to placing the benefits and risks of physical activity into perspective.

Hydroxychloroquine/Azithromycin Therapy and QT Prolongation in Hospitalized Patients With COVID-19.

OBJECTIVES: This study aimed to characterize corrected QT (QTc) prolongation in a cohort of hospitalized patients with coronavirus disease-2019 (COVID-19) who were treated with hydroxychloroquine and azithromycin (HCQ/AZM). BACKGROUND: HCQ/AZM is being widely used to treat COVID-19 despite the known risk of QT interval prolongation and the unknown risk of arrhythmogenesis in this population. METHODS: A retrospective cohort of COVID-19 hospitalized patients treated with HCQ/AZM was reviewed. The QTc interval was calculated before drug administration and for the first 5 days following initiation. The primary endpoint was the magnitude of QTc prolongation, and factors associated with QTc prolongation. Secondary endpoints were incidences of sustained ventricular tachycardia or ventricular fibrillation and all-cause mortality. RESULTS: Among 415 patients who received concomitant HCQ/AZM, the mean QTc increased from 443 ± 25 ms to a maximum of 473 ± 40 ms (87 [21%] patients had a QTc ≥500 ms). Factors associated with QTc prolongation ≥500 ms were age (p < 0.001), body mass index <30 kg/m2 (p = 0.005), heart failure (p < 0.001), elevated creatinine (p = 0.005), and peak troponin (p < 0.001). The change in QTc was not associated with death over the short period of the study in a population in which mortality was already high (hazard ratio: 0.998; p = 0.607). No primary high-grade ventricular arrhythmias were observed. CONCLUSIONS: An increase in QTc was seen in hospitalized patients with COVID-19 treated with HCQ/AZM. Several clinical factors were associated with greater QTc prolongation. Changes in QTc were not associated with increased risk of death.