Background: Information regarding the cardiac manifestations of COVID-19 is scarce. We performed a systematic and comprehensive echocardiographic evaluation of consecutive patients hospitalized with COVID-19 infection. Methods: 100 consecutive patients diagnosed with COVID-19 infection underwent complete echocardiographic evaluation within 24 hours of admission and were compared to reference values. Echocardiographic studies included left ventricular (LV) systolic and diastolic function, valve hemodynamics and right ventricular (RV) assessment, as well as lung ultrasound. A second exam was performed in case of clinical deterioration. Results: Thirty two patients (32%) had a normal echocardiogram at baseline. The most common cardiac pathology was RV dilatation and dysfunction (observed in 39% of patients), followed by LV diastolic dysfunction (16%) and LV systolic dysfunction (10%). Patients with elevated troponin (20%) or worse clinical condition did not demonstrate any significant difference in LV systolic function compared to patients with normal troponin or better clinical condition, but had worse RV function. Clinical deterioration occurred in 20% of patients. In these patients, the most common echocardiographic abnormality at follow-up was RV function deterioration (12 patients), followed by LV systolic and diastolic deterioration (in 5 patients). Femoral vein thrombosis (DVT) was diagnosed in 5 of 12 patients with RV failure. Conclusions: In COVID-19 infection, LV systolic function is preserved in the majority of patients, but LV diastolic and RV function are impaired. Elevated troponin and poorer clinical grade are associated with worse RV function. In patients presenting with clinical deterioration at follow-up, acute RV dysfunction, with or without DVT, is more common, but acute LV systolic dysfunction was noted in ≈20%.

Information regarding the use of lung ultrasound (LUS) in patients with Coronavirus disease 2019 (COVID-19) is quickly accumulating, but its use for risk stratification and outcome prediction has yet to be described. We performed the first systematic and comprehensive LUS evaluation of consecutive patients hospitalized with COVID-19 infection, in order to describe LUS findings and their association with clinical course and outcome. Methods: Between 21/03/2020 and 04/05/2020, 120 consecutive patients admitted to the Tel Aviv Medical Center due to COVID-19, underwent complete LUS within 24 h of admission. A second exam was performed in case of clinical deterioration. LUS score of 0 (best)-36 (worst) was assigned to each patient. LUS findings were compared with clinical data. Results: The median baseline total LUS score was 15, IQR [7-20]. Baseline LUS score was 0-18 in 80 (67%) patients, and 19-36 in 40 (33%) patients. The majority had patchy pleural thickening (n = 100; 83%), or patchy subpleural consolidations (n = 93; 78%) in at least one zone. The prevalence of pleural thickening, subpleural consolidations and the total LUS score were all correlated with severity of illness on admission. Clinical deterioration was associated with increased follow-up LUS scores (p = 0.0009), mostly due to loss of aeration in anterior lung segments. The optimal cutoff point for LUS score was 18 (sensitivity = 62%, specificity = 74%). Both mortality and need for invasive mechanical ventilation were increased with baseline LUS score > 18 compared to baseline LUS score 0-18. Unadjusted hazard ratio of death for LUS score was 1.08 per point [1.02-1.16], p = 0.008; Unadjusted hazard ratio of the composite endpoint (death or need for invasive mechanical ventilation) for LUS score was 1.12 per point [1.05-1.2], p = 0.0008. Conclusion: Hospitalized patients with COVID-19, at all clinical grades, present with pathological LUS findings. Baseline LUS score strongly correlates with the eventual need for invasive mechanical ventilation and is a strong predictor of mortality. Routine use of LUS may guide patients' management strategies, as well as resource allocation in case of surge capacity.

Background Large number of patients around the world are recovering from COVID-19; many of them report persistence of symptoms. Objectives We sought to test pulmonary, cardiovascular and peripheral responses to exercise in patients recovering from COVID-19. Methods We prospectively evaluated patients who recovered from COVID-19 using a combined anatomic/functional assessment. All patients underwent clinical examination, laboratory tests, and a combined stress echocardiography and cardiopulmonary exercise test. We measured left ventricular volumes, ejection fraction, stroke volume, heart rate, E/e' ratio, right ventricular function, VO 2 , lung volumes, Ventilatory efficiency, O 2 saturation and muscle O 2 extraction in all effort stages and compared them to historical controls. Results A total of 71 patients were assessed 90.6±26 days after onset of COVID-19 symptoms. Only 23 (33%) were asymptomatic. The most common symptoms were fatigue (34%), muscle weakness/pain (27%) and dyspnea (22%). VO 2 was lower among post-COVID-19 patients compared to controls (p=0.03, group by time interaction p=0.007). Reduction in peak VO 2 was due to a combination of chronotropic incompetence (75% of post-COVID-19 patients vs. 8% of controls, p<0.0001) and insufficient increase in stroke volume during exercise (p=0.0007, group by time interaction p=0.03). Stroke volume limitation was mostly explained by diminished increase in left ventricular end-diastolic volume (p=0.1, group by time interaction p=0.03) and insufficient increase in ejection fraction (p=0.01, group by time interaction p=0.01). Post-COVID-19 patients had higher peripheral O 2 extraction (p=0.004) and did not have significantly different respiratory and gas exchange parameters compared to controls. Conclusions Patients recovering from COVID-19 have symptoms associated with objective reduction in peak VO 2 . The mechanism of this reduction is complex and mainly involves a combination of attenuated heart rate and stroke volume reserve.

No abstract

The risk of fever-related AE in BrS markedly varies according to age group, sex, and ethnicity. Taking these factors into account could help the clinical management of patients with BrS with fever.

This study confirms that female patients with BrS are much rarer, display less type 1 Brugada ECG, and exhibit lower inducibility rates than do males. It shows for the first time that female patients with BrS with AE have higher SCN5A mutation rates as well as the relationship between gender vs age at the onset of AEs and ethnicity.

No abstract

Background: Polymorphic ventricular tachycardia (VT) without QT prolongation is well described in patients without structural heart disease (mainly idiopathic ventricular fibrillation and Brugada syndrome) and in patients with acute ST-elevation myocardial infarction. Methods: Retrospective study of patients with polymorphic VT related to coronary artery disease, but without evidence of acute myocardial ischemia. Results: The authors identified 43 patients in whom polymorphic VT developed within days of an otherwise uncomplicated myocardial infarction or coronary revascularization procedure. The polymorphic VT events were invariably triggered by extrasystoles with short (364±36 ms) coupling interval. Arrhythmic storms (4–16 events of polymorphic VT deteriorating to ventricular fibrillation) occurred in 23 (53%) patients. These arrhythmic storms were always refractory to conventional antiarrhythmic therapy, including intravenous amiodarone, but invariably responded to quinidine therapy. In-hospital mortality was 17% for patients with arrhythmic storm. Patients treated with quinidine invariably survived to hospital discharge. During long-term follow-up (of 5.6±6 years; range, 1 month to 18 years), 3 (16%) of patients discharged without quinidine developed recurrent polymorphic VT. There were no recurrent arrhythmias during quinidine therapy Conclusions: Arrhythmic storm with recurrent polymorphic VT in patients with coronary disease responds to quinidine therapy when other antiarrhythmic drugs (including intravenous amiodarone) fail.