Aims Patients with cardiovascular disease appear particularly susceptible to severe COVID‐19 disease, but the impact of COVID‐19 infection on patients with heart failure (HF) is not known. This study aimed to quantify the impact of COVID‐19 infection on mortality in hospitalized patients known to have HF. Methods and results We undertook a retrospective analysis of all patients admitted with a pre‐existing diagnosis of HF between 1 March and 6 May 2020 to our unit. We assessed the impact of concomitant COVID‐19 infection on in‐hospital mortality, incidence of acute kidney injury, and myocardial injury. One hundred and thirty‐four HF patients were hospitalized, 40 (29.9%) with concomitant COVID‐19 infection. Those with COVID‐19 infection had a significantly increased in‐hospital mortality {50.0% vs. 10.6%; relative risk [RR] 4.70 [95% confidence interval (CI) 2.42–9.12], P < 0.001} and were more likely to develop acute kidney injury [45% vs. 24.5%; RR 1.84 (95% CI 1.12–3.01), P = 0.02], have evidence of myocardial injury [57.5% vs. 31.9%; RR 1.81 (95% CI 1.21–2.68), P < 0.01], and be treated for a superadded bacterial infection [55% vs. 32.5%; RR 1.67 (95% CI 1.12–2.49), P = 0.01]. Conclusions Patients with HF admitted to hospital with concomitant COVID‐19 infection have a very poor prognosis. This study highlights the need to regard patients with HF as a high‐risk group to be shielded to reduce the risks of COVID‐19 infection.
Background and aimThe efficacy of pre-COVID-19 and post-COVID-19 infection 12-lead ECGs for identifying athletes with myopericarditis has never been reported. We aimed to assess the prevalence and significance of de-novo ECG changes following COVID-19 infection.MethodsIn this multicentre observational study, between March 2020 and May 2022, we evaluated consecutive athletes with COVID-19 infection. Athletes exhibiting de-novo ECG changes underwent cardiovascular magnetic resonance (CMR) scans. One club mandated CMR scans for all players (n=30) following COVID-19 infection, despite the absence of cardiac symptoms or de-novo ECG changes.Results511 soccer players (median age 21 years, IQR 18–26 years) were included. 17 (3%) athletes demonstrated de-novo ECG changes, which included reduction in T-wave amplitude in the inferior and lateral leads (n=5), inferior leads (n=4) and lateral leads (n=4); inferior T-wave inversion (n=7); and ST-segment depression (n=2). 15 (88%) athletes with de-novo ECG changes revealed evidence of inflammatory cardiac sequelae. All 30 athletes who underwent a mandatory CMR scan had normal findings. Athletes revealing de-novo ECG changes had a higher prevalence of cardiac symptoms (71% vs 12%, p<0.0001) and longer median symptom duration (5 days, IQR 3–10) compared with athletes without de-novo ECG changes (2 days, IQR 1–3, p<0.001). Among athletes without cardiac symptoms, the additional yield of de-novo ECG changes to detect cardiac inflammation was 20%.Conclusions3% of athletes demonstrated de-novo ECG changes post COVID-19 infection, of which 88% were diagnosed with cardiac inflammation. Most affected athletes exhibited cardiac symptoms; however, de-novo ECG changes contributed to a diagnosis of cardiac inflammation in 20% of athletes without cardiac symptoms.
There is a paucity of studies looking at the natural history of valvular heart disease (VHD) in exercising individuals, and exercise recommendations are largely based on expert consensus. All individuals with VHD should be encouraged to avoid sedentary behaviour by engaging in at least 150 min of physical activity every week, including strength training. There are generally no exercise restrictions to individuals with mild VHD. Regurgitant lesions are better tolerated compared with stenotic lesions and as such the recommendations are more permissive for moderate-to-severe regurgitant VHD. Individuals with severe aortic regurgitation can still partake in moderate-intensity exercise provided the left ventricle (LV) and aorta are not significantly dilated and the ejection fraction (EF) remains >50%. Similarly, individuals with severe mitral regurgitation can partake in moderate-intensity exercise if the LV end-diastolic diameter <60 mm, the EF ≥60%, resting pulmonary artery pressure <50 mm Hg and there is an absence of arrhythmias on exercise testing. Conversely, individuals with severe aortic or mitral stenosis are advised to partake in low-intensity exercise. For individuals with bicuspid aortic valve, in the absence of aortopathy, the guidance for tricuspid aortic valve dysfunction applies. Mitral valve prolapse has several clinical, ECG and cardiac imaging markers of increased arrhythmic risk; and if any are present, individuals should refrain from high-intensity exercise.
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