ABSTRACT
BACKGROUND AND AIM: The 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. METHODS: In 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. RESULTS: 511 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%. CONCLUSIONS: 3% 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.
Subject(s)
COVID-19 , Soccer , Humans , Young Adult , Adult , Prevalence , COVID-19/complications , COVID-19/epidemiology , Electrocardiography , Arrhythmias, Cardiac/diagnosis , Athletes , Inflammation , COVID-19 TestingABSTRACT
Among the multiple uncertainties surrounding the novel coronavirus disease (COVID-19) pandemic, a research letter published in The Lancet implicated drugs that antagonize the renin-angiotensin-aldosterone system (RAAS) in an unfavorable prognosis of COVID-19. This report prompted investigations to identify mechanisms by which blocking angiotensin-converting enzyme 2 (ACE2) could lead to serious consequences in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The possible association between RAAS inhibitors use and unfavorable prognosis in this disease may have been biased by the presence of underlying cardiovascular diseases. As the number of COVID-19 cases has increased worldwide, it has now become possible to investigate the association between RAAS inhibitors and unfavorable prognosis in larger cohorts. Observational studies and one randomized clinical trial failed to identify any consistent association between the use of these drugs and unfavorable prognosis in COVID-19. In view of the accumulated clinical evidence, several scientific societies recommend that treatment with RAAS inhibitors should not be discontinued in patients diagnosed with COVID-19 (unless contraindicated). This recommendation should be followed by clinicians and patients.
Subject(s)
COVID-19 , Coronavirus , Angiotensin Receptor Antagonists/adverse effects , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Humans , Peptidyl-Dipeptidase A/metabolism , Randomized Controlled Trials as Topic , Renin-Angiotensin System , SARS-CoV-2ABSTRACT
The novel coronavirus disease (COVID-19) showed increased morbidity and mortality rates and worse prognosis in individuals with underlying chronic diseases, especially cardiovascular disease and its risk factors, such as hypertension, diabetes, and obesity. There is also evidence of possible links among COVID-19, myocardial infarction, and stroke. Emerging evidence suggests a pro-inflammatory milieu and hypercoagulable state in patients with this infection. Despite anticoagulation, a large proportion of patients requiring intensive care may develop life-threatening thrombotic complications. Indeed, the levels of some markers of hemostatic activation, such as D-dimer, are commonly elevated in COVID-19, indicating potential risk of deep vein thrombosis and pulmonary thromboembolism. In this review, we critically examine and discuss aspects of hypercoagulability and inflammation in COVID-19 and the possible benefits of statins in this scenario, with emphasis on their underlying molecular mechanisms. Moreover, we present recommendations on the use of antiviral drugs in combination with statins.
Subject(s)
COVID-19 , Coronavirus , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Thrombosis , Anticoagulants/adverse effects , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Inflammation/drug therapy , SARS-CoV-2ABSTRACT
In December 2019, a new human coronavirus, called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or coronavirus disease 2019 (COVID-19) by the World Health Organization, emerged in the city of Wuhan, China. Spreading globally, it is now considered pandemic, with approximately 3 million cases worldwide at the end of April. Its symptoms include fever, cough, and headache, but the main one is shortness of breath. In turn, it is believed that there is a relationship between COVID-19 and damage to the heart muscle, and hypertensive and diabetic patients, for example, seem to have worse prognosis. Therefore, COVID-19 may worsen in individuals with underlying adverse conditions, and a not negligible number of patients hospitalized with this virus had cardiovascular or cerebrovascular diseases. Systemic inflammatory response and immune system disorders during disease progression may be behind this association. In addition, the virus uses angiotensin-converting enzyme (ACE) receptors, more precisely ACE2, to penetrate the cell; therefore, the use of ACE inhibitor drugs and angiotensin receptor blockers could cause an increase in these receptors, thus facilitating the entry of the virus into the cell. There is, however, no scientific evidence to support the interruption of these drugs. Since they are fundamental for certain chronic diseases, the risk and benefit of their withdrawal in this scenario should be carefully weighed. Finally, cardiologists and health professionals should be aware of the risks of infection and protect themselves as much as possible, sleeping properly and avoiding long working hours.
Em dezembro de 2019, um novo coronavírus humano, chamado síndrome respiratória aguda grave do coronavírus 2 (SARS-CoV-2) ou nomeado doença de coronavírus (COVID-19) pela Organização Mundial da Saúde, surgiu na cidade de Wuhan, China. Difundido globalmente, é atualmente considerado pandêmico, com aproximadamente 3 milhões de casos no mundo no final de abril. Seus sintomas incluem febre, tosse, dor de cabeça e falta de ar, esse último considerado o sintoma principal. Por sua vez, acredita-se que haja uma relação entre o COVID-19 e danos ao músculo cardíaco, e pacientes com hipertensão e diabetes, por exemplo, parecem apresentar prognóstico pior. Portanto, o COVID-19 pode piorar em indivíduos com condições adversas subjacentes. Um número não negligenciável de pacientes internados com este vírus tinham doenças cardiovasculares ou cerebrovasculares. A resposta inflamatória sistêmica e distúrbios do sistema imunológico durante a progressão da doença podem estar por trás dessa associação. Além disso, o vírus usa os receptores da enzima conversora da angiotensina (ECA), mais especificamente da ECA2, para penetrar nas células; portanto, o uso de fármacos inibidores de ECA e bloqueadores de receptores de angiotensina pode causar um aumento nestes receptores, assim facilitando a entrada do vírus na célula. No entanto, não há evidências científicas que apóiem a interrupção desses medicamentos. Considerando que são fundamentais para o manejo de certas doenças crônicas, os riscos e benefícios da sua retirada devem ser cuidadosamente ponderados neste cenário. Finalmente, cardiologistas e profissionais de saúde devem estar cientes dos riscos de infecção e se proteger o máximo possível, dormindo adequadamente e evitando longos turnos de trabalho.