Cardiovascular effects of COVID-19 lockdown in professional football players.

BACKGROUND: The COVID-19 pandemic with the stay-at-home orders and lockdown has dramatically forced athletes to stop team training and competitions, causing deep changes in habits and lifestyle. Aim of this study was to evaluate in a retrospective single center study the cardiovascular (CV) health and fitness of elite football player after COVID-19 lockdown in Italy and to compare such findings with the 2019 off-season period, in order to identify potential differences in the CV features and outcomes. METHODS: All 29 professional football players of the first male team were enrolled before resuming training and competition after COVID-19 lockdown and underwent several exams including physical examination, resting and stress electrocardiography (ECG), echocardiography, spirometry and blood tests. RESULTS: Median age was 27 years (23; 31), with no athlete being COVID-19 positive at the time of the evaluation. In comparison with the usual off-season 2-month detraining, significant differences were found for left ventricular (LV) mass (189 g [172; 212] vs. 181 g [167; 206], P=0.024) and LV Mass Index for body surface area (94 g/m2 [85; 104] vs. 88 g/m2 [79.5; 101.5], P=0.017), while LV mass/fat free mass remained unchanged (2.8 g/kg [2.6; 2.9] vs. 2.9 g/kg [2.6; 3.2], P=0.222). Respiratory function and metabolic profile were improved, while no significant changes were found in ECG findings, at rest and during exercise. CONCLUSIONS: Prolonged abstinence from training and competitions induced by lockdown elicited significant changes in comparison with off-season in parameters ascribable to detraining, as the changes in LV mass, in respiratory function and in metabolic profile.

Local immune activity in acute coronary syndrome: oxLDL abrogates LPS-tolerance in mononuclear cells isolated from culprit lesion.

BACKGROUND: OxLDL plays a major role in the initiation and progression of atherosclerotic lesions even though further factors are needed to promote fibrous cap rupture and thrombotic occlusion of the arterial lumen. Pathogens have been implicated in this process but it remains unclear how they can cooperate with oxLDL in amplifying the destructive inflammatory response. OBJECTIVE: To phenotypically analyze culprit coronary inflammatory cells, evaluate their responsiveness to endotoxins and ascertain whether oxLDL alters the sensitivity of coronary mononuclear cells to bacterial components. METHODS: Mononuclear cells isolated from culprit and non-culprit coronary blood samples of patients with ST-segment elevation myocardial infarction (STEMI) and controls were analyzed for cell-specific surface markers and cytokines by flow-cytometry. RESULTS AND CONCLUSIONS: CD14+ cells contained elevated levels of TLR4, expressed high CD80, and produced huge amounts of inflammatory cytokines in response to LPS. Using a well-established model of endotoxin tolerance, we next showed that mononuclear cells isolated from control coronary artery, but not from culprit coronary artery, were tolerant to LPS, but pre-treatment of such cells with oxLDL abrogated LPS tolerance. Flow-cytometry analysis also showed that IL-17A, IL-21 and IFN-γ were over-produced by CD4+ and CD56+ cells isolated from the culprit coronary artery. All this data indicate that monocytes circulating in the culprit coronary artery of patients with STEMI are primed to synthesize high levels of inflammatory cytokines and suggest that oxLDL can amplify the inflammatory response of such cells to endotoxins.