As our understanding of the complications of coronavirus disease–2019 (COVID-19) evolve, sub-clinical cardiac pathology such as myocarditis, pericarditis and right ventricular dysfunction in the absence of significant clinical symptoms represents a concern. The potential implications of these findings in athletes are significant given the concern that exercise, during the acute phase of viral myocarditis, may exacerbate myocardial injury and precipitate malignant ventricular arrhythmias. Such concerns have led to the development and publication of expert consensus documents aimed at providing guidance for the evaluation of athletes after contracting COVID-19 in order to permit safe return-to-play. Cardiac imaging is at the center of these evaluations. This review seeks to evaluate the current evidence regarding COVID-19associated cardiovascular disease and how multi-modality imaging may be useful in the screening and clinical evaluation of athletes with suspected cardiovascular complications of infection. Guidance is provided with diagnostic “red flags” that raise the suspicion of pathology. Specific emphasis is placed on the unique challenges posed in distinguishing athletic cardiac remodeling from sub-clinical cardiac disease. The strengths and limitations of different imaging modalities are discussed and an approach to return-to-play decision making for athletes’ post COVID-19, as informed by multi-modality imaging, is provided.
There is wide variability in the physical activity patterns of the patients in contemporary clinical cardiovascular practice. This review is designed to address the impact of exercise dose on key cardiovascular risk factors and on mortality. We begin by examining the body of literature that supports a dose-response relationship between exercise and cardiovascular disease risk factors including plasma lipids, hypertension, diabetes mellitus, and obesity. We next explore the relationship between exercise dose and mortality by reviewing the relevant epidemiological literature underlying current physical activity guideline recommendations. We then expand this discussion to critically examine recent data pertaining to the impact of exercise dose at the lowest and highest ends of the spectrum. Finally, we provide a framework for how the key concepts of exercise dose can be integrated into clinical practice.
E xercise-induced cardiac remodeling (EICR) refers to changes in cardiac structure and function that occur in response to exercise training. Numerous structural aspects of EICR (ie, athlete's heart) including ventricular chamber enlargement 1 and hypertrophy 2 have been described, and several key determinants of the EICR process including age, 3 sex, 4 ethnicity, 5 and sporting discipline 6,7 have been established. However, contemporary understanding of EICR is based largely on cross-sectional data derived from competitive athletes and instructive but relatively short duration longitudinal studies of recreational exercisers. 8,9 Therefore, the temporal progression of EICR among competitive athletes remains incompletely understood. See Clincial Perspective See Editorial by D'Silva and SharmaThe myocardial response to hemodynamic perturbation occurs in discrete phases in numerous settings. Specifically, physiological remodeling after 12 months of exercise training in previously sedentary people 9 and cardiac adaptations during pregnancy 10 occurs in different stages. In addition, numerous cardiac disease states are defined by phasic adaptations in myocardial structural and function. 11,12 Whether the EICR that occurs among competitive athletes develops in a phasic sequence remains unknown because of the lack of long-term longitudinal data. Determining the time course of EICR represents a critical step in further defining the myocardial response Background-Contemporary understanding of exercise-induced cardiac remodeling is based on cross-sectional data and relatively short duration longitudinal studies. Temporal progression of exercise-induced cardiac remodeling remains incompletely understood. Methods and Results-A longitudinal repeated-measures study design using 2-dimensional and speckle-tracking echocardiography was used to examine acute augmentation phase (AAP; 90 days) and more extended chronic maintenance phase (39 months) left ventricular (LV) structural and functional adaptations to endurance exercise training among competitive male rowers (n=12; age 18.6±0.5 years). LV mass was within normal limits at baseline (93±9 g/ m 2 ), increased after AAP (105±7 g/m 2 ; P=0.001), and further increased after chronic maintenance phase (113±10 g/m 2 ; P<0.001 for comparison to post-AAP). AAP LV hypertrophy was driven by LV dilation (ΔLV end-diastolic volume, 9±3 mL/m 2 ; P=0.004) with stable LV wall thickness (ΔLV wall thickness, 0.3±0.1 mm; P=0.63). In contrast, chronic maintenance phase LV hypertrophy was attributable to LV wall thickening (Δ LV wall thickness, 1.1±0.4 mm; P=0.004) with stable LV chamber volumes (ΔLV end-diastolic volume, 1±1 mL/m 2 ; P=0.48). Early diastolic peak tissue velocity increased during AAP (−11.7±1.9 versus −13.6±1.3 cm/s; P<0.001) and remained similarly increased after chronic maintenance phase. Conclusions-In a small sample of competitive endurance athletes, exercise-induced cardiac remodeling follows a phasic response with increases in LV chamber size, early diastolic function, and sy...
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