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Background: The relation between ventricular arrhythmia and fibrosis in mitral valve prolapse (MVP) is reported, but underlying valve-induced mechanisms remain unknown. We evaluated the association between abnormal MVP-related mechanics and myocardial fibrosis, and their association with arrhythmia. Methods: We studied 113 patients with MVP with both echocardiogram and gadolinium cardiac magnetic resonance imaging for myocardial fibrosis. Two-dimensional and speckle-tracking echocardiography evaluated mitral regurgitation, superior leaflet and papillary muscle displacement with associated exaggerated basal myocardial systolic curling, and myocardial longitudinal strain. Follow-up assessed arrhythmic events (nonsustained or sustained ventricular tachycardia or ventricular fibrillation). Results: Myocardial fibrosis was observed in 43 patients with MVP, predominantly in the basal-midventricular inferior-lateral wall and papillary muscles. Patients with MVP with fibrosis had greater mitral regurgitation, prolapse, and superior papillary muscle displacement with basal curling and more impaired inferior-posterior basal strain than those without fibrosis ( P P 6-month follow-up developed ventricular arrhythmias associated (univariable) with fibrosis, greater prolapse, mitral annular disjunction, and double-peak strain. In multivariable analysis, double-peak strain showed incremental risk of arrhythmia over fibrosis. Conclusions: Basal inferior-posterior myocardial fibrosis in MVP is associated with abnormal MVP-related myocardial mechanics, which are potentially associated with ventricular arrhythmia. These associations suggest pathophysiological links between MVP-related mechanical abnormalities and myocardial fibrosis, which also may relate to ventricular arrhythmia and offer potential imaging markers of increased arrhythmic risk.

The global pandemic of COVID-19 caused by infection with SARS-CoV-2 is now entering its fourth year with little evidence of abatement. As of December 2022, the World Health Organization Coronavirus (COVID-19) Dashboard reported 643 million cumulative confirmed cases of COVID-19 worldwide and 98 million in the United States alone as the country with the highest number of cases. Although pneumonia with lung injury has been the manifestation of COVID-19 principally responsible for morbidity and mortality, myocardial inflammation and systolic dysfunction though uncommon are well-recognized features that also associate with adverse prognosis. Given the broad swath of the population infected with COVID-19, the large number of affected professional, collegiate, and amateur athletes raises concern regarding the safe resumption of athletic activity (return to play) following resolution of infection. A variety of different testing combinations that leverage ECG, echocardiography, circulating cardiac biomarkers, and cardiovascular magnetic resonance imaging have been proposed and implemented to mitigate risk. Cardiovascular magnetic resonance in particular affords high sensitivity for myocarditis but has been employed and interpreted nonuniformly in the context of COVID-19 thereby raising uncertainty as to the generalizability and clinical relevance of findings with respect to return to play. This consensus document synthesizes available evidence to contextualize the appropriate utilization of cardiovascular magnetic resonance in the return to play assessment of athletes with prior COVID-19 infection to facilitate informed, evidence-based decisions, while identifying knowledge gaps that merit further investigation.

Background— Right ventricular (RV) and left ventricular (LV) function are closely linked due to a variety of factors, including common coronary blood supply. Altered LV perfusion holds the potential to affect the RV, but links between LV ischemia and RV performance, and independent impact of RV dysfunction on effort tolerance, are unknown. Methods and Results— The population comprised 2051 patients who underwent exercise stress myocardial perfusion imaging and echo (5.5±7.9 days), among whom 6% had echo-evidenced RV dysfunction. Global summed stress scores were ≈3-fold higher among patients with RV dysfunction, attributable to increments in inducible and fixed LV perfusion defects (all P ≤0.001). Regional inferior and lateral wall ischemia was greater among patients with RV dysfunction (both P P =0.13). In multivariable analysis, inducible inferior and lateral wall perfusion defects increased the likelihood of RV dysfunction (both P P P P P P Conclusions— Among patients with known or suspected coronary artery disease, regional LV ischemia involving the inferior and lateral walls confers increased likelihood of RV dysfunction. RV dysfunction impairs exercise tolerance independent of LV dysfunction.

Acute ST-segment–elevation myocardial infarction (STEMI) is estimated to occur in over 3 million patients each year.1 Left ventricular (LV) thrombus is a serious complication of STEMI, which has been attributed to blood stasis resulting from LV contractile dysfunction and altered geometry (aneurysm). Advances in STEMI management bear particular relevance to LV thrombus: improved coronary reperfusion has augmented myocardial salvage, resulting in improved LV function and remodeling. Newly adopted standard of care therapies, such as thienopyridines, inhibit platelet aggregation, thereby potentially decreasing risk for thrombus. However, despite widespread changes in post-STEMI care, limited data exists concerning LV thrombus in the current era. Given that LV thrombus provides a substrate for embolic events and a rationale for anticoagulation, better understanding of prevalence, predictors, and prognostic significance of post-STEMI LV thrombus is of substantial importance. See Article by Poss et al Beyond changes in clinical management, advances in noninvasive imaging provide a strong rationale for revisiting post-STEMI LV thrombus. Echocardiography (echo) has traditionally been used as the primary modality for evaluating STEMI patients because it is widely available, inexpensive, and supported by ample data demonstrating that echo-based quantification of LV structure and function stratifies post-STEMI prognosis.2,3 However, echo can be limited with respect to LV thrombus. Image quality can be compromised by near field artifacts that obscure the LV apex, a location in which thrombus is often suspected. More broadly, echo limitations may stem from the approach by which thrombus is diagnosed. Echo identifies thrombus based on morphology. This approach can be straightforward when thrombus is large or protuberant, but challenging when thrombus is small or flat (mural). Consistent with these concepts, echo studies have reported marked variability in thrombus prevalence and prognostic significance4,5 and reported substantial inter-reader variability concerning diagnosis of LV thrombus.6 Given …