Endothelial-dependent coronary artery dilation and increased blood flow in healthy subjects, and their absence in CAD patients, can now be directly visualized and quantified noninvasively. Local coronary endothelial function differs between severely and mildly diseased arteries in a given CAD patient. This novel, safe method may offer new insights regarding the importance of local coronary endothelial function and improved risk stratification in patients at risk for and with known CAD.

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Background: Knowledge gaps remain in the epidemiology and clinical implications of myocardial injury in COVID-19. Our goal was to determine the prevalence and outcomes of myocardial injury in severe COVID-19 compared to acute respiratory distress syndrome (ARDS) unrelated to COVID-19. Methods: We included intubated COVID-19 patients from 5 hospitals between March 15 and June 11, 2020 with troponin levels assessed. We compared them to patients from a cohort study of myocardial injury in ARDS. We performed survival analysis with primary outcome of in-hospital death associated with myocardial injury. We performed linear regression to identify clinical factors associated with myocardial injury in COVID-19. Results: Of 243 patients intubated with COVID-19, 51% had troponin levels > upper limit of normal (ULN). Chronic kidney disease, lactate, ferritin and fibrinogen were associated with myocardial injury. Mortality was 22.7% among COVID-19 patients with troponin < ULN and 61.5% for those with troponin levels > 10xULN (P< 0.001). The association of myocardial injury with mortality was not statistically significant after adjusting for age, sex and multi-system organ dysfunction. Compared to non-COVID ARDS patients, patients with COVID-19 were older with higher creatinine and less favorable vital signs. After adjustment, COVID-19 was associated with lower odds of myocardial injury compared to non-COVID ARDS (OR 0.55 95% CI 0.36-0.84, P=0.005). Conclusions: Myocardial injury in severe COVID-19 is a function of baseline comorbidities, advanced age and multisystem organ dysfunction similar to traditional ARDS. The adverse prognosis of myocardial injury in COVID-19 relates largely to multisystem organ involvement and critical illness.

Background and Purpose-Left ventricular dysfunction (LVD) is associated with cardiovascular mortality. Its association with ischemic stroke has been mainly documented after myocardial infarction. The stroke risk associated with LVD, especially of mild degree, in the general population is unclear. The purpose of this study was to evaluate the relationship between LVD and ischemic stroke in a multiethnic cohort. Methods-LV systolic function was assessed by transthoracic 2-dimensional echocardiography in a subset of subjects from the Northern Manhattan Study (NOMAS), 270 patients with first ischemic stroke and 288 age-, gender-and race-matched community controls. LV ejection fraction was measured by a simplified cylinder-hemiellipsoid formula, and categorized as normal (Ͼ50%), mildly (41% to 50%), moderately (31% to 40%) or severely (Յ30%) decreased. The association between impaired ejection fraction and ischemic stroke was evaluated by logistic regression analysis after adjustment for established stroke risk factors. Results-LVD of any degree was more frequent in stroke patients (24.1%) than in controls (4.9%; PϽ0.0001), as was moderate/severe LVD (13.3% versus 2.4%; PϽ0.001). A decreased ejection fraction was associated with ischemic stroke even after adjusting for other stroke risk factors. The adjusted odds ratio for any degree of LVD was 3.92 (95% CI, 1.93 to 7.97). The adjusted odds ratio for mild LVD was 3.96 (95% CI, 1.56 to 10.01) and for moderate/severe LVD 3.88 (95% CI, 1.45 to 10.39). The association between LVD of any degree and stroke was present in all age, gender and race-ethnicity subgroups. Conclusions-LVD, even of mild degree, is independently associated with an increased risk of ischemic stroke. The assessment of LV function should be considered in the assessment of the stroke risk.