Objective To evaluate the race-stratified state-level prevalence of health determinants and the racial disparities in coronavirus disease-2019 (COVID-19) cumulative incidence and mortality in the United States. Patients and Methods Age-adjusted race-stratified prevalence of comorbidities (hypertension, diabetes, dyslipidemia, obesity), preexisting medical conditions (pulmonary disease, heart disease, stroke, kidney disease, malignancy), poor health behaviors (smoking, alcohol abuse, physical inactivity), and adverse socioeconomic factors (education, household income, health insurance) was computed in 435,139 American adult participants from 2017 Behavioral Risk Factor Surveillance System survey (BRFSS). Correlation was assessed between health determinants and the race-stratified COVID-19 crude mortality and infection-fatality-ratio computed from respective state public health departments in 47 states. Results Blacks had a higher prevalence of comorbidities (63.3% [95%CI:62.4-64.2%] vs. 55.1% [95%CI:54.7-55.5]) and adverse socioeconomic factors (47.0% [95%CI:46.0-47.9%] vs. 30.9% [95%CI:30.6-31.3]) than Whites. The prevalence of preexisting medical conditions was similar among Blacks (30.4% [95%CI:28.8-32.1%]) and Whites (30.8% [95%CI:30.2-31.4%]). The prevalence of poor health behaviors was higher in Whites (57.2% [95%CI:56.3-58.0%]) than Blacks (50.2% [95%CI:46.2-54.2%]). The comorbidities and adverse socioeconomic factors were highest in the Southern region, and poor health behaviors were highest in the Western region. Cumulative incidence rate (per 100,000 persons) was three-fold higher in Blacks (1546.4) compared withwith Whites (540.4). The crude mortality (per 100,000 persons) was two-fold higher in Blacks (83.2) than Whites (33.2). However, the infection-fatality-ratio (per 100-cases) was similar between Whites (6.2) and Blacks (5.4). Within racial groups, the geographic distribution of health determinants did not correlate with state-level COVID-19 mortality and infection-fatality ratio (p>0.05 for all). Conclusions Racial disparities in COVID-19 are largely driven by the higher cumulative incidence of infection in Blacks. There is a discordance between the geographic dispersion of COVID-19 mortality and the regional distribution of health determinants.

Background The burden of insulin resistance (IR) among young American adults has not been previously assessed. We evaluated the 1) prevalence and trends of IR and cardiometabolic risk factors and, 2) assessed the association between measures of adiposity and IR among adults aged 18-44 years without diabetes and preexisting cardiovascular disease. Methods Cross-sectional survey data from six consecutive National Health and Nutrition Examination Survey (2007-2008 to 2017-2018) cycles were analyzed. IR was defined by the homeostatic model assessment for IR (HOMA-IR) of ≥2.5. The temporal trends of IR, cardiometabolic risk factors, and the relationship between IR and measures of adiposity were assessed using multivariable-adjusted regression models. Results Among 6,247 young adults aged 18-44 years, the prevalence of IR was 44.8% (95% CI: 42.0-47.6%) in 2007-2010 and 40.3% (95% CI: 36.4-44.2%) in 2015-2018 (Ptrend=0.07). There was a modest association of HOMA-IR with higher body mass index (BMI), waist circumference, total lean fat mass, and total and localized fat mass (all p<0.001). Participants with IR had a higher prevalence of hypertension (31.3% [95% CI: 29.2-33.5%] vs. 14.7% [95% CI: 13.2-16.2%]), hypercholesterolemia (16.0% [95% CI: 12.4-19.5%] vs. 7.0% [95% CI: 5.8-8.5%]), obesity (56.6% [95% CI: 53.9-59.3%] vs. 14.7% [95%CI: 13.0-16.5%]) and poor physical activity levels (18.3% [95% CI: 16.4-20.2%] vs. 11.7% [95%CI: 10.3-13.1%]) compared to participants without IR (all p<0.05). Conclusions Four-in-ten young American adults have IR, which occurs in a cluster with cardiometabolic risk factors. Nearly half of young adults with IR are non-obese. Screening efforts for IR irrespective of BMI may be required.

Background Myocardial injury is associated with excess mortality in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, and the mechanisms of injury are diverse. Coagulopathy associated with this infection may have unique cardiovascular implications. Case summary We present a case of 62-year-old male who presented after experiencing syncope and cardiac arrest. Given the clinical presentation and electrocardiographic findings, there was concern for acute coronary syndrome. However, coronary angiogram did not reveal significant coronary obstruction. Due to the unclear nature of his presentation, a bedside echocardiogram was rapidly performed and was indicative of right ventricular strain. Due to these findings, a pulmonary angiogram was performed that revealed massive pulmonary embolism. He successfully underwent catheter-directed thrombolysis and, after a prolonged hospital stay, was discharged home on lifelong anticoagulation. Discussion The impact of coronavirus disease-2019 (COVID-19) on the cardiovascular system has been prominent and multifaceted. COVID-19 can have wide-ranging effects on the cardiovascular system due to coagulopathy with resultant venous and arterial thrombo-embolism. Due to the critical condition of many patients affected by COVID-19, imaging for thrombo-embolic events is often delayed. With the use of bedside echocardiogram, observation of right ventricular strain may be critical in raising suspicion for pulmonary embolism, especially when atypical features are noted on electrocardiogram.

Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is commonly associated with myocardial injury and heart failure. The pathophysiology behind this phenomenon remains unclear, with many diverse and multifaceted hypotheses. To contribute to this understanding, we describe the underlying cardiac findings in fifty patients who died with coronavirus disease 2019 (COVID-19). Methods Included were autopsies performed on patients with a positive SARS-CoV-2 reverse-transcriptase-polymerase-chain reaction test from the index hospitalization. In the case of out-of-hospital death, patients were included if post-mortem testing was positive. Complete autopsies were performed according to a COVID-19 safety protocol, and all patients underwent both macroscopic and microscopic examination. If available, laboratory findings and echocardiograms were reported. Results The median age of the decedents was 63.5 years. The most common comorbidities included hypertension (90.0%), diabetes (56.0%) and obesity (50.0%). Lymphocytic inflammatory infiltrates in the heart were present in eight (16.0%) patients, with focal myocarditis present in two (4.0%) patients. Acute myocardial ischemia was observed in eight (16.0%) patients. The most common findings were myocardial fibrosis (80.0%), hypertrophy (72.0%), and microthrombi (66.0%). The most common causes of death were COVID-19 pneumonia in 18 (36.0%), COVID-19 pneumonia with bacterial superinfection in 12 (24.0%), and COVID-19 pneumonia with pulmonary embolism in 10 (20.0%) patients. Conclusions Cardiovascular comorbidities were prevalent, and pathologic changes associated with hypertensive and atherosclerotic cardiovascular disease were the most common findings. Despite markedly elevated inflammatory markers and cardiac enzymes, few patients exhibited inflammatory infiltrates or necrosis within cardiac myocytes. A unifying pathophysiologic mechanism behind myocardial injury in COVID-19 remains elusive, and additional autopsy studies are needed.

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Background Over the past two years, the utilization of venovenous extracorporeal membrane oxygenation (VV-ECMO) for the treatment of coronavirus disease 2019 (COVID-19) acute respiratory distress syndrome (ARDS) has increased. While supporting respiratory function, VV-ECMO requires large-bore indwelling venous cannulas, which risk bleeding and infections, including endocarditis. Case Summary We describe two adults hospitalized for COVID-19 pneumonia who developed ARDS and right ventricular failure, requiring VV-ECMO and ProtekDuo cannulation. After over 100 days with these devices, both patients developed tricuspid valve vegetations. Our first patient was decannulated from ECMO and discharged, but re-presented with a segmental pulmonary embolism and tricuspid mass. The Inari FlowTriver system was chosen to percutaneously remove both the tricuspid mass and pulmonary thromboembolism. Pathological examination of the mass demonstrated Candida albicans endocarditis in the setting of Candida fungemia. Our second patient developed a tricuspid valve vegetation which was also removed with the FlowTriever system. Pathologic examination demonstrated endocarditis consistent with Pseudomonas aeruginosa in the setting of Pseudomonas bacteremia. Both patients experienced resolution of fungemia and bacteremia after percutaneous vegetation removal. After ECMO decannulation and percutaneous debulking, both patients experienced prolonged hospital stays for ventilator weaning and were eventually discharged with supplemental oxygen. Discussion VV-ECMO and right ventricular support devices are invasive and create various risks, including bloodstream infection and infective endocarditis. Percutaneous debulking of valvular vegetations associated with these right-sided indwelling devices may be an effective means of infection source control. It is unclear whether prolonged use of VV-ECMO provides a mortality benefit in COVID-19 ARDS.

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Background: Among patients receiving percutaneous coronary intervention (PCI), the role of a genotype-guided approach for antiplatelet therapy compared with usual care is unclear. We conducted a Bayesian analysis of the entire TAILOR-PCI (Tailored Antiplatelet Initiation to Lessen Outcomes Due to Decreased Clopidogrel Response After Percutaneous Coronary Intervention) randomized clinical trial population to evaluate the effect of the genotype-guided antiplatelet therapy post-PCI compared with the usual care on the risk of major adverse cardiovascular events (MACE). Methods: The primary outcome for our study was the composite of MACE (myocardial infarction, stroke, and cardiovascular death). Secondary outcomes included cardiovascular death, stroke, myocardial infarction, stent thrombosis, and major/minor bleeding. Bayesian modeling was used to estimate the probability of clinical benefit of genotype-guided therapy using (1) noninformative priors (ie, analyzing the TAILOR-PCI trial) and (2) informative priors derived from the ADAPT, POPular Genetics, IAC-PCI, and PHARMCLO trials (ie, analyzing TAILOR-PCI trial in the context of prior evidence). Risk ratio (RR: ratio of cumulative outcome incidence between genotype-guided and conventional therapy group) and 95% credible interval (CrI) were estimated for the study outcomes, and probability estimates for RR <1 were computed. Results: Using noninformative priors, in TAILOR-PCI the RR for MACE was 0.78 (95% CrI, 0.55–1.07) in genotype-guided therapy after PCI, and the probability of RR <1 was 94%. Using noninformative priors, the probability of RR <1 for cardiovascular death (RR, 0.95 [95% CrI, 0.52–1.74]), stroke (RR, 0.68 [95% CrI, 0.44–1.06]), myocardial infarction (RR, 0.84 [95% CrI, 0.37–1.89]), stent thrombosis (RR, 0.75 [95% CrI, 0.37–1.45]), and major or minor bleeding (RR, 1.22 [95% CrI, 0.84–1.77]) were 57%, 96%, 67%, 94%, and 15%, respectively. Using informative priors, the posterior probability of RR <1 for MACE, from genotype-guided therapy, was 99% (RR, 0.69 [95% CrI, 0.57–0.84]). Using informative priors, the posterior probability of RR <1 for cardiovascular death (RR, 0.86 [95% CrI, 0.61–1.19]), stroke (RR, 0.69 [95% CrI, 0.48–0.99]), myocardial infarction (RR:0.56 [95% CrI, 0.40–0.78]), stent thrombosis (RR, 0.59 [95% CrI, 0.38–0.94]), and major or minor bleeding (RR, 0.84 [95% CrI, 0.70–0.99]) were 81%, 99%, 99%, 99%, and 99%, respectively. Conclusions: Bayesian analysis of the TAILOR-PCI trial provides clinically meaningful data on the posterior probability of reducing MACE using genotype-guided P2Y 12 inhibitor therapy after PCI.