Monthly transthoracic echocardiography in young adults for 6 months following SARS-CoV-2 infection.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can elicit acute and long-term effects on the myocardium among survivors, yet effects among otherwise healthy young adults remains unclear. Young adults with mild symptoms of SARS-CoV-2 (8M/8F, age: 21 ± 1 years, BMI: 23.5 ± 3.1 kg·m-2 ) underwent monthly transthoracic echocardiography (TTE) and testing of circulating cardiac troponin-I for months 1-6 (M1-M6) following a positive polymerase chain reaction test to better understand the acute effects and post-acute sequelae of SARS-CoV-2 on cardiac structure and function. Left heart structure and ejection fraction were unaltered from M1-M6 (p > 0.05). While most parameters of septal and lateral wall velocities, mitral and tricuspid valve, and pulmonary vein (PV) were unaltered from M1-M6 (p > 0.05), lateral wall s' wave velocity increased (M1: 0.113 ± 0.019 m·s-1 , M6: 0.135 ± 0.022 m·s-1 , p = 0.013); PV S wave velocity increased (M1: 0.596 ± 0.099 m·s-1 , M6: 0.824 ± 0.118 m·s-1 , p < 0.001); the difference between PV A wave and mitral valve (MV) A wave durations decreased (M1: 39.139 ± 43.715 ms, M6: 18.037 ± 7.227 ms, p = 0.002); the ratio of PV A duration to MV A duration increased (M1: 0.844 ± 0.205, M6: 1.013 ± 0.132, p = 0.013); and cardiac troponin-I levels decreased (M1: 0.38 ± 0.20 ng·ml-1 , M3: 0.28 ± 0.34 ng·ml-1 , M6: 0.29 ± 0.16 ng·ml-1 ; p = 0.002) over time. While young adults with mild symptoms of SARS-CoV-2 lacked changes to cardiac structure, the subclinical improvements to cardiac function and reduced inflammatory marker of cardiac troponin-I over 6 months following SARS-CoV-2 infection provide physiologic guidance to post-acute sequelae and recovery from SARS-CoV-2 and its variants using conventional TTE.

Racial and ethnic disparities in cardiometabolic disease and COVID-19 outcomes in White, Black/African American, and Latinx populations: Physiological underpinnings.

Coronavirus disease 2019 (COVID-19) is a highly contagious respiratory illness caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) that began spreading globally in late 2019. While most cases of COVID-19 present with mild to moderate symptoms, COVID-19 was the third leading cause of mortality in the United States in 2020 and 2021. Though COVID-19 affects individuals of all races and ethnicities, non-Hispanic Black and Hispanic/Latinx populations are facing an inequitable burden of COVID-19 characterized by an increased risk for hospitalization and mortality. Importantly, non-Hispanic Black and Hispanic/Latinx adults have also faced a greater risk of non-COVID-19-related mortality (e.g., from cardiovascular disease/CVD) during the pandemic. Contributors to the racial disparities in morbidity and mortality during the pandemic are multi-factorial as we discuss in our companion article on social determinants of health. However, profound racial variation in the prevalence of CVD and metabolic diseases may serve as a key driver of worse COVID-19-related and non-COVID-19-related health outcomes among racial and ethnic minority groups. Within this review, we provide data emphasizing the inequitable burden of CVD and metabolic diseases among non-Hispanic Black and Hispanic/Latinx populations. We also discuss the pathophysiology of these conditions, with a focus on how aberrant physiological alterations in the context of CVD and metabolic diseases manifest to increase susceptibility to severe COVID-19.

Racial and ethnic disparities in cardiometabolic disease and COVID-19 outcomes in White, Black/African American, and Latinx populations: Social determinants of health.

Racial and ethnic-related health disparities in the United States have been intensified by the greater burden of Coronavirus Disease 2019 (COVID-19) in racial and ethnic minority populations. Compared to non-Hispanic White individuals, non-Hispanic Black and Hispanic/Latinx individuals infected by COVID-19 are at greater risk for hospitalization, intensive care unit admission, and death. There are several factors that may contribute to disparities in COVID-19-related severity and outcomes in these minority populations, including the greater burden of cardiovascular and metabolic diseases as discussed in our companion review article. Social determinants of health are a critical, yet often overlooked, contributor to racial and ethnic-related health disparities in non-Hispanic Black and Hispanic/Latinx individuals relative to non-Hispanic White individuals. Thus, the purpose of this review is to focus on the essential role of social factors in contributing to health disparities in chronic diseases and COVID-19 outcomes in minority populations. Herein, we begin by focusing on structural racism as a social determinant of health at the societal level that contributes to health disparities through downstream social level (e.g., occupation and residential conditions) and individual level health behaviors (e.g., nutrition, physical activity, and sleep). Lastly, we conclude with a discussion of practical applications and recommendations for future research and public health efforts that seek to reduce health disparities and overall disease burden.