Stephen M. Ratchford

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.