ABSTRACT
OBJECTIVE: The longitudinal trajectories of cardiac structure and function following SARS-CoV-2 infection are unclear. Therefore, this meta-analysis aims to elucidate the effect of SARS-CoV-2 infection on cardiac function in COVID-19 survivors after recovery. METHODS: PubMed/MEDLINE, CENTRAL, and EMBASE were systematically searched for articles published up to 1st August 2022. A systematic review and meta-analysis were performed to calculate the pooled effects size and 95% confidence interval (CI) of each outcome. RESULTS: Twenty-one studies including 2394 individuals (1436 post-COVID-19 cases and 958 controls) were included in the present meta-analysis. The pooled analyses compared with control groups showed a significant association between post-COVID-19 and reduced left ventricular ejection fraction (LV EF), LV end-diastolic volume (LV EDV), LV stroke volume (LV SV), mitral annular plane systolic excursion (MAPSE), global longitudinal strain (GLS), right ventricular EF (RV EF), RV EDV, RV ESV, RV SV, tricuspid annular plane systolic excursion (TAPSE), and increased LV mass. Subgroup analysis based on the severity of COVID-19 in the acute phase and subsequent chronic outcomes revealed that LV EF, MAPSE, RV EF, and RV ESV only decreased in studies including patients with a history of intensive care unit (ICU) admission. CONCLUSION: Cardiac impairment after SARS-CoV-2 infection persisted in recovered COVID-19 patients even after one year. Future studies are warranted to determine the biological mechanisms underlying the long-term cardiovascular consequences of COVID-19. This article is protected by copyright. All rights reserved.
ABSTRACT
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.