The effect of SARS‐CoV‐2 infection on cardiac function in post‐COVID‐19 survivors: A systematic review and meta‐analysis

Abstract

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 coronavirus disease 2019 (COVID‐19) survivors after recovery. 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 of each outcome. A total of 21 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, right ventricular EF (RV EF), RV EDV, RV ESV, RV SV, tricuspid annular plane systolic excursion, 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 admission. Cardiac impairment after SARS‐CoV‐2 infection persisted in recovered COVID‐19 patients even after 1 year. Future studies are warranted to determine the biological mechanisms underlying the long‐term cardiovascular consequences of COVID‐19.

Impact of COVID-19 Infection on Cardiorespiratory Fitness, Sleep, and Psychology of Endurance Athletes– CAESAR Study

“…We conducted a study that included: a double CPET assessment, and a mental health Exclusion criteria: pulmonary condition (COPD, uncontrolled bronchial asthma, blood saturation <95%), cardiovascular disease (arrhythmia confirmed by ECG, ischemia of myocardium, QT prolongation confirmed by ECG, morphological heart abnormalities confirmed by echocardiography, uncontrolled hypertension >160/100 mmHg), [28] present mental condition, (4) an orthopedic condition that prevents EA to perform CPET, (5) deviations in CBC (leukocytosis >10,000•mm -3 , anemia with blood hemoglobin <10g•dL -1 ).…”

“…[4]. COVID-19 infection has been shown to have an adverse effect on the heart function of patients who survived the infection [5]. A greater tendency to reduced left ventricular ejection fraction, end-diastolic volume, stroke volume was found.…”

Infection with critically ill COVID‐19 increases the risk of cardioembolic stroke

“…studies have indicated the potential for individuals to experience long-term cardiovascular and cerebrovascular complications following recovery from severe COVID-19 infection. [3][4][5] Notably, the risk of stroke appears to be notably elevated in patients who have experienced severe COVID-19. 4,6 However, existing studies have certain limitations that warrant further exploration.…”

Lactate dehydrogenase contribution to symptom persistence in long COVID: A pooled analysis

“…More than three years into the COVID‐19 pandemic, and at least 65 million people are believed to be living with long COVID (also known as post‐acute sequelae of COVID‐19 (PASC) as at January 2023 1 . According to the Centre for Disease Control, long COVID is defined as a post‐COVID‐19 condition in which there is new, evolving or persistent health issues occurring ≥4 weeks after SARS‐CoV‐2 infection 2 Emerging evidence reports that fatigue (27.4%), anosmia (25%), impaired lung diffusion capacity (24.6%), alopecia (10.2%), and dyspnoea (10.1%) are the most frequent symptoms and findings in COVID‐19 survivors 2 years after SARS‐CoV‐2 infection 3 …”

“…Long COVID symptoms have been demonstrated to have a crippling effect with significant impact on patient's quality of life 1 . Globally, labour force has struggled owing to a good number of long COVID patients that are yet to return to their original work and presently, there are no known effective pharmacological or non‐pharmacological interventions 1,3,9 . Though myriads of pathophysiological factors have been implicated including dysregulated immune response that results in some degree of tissue damage, 10 the exact cause of residual symptoms remains unclear 11 …”