Key result
Severe acute COVID-19 is linked to ~3-fold higher 4-year risk of LV systolic dysfunction.
Why the study?
Myocardial injury is observed during acute COVID-19 infection, but whether it persists at long-term follow-up and is associated with acute infection severity remained unclear.
Does increasing acute COVID-19 infection severity worsen long-term cardiac structure and function at 4 years in patients with prior confirmed COVID-19?
Cohort (n=695)
Does increasing acute COVID-19 infection severity worsen long-term cardiac structure and function at 4 years in patients with prior confirmed COVID-19?
Greater acute COVID-19 severity is associated with persistent echocardiographic abnormalities in left and right ventricular function as well as pulmonary congestion and dyspnea up to 4 years post-infection.
May support targeted echo surveillance after severe COVID-19; leaves open whether findings warrant routine screening or alter management.
Introduction Myocardial injury has been observed during the acute phase of COVID-19 infection. Whether this persists at long-term follow-up and if there is an association with acute COVID-19 severity is unclear. Aim To investigate the long-term effects of acute COVID-19 infection severity on cardiac structure and function. Method This study included patients with prior confirmed COVID-19 infection who underwent a standardized clinical follow-up approximately 4 years after infection, including transthoracic echocardiography, lung ultrasound (LUS), and symptom questionnaire. Acute COVID-19 severity was categorized as: mild (managed at home), moderate (hospitalised), or severe (intensive care unit (ICU) admission). Associations were examined using linear and logistic regression models adjusted for age, sex, body mass index, and comorbidities, with tests for linear trend across increasing severity class. Results A total of 695 patients were included (52.5% female, median age 61 years [51;70]), distributed in the following severity groups: mild (n=468), moderate (n=179), and severe (n=48). Prevalent comorbidities included hypertension (37.3%), dyslipidaemia (36.7%), asthma (17.1%), atrial fibrillation (11.1%), diabetes (7.9%), and ischemic heart disease (7.8%). (Table 1). The prevalence of ≥3 B-lines on LUS and NYHA ≥II was higher with increasing COVID-19 severity (home, hospital, ICU) (6.4%, 14.4%, 25.6%, p <0.05, and 28.2%, 74.1%, 69.2% p <0.001) (Table 1). Increasing COVID-19 severity was associated with a higher prevalence of left ventricular systolic dysfunction; GLS < 16% (9.7%, 18.0%, 33.3%, p <0.05), LVEF (40-49%) (17.8, 27.7, 30.3%, p <0.05) and LVEF (<40%) (5.9%, 11.8%, and 12.1%, p<0.05) (Figure 1). Prevalence of LV diastolic dysfunction (E/e’ ratio >14) was similar across groups (p=0.35) but became significantly different after adjustment (p <0.05). Right ventricular (RV) function was worse in higher severity groups according to RV fractional area change (42.5% (10.4), 38.5% (11.0), 35.2% (9.1), p <0.001), with association persisting after adjustment. Left atrial (LA) parameters were also worse in higher severity groups (peak atrial longitudinal strain (36.2 [30;44], 32.9 [26;41], 27.5 [24;36], p < 0.001), and LA conduit strain (17.9 [13;24], 14.7 [10;20], 11.0 [9;16], p <0.001), however these trends were attenuated after adjustment. Conclusion Increasing severity of acute COVID-19 infection was associated with long-term echocardiographic signs of worse RV, LA, and LV systolic function, and higher number of B-lines on LUS.Figure 1Table 1
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Andersen et al. (2026) conducted a cohort in Prior confirmed COVID-19 infection (n=695). Severe acute COVID-19 infection (ICU admission) vs. Mild acute COVID-19 infection (managed at home) and moderate (hospitalised) was evaluated on Left ventricular systolic dysfunction (GLS < 16%) (p=<0.05). Increasing acute COVID-19 severity (mild, moderate, severe) was associated with higher 4-year prevalence of LV systolic dysfunction (GLS <16%: 9.7%, 18.0%, 33.3%, p<0.05) and worse RV function.
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