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Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Clin+Microbiol+Infect 2021 ; 27 (9): 1250-1261 Nephropedia Template TP
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Cardiac sequelae after coronavirus disease 2019 recovery: a systematic review #MMPMID34171458
Ramadan MS; Bertolino L; Zampino R; Durante-Mangoni E
Clin Microbiol Infect 2021[Sep]; 27 (9): 1250-1261 PMID34171458show ga
BACKGROUND: Coronavirus disease 2019 (COVID-19) has been implicated in a wide spectrum of cardiac manifestations following the acute phase of the disease. OBJECTIVES: To assess the range of cardiac sequelae after COVID-19 recovery. DATA SOURCES: PubMed, Embase, Scopus (inception through 17 February 2021) and Google scholar (2019 through 17 February 2021). STUDY ELIGIBILITY CRITERIA: Prospective and retrospective studies, case reports and case series. PARTICIPANTS: Adult patients assessed for cardiac manifestations after COVID-19 recovery. EXPOSURE: Severe acute respiratory syndrome coronavirus 2 infection diagnosed by PCR. METHODS: Systematic review. RESULTS: Thirty-five studies (fifteen prospective cohort, seven case reports, five cross-sectional, four case series, three retrospective cohort and one ambidirectional cohort) evaluating cardiac sequelae in 52 609 patients were included. Twenty-nine studies used objective cardiac assessments, mostly cardiac magnetic resonance imaging (CMR) in 16 studies, echocardiography in 15, electrocardiography (ECG) in 16 and cardiac biomarkers in 18. Most studies had a fair risk of bias. The median time from diagnosis/recovery to cardiac assessment was 48 days (1-180 days). Common short-term cardiac abnormalities (<3 months) included increased T1 (proportion: 30%), T2 (16%), pericardial effusion (15%) and late gadolinium enhancement (11%) on CMR, with symptoms such as chest pain (25%) and dyspnoea (36%). In the medium term (3-6 months), common changes included reduced left ventricular global longitudinal strain (30%) and late gadolinium enhancement (10%) on CMR, diastolic dysfunction (40%) on echocardiography and elevated N-terminal proB-type natriuretic peptide (18%). In addition, COVID-19 survivors had higher risk (risk ratio 3; 95% CI 2.7-3.2) of developing heart failure, arrythmias and myocardial infarction. CONCLUSIONS: COVID-19 appears to be associated with persistent/de novo cardiac injury after recovery, particularly subclinical myocardial injury in the earlier phase and diastolic dysfunction later. Larger well-designed and controlled studies with baseline assessments are needed to better measure the extent of cardiac injury and its clinical impact.