key: cord-0742431-segts6ca authors: Mahajan, Sudhanshu; Kunal, Shekhar; Shah, Bhushan; Garg, Shobhit; Palleda, Girish M.; Bansal, Ankit; Batra, Vishal; Yusuf, Jamal; Mukhopadhyay, Saibal; Kumar, Suresh; Tyagi, Sanjay; Gupta, Anubha; Gupta, Mohit D. title: Left ventricular global longitudinal strain in COVID‐19 recovered patients date: 2021-09-23 journal: Echocardiography DOI: 10.1111/echo.15199 sha: 5603c8a83504442cc2897b07937dd639abf6a417 doc_id: 742431 cord_uid: segts6ca OBJECTIVES: Myocardial injury during active coronavirus disease‐2019 (COVID‐19) infection is well described; however, its persistence during recovery is unclear. We assessed left ventricle (LV) global longitudinal strain (GLS) using speckle tracking echocardiography (STE) in COVID‐19 recovered patients and its correlation with various parameters. METHODS: A total of 134 subjects within 30–45 days post recovery from COVID‐19 infection and normal LV ejection fraction were enrolled. Routine blood investigations, inflammatory markers (on admission) and comprehensive echocardiography including STE were done for all. RESULTS: Of the 134 subjects, 121 (90.3%) were symptomatic during COVID‐19 illness and were categorized as mild: 61 (45.5%), moderate: 50 (37.3%) and severe: 10 (7.5%) COVID‐19 illness. Asymptomatic COVID‐19 infection was reported in 13 (9.7%) patients. Subclinical LV and right ventricle (RV) dysfunction were seen in 40 (29.9%) and 14 (10.5%) patients, respectively. Impaired LVGLS was reported in 1 (7.7%), 8 (13.1%), 22 (44%) and 9 (90%) subjects with asymptomatic, mild, moderate and severe disease, respectively. LVGLS was significantly lower in patients recovered from severe illness(mild: ‐21 ± 3.4%; moderate: ‐18.1 ± 6.9%; severe: ‐15.5 ± 3.1%; p < 0.0001). Subjects with reduced LVGLS had significantly higher interleukin‐6 (p < 0.0001), C‐reactive protein (p = 0.001), lactate dehydrogenase (p = 0.009), serum ferritin (p = 0.03), and troponin (p = 0.01) levels during index admission. CONCLUSIONS: Subclinical LV dysfunction was seen in nearly a third of recovered COVID‐19 patients while 10.5% had RV dysfunction. Our study suggests a need for closer follow‐up among COVID‐19 recovered subjects to elucidate long‐term cardiovascular outcomes. The ongoing coronavirus disease-2019 (COVID-19) pandemic continues to cause considerable morbidity and mortality worldwide. 1 Cardiovascular manifestations in COVID-19 include myocarditis, acute coronary syndrome, cardiac arrhythmias, heart failure, cardiogenic shock and venous thromboembolism. 2, 3 Acute cardiac injury (defined by elevated cardiac troponin levels) has been reported in 8-28% of patients with COVID-19 and is associated with worse clinical outcomes. 2, [4] [5] [6] In addition, few studies have observed subclinical myocardial dysfunction in COVID-19 patients. 7, 8 However, there is paucity of data regarding myocardial dysfunction in COVID-19 recovered patients. Initial studies using cardiac magnetic resonance (CMR) imaging have shown relatively high prevalence of subclinical left ventricle (LV) dysfunction in recovered COVID-19 patients. [9] [10] [11] Despite being the "gold standard", CMR is often limited by its availability, longer imaging time and feasibility especially in light of ongoing pandemic. Hence, there is an urgent need for a systematic study to identify the prevalence of subclinical myocardial dysfunction using simple bedside tools. Global longitudinal strain (GLS) obtained by two-dimensional speckle tracking echocardiography (STE) is a sensitive and validated method for detection of subclinical LV dysfunction compared with ejection fraction (EF). 12 In the present study, we assessed LVGLS in recovered COVID-19 patients and its correlation with various laboratory parameters and inflammatory markers. This was a prospective single center study in a tertiary care center of Continuous data was expressed as mean ± standard deviation (SD) and categorical data was represented as proportions. Normality of distri- The baseline demographic characteristics of 134 subjects is depicted in There was no significant difference in the prevalence of hypertension and diabetes mellitus between the three groups. Patients in severe COVID-19 illness group had significantly higher levels of A longer duration of hospital stay (greater in severe COVID-19 infection) and male sex were the important predictors of reduced strain (Table 2) (Table 2) . Additionally, these subjects were more likely to have a lower TAPSE and a higher RV basal diameter. No significant difference was observed between the groups with respect to other echocardiographic parameters (LVEF, LVEDd, LVESd, LA size, RVSP and diastolic dysfunction). On Multivariate logistic regression, raised CRP (> 5 mg/L), raised IL-6 (> 7 ρg/ml) and severity of COVID-19 illness were the independent predictors of reduced LVGLS in COVID-19 recovered subjects (Figure 4 ). The present study evaluated the presence of subclinical myocardial dysfunction using two-dimensional strain analysis via STE in COVID- LVGLS serves as a more sensitive and earlier predictor of LV systolic dysfunction as compared to LVEF. 20 Additionally, it has also been shown to predict subclinical myocardial dysfunction because of its abil-ity to detect myocardial fibrosis early in the disease process. 19 Initial studies have shown the utility of LVGLS in predicting cardiac involvement patients with active COVID-19 infection. 8, 21, 22 There is a limited evidence regarding the role of LVGLS in COVID-19 recovered patients. In a small study from Turkey, LVGLS was impaired in 28 (37.8%) patients one month post discharge following COVID-19 infection. 23 to understand the natural progression of persistent myocardial damage and subclinical LV dysfunction. It will be of interest to see whether abnormal strain in recovered patients is an adverse prognostic marker. It was a single center study with a relatively small sample size. One of the inherent limitations of STE is the large number of clinical conditions and imaging quality which can impact the LVGLS. Hence, subjects with these confounding clinical conditions were excluded and STE was performed in a select subset of COVID-19 recovered patients. One of the other limitations possibly could be a lack of baseline echocardiography during the active COVID-19 infection due to the logistic issues in resource limited countries such as ours in the initial phases of the pandemic. Lack of data for cardiac troponins for some patients in our study was another limitation. Additionally, there was a lack of use of CMR imaging in our study. The COVID-19 recovered patients in our study are being followed-up longitudinally with STE at three monthly intervals for a period of one year to sequentially assess their strain pattern and determine the natural course of subclinical LV dysfunction following recovery from COVID-19. The present study provides important insights into the prevalence of subclinical myocardial dysfunction in recovered COVID-19 subset. Nearly a third of patients recovering from COVID-19 had subclinical LV dysfunction while 10.5% of them had RV dysfunction. The presence of such persistent myocardial dysfunction in recovered subjects suggests cardiac involvement as a possible lasting consequence of COVID- 19 . This study reiterates the importance of STE as a practical imaging modality for detection of subclinical myocardial dysfunction especially amidst the huge burden of recovered patients. It also highlights the need for long term follow-up of these subjects to unmask long-term cardiovascular consequences of COVID-19 infection. None. 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