Introduction: Left atrium (LA) dilates and its function decreases as a chronic secondary change in hypertrophic cardiomyopathy (HCM). LA strain is a more sensitive measure of LV filling pressure than LA volume and can be used to predict the functional capacity in HCM. Objective: To analyse LA strain in patients with HCM and its correlation with exercise tolerance. Methods: A total of 113 patients with HCM were enrolled. All patients underwent detailed clinical evaluation, 24-hour Holter monitoring, exercise stress testing, two dimensional echocardiography with LA strain analysis using speckle tracking imaging. Assessment of functional capacity was done in terms of metabolic equivalents (METS). HCM patients with METS > 6.0 were included in group A while those with METS ≤ 6.0 were included group B. Correlation of various parameters of LA strain (LASr, LAScd and LASct) was done with functional capacity. Results: Mean age of the study population was 47±10.77 years with majority of them being males (71.9%). Group B patients had significantly lower LASr (12.95 ±8.61% vs 22.16±16%; P<0.001), LAScd (-7.28 ±6.29% vs -12.74±8.40%; P<0.001) and LASct (-7.44 ±4.46 vs -11.19±6.53; P<0.001). Multivariable linear regression analysis reported LASr to be an independent predictor of METs (P = 0.04). LASr was strongest echocardiographic predictor of reduced METS with an AUC of 0.78 (95% CI: 0.68 to 0.88), sensitivity of 71.8% and specificity of 82.9%. Conclusion: LA strain parameters are associated with functional capacity in patients with HCM with lower LA strain values being associated with poor functional capacity.

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 studied 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) and serum ferritin (P = 0.03) 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.