To our knowledge, this is the first study in the literature evaluating LV mechanics by STE in long-term follow-up of recovered COVID-19 patients.
Indices of longitudinal strain are known to strongly correlate with the levels of lymphocytic infiltrates in endomyocardial biopsy (EMB) samples  and with the amount of edema detected by cardiac magnetic resonance (CMR) . Moreover, the diagnostic performance of LS in acute myocarditis has been validated by showing preferential alteration of subepicardial deformation that was consistent with tissue characteristics established by CMR . So, although CMR and EMB are the gold standards for the diagnosis of myocarditis, the evidence shows a good correlation between echocardiographic strain and CMR .
Speckle-tracking echocardiography works as a “digital biopsy” and it could become an essential diagnostic tool for myocarditis and other cardiomyopathies .
Previous report using CMR in 100 individuals recovered from COVID-19 detected cardiovascular involvement in 78 of them, irrespective or preexisting conditions, the severity and overall course of the COVID-19 presentation, the time from the original diagnosis, or the presence of cardiac symptoms . This study was corroborated by another autopsy study .
There are a few studies showing reduction in GLS during acute hospitalized patients, regardless of the severity of the COVID-19, even in the presence of normal LVEF [5,9,18,28-31] compatible with subclinical LV dysfunction.
In corroboration to our findings, other studies using STE for diagnosis of cardiac involvement during acute COVID-19 showed reduction of LS in more than one of the basal LV segments [9,32], despite normal LVEF and even in the presence of normal GLS. And in one study abnormal LV deformation patterns were still observed in 3 patients after recovery from acute stage, indicating residual myocardial involvement . Furthermore, CMR showed late enhancement predominantly in the basal inferolateral/anterolateral LV segments indicating myocardial fibrosis or scars, respectively [8,9,33]. This basal injury pattern reflects the susceptibility of certain myocardial regions to inflammatory or systemic stressors rather than a geographic predilection specific to COVID-19.
Another plausible hypothesis, more specific to COVID-19, involves the viral receptor, angiotensin-converting enzyme 2 (ACE2). This membrane-bound enzyme is responsible for production of angiotensin [1-7], leading to well-described anti-inflammatory and anti-thrombotic effects . ACE2 is highly expressed in fat, and epicardial adipose tissue (EAT) is more prominent in the atrioventricular groove and lateral LV wall, closer to the basal segments . Loss of ACE2 has been shown to result in heart failure with preserved LVEF, mediated in part by EAT inflammation. Thus, COVID-19 binding of ACE2 may occur more prominently in areas of high EAT, such as the basal LV, and cause subclinical dysfunction via inflammatory downstream effects .
Case reports and series of patients with various forms of myocarditis, including influenza myocarditis, have described a similar pattern of reduced basal strain on STE [36,37]. Abnormal basal LS has also been seen in infiltrative cardiomyophaties including, Anderson-Fabry disease .