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 [21] and with the amount of edema detected by cardiac magnetic resonance (CMR) [22]. 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 [23]. 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 [24].
Speckle-tracking echocardiography works as a “digital biopsy” and it could become an essential diagnostic tool for myocarditis and other cardiomyopathies [25].
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 [26]. This study was corroborated by another autopsy study [27].
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 [9]. 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 [34]. 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 [35]. 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 [32].
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 [38].