Discussion
myocardial damage, fatigue, early-stage myocardial fibrosis, COVID-19 infection, myocardial dysfunction, systolic dysfunction, cardiac abnormalities
VIRUS, NEUROLOGICAL DISEASE, LEFT VENTRICULAR DYSFUNCTION, POST-ACUTE COVID-19 SYNDROME, COVID-19 INFECTION, CARDIAC COMPLICATIONS, MYOCARDIAL DYSFUNCTION, SYSTOLIC DYSFUNCTION
The current randomized controlled trial demonstrates a subtle systolic dysfunction of GLS lower than − 20%, in about half (48.3%) of the post-COVID-19 syndrome patients, which was significantly improved by HBOT. This recovery in GLS by HBOT exceeded the natural recovery rate observed in the sham group.Previous studies have documented cardiac abnormalities in post-acute COVID-19 syndrome with transthoracic echocardiography (TTE). In 80% of patients who underwent echocardiography examination during hospitalization with COVID-19, GLS was reducedGLS has also been shown to allow the detection of subclinical myocardial dysfunction due to its ability to predict early-stage myocardial fibrosis in correlation with CMRThe principal pathophysiological mechanisms considered responsible for the myocardial damage caused by COVID-19 infection are related mostly to direct virus-induced injury due to a high distribution of ACE2 receptors on cardiac myocytes which are binding sites for virus particlesIn the past decade, novel HBOT protocols have been shown to induce both regenerative and anti-inflammatory effectsIn the current study, GLS significantly improved following HBOT, compared to the sham protocol. However, the significant mixed model interaction was significant in the post-hoc analysis for patients with reduced GLS. In other words, the regenerative effect of HBOT was beneficial in dysfunctional cardiac tissue, compared to supposedly healthy functional cardiac tissue. This finding has been validated in studies of non-healing wounds using HBOT, as well as recently in neurological diseases with dysfunctional (but non-necrotic) brain tissue. Recently, Robbins et al. reported a significant improvement in fatigue following HBOT sessions in post-COVID-19 patientsThe study has several strengths and limitations. The primary strength of this study is the sham protocol for the control arm. The main limitation lies in the relatively small sample size. A second limitation is that echocardiographic evaluation is operator-dependent. However, all the echocardiography examinations were performed by experienced sonographers and evaluated by the same senior cardiologists, who were blinded to the patient's allocation. Third, although the HBOT protocol included 40 sessions, an optimal number of sessions for maximal therapeutic effect has yet to be determined. Fourth, the SARS-CoV-2 different variants are not routinely tested in clinical practice, and therefore the data were unavailable as a possible co-factor. Lastly, results were collected 1–3 weeks after the last HBOT session. Long-term results as well as possible long-term clinical cardiac complications remain to be collected.In conclusion, in post-COVID-19 patients, slightly reduced GLS despite normal EF is a frequent finding and can indicate subclinical left ventricular dysfunction. HBOT promotes cardiac systolic function recovery in patients suffering from the post-COVID-19 condition. Further studies are needed to optimize patient selection and to evaluate long-term outcomes.