ABSTRACT
Background: A significant proportion of patients recovering from SARS-CoV-2 infection (Covid-19) complain a wide variety of bothersome symptoms, including symptoms potentially related to cardiac involvement, that may significantly impair their quality of life (post-Covid or long-Covid syndrome). However, full diagnostic investigation usually does not reveal significant structural or functional cardiac abnormalities. Whether cardiac autonomic dysfunction and/or endothelial dysfunction may play a role in post-COVID-19 symptoms, however, has poorly been investigated. Method(s): We prospectively enrolled 63 young adult patients (age 18-55 years) without any previous cardiovascular disease, referred to our "Post-COVID-19" Day Hospital ward for a clinical follow-up after 3 months from SARS-CoV-2 infection. In all patients endothelium-dependent vasodilator function was assessed noninvasively by measuring the change of brachial artery diameter in response to hyperaemia after 5 minutes of forearm ischemia (flow-mediated dilatation, FMD);furthermore, endothelium-independent vasodilator function was assessed by measuring the change of brachial artery diameter in response to sublingual nitroglycerine (25 mug) (nitrate-mediated dilatation, NMD). A 24-hour ECG Holter monitoring (HM) was performed to assess cardiac autonomic function by obtaining timedomain and frequency-domain parameters of heart rate variability (HRV). Result(s): Symptoms of potential cardiac origin (dyspnoea on exertion, chest pain, arrhythmic symptoms) were referred by 47 patients (74.6%, Group 1), whereas 16 (25.4%, Group 2) were free from any possible cardiac symptom. The two groups did not differ in age, sex and cardiovascular risk factors. FMD was 7.29+/-3.4% and 7.01+/-2.3% in Group 1 and 2, respectively (p=0.77), whereas NMD was 11.1+/-3.8% and 14.2+/-4.9 in the two groups, respectively (p=0.013). No significant differences were observed for HRV parameters between the two groups (see Table). Conclusion(s): Our data do not support a role for both endothelial dysfunction and cardiac autonomic dysfunction in the persistence of symptoms of potential cardiac origin in patients with a recent SARS-CoV-2 infection. The lower endothelium-independent arterial vasodilator found in these patients, however, deserves further investigation.