Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such N-terminal pro–B-type natriuretic peptide (NT-pro-BNP), creatine kinase-myocardial band (CK-MB) and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. The purpose of this review is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes.

Background: It has been widely reported that the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) attaches human cells by using the Angiotensin Converting Enzyme 2 (ACE2) receptor, but vascular impairment described during coronavirus disease 2019 (COVID-19) infection is primarily due to the direct involvement of the endothelial cells by the virus or secondarily to the inflammatory host response is currently unknown. Methods: We therefore aimed to demonstrate in vivo the presence of endothelial dysfunction in six COVID-19 patients without cardiovascular risk factors or pre-existing cardiac condition, using the Endo-PAT 2000, a device able to measure endothelial vasodilation function in a rapid and non-invasive way. Results: Four patients were positive for endothelial dysfunction, with RHI values between 1.13-1.56 (average value 1.32, normal values >1.67); in one of the two negative patients the reported RHI value was slightly above the cutoff (1.72). Conclusion: Our findings confirm that COVID-19 patients are at higher risk of developing endothelial dysfunction. In addition, our results demonstrate that endothelial impairment may occur even in the absence of cardiovascular risk factors.

Mitral annular disjunction (MAD) is a structural abnormality of the mitral annulus, defined by a detachment of the atrial wall-mitral valvular junction from the left ventricular (LV) free wall. This structural abnormality in mitral annulus fibrosus is significantly associated with the presence of mitral valve prolapse (MVP) [1], but it can be also detected in normal cases as an anatomical variation of the mitral annulus fibrosus [2]. The main tools to detect MAD are echocardiography and cardiac magnetic resonance. Prevalence of MAD in the general population ranges from 7% [1] to 9% [2]. Several studies proved an association between MAD and arrhythmic events, independently of concomitant mitral valve abnormalities, suggesting the existence of a novel entity: MAD arrhythmic syndrome [3]. Herein we describe a case report of a middle age man with MAD who experienced ventricular arrhythmias and placement of an implantable cardioverter-defibrillator (ICD).