Since an association between myocardial infarction (MI) and respiratory infections has been described for influenza viruses and other respiratory viral agents, understanding possible physiopathological links between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and acute coronary syndromes (ACS) is of the greatest importance. The initial data suggest an underestimation of ACS cases all over the world, but acute MI still represents a major cause of morbidity and mortality worldwide and should not be overshadowed during the coronavirus disease (Covid-19) pandemic. No common consensus regarding the most adequate healthcare management policy for ACS is currently available. Indeed, important differences have been reported between the measures employed to treat ACS in China during the first disease outbreak and what currently represents clinical practice across Europe and the USA. This review aims to discuss the pathophysiological links between MI, respiratory infections, and Covid-19; epidemiological data related to ACS at the time of the Covid-19 pandemic; and learnings that have emerged so far from several catheterization labs and coronary care units all over the world, in order to shed some light on the current strategies for optimal management of ACS patients with confirmed or suspected SARS-CoV-2 infection.

COVID-19 infection may lead to an Acute Respiratory Distress Syndrome where severe gas exchange derangements may be associated, at least in the early stages, only with minor pulmonary infiltrates. This suggests that the shunt associated to the gasless lung parenchyma is not sufficient to explain CARDS hypoxemia. We designed an algorithm (VentriQlar), based on the same conceptual grounds described by J.B West in 1969. We set 499 ventilation-perfusion (VA/Q) compartments and, after calculating their blood composition (PO2, PCO2 and pH), we randomly chose 106 combinations of five parameters controlling a bimodal distribution of blood flow. The solutions were accepted if the predicted PaO2 and PaCO2 were within 10% of the patient's values. We assumed that shunt fraction equaled the fraction of non-aerated lung tissue at the CT quantitative analysis. Five critically-ill patients later deceased were studied. The PaO2/FiO2 was 91.1±18.6 mmHg and PaCO2 69.0±16.1 mmHg. Cardiac output was 9.58±0.99 l/min. The fraction of non-aerated tissue was 0.33±0.06. The model showed that a large fraction of the blood flow was likely distributed in regions with very low VA/Q (Qmean=0.06±0.02) and a smaller fraction in regions with moderately high VA/Q. Overall LogSD, Q was 1.66 ± 0.14, suggestive of high VA/Q inequality. Data suggest that shunt alone cannot completely account for the observed hypoxemia and a significant VA/Q inequality must be present in COVID-19. The high cardiac output and the extensive microthrombosis later found in the autopsy further support the hypothesis of a pathological perfusion of non/poorly ventilated lung tissue.

Background: Electroanatomic voltage mapping (EVM) is a promising modality for guiding endomyocardial biopsies (EMB). However, few data support its feasibility and safety. We now report the largest cohort of patients undergoing EVM-guided EMB in order to show its diagnostic yield and to compare it with a cardiac magnetic resonance (CMR) guided approach. Methods: One-hundred and sixty-two consecutive patients undergoing EMB at our Institution from 2010 to 2019 were included. EMB was performed in pathological areas identified at EVM and CMR. According to EMB results, CMR and EVM sensitivity and specificity regarding the identification of pathological substrates of myocardium were evaluated. Results: Pre-operative CMR showed late gadolinium enhancement (LGE) in 70% of the patients, while EVM identified areas of low voltages in 61%. Right (73%), left (19%) or both ventricles (8%) underwent sampling. EVM proved to have similar sensitivity to CMR (74% vs. 77%), with specificity being respectively 70% and 47%. In 12 patients with EMB-proven cardiomyopathy, EVM identified pathological areas, which had been undetected at CMR evaluation. Sensitivity of pooled EVM and CMR was as high as 95%. EMB analysis allowed to reach a new diagnosis, different from the suspected clinical diagnosis, in 39% of patients. Complications rate was low, mostly vascular access related, with no patients requiring urgent management. Conclusions: EVM proved to be a promising tool for targeted-EMB due to its sensitivity and specificity for identification of myocardial pathological substrates. EVM demonstrated to have an accuracy similar to CMR. EVM and CMR together conferred EMB a positive predictive value of 89%.