Biomarkers Predict In-Hospital Major Adverse Cardiac Events in COVID-19 Patients: A Multicenter International Study

Background: The COVID-19 pandemic carries a high burden of morbidity and mortality worldwide. We aimed to identify possible predictors of in-hospital major cardiovascular (CV) events in COVID-19. Methods: We retrospectively included patients hospitalized for COVID-19 from 10 centers. Clinical, biochemical, electrocardiographic, and imaging data at admission and medications were collected. Primary endpoint was a composite of in-hospital CV death, acute heart failure (AHF), acute myocarditis, arrhythmias, acute coronary syndromes (ACS), cardiocirculatory arrest, and pulmonary embolism (PE). Results: Of the 748 patients included, 141(19%) reached the set endpoint: 49 (7%) CV death, 15 (2%) acute myocarditis, 32 (4%) sustained-supraventricular or ventricular arrhythmias, 14 (2%) cardiocirculatory arrest, 8 (1%) ACS, 41 (5%) AHF, and 39 (5%) PE. Patients with CV events had higher age, body temperature, creatinine, high-sensitivity troponin, white blood cells, and platelet counts at admission and were more likely to have systemic hypertension, renal failure (creatinine ≥ 1.25 mg/dL), chronic obstructive pulmonary disease, atrial fibrillation, and cardiomyopathy. On univariate and multivariate analysis, troponin and renal failure were associated with the composite endpoint. Kaplan–Meier analysis showed a clear divergence of in-hospital composite event-free survival stratified according to median troponin value and the presence of renal failure (Log rank p < 0.001). Conclusions: Our findings, derived from a multicenter data collection study, suggest the routine use of biomarkers, such as cardiac troponin and serum creatinine, for in-hospital prediction of CV events in patients with COVID-19.

Long SARS-CoV-2 with Hypoxic Leukoencephalopathy, Cardiocirculatory Arrest and Severe Interstitial Pneumonia: The Role of Timely Nuclear Magnetic Resonance for the Early Diagnosis and Regression of this Dramatic Complication

In December 2019, a devastated novel coronavirus, Severe Acute Respiratory Syndrome coronavirus-2 (SARS-CoV-2), was identified as the causative agent of the acute atypical cluster of pneumonia cases in the city of Wuhan, China [1]. In February 2020, the World Health Organization (WHO) named the disease COVID-19. Currently, the SARS-CoV-2 pandemic is of a scale not seen since the 1918 influenza pandemic and has already infected more than 156 million people worldwide and resulted in 3.2 million deaths, and cancer is a major risk factor for death associated with COVID-19. Although the predominant clinical presentation is with respiratory disease, Human coronaviruses exhibit neuroinvasive potential, and the systemic disorders that are the hallmark of COVID-19, such as hypoxia, inflammation, and acquired thrombophilia, may impose a high risk of CNS complications [2]. However, it is not clear which of these complications are consequences of direct neurological injury of SARS-CoV-2 or events secondary to the systemic dysfunctional state. New information about the neurological entities arising in patients with COVID-19 is needed to delineate better the clinical implications of this disease. We report a case of a patient with Hypoxic Leukoencephalopathy after Cardiocirculatory Arrest in patient SARS-CoV-2 and Severe Interstitial Pneumonia.