Transthoracic Echocardiography-Based Prediction Model of Adverse Event Risk in Patients with COVID-19.

Cardiopulmonary disorders cause a significant increase in the risk of adverse events in patients with COVID-19. Therefore, the development of new diagnostic and treatment methods for comorbid disorders in COVID-19 patients is one of the main public health challenges. The aim of the study was to analyze patient survival and to develop a predictive model of survival in adults with COVID-19 infection based on transthoracic echocardiography (TTE) parameters. We conducted a prospective, single-center, temporary hospital-based study of 110 patients with moderate to severe COVID-19. All patients underwent TTE evaluation. The predictors of mortality we identified in univariate and multivariable models and the predictive performance of the model were assessed using receiver operating characteristic (ROC) analysis and area under the curve (AUC). The predictive model included three factors: right ventricle (RV)/left ventricle (LV) area (odds ratio (OR) = 1.048 per 1/100 increase, p = 0.03), systolic pulmonary artery pressure (sPAP) (OR = 1.209 per 1 mm Hg increase, p < 0.001), and right ventricle free wall longitudinal strain (RV FW LS) (OR = 0.873 per 1% increase, p = 0.036). The AUC-ROC of the obtained model was 0.925 ± 0.031 (95% confidence interval (95% CI): 0.863-0.986). The sensitivity (Se) and specificity (Sp) measures of the models at the cut-off point of 0.129 were 93.8% and 81.9%, respectively. A binary logistic regression method resulted in the development of a prognostic model of mortality in patients with moderate and severe COVID-19 based on TTE data. It may also have additional implications for early risk stratification and clinical decision making in patients with COVID-19.

Evolution of Echocardiographic Abnormalities Identified in Previously Healthy Individuals Recovering from COVID-19.

(1) Background: Although the infection with the SARS-CoV-2 virus affects primarily the lungs, it is well known that associated cardiovascular (CV) complications are important contributors to the increased morbidity and mortality of COVID-19. Thus, in some situations, their diagnosis is overlooked, and during recovery, some patients continue to have symptoms enclosed now in the post-acute COVID-19 syndrome. (2) Methods: In 102 patients, under 55 years old, and without a history of CV diseases, all diagnosed with post-acute COVID-19 syndrome, we assessed by transthoracic echocardiography (TTE) four patterns of abnormalities frequently overlapping each other. Their evolution was followed at 3 and 6 months. (3) Results: In 35 subjects, we assessed impaired left ventricular function (LVF), in 51 increased systolic pulmonary artery pressure, in 66 diastolic dysfunction (DD) with normal LVF, and in 23 pericardial effusion/thickening. All TTE alterations alleviated during the follow-up, the best evolution being observed in patients with pericarditis, and a considerably worse one in those with DD, thus with a reduction in severity (4) Conclusions: In patients with post-acute COVID-19 syndrome, several cardiac abnormalities may be assessed by TTE, most of them alleviating in time. Some of them, especially DD, may persist, raising the presumption of chronic alterations.

Early echocardiographic findings in patients hospitalized for COVID-19 pneumonia: a prospective, single center study.

BACKGROUND: Cardiac dysfunction, mainly assessed by biomarker alterations, has been described in COVID-19 infection. However, there are still areas of uncertainty regarding its effective role in disease evolution. Aim of this study was to evaluate early echocardiographic parameters in COVID pneumonia and their association with severity disease and prognosis. METHODS: An echocardiographic examination was performed within 72 h from admission in 64 consecutive patients hospitalized for COVID-19 pneumonia in our medium-intensity care unit, from March 30th to May 15th 2020. Six patients were excluded for inadequate acoustic window. RESULTS: Fifty-eight consecutive patients were finally enrolled, with a median age of 58 years. Twenty-two (38%) were classifiable as severe COVID-19 disease. Eight out of 58 patients experienced adverse evolution (six died, two were admitted to ICU and received mechanical ventilation), all of them in the severe pneumonia group. Severe pneumonia patients showed higher troponin, IL-6 and D-Dimer values. No significant new onset alterations of left and right ventricular systolic function parameters were observed. Patients with severe pneumonia showed higher mean estimated systolic pulmonary artery pressure (sPAP) (30.7 ± 5.2 mmHg vs 26.2 ± 4.3 mmHg, p = 0.006), even if in the normality range values. No differences in echocardiographic parameters were retrieved in patients with adverse events with respect to those with favorable clinical course. CONCLUSION: A mild sPAP increase in severe pneumonia patients with respect to those with milder disease was the only significant finding at early echocardiographic examination, without other signs of new onset major cardiac dysfunction. Future studies are needed to deepen the knowledge regarding minor cardiac functional perturbation in the evolution of a complex systemic disorder, in which the respiratory involvement appears as the main character, at least in non-ICU patients.

Characteristics of 24-hour ambulatory blood pressure monitoring in a COVID-19 survivor.

COVID-19 infection primarily causes severe pneumonia complicated by acute respiratory distress syndrome and multiorgan failure requiring a ventilator support. We present a case of a 55-year-old male, admitted with COVID-19. He was obese but had no other medical conditions. His blood pressure was measured by his general physician on several occasions in the past, all values being normal (<140/90 mmHg). He developed multiorgan failure, requiring vasopressor and ventilator support for 17 days. A prone positioning improved the arterial oxygenation, and reduced the need for supplemental oxygen. After recovery, he showed persistently elevated blood pressure and sinus tachycardia both in clinic and out-of-clinic. The activation of the renin-angiotensin-aldosterone and sympathetic systems, volume-overload, hyperreninemia and cytokine storm might have contributed to the exaggerated cardiovascular response.