Abstract:Backgrounds
Patients at greatest risk of severe clinical conditions from coronavirus disease 2019 (COVID-19) and death are elderly and comorbid patients. Increased levels of cardiac troponins identify patients with poor outcome. The present study aimed to describe the clinical characteristics and outcomes of a cohort of Italian inpatients, admitted to a medical COVID-19 Unit, and to investigate the relative role of cardiac injury on in-hospital mortality.
Methods and results
We analyzed all consecutive patie… Show more
“…Although it seems to spare the cardiovascular system as the primary site of infection, there is increasing evidence linking COVID-19 with cardiovascular morbidity [2]. A discrete prevalence of cardiac damage, defined by troponin elevation independently from electrocardiographic and echocardiographic findings, has been reported in patients hospitalized for COVID infection, with significant correlation with mortality [3][4][5]. Several pathways have been proposed for cardiovascular involvement during COVID illness.…”
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.
“…Although it seems to spare the cardiovascular system as the primary site of infection, there is increasing evidence linking COVID-19 with cardiovascular morbidity [2]. A discrete prevalence of cardiac damage, defined by troponin elevation independently from electrocardiographic and echocardiographic findings, has been reported in patients hospitalized for COVID infection, with significant correlation with mortality [3][4][5]. Several pathways have been proposed for cardiovascular involvement during COVID illness.…”
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.
Background
With the continuance of the global COVID-19 pandemic, cardiovascular disease (CVD) and cardiac injury have been suggested to be risk factors for severe COVID-19.
Objective
The aim is to evaluate the mortality risks associated with CVD and cardiac injury among hospitalized COVID-19 patients, especially in subgroups of populations in different countries.
Methods
A comprehensive systematic literature search was performed using 9 databases from November 1, 2019 to November 9, 2020. Meta-analyses were performed for CVD and cardiac injury between non-survivors and survivors of COVID-19.
Results
Although the prevalence of CVD in different populations was different, hospitalized COVID-19 patients with CVD were at a higher risk of fatal outcomes (OR = 2.72; 95% CI 2.35–3.16) than those without CVD. Separate meta-analyses of populations in four different countries also reached a similar conclusion that CVD was associated with an increase in mortality. Cardiac injury was common among hospitalized COVID-19 patients. Patients with cardiac injury had a significantly higher mortality risk than those without cardiac injury (OR = 13.25; 95% CI: 8.56–20.52).
Conclusions
Patients' CVD history and biomarkers of cardiac injury should be taken into consideration during the hospital stay and incorporated into the routine laboratory panel for COVID-19.
“…Additionally, in a study completed in Illinois, 673 patients with elevated troponin had significantly increased odds of critical illness (OR 3.65; 95% CI 2.03-6.57) [62]. Not only is cTnI an independent predictor of disease severity and ICU admission, but it is also, unsurprisingly, associated with increased patient mortality [63][64][65]. For example, in a study of 1919 patients in Wuhan, patients with acute cardiac injury, defined as serum hs-cTnI above the 99th percentile upper reference limit, had an odds ratio of 80.07 for in-hospital mortality, and nonsurvivors had significantly higher levels of hs-cTnI (nearly tenfold) than survivors [66].…”
Section: Troponin As a Prognostic Factormentioning
There has been strong evidence of myocardial injury in coronavirus disease 2019 (COVID-19) patients with significantly elevated serum cardiac troponin (cTn). While the exact mechanism of injury is unclear, possible suggested pathological mechanisms of injury are discussed. These include increased susceptibility of the myocardium and endothelium to viral invasion, underlying hyperinflammatory state and subsequent cytokine storm, a hypercoagulable and prothrombotic state, and indirect myocardial injury due to hypoxemia. As a result of these pathological mechanisms in COVID-19 patients, cTn may be elevated largely due to myocarditis, microangiopathy or myocardial infarction. The utility of cTn as a biomarker for measuring myocardial injury in these patients and assessing its ability as a prognostic factor for clinical outcome is also discussed.
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