Cardiac injury occurs in about 20-30% of patients hospitalized for COVID-19 and influence the prognosis but many aspects like the role of age and magnitude of cardiac damage in determining the prognosis, remains vague.Hypothesis: Age and magnitude of cardiac damage may influence the mortality of patients hospitalized for COVID-19.
Methods: We considered all patients consecutively admitted at a third-level European Hospital for COVID-19 between February and June 2020.
Cardiac injury was defined as a high-sensitivity cardiac Troponin I (hs-cTnI) value greater than the upper reference limit (URL) of 47 ng/dL.
Firstly, we analyzed the data by hs-cTnI across age tertiles (<62 years, 62-73 years and >73 years). Then, we compared patients with no-damage, mid-damage (hs-cTnI up to 10-fold URL) and high-damage (more than 10-fold URL).
The primary endpoint was in-hospital mortality.
Results: We enrolled 543 patients (median age 69, 67% males); hs-cTnI was available in 509. The survival was lower in elderly patients and high levels of hs-cTnI worsened the prognosis across all age tertiles.
Surprisingly, the magnitude of cardiac damage did not influence the overall in-hospital mortality, but patients with high-damage died earlier (survival at 15 days: 86% no-damage vs 61% mid-damage vs 49% high-damage; p<0.001).
Of note, among patients with high-damage, only 7 received coronary angiography, cardiac magnetic resonance or heart biopsy.
Conclusions: Cardiac injury dramatically increased the mortality across all ages in patients hospitalized for COVID-19.
The magnitude of cardiac damage did not influence overall in-hospital mortality but almost all patients with high-damage died within 15 days from admission.
A second-level diagnostic test was performed seldomly in high-damage patients, suggesting that the unexpected high burden of the first COVID-19 wave negatively influenced the health system and our clinical daily practice.
Of 5789 Out-Of-Hospital Cardia Arrest (OHCA) patients included from 6 studies, patients who were COVID-19 positive comprised of 61.46% males while COVID-19 negative patients included 63.37% of males (p=0.2). COVID-19 OHCA patients were younger (Mean±SD, 68.94±17.93 vs 70.23±17.93, p=0.03) compared to COVID-19 negative patients. Incidence of OHCA at home/private address was higher (OR=1.92, 95%CI:1.52-2.43), while shockable rhythm (OR=0.34, 95%-CI:0.24-0.46) and use of AED (OR=0.77, 95%CI 0.61-0.97) were less frequently noted in COVID-19 patients (p<0.0001). As shown
Rreturn of spontaneous circulation did not differ significantly (OR=1.01, 95%CI:0.85-1.20, p<0.92); however, survival to admission (OR=0.64, 95%CI:0.48-0.86, p<0.01), and survival to discharge (OR=0.28, 95%CI:0.13-0.59, p<0.01) were significantly lower in COVID-19 OHCA admissions compared to non-COVID-19 OHCA admissions.
Platelets Contribute to Disease Severity in Covid-19
Objective: Heightened inflammation, dysregulated immunity, and thrombotic events are characteristic of hospitalized COVID-19 patients. Platelets are key regulators of thrombosis, inflammation, immunity and are prime candidates for a role in the pathogenesis of COVID-19. The objective of this study was to analyze the platelet phenotype in COVID-19.
Approach and Results: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is detected in human megakaryocytes and platelets in COVID-19 patients and following incubation with the virus in vitro.
We show a direct interaction between SARS-CoV-2 and megakaryocytes that alters the platelet transcriptome and platelet activity. COVID-19 platelets are hyperreactive and have a distinct transcriptomic profile characteristic of prothrombotic large and immature platelets.
We find transcriptomic changes mediated by SARS-CoV-2 do not occur following exposure of megakaryocytes with a coronavirus responsible for the common cold, CoV-OC43. In a cohort of 3,915 hospitalized COVID-19 patients, we analyzed blood platelet indices collected at hospital admission.
Following adjustment for demographics, clinical risk factors, medication use, and biomarkers of inflammation and thrombosis, platelet count, size, and immaturity are each associated with increased critical illness and all-cause mortality.
Conclusions: Our findings demonstrate that SARS-CoV-2 virions invade megakaryocytes and platelets, inducing alterations to the platelet transcriptome and activation profile, which correlate with critical illness and mortality in hospitalized COVID-19 patients.