Background: The scope of pericardial involvement in COVID‐19 infection is unknown. We aimed to evaluate the prevalence, associates, and clinical impact of pericardial involvement in hospitalized patients with COVID‐19. Methods and Results: Consecutive patients with COVID‐19 underwent clinical and echocardiographic examination, irrespective of clinical indication, within 48 hours as part of a prospective predefined protocol. Protocol included clinical symptoms and signs suggestive of pericarditis, calculation of modified early warning score, ECG and echocardiographic assessment for pericardial effusion, left and right ventricular systolic and diastolic function, and hemodynamics. We identified predictors of mortality and assessed the adjunctive value of pericardial effusion on top of clinical and echocardiographic parameters. The study included 530 patients. Pericardial effusion was found in 75 (14%), but only 17 patients (3.2%) fulfilled the criteria for acute pericarditis. Pericardial effusion was independently associated with modified early warning score, brain natriuretic peptide, and right ventricular function. It was associated with excess mortality (hazard ratio [HR], 2.44; P =0.0005) in nonadjusted analysis. In multivariate analysis adjusted for modified early warning score and echocardiographic and hemodynamic parameters, it was marginally associated with mortality (HR, 1.86; P =0.06) and improvement in the model fit ( P =0.07). Combined assessment for pericardial effusion with modified early warning score, left ventricular ejection fraction, and tricuspid annular plane systolic excursion was an independent predictor of outcome (HR, 1.86; P =0.02) and improved model fit ( P =0.02). Conclusions: In hospitalized patients with COVID‐19, pericardial effusion is prevalent, but rarely attributable to acute pericarditis. It is associated with myocardial dysfunction and mortality. A limited echocardiographic examination, including left ventricular ejection fraction, tricuspid annular plane systolic excursion, and assessment for pericardial effusion, can contribute to outcome prediction.

Most patients with significant (defined as ≥ moderate) tricuspid regurgitation (TR) are treated conservatively. Individual mortality rates are markedly variable. We developed a risk score based on comprehensive clinical and echocardiographic evaluation, predicting mortality on an individual patient level. The cohort included 1701 consecutive patients with significant TR, half with isolated TR, admitted to a single hospital, treated conservatively. We derived a scoring system predicting 1-year mortality and validated it using k-fold cross-validation and with external validation on another cohort of 5141 patients. Score utility was compared with matched patients without significant TR. One-year mortality rate was 31.3%. The risk score ranged 0–17 points and included 11 parameters: age (0–3), body mass index ≤ 25 (0–1), history of liver disease (0–2), history of chronic lung disease (0–2), estimated glomerular filtration rate (0–5), haemoglobin (0–2), left-ventricular ejection fraction (0–1), right-ventricular dysfunction (0–1), right atrial pressure (0–2), stroke volume index (SVI) (0–1) and left-ventricular end-diastolic diameter (0–1). One-year mortality rates increased from 0 to 100%, as the score increased up to ≥16. Areas under the receiver operating curves were 0.78, 0.70, and 0.73, for the original, external validation, and external validation with SVI measured cohorts. The score remained valid in subpopulations of patients with quantified RV function, quantified TR and isolated TR. Significant TR compared to no TR, affected 1-year mortality stronger with higher scores, with a significantly positive interaction term. We suggest a robust risk score for inpatients with significant TR, assisting risk stratification and decision-making. Our findings underscore the burden of TR providing benchmarks for clinical trial design.

Background: Information about the cardiac manifestations of the Omicron variant of COVID‐19 is limited. We performed a systematic prospective echocardiographic evaluation of consecutive patients hospitalized with the Omicron variant of COVID‐19 infection and compared them with similarly recruited patients were propensity matched with the wild‐type variant. Methods and Results: A total of 162 consecutive patients hospitalized with Omicron COVID‐19 underwent complete echocardiographic evaluation within 24 hours of admission and were compared with propensity‐matched patients with the wild‐type variant (148 pairs). Echocardiography included left ventricular (LV) systolic and diastolic, right ventricular (RV), strain, and hemodynamic assessment. Echocardiographic parameters during acute infection were compared with historic exams in 62 patients with the Omicron variant and 19 patients with the wild‐type variant who had a previous exam within 1 year. Of the patients, 85 (53%) had a normal echocardiogram. The most common cardiac pathology was RV dilatation and dysfunction (33%), followed by elevated LV filling pressure (E/e′ ≥14, 29%) and LV systolic dysfunction (ejection fraction <50%, 10%). Compared with the matched wild‐type cohort, patients with Omicron had smaller RV end‐systolic areas (9.3±4 versus 12.3±4 cm ² ; P =0.0003), improved RV function (RV fractional‐area change, 53.2%±10% versus 39.7%±13% [ P <0.0001]; RV S′, 12.0±3 versus 10.7±3 cm/s [ P =0.001]), and higher stroke volume index (35.6 versus 32.5 mL/m ² ; P =0.004), all possibly related to lower mean pulmonary pressure (34.6±12 versus 41.1±14 mm Hg; P =0.0001) and the pulmonary vascular resistance index ( P =0.0003). LV systolic or diastolic parameters were mostly similar to the wild‐type variant‐matched cohort apart from larger LV size. However, in patients who had a previous echocardiographic exam, these LV abnormalities were recorded before acute Omicron infection, but not in the wild‐type cohort. Numerous echocardiographic parameters were associated with higher in‐hospital mortality (LV ejection fraction, stroke volume index, E/e′, RV S′). Conclusions: In patients with Omicron, RV function is impaired to a lower extent compared with the wild‐type variant, possibly related to the attenuated pulmonary parenchymal and/or vascular disease. LV systolic and diastolic abnormalities are as common as in the wild‐type variant but were usually recorded before acute infection and probably reflect background cardiac morbidity. Numerous LV and RV abnormalities are associated with adverse outcome in patients with Omicron.

Objective: Subclinical myocardial dysfunction has been reported to occur early in systemic lupus erythematous (SLE). The study aim was to search for biomarkers of subclinical myocardial dysfunction which may correlate with disease activity in SLE patients. Methods: This is a prospective, controlled, cross-sectional study of 57 consecutive patients with SLE and 18 controls. Serum samples were obtained to determine serum soluble ST2 (sST2), CXCL-10 and high-sensitivity troponin (hs-troponin) levels. All participants underwent an echocardiographic tissue Doppler study. Results: sST2, CXCL-10 and hs-troponin levels were higher in patients with higher SLE disease activity (SLEDAI). sST2 and CXCL-10 levels were higher in patients with more disease damage as measured by the SLE damage index. Measures of diastolic dysfunction, as assessed by echocardiographic tissue Doppler negatively correlated with log CXCL-10: including E/A; E/e′_lateral and E/e′_septal, while E/e′ positively correlated with CXCL-10. Diastolic dysfunction parameters also correlated with log sST2 levels, a negative correlation was seen with E/e′_lateral and a positive correlation was seen with E/e′. Systolic dysfunction parameters positively correlated with hs-troponin: LVED, LVES, IVS, LVMASS and LVMASS index. In a multivariate analysis, sST2 and CXCL-10 were found to be significantly different in SLE vs. healthy controls, independent of each other and independent of cardiovascular risk factors. Conclusions: Soluble ST2 and CXCL-10 are markers of disease activity and accrued damage in SLE and may serve as sensitive biomarkers for detection of subclinical diastolic dysfunction, independent of traditional cardiovascular risk factors.

Preliminary data suggested that patients with Omicron-type-Coronavirus-disease-2019 (COVID-19) have less severe lung disease compared with the wild-type-variant. We aimed to compare lung ultrasound (LUS) parameters in Omicron vs. wild-type COVID-19 and evaluate their prognostic implications. One hundred and sixty-two consecutive patients with Omicron-type-COVID-19 underwent LUS within 48 h of admission and were compared with propensity-matched wild-type patients (148 pairs). In the Omicron patients median, first and third quartiles of the LUS-score was 5 [2–12], and only 9% had normal LUS. The majority had either mild (≤5; 37%) or moderate (6–15; 39%), and 15% (≥15) had severe LUS-score. Thirty-six percent of patients had patchy pleural thickening (PPT). Factors associated with LUS-score in the Omicron patients included ischaemic-heart-disease, heart failure, renal-dysfunction, and C-reactive protein. Elevated left-filling pressure or right-sided pressures were associated with the LUS-score. Lung ultrasound-score was associated with mortality [odds ratio (OR): 1.09, 95% confidence interval (CI): 1.01–1.18; P = 0.03] and with the combined endpoint of mortality and respiratory failure (OR: 1.14, 95% CI: 1.07–1.22; P < 0.0001). Patients with the wild-type variant had worse LUS characteristics than the matched Omicron-type patients (PPT: 90 vs. 34%; P < 0.0001 and LUS-score: 8 [5, 12] vs. 5 [2, 10], P = 0.004), irrespective of disease severity. When matched only to the 31 non-vaccinated Omicron patients, these differences were attenuated. Lung ultrasound-score is abnormal in the majority of hospitalized Omicron-type patients. Patchy pleural thickening is less common than in matched wild-type patients, but the difference is diminished in the non-vaccinated Omicron patients. Nevertheless, even in this milder form of the disease, the LUS-score is associated with poor in-hospital outcomes.