Background: In-hospital mortality for patients presenting with acute pulmonary embolism (PE) has been reported to be up to 7 times higher for patients with decreased estimated glomerular filtration rate (eGFR). However, few studies have assessed its effect on long-term mortality. Objective: To determine the impact of eGFR and creatinine clearance (CrCl) on long-term all-cause mortality following acute PE in association with other routine laboratory analyses and comorbidities. Patients/Methods: The prospective study enrolled 141 consecutive patients presenting with objectively confirmed acute PE. Demographic, clinical data, comorbidities, and laboratory values were recorded. CrCl and GFR were estimated using the Cockcroft-Gault, MDRD, and chronic kidney disease (CKD)-EPI equations. Patients were followed up at 90 days and 1 year after the event. Results: In univariate analyses, age, active cancer, PE severity index (PESI), CrCl and eGFR, D-dimer value, and high-density lipoprotein level were found to be significantly associated with mortality in 90 days and 1 year. Additionally, body mass index was significant in the 1-year follow-up. CrCl by Cockcroft-Gault (90-day: area under the curve [AUC] 0.763; 1-year: AUC 0.718) demonstrated higher discriminatory power for predicting mortality than eGFR by the MDRD (AUC 0.686; AUC 0.609) and CKD-EPI (AUC 0.697; AUC 0.630) equations. In multivariate analyses, active cancer, CrCl by Cockcroft-Gault (90-day: hazard ratio [HR] 0.948, 95% CI 0.919–0.979; 1-year: HR 0.967, 95% CI 0.943–0.991), eGFR by CKD-EPI (90-day: HR 0.948, 95% CI 0.915–0.983; 1-year: HR 0.971, 95% CI 0.945–0.998) were found to be independent predictors of mortality. eGFR by MDRD, D-dimer, and PESI value were significant prognostic factors for 90-day mortality. Conclusion: Decreased renal function is a prognostic factor for increased all-cause mortality 90 days and 1 year after acute PE.

Right ventricular (RV) and left ventricular (LV) dysfunction is common in a significant number of hospitalized coronavirus disease 2019 (COVID-19) patients. This study was conducted to assess whether the improved mitochondrial bioenergetics by cardiometabolic drug meldonium can attenuate the development of ventricular dysfunction in experimental RV and LV dysfunction models, which resemble ventricular dysfunction in COVID-19 patients. Effects of meldonium were assessed in rats with pulmonary hypertension-induced RV failure and in mice with inflammation-induced LV dysfunction. Rats with RV failure showed decreased RV fractional area change (RVFAC) and hypertrophy. Treatment with meldonium attenuated the development of RV hypertrophy and increased RVFAC by 50%. Mice with inflammation-induced LV dysfunction had decreased LV ejection fraction (LVEF) by 30%. Treatment with meldonium prevented the decrease in LVEF. A decrease in the mitochondrial fatty acid oxidation with a concomitant increase in pyruvate metabolism was noted in the cardiac fibers of the rats and mice with RV and LV failure, respectively. Meldonium treatment in both models restored mitochondrial bioenergetics. The results show that meldonium treatment prevents the development of RV and LV systolic dysfunction by enhancing mitochondrial function in experimental models of ventricular dysfunction that resembles cardiovascular complications in COVID-19 patients.

The current predictive score, based on data during the index pulmonary embolism, is not sensitive enough in a chronic thromboembolic pulmonary hypertension (CTEPH) rule-out strategyhttp://ow.ly/8fGy30iIjgN