Pulmonary hypertension (PH) caused by left heart disease, also known as post-capillary PH, is the most common etiology of PH. Left heart disease due to systolic dysfunction or heart failure with preserved ejection fraction, valvular heart disease, and left atrial myopathy due to atrial fibrillation are causes of post-capillary PH. Elevated left-sided filling pressures cause pulmonary venous congestion due to backward transmission of pressures and post-capillary PH. In advanced left-sided heart disease or valvular heart disease, chronic uncontrolled venous congestion may lead to remodeling of the pulmonary arterial system, causing combined pre-capillary and post-capillary PH. The hemodynamic definition of post-capillary PH includes a mean pulmonary arterial pressure > 20 mmHg, pulmonary vascular resistance < 3 Wood units, and pulmonary capillary wedge pressure > 15 mmHg. Echocardiography is important in the identification and management of the underlying cause of post-capillary PH. Management of post-capillary PH is focused on the treatment of the underlying condition. Strategies are geared towards pharmacotherapy and guideline-directed medical therapy for heart failure, surgical or percutaneous management of valvular disorders, and control of modifiable risk factors and comorbid conditions. Referral to centers with advanced heart and pulmonary teams has shown to improve morbidity and mortality. There is emerging interest in the use of targeted agents classically used in pulmonary arterial hypertension, but current data remain limited and conflicting. This review aims to serve as a comprehensive summary of postcapillary PH and its etiologies, pathophysiology, diagnosis, and management, particularly as it pertains to advanced heart failure.

International Statistical Classification of Disease and Related Health Problems, 10th Revision codes (ICD‐10) are used to characterize cohort comorbidities. Recent literature does not demonstrate standardized extraction methods. Objective: Compare COVID‐19 cohort manual‐chart‐review and ICD‐10‐based comorbidity data; characterize the accuracy of different methods of extracting ICD‐10‐code‐based comorbidity, including the temporal accuracy with respect to critical time points such as day of admission. Design: Retrospective cross‐sectional study. Measurements: ICD‐10‐based‐data performance characteristics relative to manual‐chart‐review. Results: Discharge billing diagnoses had a sensitivity of 0.82 (95% confidence interval [CI]: 0.79–0.85; comorbidity range: 0.35–0.96). The past medical history table had a sensitivity of 0.72 (95% CI: 0.69–0.76; range: 0.44–0.87). The active problem list had a sensitivity of 0.67 (95% CI: 0.63–0.71; range: 0.47–0.71). On day of admission, the active problem list had a sensitivity of 0.58 (95% CI: 0.54–0.63; range: 0.30–0.68)and past medical history table had a sensitivity of 0.48 (95% CI: 0.43–0.53; range: 0.30–0.56). Conclusions and Relevance: ICD‐10‐based comorbidity data performance varies depending on comorbidity, data source, and time of retrieval; there are notable opportunities for improvement. Future researchers should clearly outline comorbidity data source and validate against manual‐chart‐review.

Objective COVID-19 has disproportionately affected low-income communities and people of color. Previous studies demonstrated that race/ethnicity and socioeconomic status (SES) are not independently correlated with COVID-19 mortality. The purpose of our study is to determine the effect of race/ethnicity and SES on COVID-19 30-day mortality in a diverse, Philadelphian population. Methods This is a retrospective cohort study in a single center tertiary care hospital in Philadelphia, PA. The study includes adult patients hospitalized with polymerase-chain-reaction-confirmed COVID-19 between March 1^st, 2020 and June 6^th, 2020. The primary outcome was a composite of COVID-19 death or hospice discharge within 30 days of discharge. The secondary outcome was intensive care unit (ICU) admission. Results The study included 426 patients. 16.7% died, 3.3% were discharged to hospice, and 20.0% were admitted to the ICU. Using multivariable analysis, race/ethnicity was not associated with the primary nor secondary outcome. In Model 4, age greater than 75 (Odds Ratio [OR], 11.01; 95% confidence interval [CI], 1.96 to 61.97) and renal disease (OR 2.78; 95% CI, 1.31 to 5.90) were associated with higher odds of the composite primary outcome. “Very-low-income area” (OR 0.29; 95% CI, 0.12 to 0.71) and BMI 30-35 (OR 0.24; 95% CI, 0.08 to 0.69) were associated with lower odds of the primary outcome. Conclusions When controlling for demographics, SES, and comorbidities, race/ethnicity was not independently associated with the composite primary outcome. Very-low SES, as extrapolated from census-tract-level income data, were associated with lower odds of the composite primary outcome.

Nonbacterial thrombotic endocarditis (NBTE) is a noninflammatory endocarditis that occurs in hypercoagulable states. Acute promyelocytic leukemia (APL) is an aggressive form of acute leukemia associated with significant coagulopathy. A 45-year-old woman with new pulmonary emboli and progressive heart failure developed pancytopenia, leading to diagnosis of APL and cardiogenic shock secondary to NBTE of the mitral valve. APL was treated with induction chemotherapy, alongside inotropic support for cardiogenic shock. After cancer remission, she underwent mitral valve replacement, resolving the cardiogenic shock. NBTE is a recognized complication of solid malignancy but is rarely associated with leukemia. Fewer than 5 cases have been reported in APL. This case highlights 2 critical complications of each disease process: cardiogenic shock and disseminated intravascular coagulation. APL and NBTE can present as oncologic and cardiac emergencies. Co-managing these conditions requires a multidisciplinary approach integrating specialized care in both cardiology and oncology.