Cocaine is an established cardiovascular toxin, but the impact of cocaine use on clinical outcomes in heart failure (HF) remains unknown. Although nonselective β-blocker use in cocaine users with HF and reduced ejection fraction (HFrEF) appears to be safely tolerated, selective β-blockers have not been evaluated. This study aimed to assess whether cocaine use is associated with worse clinical outcomes in patients with HF and evaluate the safety of β-blocker prescription upon discharge in cocaine users with HFrEF. This was a single-center retrospective cohort study of patients with incident HF hospitalization at a safety-net hospital. Primary outcomes included all-cause mortality and readmissions, including HF. Cocaine users were compared with nonusers matched by age, gender, and year of index admission. In cocaine users with HFrEF, outcomes were compared according to β-blocker prescription at discharge. From 2001 to 2019, 738 cocaine users were identified and compared with 738 matched nonusers. Cocaine use was associated with increased mortality (adjusted hazard ratio [HR] 1.21; 95% confidence interval [CI] 1.00 to 1.48) and 90-day readmission (all-cause: adjusted HR 1.49; 95% CI 1.20 to 1.85; HF: adjusted HR 1.49; 95% CI 1.10 to 2.01), persisting at 1 year. In cocaine users who were prescribed metoprolol, carvedilol, or no β-blocker at discharge, the rates of 1-year mortality and 30-day readmission were similar. In conclusion, cocaine use is associated with increased all-cause mortality, HF readmission, and all-cause readmission. Both nonselective and selective β-blocker may be safe in managing patients with HFrEF and cocaine use.

BACKGROUND: Routine long-term anticoagulation in pulmonary arterial hypertension (PAH) is controversial. To date, anticoagulation has been found to be beneficial or neutral in idiopathic disease (IPAH) and neutral-to-harmful in connective tissue disease (CTD-PAH). We sought to examine the association between anticoagulation and mortality, healthcare utilization, and quality of life (QoL) in PAH. METHODS: The PHAR is a prospective registry of PAH patients referred to 58 pulmonary hypertension care centers in the United States. We compared patients who received anticoagulation during enrollment (questionnaire documented) to those who did not. Cox proportional hazard models were used for mortality, Poisson multivariate regression models for healthcare utilization, and generalized estimating equations for QOL RESULTS: Of 1175 patients included, 316 patients were treated with anticoagulation. IPAH/hereditary PAH (HPAH) comprised 46% of the cohort and CTD-PAH comprised 33%. After adjustment for demographics, clinical characteristics, site and disease severity, anticoagulation was not associated with mortality in the overall population (HR, 1.00; 95% CI, 0.72-1.36), IPAH/HPAH (HR, 1.19; 95% CI, 0.74-1.94), or CTD-PAH (HR 0.87; 95% CI, 0.53-1.42). Anticoagulation was associated with an increased rate of emergency department visits (IRR: 1.41), hospitalizations (IRR: 1.30), and hospital days (IRR 1.33). QOL measured by emPHasis-10 score was worse in patients receiving anticoagulation (mean difference 1.74; 95% CI 0.40-3.09). CONCLUSIONS: Anticoagulation is not associated with higher mortality, but is associated with increased healthcare utilization in the PHAR. PAH-specific QoL may be worse in patients receiving anticoagulation. The risks and benefits surrounding routine prescription of anticoagulation for PAH should be carefully considered.