Effect of Chronic Digoxin Use on Mortality and Heart Failure Hospitalization in Pulmonary Arterial Hypertension.

Background Digoxin acutely increases cardiac output in patients with pulmonary arterial hypertension (PAH) and right ventricular failure; however, the effects of chronic digoxin use in PAH are unclear. Methods and Results Data from the Minnesota Pulmonary Hypertension Repository were used. The primary analysis used likelihood of digoxin prescription. The primary end point was a composite of all-cause mortality or heart failure (HF) hospitalization. Secondary end points included all-cause mortality, HF hospitalization, and transplant-free survival. Multivariable Cox proportional hazards analyses determined the hazard ratios (HR) and 95% CIs for the primary and secondary end points. Among 205 patients with PAH in the repository, 32.7% (n=67) were on digoxin. Digoxin was more often prescribed to patients with severe PAH and right ventricular failure. After propensity score-matching, 49 patients were digoxin users, and 70 patients were nonusers; of these 31 (63.3%) in the digoxin group and 41 (58.6%) in nondigoxin group met the primary end point during a median follow-up time of 2.1 (0.6-5.0) years. Digoxin users had a higher combined all-cause mortality or HF hospitalization (HR, 1.82 [95% CI, 1.11-2.99]), all-cause mortality (HR, 1.92 [95% CI, 1.06-3.49]), HF hospitalization (HR, 1.89 [95% CI, 1.07-3.35]), and worse transplant-free survival (HR, 2.00 [95% CI, 1.12-3.58]) even after adjusting for patient characteristics and severity of PAH and right ventricular failure. Conclusions In this retrospective, nonrandomized cohort, digoxin treatment was associated with greater all-cause mortality and HF hospitalization, even after multivariate correction. Future randomized controlled trials should assess the safety and efficacy of chronic digoxin use in PAH.

Chest Pain Severity Rating Is a Poor Predictive Tool in the Diagnosis of ST-Segment Elevation Myocardial Infarction.

Current ST-segment elevation myocardial infarction (STEMI) guidelines require persistent electrocardiogram ST-segment elevation, cardiac enzyme changes, and symptoms of myocardial ischemia. Chest pain is the determinant symptom, often measured using an 11-point scale (0-10). Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis. This retrospective observational cohort study considered consecutive STEMI patients from May 02, 2009 to December 31, 2018. Analysis of standard STEMI metrics included positive electrocardiogram-to-device and first medical contact-to-device times, presence of comorbidities, false-positive diagnosis, 30-day and 1-year mortality, and 30-day readmission. Chest pain severity was assessed upon admission to the primary percutaneous coronary intervention hospital. We analyzed 1409 STEMI activations (69% male, 66.3 years old ± 13.7 years). Of these, 251 (17.8%) had no obstructive lesion, consistent with false-positive STEMI. Four hundred sixty-six (33.1%) reported chest pain rating of 0 on admission, 378 (26.8%) reported mild pain (1-3), 300 (21.3%) moderate (4-6), and 265 (18.8%) severe (7-10). Patients presenting without chest pain had a significantly higher rate of false-positive STEMI diagnosis. Increasing chest pain severity was associated with decreased time from first medical contact to device, and decreased in-hospital, 30-day and 1-year mortality. Severity of chest pain on admission did not correlate to the likelihood of a true-positive STEMI diagnosis, although it was associated with improved patient prognosis, in the form of improved outcomes, and shorter times to reperfusion.