Our study has a relatively small sample size, compared with contemporary studies of hemodynamic variables in PAH, but it is the first to Bcl2 inhibitor report the response of RVSWI and PC to therapy. Patients who died or were lost from the study before follow-up catheterization were excluded from this analysis, which might limit the prognostic value of our findings and bias to the null hypothesis. The RVSWI is an imperfect measure of

RV function and reflects influences from both afterload and preload. However, it is used clinically in patients with left heart disease and has prognostic value in patients with PAH 9 and 21. In addition, our detailed analysis suggests that it might add incremental value to interpretation of its individual components. Echocardiographic data would have provided an additional measure of RV function but were not available for analysis in our cohort over the extended period of the study. In this study of serial hemodynamic measurements in patients with PAH we have shown

that RV function improves after prostanoid therapy but not after therapy with oral medications. Patients with the least compensated RV function at diagnosis had the greatest post-therapy improvement in RV function and might derive the most benefit from therapy. Larger studies are needed to validate these findings LGK974 and determine the clinical utility MG-132 nmr of RVSWI and PC versus conventional hemodynamic parameters. Further study is also needed to explore the potential of prostanoid therapy to directly improve RV function. “
“Atrial fibrillation (AF) is the most common cardiac arrhythmia and is frequently observed in chronic heart failure/reduced ejection fraction (HFREF) populations (1), where the incidence is several-fold higher than in patients

without heart failure (2). In the Framingham cohort, new-onset AF was associated with an increase in mortality in patients with heart failure (3). However, in HFREF patients, rhythm control strategies with current antiarrhythmic medications have not been associated with improved outcomes (4). This may be due to multiple adverse effects of current antiarrhythmic agents in HFREF populations (5). A drug treatment capable of decreasing the incidence of new-onset AF with an improved safety profile would benefit HFREF patients, particularly if such therapy also favorably affected the underlying pathophysiologic mechanisms that predispose patients to AF. β-blockers are candidates for such a therapy because they both improve heart failure outcomes (6) and have efficacy for AF prevention (7), likely due in part to reverse remodeling in both ventricular (8) and atrial 9 and 10 chambers. However, currently approved β-blockers exhibit only modest efficacy for reducing new-onset AF in HFREF patients (7).