Background: Nearly two-third of patients with heart failure with reduced ejection fraction (HFrEF) have right ventricular (RV) dysfunction, which has previously been identified as an independent predictor of reduced functional capacity and poor prognosis. However, RV has received little attention in the past. Beta-blocker therapy (β-BT) has been shown to improve mortality and reduce hospitalizations in patients with HFrEF, being approved as first-line therapy irrespective to RV function. Less is known about the sympathetic nervous system' role in RV dysfunction and the potential usefulness (or harmfulness) of β-BT in these patients is still unclear.
Objectives: Our study aimed to evaluate the medium-term effect of β-BT discontinuation on functional capacity and RV remodelling based on cardiopulmonary exercise testing (CPET), echocardiography and serum biomarkers in patients with clinically stable HFrEF and RV dysfunction.
Methods: Seventeen outpatients were prospectively enrolled using the following criteria: presence of signs and symptoms of HF while on optimal medical therapy (including β-BT); LVEF ≤40%; echocardiographic criteria of RV dysfunction. Patients were randomized 1:1, either to withdraw (group 0) or prosecute (group 1) β-BT. In group 0 optimal heart rate was obtained with digoxine or ivabradine. Echo and serum biomarkers were performed at baseline, after 3 and 6 months; CPET was performed at baseline and 6 months.
Results: After six months follow up, RV systolic function improved based on S’-DTI in group 0 (∆S’: 1.01 vs. -0.92cm/s; P=.03). Conversely, worsening of estimated PAPs (∆PAPs: 0.8 vs. -7.5mmHg; P =.04) and echo LV-remodelling (∆EDVi: 19.55 vs. -0.96mL/mq P=.03) were observed. No significant improvements in term of functional capacity were obtained. The only variables significantly affected by β-BT withdrawal were LV EDV and ESV, appearing worse in group 0 (meanEDVi 115 vs. 84mL/mq; meanESVi 79 vs. 53mL/mq, P=.03).
Conclusions: β-BT discontinuation did not produced any beneficial effect. Additionally, despite maintenance of optimal heart rate control, β-BT withdraw worsened LV remodelling. Our study corroborates the hypothesis that improvement in LV function may be a major determinant for improvement in RV function, reducing pulmonary wedge pressure and RV afterload, with only a marginal action of its negative inotropic effect. In conclusion, β-BT might be beneficial also in heart failure patients with biventricular dysfunction.