Key result
Adding ivabradine to optimized medical therapy in stable CHF patients reduced the prevalence of impaired ventricular-arterial coupling from 73% to 40% after 4 months.
Why the study?
Does ivabradine improve ventricular-arterial coupling, aortic stiffness, and endothelial function in stable patients with chronic heart failure?
Cohort (n=30)
Does ivabradine improve ventricular-arterial coupling, aortic stiffness, and endothelial function in stable patients with chronic heart failure?
Adding ivabradine to standard medical therapy in stable HFrEF patients improves surrogate markers of vascular health, including endothelial function, aortic stiffness, and ventricular-arterial coupling.
Answers are grounded in this paper and cite their sources.
May improve VAC surrogates in stable HFrEF; hypothesis-generating and leaves open effects on outcomes.
Summary Aim Heart rate ( HR ) is an important prognostic factor in patients affected by chronic heart failure ( CHF ); ivabradine has been demonstrated to significantly reduce nonfatal myocardial infarction and hospitalization rate for acute heart failure and to improve left ventricular ( LV ) reverse remodeling, quality of life, exercise capacity, and arterial elastance (Ea) in these patients. We aimed at evaluating the short‐term effects of ivabradine on ventricular‐arterial coupling ( VAC ), aortic stiffness, and endothelial function in stable patients with CHF . Methods We evaluated 30 consecutive CHF patients ( LVEF ≤ 35%, NYHA class II ) with sinus rhythm and HR ≥ 70 bpm on optimized pharmacological therapy. All of them underwent both transthoracic echocardiogram to assess aortic elastic properties (aortic distensibility, AD ; aortic stiffness index, ASI ; systolic aortic strain, SAS ) and VAC , and peripheral arterial tonometry to measure endothelial function. Therapy with ivabradine 5 mg bid was added and each patient was evaluated with the same examinations after 4 months. Results At the baseline, 73% of patients had impaired VAC and 63% endothelial dysfunction. After 4 months, there was a significant improvement in the VAC value (Δ VAC −0.10 ± 0.18, P = .021), mainly linked to Ea (ΔEa −0.40 ± 0.23 mm Hg/ mL ; P = .003). All the parameters of aortic elasticity underwent significant improvement (Δ AD 1.82 ± 1.43 cm² × dyn − ¹, P = .004; Δ ASI −4.73 ± 6.07, P = .033; Δ SAS −7.98 ± 4.37%, P = .003). Lastly, we also noted a significant improvement of endothelial function (Δ RHI 0.35 ± 0.35; P < .001). At follow‐up 40% of patients had impaired VAC ( P = .018) and 33% endothelial dysfunction ( P = .038). Conclusion In patients with CHF adding ivabradine on top to the standard optimized medical therapy, when indicated, seems to improve endothelial function, aortic properties, and VAC .
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Bonadei et al. (2018) conducted a cohort in chronic systolic heart failure (n=30). ivabradine vs. baseline was evaluated on impaired ventricular-arterial coupling (VAC) (p=0.018). Adding ivabradine to optimized medical therapy in stable CHF patients reduced the prevalence of impaired ventricular-arterial coupling from 73% to 40% after 4 months.
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