Abstract
Background Residual angina after PCI is a frequently occurring disease. Ivabradine improves symptoms but its role in patients without left ventricular systolic dysfunction is still unclear. The aim was to quantify the effects of ivabradine in terms of MVO2 indicators and diastolic function. Methods Twenty-eight consecutive patients with residual angina after PCI were randomized to ivabradine 5 mg twice/day (IG) or standard therapy (CG). All patients performed a stress echocardiography at the enrollment and after 30 days. MVO2 was estimated from double product (DP) and triple product (TP) integrating DP with ejection time (ET). Diastolic function was evaluated determining E and A waves, E′ measurements, and E/E′ ratio both at rest and at the peak of exercise. Results The exercise time was longer in IG 9′49″ ± 48″ vs 8′09″ ± 59″ in CG (p=0.0001), reaching a greater workload (IG 139.3 ± 13.4 vs CG 118.7 ± 19.6 Watts; p=0.003). MVO2 expressed with DP and TP was significantly higher in IG (DP: IG 24194 ± 2697 vs CG 20358 ± 4671.8, p=0.01; TP: IG 17239 ± 4710 vs CG 12206 ± 4413, p=0.007). At peak exercise, the ET was diminished in IG than CG. The analysis of diastolic function after the exercise revealed an increase of E and A waves, without difference in the E/A ratio. The E′ wave was higher in IG than CG, and in the same group, the differences between baseline and peak exercise were greater (∆E′3.14 ± 0.7 vs 2.4 ± 1.13, p=0.047). The E/E′ ratio was reduced in patients treated with ivabradine (IG 10.2 ± 2.0 vs CG 7.9 ± 1.6, p=0.002). Conclusions Ivabradine seems to produce a significant improvement of ischemic threshold, chronotropic reserve, and diastolic function.
Highlights
Stable angina is a syndrome characterized by a transitory condition of acute myocardial ischemic attacks caused by an imbalance between myocardial perfusion and metabolic demand [1]. e antianginal drugs and the percutaneous coronary revascularization are essential to treat the persistent symptoms
Heart rate is the major determinant of cardiac output and myocardial oxygen consumption; the reduction of the heart rate in patients with stable angina can be considered a goal of the therapy [2]
We investigated the efficacy of treatments with ivabradine in addition to full anti-ischemic therapy compared with the latter alone in patients with signs or symptoms of residual angina underwent percutaneous coronary intervention plus stent implantation. e main purpose was to evaluate if addition of ivabradine to standard therapy might increase the threshold for angina improving the stress tolerance and exercise duration in terms of double product (DP) and triple product (TP), respectively, calculated as a product between HR and systolic blood pressure and the product between DP and ejection time
Summary
Stable angina is a syndrome characterized by a transitory condition of acute myocardial ischemic attacks caused by an imbalance between myocardial perfusion and metabolic demand [1]. e antianginal drugs and the percutaneous coronary revascularization are essential to treat the persistent symptoms. Ivabradine reduced anginal symptomatology but has not clearly demonstrated improvements of the outcomes in patients with chronic ischemic disease without left ventricular systolic dysfunction [5,6,7]. In CONTROL-2 Study, in patients with stable angina, the combination of the two therapies ivabradine and β-blockers together demonstrated good tolerability, safety, Cardiology Research and Practice and pronounced clinical improvements, compared to β-blockers up-titration [8]. Twenty-eight consecutive patients with residual angina after PCI were randomized to ivabradine 5 mg twice/day (IG) or standard therapy (CG). Diastolic function was evaluated determining E and A waves, E′ measurements, and E/E′ ratio both at rest and at the peak of exercise. E analysis of diastolic function after the exercise revealed an increase of E and A waves, without difference in the E/A ratio. Ivabradine seems to produce a significant improvement of ischemic threshold, chronotropic reserve, and diastolic function
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