Therapeutic Effect on Heart Rate: Visible Simplicity and Real Difficulty

Гиляревский, Р.; Голшмид, В.; Кузьмина, М.

doi:10.21518/2079-701x-2016-13-74-80

Cited by 1 publication

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References 36 publications

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“…Одним из механизмов их действия является уменьшение частоты сердечных сокращений (ЧСС) и систолического напряжения миокарда, что снижает потребность миокарда в кислороде и предупреждает развитие и прогрессирование ХСН. Однако с учетом известных их противопоказаний не всегда они могут быть использованы или применены в необходимых дозах для лечения коморбидных пациентов в постинфарктном периоде [2,3]. Альтернативным препаратом в таких случаях может быть ивабрадин -селективный блокатор I f -каналов синусового узла, уменьшающий ЧСС, не влияя на сократительную способность миокарда.…”

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The effect of ivabradine as part of standard therapy on vascular endothelial function and cardiac electrical instability in patients with post-infarction cardiosclerosis and heart failure

et al. 2020

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Aim. To reveal the equivalence of nebivolol replacement with ivabradine in the prevention of endothelial dysfunction and cardiac electrical instability in patients with heart failure with reduced ejection fraction (HFrEF).Material and methods. In current observational study, 126 patients with HFrEF in the postinfarction period were randomized into two groups for six-month treatment: group 1 (n=62) — standard therapy (acetylsalicylic acid 0,1 g/day, clopidogrel 75 mg/day, veroshpiron 50 mg/day, nebivolol 5 mg/day, perindopril 5 mg/day and rosuvastatin 20 mg/day; group 2 (n=66) — the same therapy with nebivolol replacement with ivabradine 10 mg/day. Initially and after 6 months, 24-hour Holter monitoring was performed, heart rate variability was determined. We also investigated endothelial dysfunction using the photoplethysmographic technique with post-occlusive reactive hyperemia (PORH) test.Results. The heart rate, the number of episodes and the duration of symptomatic and silent myocardial ischemia, total myocardial ischemia were significantly decreased in both groups (p<0,001). The decrease of supraventricular extrasystole frequency in both groups had not statistical significance (p>0,05). In both groups, after therapy, parameters of heart rate variability were improved with the parasympathetic predominance (p<0,01). In both groups, the PORH test revealed the increase of brachial artery diameter (group 1 — 5,90Ѓ}3,15% and group 2 — 5,88Ѓ}1,82%) and pulse wave amplitude (group 1 — 1,81Ѓ}0,78 and group 2 — 1,73Ѓ}0,90 times), which indicates a trend towards an improvement in endothelial function. Intergroup comparisons did not reveal significant differences.Conclusion. Ivabradine is equivalent to nebivolol in preventing ventricular extrasystole and reducing heart rate, number of episodes of symptomatic and silent ischemia and the duration of total myocardial ischemia in patients with HFrEF. Ivabradine equivalently to nebivolol improves endothelial function and heart rate variability with reducing the sympathetic activity.

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