Abstract
Purpose Ivabradine has emerged as a new antiarrhythmic agent that could compete with the traditional ones, such as beta-blockers. This experimental study aims to ascertain whether ivabradine directly interferes with the myocardial contractility in an in vitro environment. Methods Myocardial tissues from the right atrial appendages of patients undergoing cardiac surgery were dissected to obtain 40 specimens from 20 patients (length: 3 mm), which were exposed to electrical impulses at a frequency of 75 bpm for 30 min to reach a steady state. Specimens were then categorised into four groups (each including five patients). The first group was the control, whereas the second, third, and fourth were treated with 60 nM, 200 nM, and 2 μM ivabradine, respectively. We assessed five different contraction parameters before and after a 15 min treatment and calculated their relative changes, which were then compared to the control group. Results Ivabradine has affected the force of contraction significantly in vitro (p=0.009). However, force of contraction decreased in both the control group (93.5 ± 4.7%) and the second group (94.1 ± 4.5%, p=0.8) and force of contraction remained unchanged in the third group (101.0 ± 4.1%, p=0.24) and increased significantly in the fourth group (108.9 ± 11.6%, p=0.008). There was no change in other contraction parameters, such as passive tension force (97.1 ± 5.1%, p=0.368), duration of contraction (99.1 ± 4.3%, p=0.816), time to peak (96.6 ± 3.0%, p=0.536), and time to relaxation (101.2 ± 7.0%, p=0.564). Conclusions Ivabradine did not interfere with the contractile behaviour of human atrial tissue when it was used in therapeutic dosages in vitro. However, it increased the contractility slightly, when it was used in supratherapeutic dosage.
Highlights
Heart rate reduction (HRR), a cornerstone of the modern heart failure therapy [1,2,3], enhances the balance between the cardiac oxygen demand and supply by augmenting the coronary blood flow through a longer diastolic phase and decreasing the oxygen consumption owing to lowering the frequency
The heart rate decline leads to a better ventricular filling through an extended diastolic phase and an enhanced diastolic function because of better myocardial oxygen supply
Ere was no change in other contraction parameters, such as passive tension force (97.1 ± 5.1%, p 0.368), duration of contraction (99.1 ± 4.3%, p 0.816), time to peak (96.6 ± 3.0%, p 0.536), and time to relaxation (101.2 ± 7.0%, p 0.564)
Summary
Heart rate reduction (HRR), a cornerstone of the modern heart failure therapy [1,2,3], enhances the balance between the cardiac oxygen demand and supply by augmenting the coronary blood flow through a longer diastolic phase and decreasing the oxygen consumption owing to lowering the frequency. A controlled reduction in the heart rate without interfering with the systolic cardiac function is needed frequently. Cardiology Research and Practice node, and Purkinje fibers [13,14,15]. By blocking these channels, ivabradine can exert a selective negative chronotropic effect upon the heart without interfering with the systolic function [16]. Is study aims to investigate the effect of ivabradine on the cardiac contractility independently from the HRR. It used a well-established in vitro model to analyse the contractility of human atrial cardiac tissues in the presence and absence of ivabradine
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