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Evaluation of Coronary Flow Reserve After Myocardial Ischemia Reperfusion in Rats
Published on: June 28, 2019
Ivabradine improves coronary flow reserve in patients with stable coronary artery disease
Emmanouil I Skalidis1, Michalis I Hamilos, Gregory Chlouverakis
1Cardiology Department, University Hospital of Heraklion, and Biostatistics Lab, University of Crete, Crete, Greece. skalides@med.uoc.gr
Insights
Ivabradine treatment improves coronary flow and reserve in stable coronary artery disease patients. These benefits persist even when heart rate is normalized, suggesting enhanced microvascular function.
Area of Science:
- Cardiology
- Pharmacology
- Vascular Physiology
Background:
- Ivabradine is known to reduce hospital admissions for myocardial infarction and revascularization.
- However, its impact on coronary circulation has not been previously investigated.
Purpose of the Study:
- To evaluate the effects of ivabradine on coronary flow velocity and coronary flow reserve (CFR) in patients with stable coronary artery disease (CAD).
Main Methods:
- Twenty-one patients with stable CAD underwent coronary angiography with Doppler guidewire measurements of coronary flow velocity at rest and during hyperemia.
- Measurements were repeated after one week of ivabradine treatment (5 mg twice daily), with and without heart rate pacing.
- Coronary flow reserve (CFR) was calculated as the ratio of hyperemic to resting average peak flow velocity (h-APV/r-APV).
Main Results:
- Ivabradine significantly reduced heart rate (78±14 bpm to 65±9 bpm).
- Resting flow velocity (r-APV) decreased, while hyperemic flow velocity (h-APV) increased, leading to a significant improvement in CFR (2.78±0.61 to 3.51±0.81).
- Even after pacing heart rate to baseline levels, hyperemic flow velocity and CFR remained significantly improved, indicating enhanced microvascular function.
Conclusions:
- Ivabradine treatment significantly enhances hyperemic coronary flow velocity and CFR in patients with stable CAD.
- The observed improvements in CFR persist after heart rate correction, suggesting a direct positive effect on coronary microvascular function.
Objectives:
Although treatment with ivabradine reduces the incidence of hospital admissions for myocardial infarction and coronary revascularisation, there are no data concerning its effect on coronary circulation. The purpose of this study was to assess the effects of ivabradine on coronary flow velocity and flow reserve (CFR) in patients with stable coronary artery disease (CAD).
Methods:
During diagnostic coronary angiography (baseline), twenty-one patients with stable CAD underwent coronary flow velocity measurements (APV cm/s) in a non-culprit vessel, using a Doppler guidewire, at rest (r) and after adenosine administration to achieve maximal hyperaemia (h). During programmed coronary intervention in the culprit vessel, the same measurements were repeated one week after treatment with ivabradine (5 mg twice daily), both at the intrinsic heart rate and at a paced heart rate identical to that before treatment. CFR was defined as h-APV/r-APV.
Results:
Heart rate was significantly lower after treatment with ivabradine (78±14 bpm vs 65±9 bpm, p<0.001). Also, a reduction of r-APV (17.0±5.5 vs 19.7±7.6, p=0.003) and augmentation of h-APV (57.9±17.8 vs 53.5±21.4, p=0.009) leading to CFR improvement (3.51±0.81 vs 2.78±0.61, p<0.001) were observed. During pacing, although r-APV reverted to values similar to those before treatment (20.0±6.5 vs 19.7±7.6, p=NS), a sustained improvement in h-APV was observed (59.5±19.7 vs 53.5±21.4, p=0.007) and CFR remained higher than before treatment (3.04±0.66 vs 2.78±0.61, p<0.001).
Conclusions:
Ivabradine treatment significantly improves hyperaemic coronary flow velocity and CFR in patients with stable CAD. These effects remain even after heart rate correction indicating improved microvascular function.
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