Abstract 1591: Ivabradine But Not Atenolol Attenuates The Decline In Ejection Fraction And Preserves Coronary Reserve In Post-infarcted Middle-aged Rats
We compared the effects of heart rate reduction (HRR) by the If channel inhibitor, ivabradine (MI+IVA) and the β-blocker, atenolol (MI+ATEN) on ventricular remodeling and perfusion after myocardial infarction (MI). MI was induced in 12-mo.-old male Sprague-Dawley rats by left coronary artery ligation. Sham-operated rats (Sham) served as age-matched controls. Rats were treated for 1– 4 weeks and the drug doses were adjusted so that HRR would be comparable in the two groups; mean HRR ± SEM was 19.5 ± 1.1% for MI + IVA and 19.0 ± 0.8% for MI ± ATEN. Infarct areas (% of LV free wall) were not significantly different between groups: MI 64 ± 3; MI ± IVA 56 ± 3; MI ± ATEN 62 ± 3. Coronary reserve (fold increase in conductance during maximal vasodilation in response to dipyridamole), volume to mass ratio and ejection fraction (determined by echocardiograms 4 weeks after ligation) revealed the following values (*, p<0.05 vs. MI): Plasma levels of Ang II (pg/ml) 2 weeks after coronary artery ligation were significantly lower in both treatment groups compared to MI rats: Sham, 43 ± 7; MI 70 ± 10; MI+IVA 42 ± 8; MI+ATEN 21 ± 5 in the free wall. Ivabradine, but not atenolol, preserves coronary reserve, attenuates the decline in ejection fraction and the increase in left ventricular volume/mass ratio after myocardial infarction. These favorable modifications with ivabradine therapy occur despite similar increases in LVEDV after either HRR treatment. However, both ivabradine and atenolol are effective in decreasing plasma levels of Ang II.