Key result
Cilostazol preserved left ventricular systolic function in post-myocardial infarction rats exposed to restraint stress, resulting in a higher LVEF at 5 weeks compared to control (66.93% vs 47.00%, p=0.029).
Why the study?
The study was aimed to examine in vivo the effects of cilostazol treatments on myocardial function, myocardial remodeling, and neurohormonal status in a myocardial infarction with restrained stress rat model.
Does cilostazol improve myocardial function and remodeling in a post-myocardial infarction rat model exposed to restraint stress?
Does cilostazol improve myocardial function and remodeling in a post-myocardial infarction rat model exposed to restraint stress?
Absolute Event Rate: 66.93% vs 47%
p-value: p=0.029
Cilostazol preserves left ventricular systolic function and attenuates stress-induced remodeling in a post-myocardial infarction rat model.
Should not change practice; hypothesis-generating for cilostazol in stressed post-MI models.
associated catecholamine secretion. The study was aimed to examine, in vivo, the effects of cilostazol treatments on myocardial function, myocardial remodeling, and neurohormonal status in myocardial infarction (MI) with restrained stress rat model. Male Sprague Dawley rats, subjected to coronary artery ligation to induce myocardial infarction (MI), received either a standard rat chow alone (control, n=5) or combined with cilostazol (cilostazol, n=5; 5 mg/kg×5 weeks). They were exposed to repeated restraint stress (2 h×2 times/day) for 10 days beginning 1 week after surgery. Left ventricular ejection fraction (LVEF), LV mass by heart weight/body weight ratio and level of tissue brain natriuretic peptide (BNP) expression by immunoblotting were determined. Plasma epinephrine and norepinephrine levels were also measured. Mean LVEF was higher in the cilostazol group than in the control group (66.9±14.3 vs 47.0±17.1, p<0.05) at 5 weeks after MI. However, LV mass and tissue BNP expression were significantly lower in the cilostazol than in the control group (p<0.05). Plasma epinephrine and norepinephrine levels were also lower in the cilostazol group compared with the control (p<0.05). Cilostazol preserves left ventricular systolic function and attenuates stress induced remodeling in postinfarct rats. Its beneficial effects were associated with reduced plasma catecholamine levels during postinfarct remodeling.
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Lee et al. (2020) studied Myocardial infarction with restraint stress (n=10). Cilostazol vs. Standard rat chow alone was evaluated on Left ventricular ejection fraction (LVEF) at 5 weeks (p=0.029). Cilostazol preserved left ventricular systolic function in post-myocardial infarction rats exposed to restraint stress, resulting in a higher LVEF at 5 weeks compared to control (66.93% vs 47.00%, p=0.029).
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