All-cause mortality and cardiovascular events with nicorandil in patients with IHD: Systematic review and meta-analysis of the literature

Luo, Biao; Wu, Peng; Bu, Tong; Zeng, Zicheng; Lü, Dagang

doi:10.1016/j.ijcard.2014.07.007

Cited by 15 publications

(16 citation statements)

References 50 publications

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“…These previous reports [13,14] are partially concordant with our results. Several favorable effects of nicorandil on cardiovascular system have been reported, such as reduction in preload and afterload, improvement of myocardial perfusion, protection of cardiomyocytes from ischemic damage, prevention of Ca 2+ overload by opening adenosine triphosphate-sensitive potassium channels, anti-inflammatory and anti-proliferative effects, anti-apoptosis, anti-arrhythmic effects, protection of endothelial, mitochondrial, and energy-modulating functions, and preservation of kidney function [11,13,14].…”

Section: Discussionmentioning

confidence: 99%

“…A more comprehensive approach is necessary to refocus preventive and therapeutic strategies, and to decrease ischemic HF morbidity and mortality. Nicorandil, a combination of nitrate components and sarcolemmal adenosine triphosphatesensitive potassium channel opener, is a potent vasodilator of coronary and peripheral vessels and has been used as an antianginal agent [11]. A recent meta-analysis revealed that nicorandil treatment in patients with ischemic heart disease did not reduce revascularization (relative risk, RR 0.95, 95% CI 0.70-1.29) or all-cause mortality (RR 0.81, 95% CI 0.64-1.02), but did reduce cardiovascular events (RR 0.77, 95% CI 0.69-0.86) [11].…”

Section: Introductionmentioning

confidence: 99%

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Decreased cardiac mortality with nicorandil in patients with ischemic heart failure

2017

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Background: Effective treatments in heart failure (HF) patients with ischemic etiology have not been fully established. Nicorandil, combination of nitrate component and sarcolemmal adenosine triphosphate-sensitive potassium channel opener, is a potent vasodilator of coronary and peripheral vessels and has been used as an antianginal agent. Therefore, we examined impacts of nicorandil on cardiac mortality in ischemic HF patients. Methods: Consecutive 334 HF patients with ischemic etiology were retrospectively registered and divided into 2 groups based on oral administration of nicorandil: nicorandil group (n = 116) and non-nicorandil group (n = 218). We retrospectively examined cardiac mortality.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Decreased cardiac mortality with nicorandil in patients with ischemic heart failure

2017

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“…However, in addition to relieving ischemic symptoms, nicorandil exhibits numerous potential cardioprotective properties and actions, such as ischemic preconditioning, prevention of mitochondrial calcium overload, restoration of cardiac blood flow to the no-reflow phenomenon, attenuation of cardiac sympathetic nerve injury, and improvement of coronary microvasculature function, by opening the mitoKATP channel [3,[48][49][50][51][52][53] . Clinically, nicorandil has been shown to effectively reduce major coronary events in patients with stable angina or acute myocardial infarction, myocardial ischemia-reperfusion injury, and heart failure [2,7,50,[54][55][56] . Furthermore, human and animal studies have shown that long-term nicorandil treatment reduces coronary atherosclerotic lesions and plaque necrosis [9] .…”

Section: Discussionmentioning

confidence: 99%

“…Nicorandil (N-(2-hydroxyethyl)-nicotinamide nitrate), a mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channel opener, nitric oxide (NO) donor, and potent antioxidant, is effective in treating ischemic heart disease [1,2] . Nicorandil plays a crucial role not only in dilating the coronary artery, which is mainly attributed to its nitrate-like activity, but also in protecting cardiomyocytes against ischemia-reperfusion injury and endothelium against reactive oxygen species (ROS)-induced injury through the activation of mito-KATP channels in the myocardium [3][4][5][6] .…”

Section: Introductionmentioning

confidence: 99%

Nicorandil Inhibits Cyclic Strain-Induced Interleukin-8 Expression in Human Umbilical Vein Endothelial Cells

et al. 2016

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Background: Nicorandil, a mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channel opener, exerts protective effects on the cardiovascular system. This study examined the effect of nicorandil on cyclic strain-induced interleukin-8 (IL-8) expression in human umbilical vein endothelial cells (HUVECs). Methods: Cultured HUVECs were exposed to cyclic strain in the presence or absence of nicorandil (1-10 μmol/l); we then analyzed IL-8 expression. We also assessed the effects of nicorandil on heme oxygenase-1 (HO-1) expression and cyclic strain-modulated IL-8 expression after HO-1 silencing in HUVECs. Summary: HUVECs exposed to cyclic strain showed increased IL-8 messenger RNA expression and protein secretion. Nicorandil (1-10 μmol/l) inhibited cyclic strain-induced IL-8 expression, whereas 5-hydroxydecanoate (100 μmol/l), a selective inhibitor of the mitoKATP channel, completely reversed the inhibitory effects of nicorandil on cyclic strain-induced IL-8 expression. We demonstrated that nicorandil increased HO-1 expression in HUVECs. In addition, cobalt protoporphyrin (10 μmol/l), an inducer of HO-1 expression, mimicked the effects of nicorandil and inhibited IL-8 expression under cyclic strain, whereas zinc protoporphyrin IX (10 μmol/l), an inhibitor of HO-1 expression, antagonized the effect of nicorandil. HO-1 silencing significantly abrogated the inhibitory effects of nicorandil on cyclic strain-induced IL-8 expression, suggesting that HO-1 plays a role in the mechanism of action of nicorandil. Key Messages: This study is the first to report that nicorandil inhibits cyclic strain-induced IL-8 expression through the induction of HO-1 expression in HUVECs. This finding provides valuable new insight into the molecular pathways contributing to the vasoprotective effects of nicorandil.

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“…A more comprehensive approach is necessary to refocus preventive and therapeutic strategies, and to decrease ischemic HF morbidity and mortality. Nicorandil, a combination of nitrate components and sarcolemmal adenosine triphosphate-sensitive potassium channel opener, is a potent vasodilator of coronary and peripheral vessels and has been used as an antianginal agent [11]. A recent meta-analysis revealed that nicorandil treatment in patients with ischemic heart disease did not reduce revascularization (relative risk, RR 0.95, 95% CI 0.70–1.29) or all-cause mortality (RR 0.81, 95% CI 0.64–1.02), but did reduce cardiovascular events (RR 0.77, 95% CI 0.69–0.86) [11].…”

Section: Introductionmentioning

confidence: 99%

Decreased cardiac mortality with nicorandil in patients with ischemic heart failure

Yoshihisa

Sato

Watanabe

et al. 2017

BMC Cardiovasc Disord

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BackgroundEffective treatments in heart failure (HF) patients with ischemic etiology have not been fully established. Nicorandil, combination of nitrate component and sarcolemmal adenosine triphosphate-sensitive potassium channel opener, is a potent vasodilator of coronary and peripheral vessels and has been used as an antianginal agent. Therefore, we examined impacts of nicorandil on cardiac mortality in ischemic HF patients.MethodsConsecutive 334 HF patients with ischemic etiology were retrospectively registered and divided into 2 groups based on oral administration of nicorandil: nicorandil group (n = 116) and non-nicorandil group (n = 218). We retrospectively examined cardiac mortality.ResultsIn the Kaplan-Meier analysis (mean follow-up period 963 days), cardiac mortality was significantly lower in the nicorandil group than in the non-nicorandil group (11.2% vs. 19.7%, P = 0.032). In the Cox proportional hazard analysis, usage of nicorandil was a suppressor of cardiac mortality (hazard ratio 0.512, 95% confidence interval 0.275–0.953, P = 0.035), and this result was consistent in several subgroup analyses, such as left ventricular ejection fraction, percutaneous coronary intervention, coronary artery bypass graft, diabetes, β-blockers, and statins.ConclusionNicorandil is potentially effective for reducing mortality in patients with ischemic heart failure.Trial registrationThis was a retrospective study.

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All-cause mortality and cardiovascular events with nicorandil in patients with IHD: Systematic review and meta-analysis of the literature

Cited by 15 publications

References 50 publications

Decreased cardiac mortality with nicorandil in patients with ischemic heart failure

Decreased cardiac mortality with nicorandil in patients with ischemic heart failure

Nicorandil Inhibits Cyclic Strain-Induced Interleukin-8 Expression in Human Umbilical Vein Endothelial Cells

Decreased cardiac mortality with nicorandil in patients with ischemic heart failure

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