Literature DB >> 15459610

Nicorandil improves cardiac function and clinical outcome in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention: role of inhibitory effect on reactive oxygen species formation.

Hirotsugu Ono1, Tomohiro Osanai, Hiroshi Ishizaka, Hiroyuki Hanada, Takaatsu Kamada, Hiroyuki Onodera, Norio Fujita, Shingo Sasaki, Toshiro Matsunaga, Ken Okumura.   

Abstract

BACKGROUND: Early reperfusion therapy improves the clinical outcomes of patients with acute myocardial infarction (AMI), but benefits are limited by reperfusion injury in some patients. We examined the effect of nicorandil, a hybrid of K(ATP) channel opener and nicotinamide nitrate, on reactive oxygen species (ROS) formation and clinical outcomes after primary percutaneous coronary intervention (PCI) for AMI.
METHODS: Fifty-eight patients with AMI were randomized into control (n = 25) and nicorandil pretreatment groups (n = 33). In the nicorandil group, nicorandil (4 mg as a bolus injection followed by constant infusion at 8 mg/hour for 24 hours) was administered just after admission. ROS formation was assessed by measuring urinary excretion of 8-epi-prostaglandin F2alpha (PGF2alpha) and compared between the 2 groups. Cardiac function and the incidence of reperfusion injury and cardiac events were also compared.
RESULTS: Urinary 8-epi-PGF2alpha excretion was increased 2-fold at 60 to 90 minutes after PCI in the control group, whereas it was unchanged after PCI in the nicorandil group (P <.0001 between the 2 groups). The incidence of no-reflow phenomenon was lower in the nicorandil group than in the control group. Left ventricular ejection fraction and cardiac index at 6 months were greater in the nicorandil group than in controls. Plasma brain natriuretic peptide level at 6 months was lower in the nicorandil group. Incidences of inhospital cardiac events and rehospitalization were lower in the nicorandil group than in controls.
CONCLUSIONS: Nicorandil improves cardiac function and clinical outcomes in patients with AMI. Suppression of ROS formation may be involved in the mechanism.

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Year:  2004        PMID: 15459610     DOI: 10.1016/j.ahj.2004.05.014

Source DB:  PubMed          Journal:  Am Heart J        ISSN: 0002-8703            Impact factor:   4.749


  25 in total

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Authors:  Takayuki Fujiwara; Toshiro Matsunaga; Kunihiko Kameda; Naoki Abe; Hirotsugu Ono; Takumi Higuma; Jin Yokoyama; Hiroyuki Hanada; Tomohiro Osanai; Ken Okumura
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Review 5.  Inhibition of mitochondrial membrane permeability as a putative pharmacological target for cardioprotection.

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6.  Left circumflex coronary artery is protected against no-reflow phenomenon following percutaneous coronary intervention for coronary artery disease.

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7.  Effect of Thrombus Composition and Viscosity on Sonoreperfusion Efficacy in a Model of Micro-Vascular Obstruction.

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Review 8.  Reperfusion injury as a therapeutic challenge in patients with acute myocardial infarction.

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9.  Altered serum creatine kinase level and cardiac function in ischemia-reperfusion injury during percutaneous coronary intervention.

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Review 10.  Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity.

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Journal:  Oxid Med Cell Longev       Date:  2021-07-03       Impact factor: 6.543

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