Drug-eluting balloon (DEB) with angioplasty a paclitaxel-coated balloon catheter is an effective treatment option in patients with in-stent restenosis (ISR) after a drug-eluting stent (DES). We describe a case in which 'no-reflow' phenomenon developed after DEB angioplasty of a DES ISR lesion. Coronary flow was restored after intracoronary administration of nicorandil.
Angioplasty ; Catheters ; Coronary Restenosis ; Drug-Eluting Stents ; Humans ; Nicorandil ; No-Reflow Phenomenon

The effects of oral nicorandil were evaluated in 32 patients with angina pectoris who were diagnosed by typical chest pain and postitive treadmill exercise test from December 1986 throught May 1987. The effects were measured by clinical improvement rating at 4 and 8 weeks after administration of nicorandil, and by repeated treadmill exercise test in 16 patients. The results were as follow's: 1) Clinical improvement was observed in 23(71.5%) and 25(78%) of 32 patients at 4 and 8 weeks after oral nicorandil. 2) Repeated treadmill exercise test of 16 patients showed significant prolongation of exercise duration (464+/-148 seconds vs. 526+/-174, p<0.05). 3) Hemodynamic data like blood pressure or heart rate were independent of nicorandil administration. 4) Three patients complained of headache, and one of them discontinued nicorandil. Mild indigestion was also found in another one patient.
Angina Pectoris* ; Blood Pressure ; Chest Pain ; Dyspepsia ; Exercise Test ; Headache ; Heart Rate ; Hemodynamics ; Humans ; Nicorandil*

BACKGROUND AND OBJECTIVES: A radial artery spasm is one of the most common complications of coronary angiography during a transradial, causing considerable patient discomfort, which sometimes disturbs the procedure. This study was designed to evaluate the effects of nicorandil in the prevention of a radial artery spasm during coronary angiography. SUBJECTS AND METHODS: This was a randomized study to compare 4 mg of nicorandil and a 10 mL cocktail solution performed in 100 patients. Vasospasms of the radial artery, which were expressed as stenosis of the vessel diameter with a transradial approach and radial artery patency by pulse oximetry analysis one month later, were examined. RESULTS: Reductions in the systolic and diastolic blood pressures after administration of the spasmolytic agents were 15.8+/-11.8/ 8.4+/-8.0 and 20.5+/-13.6/6.7+/-6.2 in the for nicorandil and cocktail groups, respectively. Nicorandil induced a lesser decrease in the systolic BP than the cocktail, but without statistical significance (p=0.07). Both vasodilating agents showed a significant radial artery vasodilation following their intra-arterial administration (p<0.001 for all). The diameter of the radial artery showed a significant decrease in both groups following catheterization (p<0.05 for all). There were no significant differences between the two groups in terms of radial artery spasms (46 vs. 58% in nicorandil and cocktail groups, respectively, p=0.709). CONCLUSION: Nicorandil, with vasodilatory effects due to a dual mechanism was as effective as the cocktail solution in the vasodilation of the radial artery.
Catheterization ; Catheters ; Constriction, Pathologic ; Coronary Angiography* ; Humans ; Nicorandil* ; Oximetry ; Radial Artery* ; Spasm* ; Vasodilation

The antianginal effect of oral nicorandil was examined on 15 subjects with angina pectoris who had not been improved by previous treatment with beta blocker and/or calcium antagonists. Nicorandil, 5mg tid, was added to their previous regimen which were composed of beta blocker and/or calcium antagonists, and patients were followed up at least for 6 weeks. The following results were obtained; 1) Frequences of anginal attack were markedly reduced in 11(73%) of 15 patients after the use of nicorandil. 2) After the use of nicorandil, ST segment depression and T wave inversions were improved in 10(66.7%) of 15 patients. 3) In 10 patients who had been taken nicorandil over 12 weeks, 9 patients showed sustained improvement in clinical status, but no significant side effect was noted. 4) In two patients who had undergone exercise tolerance test, significant prolongation in exercise duration were noted. 5) The adverse effects of nicorandil were as follows; headache in 3, insomnia in 3, excessive perspiration, dizziness, thirst, constipation and facial fiushing in 1, respectively.
Angina Pectoris* ; Calcium ; Constipation ; Depression ; Dizziness ; Exercise Tolerance ; Headache ; Humans ; Nicorandil* ; Sleep Initiation and Maintenance Disorders ; Thirst

BACKGROUND: This study was designed to evaluate the role of KATP channel activation and change of monophasic action potential duration on cardioprotective effect of ischemic preconditioning in cat. METHODS: 34 cats were divided into 4 groups: control (n=10), ischemic preconditioning(n=8), glibenclamide pre-treated(n=8) and nicorandil pre-treated group(n=8). Ischemic preconditioning was done in ischemic preconditioning and glibenclamide pre-treated groups by 3 episodes of 5 min ischemia and 10 min reperfusion. All subjects underwent 40 min of ischemia and 40 min reperfusion. The KATP channel antagonist glibenclamide was given as intravenous bolus (0.5mg/kg) 10 min before ischemic precondtioning and infused (5 microgram/min) during ischemic preconditioning. Nicorandil, a KATP channel opener was injected as intravenous bolus (0.5mg/kg) before 40 min ischemic procedure. Monophasic action potential duration at 50% repolarization(MAP50) was measured in the ischemic and non-ischemic area respectively by epicardial probe throughout the experiment. The effects of ischemic preconditioning were determined by infarct size (% area at risk). RESULTS: Ischemic preconditioning or pretreatment with nicorandil prior to 40 min ischemia demonstrated a significant reduction in infarct size(26.6+/-7%, 33+/-8% infarction of the risk zone, respectively, p<0.01, p<0.05 vs. control) with respect to control(42+/-7% infarction of the risk zone). Pretreatment with glibenclamide abolished the effect of ischemic preconditioning(40+/-8% infarction of the risk zone, p=NS vs. control) Ischemic preconditioning group exhibited a significant reduction of ischemic area MAP50 duration in the ischemic area during preconditioning; at first preconditioning 123+/-9msec vs. 137+/-19msec control(p=NS), at second preconditioning 105+/-16msec vs. 140+/-19msec control(p<0.01), at third preconditioning 109+/-15msec vs. 138+/-19msec control(p<0.05). Pretreatment with glibenclamide prevented the reduction of MAP50 in the ischemic area during ischemic preconditioning. During 40 minutes ischemia, MAP50 shortening was more pronounced in the preconditioned group than in control group; at 10 min 85+/-22 msec vs. 131+/-31msec control(p<0.05), at 20 min 88+/-21msec vs. 130+/-32msec control(p<0.05), and at 30 min 103+/-24msec vs. 136+/-30msec control(p<0.05). This shortening effect was prevented by glibenclamide pretreatment. Nicorandil pretreatment pronounced the ischemic shortening of MAP50 in ischemic area and the nicorandil effect was most significant during early ischemic period; at 10 min 97+/-21msec(p<0.05 vs. control), at 20 min 104+/-32msec (p=NS vs. control), and at 30 min 134+/-28msec(p=NS vs. control). MAP50 measured in non-ischemic area was not significantly different between groups. CONCLUSION: We conclude that KATP channel activation and monophasic action potential duration shortening play a important role in myocardial protection during ischemic injury.
Action Potentials* ; Animals ; Cats* ; Glyburide ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Nicorandil ; Reperfusion

We evaluated the clinical effects of Nicorandil in 27 patients (17 male and 10 female) with ischemic heart disease (17 patients of stable effort angina, 3 patients of unstable effort angina, 6 patients of spontaneous angina, 1 patient of variant angina) in terms of the effect on the anginal pain, electrocardiographic changes and side effects. The results obtained were as follows; 1. The pulse rate was not changed by the drug administration and blood pressure were decreased slightly by Nicorandil in a daily dose of 15 mg divided into 3 dose, but these decrease were not significant in statistical meaning. 2. Improvement in EKG changes was observed in 9 patients (69%) among the 13 patients who showed abnormal EKG initially. 3. Anti-anginal effect of nicorandil were excellent in 14 patients, good in 8 patients, fair in 3 patients and so the rate of global improvement was 82%. 4. Nicorandil had side effects in 7 patients, headache (4 patients), palpitation, ocular pain, edema, but these were transitory and tolerable except of one case who could not be continued because of severe headache.
Angina Pectoris* ; Blood Pressure ; Edema ; Electrocardiography ; Headache ; Heart Rate ; Humans ; Male ; Myocardial Ischemia ; Nicorandil*

BACKGROUND AND OBJECTIVES: Coronary flow reserve (CFR) is the capability of coronary arteriolar bed to dilate in response to increased cardiac metabolic demand. Nocorandil, a hybrid of ATP-sensitive K+ channel opener and nitrates, causes coronary vasodilation of both epicardial and resistance vessels. We investigated the feasibility and safety of nicorandil as compared to adenosine in the measurement of CFR using a Doppler guide wire. SUBJECTS AND METHODS: We measured CFR in 26 consecutive patients (mean age 52+/-19 years, M:F=16:10) during coronary intervention with a 0.014-inch Doppler guide wire. We recorded the baseline average peak velocity (APV) and the hyperemic APV induced by intracoronary adenosine or nicorandil. The heart rate, mean aortic pressure and the time interval from maximal APV to baseline APV were also recorded. RESULTS: There were no significant differences between APV, diastole/systole velocity ratio and CFR induced by adenosine and those induced by nicorandil (44.4 +/- 17.3 vs 45.5 +/- 17.6, p=0.78, 1.59 +/- 0.51 vs 1.57 +/- 0.52 p=0.78, 2.22 +/- 0.89 vs 2.27 +/- 0.94, p=0.36). The CFR and diastole/systole velocity ratio induced by nicorandil showed a strong positive linear correlation with those by adenosine (r2=0.77, p=0.0001, r2=0.83, p=0.0001). Adenosine significantly decreased the heart rate as compared to nicorandil =-25.5 +/- 9.7 vs -8.7 +/- 4.9 bpm, p=0.001). There were no differences in the changes of mean aortic pressure between adenosine and nicorandil (-7 +/- 9 vs -2 +/- 3 mmHg, p=0.17). Nicorandil prolonged the time interval from maximal APV to baseline APV compared to adenosine (194 +/- 62 vs 37 +/- 12 sec, p=0.001). CONCLUSION: Nicorandil is feasible and safe for use in measuring CFR using a Doppler guide wire and may replace adenosine.
Adenosine* ; Arterial Pressure ; Blood Flow Velocity ; Heart Rate ; Humans ; Nicorandil* ; Nitrates ; Ultrasonography ; Vasodilation

BACKGROUND AND OBJECTIVES: Intravenous nicorandil infusion with percutaneous coronary intervention (PCI) has been reported to reduce reperfusion injury events and to improve cardiac function in patients with an acute myocardial infarction. However, there is limited information on the use of intra-coronary nicorandil. A prospective randomized single center study was designed to evaluate the efficacy of the use of intra-coronary nicorandil. SUBJECTS AND METHODS: Seventy-three patients with an acute ST segment elevation myocardial infarction were randomly assigned to the nicorandil group (n=37) or a control group (n=36); all patients received a PCI. In the nicorandil group of patients, 4 mg of intra-coronary nicorandil was infused directly into the infarct area prior to reperfusion (2 mg before ballooning, 2 mg before stenting). The composite endpoint was the incidence of ventricular arrhythmia, no-reflow and slow flow. We estimated the post thrombolysis in myocardial infarction (TIMI) grade, the myocardial perfusion grade after PCI and the short-term clinical outcome. RESULTS: The baseline characteristics were similar in both groups of patients. A significant difference was observed in the composite endpoint in the nicorandil group of patients as compared to the control group of patients (p=0.037). The achievement rate of post TIMI grade 3 was significantly higher in the nicorandil group of patients (p=0.019). The myocardial perfusion grade 1 was not observed in the nicorandil group of patients; however, it was observed in five patients in the control group (p=0.019). Major adverse cardiac events in hospital and in 30 days were similar between the two groups. CONCLUSION: Intra-coronary nicorandil infusion reduced the occurrence of no-reflow, slow reflow, reperfusion arrhythmia and improved the myocardial perfusion grade and TIMI flow during PCI. The results of this study showed that the use of intracoronary nicorandil improved the clinical outcome in patients with an acute myocardial infarction.
Achievement ; Arrhythmias, Cardiac ; Humans ; Incidence ; Myocardial Infarction ; Nicorandil ; No-Reflow Phenomenon ; Percutaneous Coronary Intervention ; Perfusion ; Prospective Studies ; Reperfusion ; Reperfusion Injury

The effect of oral nicorandil were evaluated by a 9-day double-blind cross-over protocol on 16 subjects with angina pectoris referred to our cardiology clinic from June '84 through September '85. total daily doses were 15-45mg. The effects were measured by 3 seperate treadmill exercise EKG tests and symptom reviews on each patient. The following results were obtained. 1) The mean age of the patients was 57.4+/-7.2 years. These were 14 male and 2 female patients. 2) Resting heart rate on nicorandil was 73.6+/-14.0 beats/min and 70.5+/-14.0 beats/min in placebo(P<0.05). There were no significant effects of nicorandil on resting blood pressure and heart rate-blood pressure product. 3) Peak exercise heart rate was 126.4+/-22.5 beats/min on nicorandil and 121.8+/-21.4 beats/min on placebo(P<0.05). There were no significant effects of nicorandil on blood pressure after exercise and peak heart rate-blood pressure product(x10(-3)) after nocorandil was 20.2+/-5.0 and 18.9+/-4.6 on placebo(P>0.05). 4) Exercise duration was 485.8+/-107.7 sec on nicorandil and 423.3+/-101.9 sec on placebo(P<0.001). 5) The exercise duration was prolonged in 11 cases(68.7%), showed on change in 2 cases(12.5%), and shortened in 3(18.8%). 6) There were attacks of chest pain during placebo period in 2 cases, but none developed during nicorandil period. 7) Headache was noted in 2 patients, and in one of them, it was so severe as to discontinue nicorandil stydy. No other side effects were noted. In conclusion, additional therapeutic benefit can be obtained by nicorandil in patients with severe angina in spite of conventional antianginal agents already being administered.
Angina Pectoris* ; Blood Pressure ; Cardiology ; Chest Pain ; Cross-Over Studies* ; Electrocardiography ; Female ; Headache ; Heart ; Heart Rate ; Humans ; Male ; Nicorandil*

Potassium channels and transporters maintain potassium homeostasis and play significant roles in several different biological actions via potassium ion regulation. In previous decades, the key revelations that potassium channels and transporters are involved in the production of gastric acid and the regulation of secretion in the stomach have been recognized. Drugs used to treat peptic ulceration are often potassium transporter inhibitors. It has also been reported that potassium channels are involved in ulcerative colitis. Direct toxicity to the intestines from nonsteroidal anti-inflammatory drugs has been associated with altered potassium channel activities. Several reports have indicated that the long-term use of the antianginal drug Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, increases the chances of ulceration and perforation from the oral to anal regions throughout the gastrointestinal (GI) tract. Several of these drug features provide further insights into the role of potassium channels in the occurrence of ulceration in the GI tract. The purpose of this review is to investigate whether potassium channelopathies are involved in the mechanisms responsible for ulceration that occurs throughout the GI tract.
Adenosine ; Channelopathies* ; Colitis, Ulcerative ; Gastric Acid ; Gastrointestinal Tract ; Homeostasis ; Intestines ; Nicorandil ; Peptic Ulcer ; Potassium Channels ; Potassium* ; Stomach ; Ulcer*