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Biomedical subjects

M Yasutake

Publications and source records attributed to M Yasutake.

32 records · Page 2Linked to original sources
PubMed1995

Exacerbation of reperfusion arrhythmias by alpha 1 adrenergic stimulation: a potential role for receptor mediated activation of sarcolemmal sodium-hydrogen exchange.

OBJECTIVE: Stimulation of myocardial alpha 1 adrenoceptors causes (1) exacerbation of reperfusion induced arrhythmias, and (2) stimulation of sarcolemmal Na+/H+ exchange. The aims of this study were to identify the alpha 1 adrenoceptor subtype involved in the former effect and to determine whether stimulation of the Na+/H+ exchanger may play a role in this phenomenon. METHODS: Isolated rat hearts were subjected to independent perfusion of the left and right coronary beds. After 15 min of aerobic perfusion of both beds, the alpha 1 adrenoceptor agonist phenylephrine (0.1, 1, or 10 microM) was infused selectively into the left coronary bed for 2 min. The left coronary bed was then subjected to 7 min of zero flow ischaemia and 5 min of reperfusion. RESULTS: The incidence of reperfusion induced ventricular fibrillation was increased from 0% in controls to 8%, 42%*, and 75%* with 0.1, 1, and 10 microM phenylephrine (*P < 0.05); this dose dependent effect occurred in the absence of significant intergroup differences in vascular resistance or heart rate. Similar infusion of methoxamine at 10 microM also increased the incidence of reperfusion induced ventricular fibrillation from 13% to 88%*. Infusion of 10 microM phenylephrine during reperfusion alone did not affect the incidence of reperfusion induced ventricular fibrillation. Infusion of the selective alpha 1A adrenoceptor antagonist WB4101 at 0.1, 1, or 10 microM for 2 min immediately before ischaemia (concomitantly with 10 microM phenylephrine) reduced the incidence of reperfusion induced ventricular fibrillation from 83% to 75%, 25%*, and 0%*. Similar infusion of the selective alpha 1B adrenoceptor antagonist chloroethylclonidine (0.1 or 1 microM) or the selective beta 1 adrenoceptor antagonist atenolol (0.1 or 1 microM) did not reduce the incidence of reperfusion induced ventricular fibrillation. The novel NHE-1 selective Na+/H+ exchange inhibitor HOE694 (10 microM), when infused into the left coronary bed before ischaemia (concomitantly with 10 microM phenylephrine) and throughout reperfusion, reduced the incidence of reperfusion induced ventricular fibrillation from 83% to 25%*. In hearts that received 10 microM phenylephrine before ischaemia. HOE694 (10 microM) was partially effective when infused during reperfusion alone (ventricular fibrillation incidence reduced from 83% to 42%). CONCLUSIONS: (1) the exacerbation of reperfusion induced arrhythmias by alpha 1 adrenergic stimulation during ischaemia is mediated by the alpha 1A adrenoceptor subtype, and (2) increased Na+/H+ exchanger activity during ischaemia and reperfusion may play a causal role in this phenomenon.

Animals↗
PubMed1994

Na+/H+ exchange and reperfusion arrhythmias: protection by intracoronary infusion of a novel inhibitor.

Activation of sarcolemmal Na+/H+ exchange has been proposed as a causal factor in reperfusion arrhythmogenesis. To test this hypothesis, we determined the antiarrhythmic efficacy of two structurally distinct but equipotent Na+H+ exchange inhibitors, 5-(N-ethyl-N-isopropyl)amiloride (EIPA) and the novel drug, 3-methylsulfonyl-4-piperidinobenzoyl guanidine (HOE-694), in isolated rat hearts (n = 12/group) subjected to independent dual coronary perfusion. After 15 min of aerobic perfusion of both beds, flow to the left coronary bed (LCB) was terminated for 10 min; this was followed by 5 min of reperfusion. Various concentrations of each drug were selectively infused into the LCB either during the 5-min period preceding ischemia plus during reperfusion or during reperfusion alone. With the former protocol, 0.01, 0.1, 1, and 10 microM EIPA reduced the incidence of reperfusion-induced ventricular fibrillation (VF) from 92% in controls to 83, 83, 50, and 0% (P < 0.05); the number of hearts in sinus rhythm at the end of reperfusion was increased from 17 to 42, 25, 83 (P < 0.05), and 100% (P < 0.05). HOE-694, at the same concentrations, reduced VF incidence from 92% in control to 83, 58, 50, and 8% (P < 0.05); 25, 67, 75 (P < 0.05), and 100% (P < 0.05) of hearts were in sinus rhythm, compared with 17% of controls, at the end of reperfusion. Even when infused during reperfusion alone, both drugs afforded significant protection against reperfusion-induced VF, which did not differ significantly from that observed when the drugs were also given before ischemia. The similar antiarrhythmic efficacy of EIPA and HOE-694 is consistent with an arrhythmogenic role for activation of Na+/H+ exchange during early reperfusion.

Amiloride↗
PubMed1992

Two cases of variant form angina pectoris associated with myocardial bridge--a possible relationship among coronary vasospasm, atherosclerosis and myocardial bridge.

Myocardial bridge (MB) is a congenital anomaly of the coronary artery and may occur in 5 to 12% of the human population. However, the mechanism of MB-induced myocardial ischemia is still speculative. We report 2 cases of variant form angina pectoris associated with MB in which myocardial ischemia seemed to be related to the interaction between coronary perfusion and MB. In case 1, electrocardiography during anginal attack at rest showed ST elevation in the inferior leads and MB was observed after percutaneous transluminal coronary angioplasty at the site of the right coronary artery lesion following successful dilatation. In case 2, MB of the left anterior descending coronary was located in the identical portion where coronary vasospasm was induced by intracoronary acetylcholine injection, although ischemia during the spontaneous anginal attack was limited to the inferior area of myocardium. These 2 cases suggest that MB can be, at least in some patients, one of the possible causes of the endothelial damage which seems to be related to coronary vasospasm; this was documented in both cases.

Angina Pectoris, Variant↗
PubMed1992

[Silent myocardial ischemia in myocardial infarction patients: its prognostic significance].

To evaluate the prognostic and clinical significance of silent myocardial ischemia (SMI), we examined cardiac events in 160 patients with old myocardial infarction who underwent ambulatory Holter monitoring, treadmill exercise testing and coronary angiography. Using the Cox's proportional hazard regression model and the survival curves with the Kaplan-Meier method, we identified the predictors of cardiac events. The incidence of cardiac events for all the patients during the 44-month follow-up period was 18%. The significant predictors of unfavorable outcomes were severe coronary lesions and SMI. The incidence of SMI was 38%. The cardiac event rate in patients with SMI was higher than in those without SMI (32 vs 9%, p < 0.05). The most frequent cardiac event in patients with SMI was reinfarction, and the significant predictors of cardiac events for these SMI patients were lower ejection fraction and maximum ST depression on Holter monitoring. In conclusion, SMI proved to be a significant predictor of unfavorable outcome in patients with old myocardial infarction. It was, therefore, suggested that revascularization (PTCA/CABG) should be used as early as possible in patients with SMI whether anginal symptoms are present or not.

Aged↗
PubMed1991

A new strategy for the reduction of acute myocardial infarction in variant angina.

To study the effects of stepwise early treatment in variant angina pectoris, frequencies of cardiac events and complications were examined after three different types of treatment. The subjects of the study consisted of 159 consecutive patients with variant angina pectoris, who were in need of hospitalization. The three treatment modalities were the introduction of calcium antagonists, nicorandil and nitroglycerin infusion, and percutaneous transluminal coronary angioplasty (PTCA), respectively. The cardiac event rate for this series of patients was 16% (25 of 159). The cumulative cardiac event rate was 22% at 1 year and 23% at 3 years in the first treatment period; 11% at the same intervals in the second treatment period; and 6% at the same intervals in the third treatment period. Our results suggest that it is important in the treatment of variant angina pectoris not only to prevent anginal attacks by the use of fast-acting coronary vasodilators, but also to initiate early revascularization.

Adult↗
PubMed1991

[Stress myocardial scintigraphy in coronary artery disease: its clinical significance].

To evaluate the clinical significance of asymptomatic ischemic heart disease, exercise electrocardiography and stress myocardial scintigraphy were performed. These were correlated with symptoms during exercise tests and histories of myocardial infarction (MI). The study subjects consisted of 70 patients with coronary artery disease, including 34 with MI, and 36 without MI but with angina pectoris. Stress tests were performed using bicycle ergometer under electrocardiographic monitoring throughout the test. Transient myocardial ischemia was confirmed by perfusion defects on thallium myocardial imaging demonstrated immediately after exercise, but not 3 hours after the stress test. Asymptomatic ST depression was observed in 18 of 34 patients with MI (53%) and in 21 of the 36 patients with angina (58%); however, transient myocardial perfusion defects were confirmed in 61% of the patients with MI (11 of 18 patients), but in only 33% of those with angina (7 of 21 patients). The difference was statistically significant (p less than 0.05). It was suggested that there are some differences in the clinical significance of asymptomatic ST depression between the patients with MI and those without MI but with angina pectoris.

Aged↗
PubMed1991

[A case of mitral stenosis developing infective endocarditis 18 months after PTMC].

We presented here a case of mitral stenosis developing infective endocarditis 18 months after PTMC. A 33-year-old male was admitted to our hospital for the evaluation of mitral stenosis with signs of congestive heart failure. The use of PTMC was adequately indicated based on the data of previous cardiac catheterization and was successfully performed. The post-operative clinical course was good leaving only slight mitral regurgitation demonstrated by post-valvuloplasty LVG. About 18 months after PTMC, the patient developed a high fever and erythema with tenderness on his leg, so he was admitted again. Blood culture was positive for streptococcus viridans. Moreover, echocardiogram revealed valvular vegetation on the anterior mitral leaflet, which is the characteristic finding of infective endocarditis. Antibiotics were so effective that his clinical course was relatively good with minor cerebral infarction during chemotherapy. Little is known about the prognosis and late complication of PTMC. However, our reported case may suggest that prophylactic chemotherapy might be recommended at least in some cases showing mitral regurgitation after PTMC.

Adult↗
PubMed1990

Angiographic response to a vasodilating drug, nicorandil, in patients with coronary artery disease.

To investigate the usefulness of nicorandil as an antianginal drug, we compared the coronary vasodilatory response in nonstenotic coronary artery segments and the hemodynamic response in 26 coronary artery disease patients. Both responses were studied prior to sublingual administration of 10 mg of this drug and 10, 30 and 60 min afterward. The plasma nicorandil concentration was determined up to 120 min after administration. The mean coronary dilating ratio of nicorandil was 117% 30 min after administration (p less than 0.01) and showed a good correlation to the plasma nicorandil concentration. The mean maximum dilating ratio of each patient was 125%. There was no difference between individual coronary arteries or between proximal and distal segments in terms of the coronary artery dilating ratio. The plasma nicorandil concentration required for 120% dilation of the coronary arteries was 26 ng/ml, 89 ng/ml and 142 ng/ml for those cases with variant angina, exertional angina and postinfarction angina, respectively. Hemodynamic changes due to administration of this drug included a decrease in blood pressure, and a reduction in total peripheral resistance, rate-pressure product, pulmonary capillary pressure and stroke-work index. These results indicate that the antianginal effects of nicorandil are derived from its coronary vasodilatory action and an inhibitory effect on myocardial oxygen consumption.

Administration, Sublingual↗
PubMed1987

Factors influencing the clinical course and the long-term prognosis of patients with variant angina.

The purpose of this study was to clarify the factors influencing the clinical course and prognosis in variant angina. Also, the mechanism of acute myocardial infarction in variant angina is reviewed. The subjects were 110 patients with variant angina who, after the initial visit or admission, were observed for a period of at least 2 months, the average observation period being 68 +/- 49 months (range: 2 months-16 years). The incidence of acute myocardial infarction was 21.8% of these patients and 87.5% of the infarctions occurred within 1 month of the initial visit or admission. In variant angina, the average rate over 1 year was 2.2%; however, in classical angina the rate was 3.7% and in postinfarction angina 5.0%. The mortality rate was 5.5%, with death in the majority of cases occurring within 1 month, as in myocardial infarction. When treatment was stopped, spontaneous remission occurred in at least 26 of the 110 cases (23.6%). Beyond 3 months, the remission continued in 19 of these 26 cases. Seven cases had acute myocardial infarction in spite of the suppression of anginal attacks with administration of calcium antagonists. Apparently coronary spasm is the cause of anginal attacks, and the cause of acute myocardial infarction in patients with variant angina appears to be coronary thrombus formation.

Adult↗
PubMedDate not supplied

Effects of selective alpha 1A-adrenoceptor antagonists on reperfusion arrhythmias in isolated rat hearts.

Stimulation of alpha 1-adrenoceptors (AR) during ischaemia in the rat heart by exogenous phenylephrine exacerbates reperfusion arrhythmias, an effect apparently mediated by the alpha 1A-AR subtype. We tested whether alpha 1A-AR stimulation by endogenous catecholamines, released during ischaemia, could modulate reperfusion arrhythmias, using as pharmacological tools the selective alpha 1A-AR antagonists abanoquil (UK52046) and WB4101. Isolated rat hearts (n = 12/group) were subjected to dual coronary perfusion. After 15 min of aerobic perfusion of both coronary beds, abanoquil or WB4101 was infused selectively into the left coronary bed (LCB) for 5 min. The LCB was then subjected to 10 min of zero-flow ischaemia and 5 min of reperfusion. Effects on PR interval, width of the ventricular complex (QRST90) and reperfusion arrhythmias were assessed. Abanoquil at concentrations of 0.03, 0.1 and 0.3 microM tended to reduce the incidence of reperfusion-induced ventricular fibrillation (VF) in a dose-dependent manner from 75% in controls to 58, 33 and 25%, but this effects did not achieve statistical significance. Similarly, WB4101 at 0.1, 0.3 and 1 microM also tended to reduce VF incidence from 67% in controls to 67, 42% and 33% (NS). The incidence of ventricular tachycardia (VT) was 100% in all groups and ECG parameters were not altered significantly by either drug. These results suggest that, in this denervated isolated heart preparation, alpha 1A-AR stimulation during ischaemia by endogenous catecholamines does not significantly modulate reperfusion arrhythmias.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Combination of ambulatory electrocardiographic monitoring and psychological testing in coronary artery disease patients.

Ambulatory electrocardiographic monitoring and psychological testing were performed in 100 patients with chronic stable myocardial infarction. These patients were divided into four groups according to their chest pain and transient ST-segment depression by Holter monitoring during the follow-up period: group A, 40 patients without complications; group B, 20 patients with silent myocardial ischemia; group C, 14 patients with episodes of chest pain alone; and group D, 26 patients with postinfarction angina. Whereas group B had silent myocardial ischemia and extroversion, groups C and D were characterized by introversion and neuroticism. The frequency of multi-vessel disease was 41% for group A, 53% for group B, 8% for group C and 70% for group D. The patients of group B not only received treatment for coronary artery disease but also behavioral counseling and those of group C received psychotherapy. The results support the view that a combination of Holter monitoring and psychological testing is clinically useful for the development of therapeutic strategies for coronary artery disease.

Aged↗