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Dive into the research topics where Haruo Araki is active.

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Featured researches published by Haruo Araki.


Journal of Electrocardiology | 1990

Arrhythmia analysis by successive RR plotting.

Tsuyoshi Anan; Kenji Sunagawa; Haruo Araki; Motoomi Nakamura

A successive RR interval plot was developed to analyze arrhythmia. The plot consisted of a set of points with the x-value of (N)th RR interval and the y-value of (N + 1)th RR interval. This method was applied in the arrhythmia analysis of Holter electrocardiograms obtained from 35 patients. In the analysis of ventricular premature contractions (VPCs) this method was useful not only in detecting VPCs but also in demonstrating coupling interval-dependent characteristics of VPCs. In the analysis of atrial fibrillation the successive RR plot enabled the authors to estimate the functional refractory period of the atrioventricular conduction. In conclusion, despite its simplicity, the successive RR plot was found to be powerful in analyzing arrhythmia. Specifically, the potential to analyze integrally the coupling interval-dependent properties of various types of arrhythmia makes it attractive as a clinical tool.


American Heart Journal | 1986

Effects of nicorandil on exercise tolerance in patients with stable effort angina: a double-blind study

Nobu Hayata; Haruo Araki; Motoomi Nakamura

Effects of nicorandil, a recently introduced 2-nicotinamidethyl nitrate, on exercise performance were studied in 11 patients with stable effort angina. The duration of exercise before the onset of angina and time to the onset of ischemic ST depression 30 minutes after 20 mg of oral nicorandil were compared with events 30 minutes after oral placebo and 5 minutes after 0.3 mg of sublingual nitroglycerin. Nicorandil and placebo were given according to the randomized double-blind method. Nicorandil prolonged the duration of exercise in all 11 patients by 2.3 +/- 2.2 minutes (mean +/- SD, p less than 0.01) and delayed the onset of ischemic ST depression by 2.3 +/- 1.7 minutes compared to placebo (p less than 0.01). The increment of the duration of exercise and the time to the onset of ischemic ST depression following 20 mg of oral nicorandil were almost equivalent to findings after sublingual nitroglycerin (by 2.0 +/- 1.8 and 2.5 +/- 1.7 minutes, respectively). Nicorandil also increased the pressure-rate product at the time of angina compared with placebo (20,420 +/- 480 vs 17,480 +/- 370, p less than 0.05). These results indicate that oral administration of nicorandil should be considered for the clinical treatment of effort angina.


Basic Research in Cardiology | 1985

Vasoconstrictor agents correlatively alter diameter and tension development in isolated pig coronary arteries

Yoshiyuki Nagata; Haruo Araki; Hitonobu Tomoike; Motoomi Nakamura

SummaryOuter diameter of the isolated pig coronary artery was measured under isotonic conditions using a sonomicrometer, and tension development of a ring preparation was assessed isometrically by a strain gauge transducer. Potassium chloride (KCl), acetylcholine (ACh) and 5-hydroxytryptamine dose-dependently reduced the coronary outer diameter. There was a direct linear relation between the reduction of diameter and tension development by these agents (r=0.91, n=15, p<0.001). KCl was one of the most potent vasoconstrictors tested and reduced the outer diameter by 35±1% (n=15, mean ± SEM) at 120 mM. ACh produced a transient increase in isometric tension and the reduction of the coronary diameter by ACh was smaller than that seen with KCl, even with a dose which produced the similar peak level of isometric tension by KCl and ACh. It is concluded that changes in the coronary diameter do closely correlate with those in tension development, however, the reduction of coronary diameter after exposure to vasoconstrictive agents is less in phasic than tonic contraction. The latter evidence suggests the importance of both the sterngth and duration of active vasoconstriction in eliciting coronary spasm.


American Heart Journal | 1984

Reflex heart rate and blood pressure changes during ST segment elevation in patients with variant angina

Haruo Araki; Tsuyoshi Anan; Yasushi Koiwaya; Osamu Nakagaki; Akira Takeshita; Motoomi Nakamura

Responses of heart rate and blood pressure to transient myocardial ischemia were analyzed in patients with variant angina. Heart rate changes during ST segment elevation were examined by means of a Holter ECG monitoring system. All 27 ST segment elevations from 10 patients with anterior ischemia were accompanied by an increase in heart rate by 12 +/- 2 bpm (mean +/- SEM, p less than 0.001) at peak ST segment elevation. With inferior ischemia in nine patients, heart rate decreased significantly by 4 +/- 1 bpm (n = 28, p less than 0.001). However, 9 of these 28 ST segment elevations showed a biphasic response of heart rate, that is, an initial increase and subsequent decrease. Such heart rate changes were not different between ST segment elevations with and without chest pain. With chest pain systolic blood pressure rose in anterior ischemia by 42 +/- 5 mm Hg (n = 10, p less than 0.001) but fell in inferior ischemia by 22 +/- 8 mm Hg (n = 7, p less than 0.05). We conclude that a different cardiovascular reflex occurs in response to inferior versus anterior ischemia and it is independent of chest pain.


Angiology | 1988

Prevention of Vasospastic Angina by Alcohol Ingestion: Report of 2 Cases

Takeyuki Matsuguchi; Haruo Araki; Naonori Nakamura; Yasuyuki Etoh; Shuichi Okamatsu; Akira Takeshita; Motoomi Nakamura

The authors report 2 patients with vasospastic angina in whom alcohol ingestion was effective in preventing angina. Coronary angiography revealed no organic coronary stenosis but demonstrated coronary artery spasm during angina attacks. In 1 patient, alcohol ingestion every six hours completely suppressed frequent spontaneous angina. In the other patient, alcohol ingestion markedly prolonged the duration of the exercise on treadmill testing by preventing exercise-induced coronary spasm.


American Heart Journal | 1986

Prevalence of ventricular tachycardia in patients with different underlying heart diseases: A study by Holter ECG monitoring

Akiko Suyama; Tsuyoshi Anan; Haruo Araki; Akira Takeshita; Motoomi Nakamura

Twenty-four-hour Holter ECGs were recorded in 1089 patients. Ventricular tachycardia (VT) was observed in 184 tapes obtained from 81 patients (73 men and 8 women). Underlying heart diseases were present in 72 patients and no organic heart diseases were found in nine patients. The analysis of continuous 1-hour rhythm strips immediately before VT revealed that, in ischemic heart disease and hypertrophic cardiomyopathy, there was no correlation between the incidence of VT and the number or complexity of premature ventricular complexes (PVCs) within 1 hour before VT. In contrast, frequent or multiform PVCs were often observed during the pre-VT period in the patients with rheumatic heart disease or dilated cardiomyopathy. These findings suggest that the mechanism of VT may be different among the various underlying heart diseases. In addition, the mode of initiation of VT was evaluated. Only few episodes of VT occurred with the prematurity index value smaller than 1.0 or the vulnerability index value greater than 1.1. The correlation between the rate of VT and the preceding sinus rate was not significant, and the correlation between the rate of VT and the coupling interval of VT was weak. These facts suggest that the malignancy of VT, represented by the rate of VT, cannot be predicted by the preceding sinus rate or by the coupling interval of VT.


American Heart Journal | 1985

Acute myocardial infarction following asymptomatic ST elevation despite diltiazem therapy

Kensuke Egashira; Haruo Araki; Yasushi Koiwaya; Akira Takeshita; Motoomi Nakamura

8. Dessertenne F: La tachycardie ventriculaire a deux foyers opposes variables. Arch Ma1 Coeur 59:263, 1966. Smith WM, Gallagher JJ: “Les torsades de pointes”: An unusual ventricular arrhythmia. Ann Intern Med 93:578, 1980. Kirkler DM, Curry PVL: Torsades de pointes, an atypical ventricular tachycardia. Br Heart J 38:117, 1976. Kossman CE: Torsades de pointes: An addition to the nosography of ventricular tachycardia. Am J Cardiol42:1054, 1978. Horowitz LN, Greenspan AM, Spielman SR, Josephson ME: Torsades de pointes: Electrophysiologic studies in patients without transient pharmacologic or metabolic abnormalities. Circulation 63:1120, 1981. Ejvinsson G, Orinius E: Prodromal ventricular premature beats preceded by a diastolic wave. Acta Med Stand 208:445, 1980. Koster RW, Wellens HJJ: Quinidine-induced ventricular flutter and fibrillation without digitalis therapy. Am J Cardiol 38:519, 1976. Tzivoni D, Keren A, Stern S, Gottlieb S: Disopyramideinduced torsades de pointes. Arch Intern Med 141:946, 1981.


European Heart Journal | 1984

Provocation of variant angina by alcohol ingestion

Takeyuki Matsuguchi; Haruo Araki; Tsuyoshi Anan; Nobu Hayata; Osamu Nakagaki; Akira Takeshita; Motoomi Nakamura


International Journal of Cardiology | 1984

Diurnal variation of variant angina.

Haruo Araki; Motoomi Nakamura


Japanese Heart Journal | 1985

Right ventricular systolic and diastolic function at rest in patients with coronary artery disease. Assessment with equilibrium radionuclide ventriculography.

Nail M. Caglar; Haruo Araki; Yuji Taira; Takaya Fukuyama; Motoomi Nakamura

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