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O Nishiyama

Publications and source records attributed to O Nishiyama.

16 recordsLinked to original sources
PubMed1995

[Preventive effect of pravastatin on restenosis following coronary angioplasty: prospective randomized trial].

This study investigated the preventive effect of pravastatin on restenosis following successful transluminal coronary angiography (PTCA) in 109 consecutive patients. Patients were randomly and prospectively assigned to the pravastatin group (group P, n = 57) or the control group (group C, n = 52). The former received 10 mg/day pravastatin from the day of PTCA for 3 months. Restenosis was defined as a > or = 50% diameter stenosis at follow-up angiography with a > or = 15% reduction in luminal diameter compared to post-PTCA. The effect of pravastatin was analyzed in association with 7 clinical and 15 angiographic factors. Follow-up rate, serum lipid levels (total cholesterol, triglyceride, and HDL-cholesterol), and clinical and angiographic backgrounds except age and angularity of the lesions were not significantly different between the two groups at PTCA. Three months later, total cholesterol decreased from 222.3 +/- 35.1 to 179.2 +/- 31.2 mg/dl in group P, but was unchanged in group C (from 226.0 +/- 33.7 to 211.7 +/- 30.9 mg/dl). The restenosis rate was not different between the two groups (35.6 vs 35.7% per patient, 32.0 vs 33.3% per lesion). Moreover, no relationship between restenosis rate and serum total cholesterol level at follow-up angiography was observed. Multivariate analysis, including 7 clinical and 15 angiographic factors, found neither pravastatin administration nor serum lipid levels were significantly correlated with decreased luminal diameter. Pravastatin (10 mg/day) did not reduce the incidence of restenosis after PTCA when administered from the day of PTCA for 3 months.

Aged↗
PubMed1992

Emergency coronary angioplasty for acute myocardial infarction--factors affecting acute restenosis in catheterization laboratory and reocclusion during hospitalization.

A total of 107 consecutive patients with acute myocardial infarction underwent emergency coronary angioplasty (PTCA). Restoration of blood flow with TIMI grade III was established by emergency PTCA in 101 patients (94.4%). "Acute restenosis" was defined as a lesion that, when dilated to less than 50%, narrowed again to more than 75% luminar reduction 5 min after the balloon inflation. Acute restenosis occurred in 39 patients (39%). Multivariate analysis selected 3 factors associated significantly with an increased rate of acute restenosis: (1) dissection, (2) small balloon/artery diameter ratio and (3) low systolic blood pressure during PTCA. Reocclusion, which was defined as a total reobstruction of the lesion during hospitalization following emergency PTCA, was examined by predischarge coronary angiography. Acute restenosis correlated significantly with an increase in reocclusion rate. The incidence of documented reocclusion was 12%. Residual stenosis, multivessel disease and irregular dilation correlated significantly with an increased rate of reocclusion. The in-hospital and postdischarge mortalities were 5.6% and 2.1%, respectively. In summary, emergency PTCA produced a high angiographic success rate. Use of adequate balloon size and sufficient dilation correlated significantly with angiographic outcome in emergency PTCA. Patients with acute restenosis, high residual stenosis, irregular dilation, and multivessel disease would have a relatively high risk of reocclusion.

Adult↗
PubMed1991

[A case of acute myocardial infarction due to simultaneous occlusion of the right coronary artery and left anterior descending coronary artery].

We reported a rare case of a 53-year-old man who experienced acute myocardial infarction due to simultaneous occlusion in the right coronary artery and the left anterior descending coronary artery. He also experienced thromboembolisms on several occasions. So anticoagulant therapy is necessary for patients with exceedingly poor LV function.

Angioplasty, Balloon, Coronary↗
PubMed1990

[Chronic intractable pericardial effusion associated with pulmonary hypertension: report of two cases].

We report two cases of chronic intractable pericardial effusion associated with pulmonary hypertension. Case 1. A 35-year-old women was admitted to our hospital because of dyspnea and edema. Chest X-ray examination showed enlargement of cardiac, and pulmonary artery shadow. An electrocardiogram with high voltage of R in V1 and deep S in V5 suggested right ventricular hypertrophy. Pericardial echo-free space with dilated right ventricle was demonstrated by echocardiography. Cardiac catheterization revealed an elevated pulmonary systolic pressure of 120 mmHg. No intracardiac shunt was calculated. A diagnosis of primary pulmonary hypertension was made. Pericardial drainage diminished pericardial effusion. Soon after discharge, however, pericardial effusion increased and the patient died. Case 2. A 65-year-old man was admitted because of dyspnea. The findings of chest X-ray and echocardiography were essentially the same as Case 1. Pericardial effusion disappeared after pericardiocentesis, but appeared again one month later. Cardiac catheterization demonstrated an elevated pulmonary systolic pressure of 73 mmHg. Pulmonary-capillary-wedge pressure was normal. Pulmonary arteriogram showed occlusion of the pulmonary artery trees. A diagnosis of chronic thromboembolic pulmonary hypertension was made. Although diuretics and vasodilators decreased pulmonary-artery pressure, pericardial effusion was unchanged. We compared these two cases with 11 control patients of pulmonary hypertension without pericardial effusion. Venous pressure was higher than that in the controls in Case 1, but not different in Case 2. Thus, venous pressure did not fully account for pericardial effusion. In summary, chronic pulmonary hypertension should be added to the list of conditions known to cause pericardial effusion. In these cases, echocardiography revealed important signs, and cardiac catheterization was essential for definite diagnosis. Pericardial effusion associated with pulmonary hypertension was refractory to diuretics and vasodilators.

Adult↗
PubMed1989

Reperfusion through balloon catheter to minimize myocardial infarction during the interval between failed percutaneous transluminal coronary angioplasty and emergency coronary artery bypass grafting.

A 65-year-old man was admitted with chest pain. A diagnosis of spastic angina was made because of symptoms of recurrent anginal attacks associated with ST-segment elevations in the electrocardiogram. A selective coronary arteriogram revealed a 90% diameter narrowing of the proximal left anterior descending coronary artery (LAD). No angiographically visible collaterals from the right coronary artery to the LAD were observed. The ventriculogram showed normal contraction of the left ventricle with an ejection fraction of 65%. Percutaneous transluminal coronary angioplasty (PTCA) failed resulting in total occlusion of the stenosis. Repeat PTCA at a higher pressure and of longer duration failed to redilate the artery. Reperfusion with the blood from the femoral artery through the balloon catheter, which was used for the PTCA, was carried out until coronary artery bypass grafting (CABG). Blood flow rate of perfusion was approximately 25 ml/min. Reperfusion through the balloon catheter reduced chest pain and ST-segment elevations in the electrocardiogram. The patient tolerated the operative procedure well and his post-operative course was uncomplicated. The interval between the acute occlusion and revascularization by CABG was approximately 4 1/4 h. The ventriculogram taken 56 days after the CABG demonstrated normal contraction of the anterior wall of the left ventricle with an ejection fraction of 63%. Abnormal Q waves did not appear in precordial leads of the electrocardiogram after the surgery. The thallium scintigram showed no perfusion defects. In conclusion, this case suggested that autologous blood reperfusion through balloon catheter would be worth attempting in some cases for minimization of myocardial infarction during the interval between failed PTCA and emergency CABG.

Angioplasty, Balloon, Coronary↗
PubMed1989

Factors influencing acute high-grade restenosis in emergency percutaneous transluminal coronary angioplasty for acute myocardial infarction.

We studied the factors which may induce acute high grade restenosis in emergency percutaneous transluminal coronary angioplasty (PTCA). PTCA was attempted in 50 patients with acute myocardial infarction, and the balloon catheter passed successfully across the occlusion site in 47 (94%) of the patients. These 47 patients were analyzed. "Acute restenosis" was defined as a lesion which was revascularized to less than 50% luminal reduction narrowed again to more than 75% luminal reduction 5 min after the balloon inflation. Univariate and multivariate analyses were used for determining factors which significantly influenced acute restenosis. The incidence of at least one restenosis episode was 45%. Multiple regression analysis selected 5 factors associated significantly with an increased rate of acute restenosis: 1) angiographic evidence of dissection, 2) lesion in the right coronary artery (RCA), 3) lack of or insufficient administration of thrombolytic agent preceding PTCA, 4) curved lesion and 5) relatively small balloon/artery diameter ratio. Acute restenosis correlated significantly with late reocclusion. This study indicates that it is important to administer a thrombolytic agent prior to emergency PTCA, and to use an adequately sized balloon to the artery when the acute restenosis occurs by using relatively smaller sized balloon. The present data also demonstrated that patients with RCA and a curved lesion have a relatively high risk of acute restenosis. This study indicates how patients with relatively high risk of acute restenosis may be identified.

Acute Disease↗
PubMed1989

[Acceleration of the left main coronary artery stenosis following PTCA: a report of a case].

Acceleration of the left main coronary artery (LMCA) stenosis induced by guiding catheter which was used for percutaneous transluminal coronary angioplasty (PTCA) was demonstrated in a 68 years old man with post-infarction angina. He underwent PTCA to a subtotal lesion in the left anterior descending coronary artery (LAD). The LMCA with mild stenosis of 18% reduction of luminal diameter was unchanged during the course of PTCA. The guiding catheter was pushed repeatedly with considerable force for introducing balloon catheter due to the rigid lesion in LAD. Progression of the LMCA stenosis to a 64% was demonstrated at 6 months later angiographic restudy. It was considered that repetitive sliding of guiding catheter through the LMCA caused subangiographic intimal trauma and facilitate subsequent progression of stenosis. We examined the guiding catheter to the LMCA diameter ratio, the angle of the tip portion of the guiding catheter with LMCA, and severity of the target lesion in this case compared with other 27 controls in whom PTCA was performed to the lesion in left coronary artery. No difference of these 3 factors between this case and other 27 controls was obtained. Thus it might be difficult to predict progression of LMCA stenosis by these angiographic factors. Although the incidence of catheter-induced progression of LMCA stenosis was as low as 1 of 160 cases (0.6%) in our experience, it is important to attend to catheter-induced progression of LMCA stenosis and to make an early detection.

Aged↗
PubMed1984

Simple technique for measuring regional contractility by a modified strain guage arch.

A simple modification of a commercially available gauge arch, namely the addition of pins to effect mechanical couplings to heart muscle rather than suturing, results in an isometric myocardial force sensor which is easy to insert, stable and relatively atraumatic to the myocardium. Compressing the pins by means of a machinist's vernier caliper which is removed after the sensor is implanted, insures controlled muscle stretch. Tests in open-chest dogs show that force sensed by this gauge is little affected by changes in heart rate, left ventricular end-diastolic pressure or aortic pressure, but faithfully reflects the inotropic effects of isoproterenol or propranolol. Thus, the modified strain gauge arch is sensitive to changes in contractility but not to changes in preload or afterload.

Animals↗
PubMed1982

Decrease in myocardial oxygen extraction with aortic constriction in the dog.

In the open-chest dog constriction of the descending thoracic aorta, which raises central aortic pressure by 30-80 mmHg, increases cardiac oxygen usage (MVO2) and coronary blood flow (CBF) but reduces heart rate and myocardial oxygen extraction [(A-V)O2]. Pacing tachycardia superimposed on aortic constriction further increases MVO2 and CBF but does not alter (A-V)O2. Atropine or vagotomy abolishes the effect of aortic constriction on (A-V)O2, whereas vagal stimulation in the presence of alpha- and beta-adrenergic blockade reduces (A-V)O2. L-propranolol and phenoxybenzamine fail to modify the effect of aortic constriction on (A-V)O2. These results indicate that aortic constriction reduces (A-V)O2 by eliciting parasympathetically-mediated coronary vasodilation.

Animals↗
PubMed1982

Right and left ventricular oxygen metabolism in open-chest dogs.

A comparison of blood flow and myocardial O2 consumption (MVO2) in the right and left ventricles was made in 21 open-chest dogs. Simultaneous measurements were made of left anterior descending (LAD) and right coronary arterial blood flow and of O2 saturation in the coronary sinus and in from one to four anterior cardiac veins. Blood flow was greater in the LAD than in the right coronary artery, 87 +/- 5 vs. 46 +/- 3 ml.min-1.100 g-1. Similarly, the O2 saturation was 51 +/- 3% in the anterior cardiac veins and 40 +/- 1% in the coronary sinus. In a subset of seven dogs, the O2 saturation in blood from anterior cardiac veins varied substantially from vein to vein. The mean MVO2 was greater for the left than for the right ventricle, 8.6 +/- 1.4 vs. 4.0 +/- 0.3 ml O2.min-1,100 g-1. Increases in LAD flow with no increase in O2 extraction accounted for enhanced MVO2 of the left ventricle due to pacing, isoproterenol, or methoxamine. In contrast, pacing, isoproterenol, or constriction of the pulmonary artery increased MVO2 of the right ventricle by both augmented O2 extraction and a rise in right coronary blood flow. We conclude that right coronary arterial blood flow is lower per 100 g tissue and is less dependent on MVO2 than is LAD blood flow. The heterogeneity of O2 saturation in anterior cardiac veins suggests that regional differences in MVO2 may exist.

Animals↗
PubMed1981

Comparative effects of heart rate and aortic blood pressure on MVO in the anesthetized open-chest dog.

Comparative effects of heart rate and aortic blood pressure on myocardial oxygen consumption (MVO2) were studied in anesthetized open-chest dogs. The left coronary artery was perfused through the external shunt with blood from the left common carotid artery. Heart rate was changed with the left atrial pacing and the constriction of the descending thoracic aorta was utilized to elevate the proximal aortic blood pressure (BP). The left ventricular enddiastolic pressure was insignificantly changed with the atrial pacing and with the aortic constriction. With the constant BP (100 +/- 5 mmHg), and unit increase in heart rate per minute augmented MVO2 by 0.027 ml/min/100 Gm of left ventricular muscle, while one mmHg elevation of BP caused 0.15 ml increment in MVO2 per minute per 100 Gm of left ventricular muscle under the constant heart rate (115 +/- 5 beats/min). Therefore an unit change in BP caused five- to six-fold greater increase in MVO2 compared with that in heart rate, indicating extremely important roles of BP in MVO2.

Animals↗
PubMed1981

[Echocardiographic and non-gated computed tomographic findings of intrapericardial tumor and mediastinal tumor adjacent to the heart (author's transl)].

UNLABELLED: Echocardiographic and computed tomographic findings of a case of intrapericardial tumor are reported, and two other cases of mediastinal tumor are presented in a discussion of the differential diagnosis of intrapericardial from mediastinal tumors. CASE REPORT: A 7-year-old male complained of cough and dyspnea. Cardiomegaly had been pointed out at a mass X-ray examination about a month prior to the admission. Two-dimensional echocardiography revealed a massive anterior pericardial effusion and a fist-sized tumor with cystic structure. The tumor pushed the heart backward at the level of the aortic root. Non-gated computed tomography of the chest disclosed the size and location of the tumor, but failed to clarify the internal structure. The patient underwent successful removal of a tumor, 12 x 10 x 8 cm in size and 350 g in weight, originating from the left atrial wall. Histologically, the tumor was a fibrosarcomatous mesothelioma. Usually, an intrapericardial tumor is easily suspected by echocardiography by the presence of pericardial effusion, although there have been a few reports of intrapericardial tumors without pericardial effusion. Echocardiographic diagnosis of the intrapericardial tumor is difficult in such cases. Identification of the pericardium is necessary to diagnose whether a tumor is intra- or extrapericardial. This identification, however, is not always easy by echocardiography when the ultrasonic beams become tangent to the pericardium. The pericardium between the tumor and the heart could not be identified by echocardiography in our two cases of mediastinal tumor. Computed tomography is helpful in diagnosing the size and location of a mediastinal tumor.

Adult↗
PubMed1980

Increase in the calculated resistance of anatomically fixed stenosis in vitro in association with decrease in distal resistance.

The effects of changes in distal resistance on stenotic resistance were studied in vitro. Physiological saline was passed through the left carotid artery obtained from the dog, flexible rubber tubing, or through solid polyethylene tubing with a constant perfusion pressure or with a constant flow rate. Various stenotic resistances were established using a screw type constrictor and the distal resistance was varied by allowing physiological saline to pass through either a 23 gauge hypodermic needle (high peripheral resistance) or 23 and 20 gauge needles (low peripheral resistance ). For arteries with anatomically fixed stenosis, the calculated resistance was increased in association with reduction of the distal resistance. The stenotic resistance in the flexible rubber tubing changed in the same manner as that of the carotid artery, while the solid polyethylene tubing showed no significant stenotic resistance changes due to altering the distal resistance. These findings suggest that the stenotic resistance change of the artery correlates with the elasticity of the vessel wall and also indicate that resistance values were of little usefulness for evaluating the effects of vasodilating stimuli on the vessel segment with a significant stenosis.

Animals↗
PubMed1979

Effect of graded coronary constriction on the flow reserve in regional myocardium in dog.

Effects of coronary constriction on the flow reserve of regional myocardium were studied in the anesthetized open-chest dogs. Regional myocardial blood flow (RMBF) was continuously measured using heated crossthermocouple method. Left circumflex coronary artery (LCX) was constricted gradually with a screw type constrictor. The coronary constriction decreased subendocardial myocardial blood flow, while subepicardial myocardial blood flow was not affected until reactive hyperemia in LCX nearly disappeared. Recovery and arrival to peak flow rate of RMBF following the release of 15-second's occlusion of LCX were progressively delayed with an increase in the constriction, especially in the subendocardial myocardium. Repayment of flow debt, however, was remained relatively well since the duration of reactive hyperemia in RMBF was prolonged by an increment of the constriction. From these findings, it might be concluded that in the heart with coronary stenosis recovery from ischemia was caused by prolonged duration of reactive hyperemia, and is suggested that the time required for recovery from ischemia or ischemic abnormalities after the cessation of stress might be an important marker for the severity of coronary insufficiency.

Animals↗