Biomedical subjects
B Takase
Publications and source records attributed to B Takase.
Preoperative clinical assessment and dipyridamole thallium-201 scintigraphy for prediction and prevention of cardiac events in patients having major noncardiovascular surgery and known or suspected coronary artery disease.
The aim of this study was to assess the relative prognostic use of clinical risk stratification and intravenous dipyridamole thallium-201 scintigraphy in patients with an intermediate to high prevalence of coronary artery disease (CAD) who have undergone major noncardiovascular surgery, and to assess the effects of medical therapy or coronary revascularization based on the result of this clinical scintigraphic screening on perioperative cardiac morbidity and mortality. Patients (n = 161) with an intermediate to high likelihood of CAD had clinical assessment and intravenous dipyridamole planar thallium-201 testing which was analyzed semiquantitatively. Cardiac events were cardiac death (n = 9), nonfatal myocardial infarction (n = 6), acute pulmonary edema (n = 6), and unstable angina (n = 4). Multiple (> or = 2) clinical risk variables predicted any cardiac event (p = 0.04). Presence of multiple (> or = 2) abnormal thallium-201 segments was the only independent predictor of cardiac death or nonfatal myocardial infarction (p < 0.001), and was the most powerful multivariate predictor of any cardiac event (p < 0.002). Patients with an abnormal dipyridamole thallium-201 scan had a higher risk of perioperative cardiac death, myocardial infarction (18% vs 2%; p < 0.001), or any perioperative cardiac event (27% vs 6%; p < 0.001) when compared with those with a normal scan. Preoperative changes in anti-ischemic therapy or coronary revascularization in 36 of 72 patients with abnormal dipyridamole thallium-201 studies reduced perioperative death or myocardial infarction from 31% to 6% (p < 0.01), and all cardiac events from 47% to 8% (p < 0.001) compared with those in patients without intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of bepridil on silent myocardial ischemia and eicosanoid metabolism in chronic stable angina pectoris after healing of myocardial infarction.
To investigate the effects of bepridil on silent myocardial ischemia and on eicosanoid metabolism, 10 patients with chronic stable angina underwent exercise treadmill testing and 48-hour ambulatory electrocardiographic monitoring both before and after 4 weeks of bepridil administration (150 mg/day). Fasting venous levels of thromboxane B2, 6-keto-prostaglandin F1 alpha, and leukotriene C4 were measured by radioimmunoassay. Bepridil decreased heart rate responses to daily activities during ambulatory monitoring, and significantly (p < 0.05) reduced the median frequency and duration of silent myocardial ischemic episodes (from 5.5 to 0 events/48 hours and from 86 to 0 minutes/48 hours respectively). Bepridil significantly decreased the blood pressure heart rate product at peak exercise and significantly prolonged the mean exercise tolerance time (from 456.6 to 527.0 second). Bepridil also significantly decreased the plasma levels of thromboxane B2 and leukotriene C4 at rest. These results suggest that bepridil may reduce silent myocardial ischemic episodes either by the reduction of cardiac oxygen demand during daily activities and exercise stress, or by controlling coronary and systemic vasomotor tone. The drug also has a salutary effect on eicosanoid metabolism, to which its efficacy on silent myocardial ischemic episodes may be related.
The effects of orally administered atenolol on the coronary hemodynamics and prostaglandin metabolism in angina pectoris patients.
The effects of oral atenolol on coronary hemodynamics and prostaglandin metabolism have been investigated in 8 chronic stable angina pectoris patients who underwent the supine bicycle ergometer. At rest, atenolol taken orally reduced the pressure-rate product significantly (P < 0.05) but did not significantly affect the coronary sinus blood flow or the coronary sinus pressure. During exercise, atenolol also reduced the pressure-rate product significantly (P < 0.05) but did not significantly affect the coronary sinus blood flow, the coronary sinus pressure, or the coronary vascular resistance. Atenolol also did not significantly affect the thromboxane B2/6-keto prostaglandin F1 alpha ratio in the arterial blood before and after exercise but did reduce this ratio in the coronary sinus blood by 15% from 1.9 +/- 1.1 to 1.5 +/- 0.46 (P < 0.10) after exercise. These results indicate that atenolol taken orally does not significantly depress the coronary hemodynamics. However, the effects of atenolol on the prostaglandin metabolism could not be clearly determined.
Usefulness of plasma beta-endorphin level, pain threshold and autonomic function in assessing silent myocardial ischemia in patients with and without diabetes mellitus.
The differences between diabetic and nondiabetic patients with silent myocardial ischemia were investigated. Based on the results of previous exercise testing, a total of 110 patients (15 diabetic and 95 nondiabetic) with exercise-induced myocardial ischemia were divided into the following 3 groups: 15 diabetics with silent myocardial ischemia, 49 nondiabetics with silent myocardial ischemia, and 46 nondiabetics with anginal symptoms. All patients underwent treadmill exercise testing and 24-hour ambulatory electrocardiographic recording. Before and during exercise, blood samples from the antecubital vein were obtained to determine the plasma beta-endorphin levels, and the pain threshold of each patient was measured with the electrical skin stimulation test. Furthermore, with regard to the ambulatory electrocardiographic recording, the mean of the SDs of all normal sinus RR intervals during successive 5-minute recording periods over 24 hours was analyzed and considered as an index of the autonomic function. The plasma beta-endorphin level during exercise was significantly greater in nondiabetic patients with silent ischemia than in diabetic ones. The SD mean was significantly less in the diabetic group than in the 2 nondiabetic ones. The findings suggest that the role of beta endorphin in diabetic patients with silent myocardial ischemia may be less significant than in nondiabetic ones; therefore, a diabetic neuropathy that affects the autonomic pain fibers that innervate the heart may be involved in the mechanism of silent myocardial ischemia in diabetics.
Comparative prognostic value of clinical risk indexes, resting two-dimensional echocardiography, and dipyridamole stress thallium-201 myocardial imaging for perioperative cardiac events in major nonvascular surgery patients.
The relative prognostic value of widely accessible resting two-dimensional echocardiographic ventricular function data has not been compared with recognized clinical and scintigraphic risk markers in patients who are unable to exercise before major nonvascular surgery. To this end, 53 consecutive patients aged 67 +/- 13 years undergoing preoperative evaluation (intraabdominal, 23%; orthopedic, 30%; thoracic, 9%; other, 38%) for known or suspected coronary artery disease were followed up to evaluate the prognostic value of these studies for the perioperative cardiac events (cardiac death [n = 4], myocardial infarction [n = 2], unstable angina [n = 3], and pulmonary edema [n = 8]) that occurred in 13 of the 53 patients (25%). Dipyridamole thallium-201 myocardial redistribution defects occurred in 15 (28%) patients. Resting echocardiographic left ventricular dysfunction was present in 21 (40%) patients. Multivariate analysis of clinical, echocardiographic, and scintigraphic risk predictors revealed that cardiac events were not predicted by clinical variables, including Goldman class or score. Cardiac events were independently predicted only by the presence of significant left ventricular dysfunction on resting two-dimensional echocardiography (p < 0.042) and dipyridamole thallium-201 defect redistribution (p < 0.026). A dipyridamole-induced reversible thallium-201 perfusion defect was predictive of subsequent cardiac death or myocardial infarction (p < 0.02), whereas left ventricular dysfunction on resting echocardiography was predictive of perioperative pulmonary edema (p < 0.023). We conclude that stress thallium-201 perfusion imaging and resting two-dimensional echocardiography provide independent prognostic information in patients undergoing major nonvascular surgery who are at significant risk for ischemic cardiac events and who are unable to perform standard exercise stress tests.(ABSTRACT TRUNCATED AT 250 WORDS)
Differences in plasma beta-endorphin and bradykinin levels between patients with painless or with painful myocardial ischemia.
To verify whether plasma beta-endorphin and bradykinin affects the pathophysiology of myocardial ischemia and the perception of cardiac pain, 35 patients with coronary artery disease were subjected to treadmill testing and 48-hour Holter ECG monitoring to measure their pain thresholds. Patients were divided into two groups during exercise testing: group 1 (N = 19) who had ST segment depression, and group 2 (N = 16), who had chest pain. Both groups were then compared with 12 age-matched control subjects. Pain thresholds were measured after Holter ECG monitoring, and blood samples were drawn before and immediately after exercise. No statistical differences were noted between groups 1 and 2 with regard to the severity of myocardial ischemia as assessed by ST segment depression or exercise tolerance time. The frequency of the episodes of silent myocardial ischemia in group 1 was found to be significantly (p less than 0.05) higher than that in group 2. The duration of the episodes of silent myocardial ischemia in group 1 was 41.9 minutes (range 3 to 343 minutes), which was significantly (p less than 0.05) longer than that in group 2 (11.5 minutes; range 0 to 74). The pain threshold in group 1 was a statistically (p less than 0.05) higher value than that in group 2. Although the resting plasma beta-endorphin level in group 1 was not statistically significantly different from values in either group 2 or the control group, during exercise the plasma beta-endorphin levels in both group 1 and the control group were significantly (p less than 0.05) elevated in comparison with their resting levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Heart rate variability in patients with diabetes mellitus, ischemic heart disease, and congestive heart failure.
The prognosis of patients with heart disease and prediction of sudden cardiac death can be assessed through heart rate variability, an indirect measure of abnormal autonomic control. The authors have evaluated the heart rate variability by 24-hour ambulatory electrocardiographic monitoring in 25 diabetic patients, 19 ischemic heart disease patients, 18 congestive heart failure patients, and 10 normal subjects. Thirteen diabetic patients had autonomic neuropathy and 12 patients did not. Heart rate variability index (mean SD) in patients with diabetes mellitus, ischemic heart disease, and congestive heart failure was significantly lower (34.5 +/- 12.6 ms, 43.7 +/- 15.4 ms, and 34.6 +/- 15.8 ms vs 65.6 +/- 16.7 ms, p less than 0.05) than that of normal subjects. Mean SD was significantly lower in patients with autonomic neuropathy as compared to patients without autonomic neuropathy (26.4 +/- 6.5 ms vs 44.2 +/- 11.0 ms, p less than 0.05) mean SD as compared to survivors: 49 +/- 7 ms in patients with mild ischemic heart disease, 48 +/- 15 ms in patients with severe ischemic heart disease, and 23 +/- 7 ms in patients who died. Similarly, the mean SD in 4 congestive heart failure patients who died was lower significantly (p less than 0.05) than in those who survived (19.0 +/- 5.6 ms vs 40.0 +/- 14.5 ms). Among congestive heart failure patients, clinical improvement by therapy was associated with a significant increase in mean SD. When the mean SD of 30 ms was used as the cutoff point for detection of autonomic dysfunction or patient death, specificity exceeded 90% and sensitivity was 75%.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of diltiazem on silent ischemic episodes, plasma bradykinin and prostaglandin metabolism.
Plasma bradykinin and prostaglandin metabolism are related to the anginal pain modulating system in patients with ischemic heart disease. We carried out a placebo controlled single blind test of diltiazem (30 mg three times a day) in 15 patients with chronic stable angina. The effect of diltiazem was evaluated by exercise treadmill testing and 48-h ambulatory electrocardiographic monitoring. Plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels were determined by radioimmunoassay prior to and during diltiazem therapy. Diltiazem significantly increased the exercise time and reduced episodes of angina. Diltiazem, however, did not appreciably improve either the frequency of silent myocardial ischemic episodes or the total duration of the silent myocardial ischemic episodes. Diltiazem also tended to decrease plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels. When ischemic episodes on ambulatory electrocardiographic monitoring are categorized according to heart rate change at the onset of episode (type A, preceded by heart rate increase > or = 5 beats/min; type B, no preceding heart rate increase), diltiazem was only effective on type A ischemic episodes as well as on symptomatic ischemia. Further, bradykinin was significantly decreased by diltiazem only in patients with exercise-induced silent ischemia or no exercise-induced ischemia, while the thromboxane B2/6-keto-prostaglandin F1 alpha ratio was unaffected by the administration of diltiazem. Thus, silent and symptomatic ischemia may be associated with different bradykinin and prostaglandin responses.
Diurnal change in heart rate variability in healthy and diabetic subjects.
We assessed the hourly coefficient of variance of RR intervals (CVRR) in 29 subjects with non-insulin-dependent diabetes mellitus and 19 age-matched healthy subjects using an ambulatory 24-hour ECG monitoring system. We also evaluated CVRR during 100 beats in both groups in the supine posture at 07:00 and 10:00 in the morning. Hourly CVRR showed an overt diurnal variation in both groups especially in the daytime and at midnight, but was significantly lower (p less than 0.05) in diabetic patients. CVRR during resting 100 beats at 07:00 was significantly higher (p less than 0.05) than that at 10:00 in both groups. These findings indicate that HRV shows an obvious diurnal variation in both groups. As a steep and marked change occurs in the morning, careful consideration is necessary to assess the test performed for a short time span at random times throughout the day, particularly in the morning.
Painless myocardial ischemia in elderly patients compared with middle-aged patients and its relation to treadmill testing and coronary hemodynamics.
We compared painless ST-segment depression (1 mm greater than or equal to 80 ms and lasting greater than or equal to 60 s) in elderly patients with coronary artery disease (greater than or equal to 65 years, mean 67 years; n = 22) and that of middle-aged patients (less than 60 years, mean 54 years; n = 20) by Holter monitoring for 24 hours to determine the relationship between episodes of painless myocardial ischemia, findings of treadmill testing, and coronary hemodynamics. Coronary arteriographic findings (Gensini score) and ejection fraction (EF) did not differ between the two groups. Painless ST-segment depression was found to be 77% in the older age group versus 45% in the middle-aged group (p less than 0.05). However, treadmill exercise score, ST-segment depression, and ST-segment integral achieved did not differ significantly between the two groups. Within 2 weeks after the above testing, coronary hemodynamic study was performed. The increment of coronary sinus flow in the older age group was 1.4 +/- 0.3 versus 1.8 +/- 0.3 in the middle-aged group (p less than 0.05), and the change of lactate extraction ratio from the basal condition in the older age group was -50 +/- 40% versus -2 +/- 15% in the middle-aged group (p less than 0.05). We conclude that episodes of painless myocardial ischemia in elderly patients with aging may be associated with the impairment of the coronary vascular reserve and easier anaerobic myocardial metabolism by pacing stress despite similar findings of coronary artery disease and EF in both groups.
The effects of trapidil on left ventricular function and platelet aggregation in patients with coronary artery disease subjected to pacing.
The effects of the intravenous administration of 100 mg of trapidil on systolic and diastolic left ventricular functions and coronary sinus blood flow, as well as on myocardial lactate metabolism and platelet aggregation, were investigated before and after pacing in 12 patients with coronary artery disease. Pacing without administration of trapidil provoked angina in 6 of these patients. During rest, trapidil decreased the mean blood pressure by an average of 5 mmHg (from 112 +/- 15 to 107 +/- 8 mmHg, p less than 0.05) and the left ventricular end-diastolic pressure by an average of 4 mmHg (from 10 +/- 3 to 6 +/- 2 mmHg, p less than 0.05). Trapidil also caused both the max dp/dt and the coronary sinus blood flow to increase slightly, although it had no significant effect on diastolic function, myocardial lactate metabolism, or platelet aggregation. During the pacing that followed trapidil administration, chest pain was not provoked in the same 6 patients who had previously experienced chest pain on pacing. The extent of ST-segment depression also improved from -1.6 +/- 0.3 to -0.9 +/- 0.7 mm (p less than 0.05) and there was a significant suppression of the production of myocardial lactate. When pacing was terminated, trapidil caused a decrease in left ventricular systolic pressure from 173 to 156 mmHg (p less than 0.05), and also caused a decrease of the left ventricular end-diastolic pressure, from 16 +/- 4 to 8 +/- 2 mmHg (p less than 0.05). Trapidil had no significant effect on platelet aggregation activity with either a 1 microM or a 2 microM dose of ADP (adenosine diphosphate). However, the beta-TG level was suppressed, decreasing from 119 +/- 14 to 99 +/- 19 ng/ml in the arterial blood (p less than 0.1) and from 114 +/- 9 to 103 +/- 17 ng/ml (p less than 0.1) in the coronary sinus blood. Reductions in the preload and afterload by trapidil were of far greater magnitude than either its coronary dilatory or positive chronotropic effects in patients with coronary artery disease. Thus trapidil, a new antianginal agent appears to inhibit the production of platelet derived growth factors and may, therefore, protect the arteries from atherosclerosis as it promotes beneficial systemic hemodynamics in patients with depressed ventricular function.
[Effects of diltiazem on hemodynamics, plasma catecholamine and renin activity during exercise in hypertension].
The effects of diltiazem on hemodynamics, plasma catecholamine and plasma renin activity were studied during treadmill exercise test in 9 cases with moderate essential hypertension. Diltiazem of 120 mg/day was orally administered for 4 weeks. At maximum exercise, significant decrease in systolic blood pressure (-32 mmHg), heart rate (-16/min), pressure-rate product (-7,883 mmHg/min), plasma norepinephrine (-195 ng/L) and plasma epinephrine (-11 ng/L) were observed; while, diastolic blood pressure, ST depression and plasma renin activity showed no significant change. Also, a significant correlation between systolic blood pressure and plasma norepinephrine (r = 0.57, p < 0.001), especially after diltiazem therapy (r = 0.68, p < 0.001), was observed. These findings indicated that diltiazem can reduce the secretion of catecholamine from the sympathetic nerves during exercise in patients with essential hypertension.
[Responses of plasma eicosanoids and hemodynamics to myocardial ischemia and the salutary effect of calcium entry blocker].
The responses of eicosanoids to acute myocardial ischemia induced by either exercise stress testing (EX) or percutaneous transluminal coronary angioplasty (PTCA) were investigated in 23 patients with effort angina pectoris (EAP). EX was useful procedure to determine the therapeutic plan in each cases, and PTCA is the novel therapeutic operation for EAP. The relations between these metabolites and either hemodynamics or coronary circulation were then evaluated. The effect of the calcium entry blocker nisoldipine (oral administration of 5 mg) was also studied in 10 patients with EAP. The plasma levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6KPGF1 alpha) and leukotriene C4 (LTC4) were determined by radioimmunoassay. in arterial and coronary sinus blood samples before and immediately after acute myocardial ischemia. The changes in hemodynamics and coronary circulation during exercise stress testing were assessed by measuring direct brachial artery pressure, cardiac output by the dye dilution method and coronary sinus flow by the thermodilution method. The TXB2/6KPGF1 alpha ratio in coronary sinus blood significantly increased after ischemia in both EX and PTCA, but there was no significant change in LTC4 levels of coronary sinus blood immediately after acute ischemia. The 6KPGF1 alpha levels in both arterial and coronary venous blood were significantly correlated to coronary perfusion pressure and mean brachial artery pressure. Arterial LTC4 levels tended to correlate to mean brachial artery pressure and coronary sinus flow. Nisoldipine improved the ischemic electrocardiography response to EX. Nisoldipine also significantly increased arterial 6KPGF1 alpha at peak exercise. It significantly decreased brachial artery pressure, pressure rate product (PRP), mean coronary sinus pressure and coronary vascular resistance both at rest and peak exercise. The response of PRP significantly correlated with the response of arterial 6KPGF1 alpha. These results suggest: 1 The imbalance of the TXB2/6KPGF1 alpha ratio may be induced more rapidly than LTC4. 2 PGI2 and LTC4 may have some role in the regulation of hemodynamics and coronary circulation during acute myocardial ischemia. 3 Nisoldipine may ameliorate myocardial ischemia through improvement of systemic hemodynamics and prostaglandin metabolism apart from through direct action on the heart.
Effects of a low, oral dose of nisoldipine on the systemic and coronary hemodynamics and the prostaglandin metabolism of ischemic heart disease patients.
This study investigated the effects of a low dose of nisoldipine (5 mg, p.o.) in 10 patients with ischemic heart disease. The patients were subjected to a 90-min exercise regimen before and after a 5 mg dose of nisoldipine, using a supine bicycle ergometer adjusted to each patient's limitations. The mean blood plasma level of nisoldipine was 3.8 +/- 3.1 (SD) ng/ml. The drug significantly decreased the systolic arterial pressure in patients throughout the experimental session, whereas a change in the diastolic arterial pressure appeared only at the submaximal stage of the exercise. Additionally, at maximal exercise, nisoldipine caused a decrease in the mean coronary sinus pressure from 11.4 +/- 7 mmHg to 6.5 +/- 5 mmHg (p less than 0.01). By contrast, while at rest, nisoldipine decreased the coronary vascular resistance from 1.5 +/- 0.7 mmHg/ml/min to 1.0 +/- 0.7 mmHg/ml/min (p less than 0.05). After exercise, the drug decreased thromboxane B2 levels from 1133 +/- 907 pg/ml to 720 +/- 379 pg/ml (p less than 0.05) in the coronary sinus blood, and increased the 6 keto-prostaglandin F1 alpha levels from 465 +/- 135 pg/ml to 559 +/- 167 pg/ml (p less than 0.05) in brachial artery blood. This suggests that a low, oral dose of nisoldipine can moderately improve the systemic and coronary hemodynamics and afterloads, and may assist in improving the prostaglandin metabolism in ischemic heart disease patients.
Plasma bradykinin and prostaglandin metabolism and exercise testing in patients with silent myocardial ischemia compared with patients with painful myocardial ischemia.
Bradykinin, alone or in combination with prostaglandin, is thought to produce pain in patients with coronary heart disease. To elucidate this further, we have investigated and compared serum bradykinin, TXB2 and 6 KPGF1 alpha levels in patients with silent myocardial ischemia (SMI, n = 18), painful myocardial ischemia (PMI, n = 8) and normal subjects (NL, n = 18). In addition, SMI and PMI subjects were given exercise testing and the results then compared. After Holter monitoring for 48 hours, exercise testing was performed. Blood was sampled in the morning between the Holter and exercise regimen. Maximal heart rate, systolic blood pressure and the double products were not significantly different between the SMI and PMI groups. The duration of exercise for the SMI group was 7.08 +/- 2.1 min vs 5.9 +/- 1.9 in the PMI group (p less than 0.10). Plasma bradykinin was 14 +/- 3 pg/ml in the SMI group and 15 +/- 3 in the PMI group (N.S), whereas it was 7 +/- 4 in the NL (p less than 0.05). The TXB2/6KPGF1 alpha for the SMI group was 1.3 +/- 0.3, which was significantly higher than that for the NL group (0.8 +/- 0.3, p less than 0.01), though this did not greatly differ from the PMI group (1.2 +/- 0.3). These results suggest that SMI patients under Holter monitoring who manifest no symptoms but show significant ST segment depressions must receive the same careful attention given to PMI patients. In both group of patients bradykinin and prostaglandin metabolism is similarly changed, as was demonstrated by exercise stress testing.
[An investigation of sudden cardiac death in apparently healthy young men by annual health examination].
We have clinically compared the health records of 58 apparently healthy men who succumbed to sudden cardiac death (SCD) against the same number of control subjects (CS) with similar physical and social backgrounds. SCD, for our purpose, was defined as a death that occurred from a non-traumatic cause within one hour after the SCD onset. The clinical examination of our SCD cases consisted of evaluating the findings derived from their health records covering a span of 13 years such as their ECGs, the blood pressure data, chest x-rays, serum chemical analysis, and their obesity indexes. Heart weights were estimated from their ECGs by the quantification of a multivariate analysis. Of the total SCD cases studied, eleven hearts also were examined pathologically. With respect to the physical conditions of the SCD cases and the CS cases, the systolic blood pressure in the SCD cases was found to be higher, whereas no significant variances in the diastolic values were found, and both the systolic and diastolic values were within normal ranges in the two groups. A greater number of hearts weighing more than 420 g were found in the SCD group. Similarly the frequency of premature contraction and the serum cholesterol level was higher. No further appreciable differences, however, were found. Myocardial cell hypertrophy, degeneration, and interstitial edema were observed in all eleven hearts. Our data have revealed that the greater the heart weight, the greater the risk of succumbing to SCD. The risk becomes more evident if the systolic and cholesterol levels are also found to be high.(ABSTRACT TRUNCATED AT 250 WORDS)
Improved regional and global diastolic performance in patients with coronary artery disease after percutaneous transluminal coronary angioplasty.
To investigate the improvement of left ventricular (LV) function after successful percutaneous transluminal coronary angioplasty (PTCA), we studied resting ejection fraction, regional ejection fraction, filling fraction as an index of early diastolic performance, and regional filling fraction in 22 patients with single-vessel coronary artery disease and technically adequate LV angiograms before and 6 months after successful PTCA without restenosis. Before PTCA, filling fraction was significantly less in patients with coronary artery disease than in the control group, although there was no significant difference in ejection fraction. Filling fraction improved significantly after PTCA. Regional filling fraction increased significantly in jeopardizing myocardium, but regional filling fraction in nonjeopardized myocardium did not change significantly. Ejection fraction and regional ejection fraction did not change significantly after PTCA. Our results indicate that the improvement of regional diastolic performance in jeopardized myocardium may contribute to the improvement of global diastolic performance after successful PTCA.