The present study measured cardiac troponin T(TnT) for the pathophysiological analysis of evolving ischemic myocardial injury in 35 patients with unstable angina (3: Class IB, 32: Class IIIB) and in 40 patients undergoing coronary reperfusion therapy for acute myocardial infarction. Serum TnT, creatine kinase (CK), CKMB, myoglobin (Mb), and myosin light chain 1 (MLC1) were measured every 2-24 h for 10 days after admission to the CCU. In patients with unstable angina, positive test results were detected in 65.7% for TnT, 20% for CK, 37.1% for CKMB, 60.9% for Mb, and 26% for MLC1. Of the 23 patients with positive TnT, 12 (52.2%) had cardiac events. Of the 12 patients with negative TnT, 11 (91.6%) were event-free. All of the patients who developed cardiac events showed a persistent (n=10) or delayed elevation (n=2) pattern 28-120 h beforehand. The sensitivity for predicting cardiac events was 92.3% for TnT, 80% for Mb, 53.8% for CKMB, and 50% for MLC1. In patients with acute myocardial infarction, TnT release kinetics showed 2 peaks after coronary reperfusion therapy. TnT values at the 1st peak significantly correlated with maximum CKMB (r=0.70, p<0.05) and early-stage left ventricular wall motion score (r=0.60, p<0.05), while 2nd-peak TnT values significantly correlated with maximum MLC1 (r=0.59, p<0.05), the T1-SPECT score (r=0.78, p<0.05) and left ventricular ejection fraction (r=-0.74, p<0.05) in the convalescent stage. The 2nd/1st-peak TnT ratio significantly correlated with the nQ/nST elevation index (ratio of the number of leads developing abnormal Q-wave 1 week after the onset to the number of leads showing ST elevation of more than 1 mm at admission) (r=0.63, p<0.05) in patients with anterior myocardial infarction. These data indicate that persistent release of TnT reflects progressive irreversible myocardial damage in unstable angina and indicates a risk of future cardiac events. In acute myocardial infarction, the 2nd/1st-peak TnT ratio in patients undergoing coronary reperfusion therapy may be useful for the quantitative evaluation of myocardial salvage. (Jpn Circ J 1996; 60: 265 - 276)

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To characterize the vasospastic angina patients with exercise-induced ischemia, we measured hemostasis (platelet factor 4; PF4, fibrinopeptide A; FPA) and fibrinolytic parameters (tissue plasminogen activator antigen; t-PA, free plasminogen activator inhibitor-1 antigen; free PAI-1) in 15 normal subjects and 33 vasospastic angina patients without significant coronary artery stenosis (less than 50% stenosis). All of the vasospastic angina patients began to feel chest pain within 3 months before diagnostic coronary angiography. Blood samples were obtained from all of the study patients at 8:30-9:30 am before exercise ²⁰¹Tl emission computed tomography. Vasospastic angina patients were divided into 2 groups; 15 patients with exercise-induced ischemia (group 1) and 18 patients without exercise-induced ischemia (group 2). On coronary angiography, the severity of coronary artery stenosis at the site of spasm in group 1 (34±5%) was greater than that in group 2 (18±3%). Plasma FPA and PF 4 Ievels in group 1 were also significantly higher than those in normal subjects and group 2. Plasma t-PA and free PAI-1 Ievels in group 1 were significantly higher than those in normal subjects and group 2. Plasma levels of free PAI-1 in group 2 were also significantly higher than those in normal subjects. The present study demonstrated that all of the patients with vasospastic angina had impaired fibrinolysis, and these patients with exercise-induced ischemia showed enhanced platelet activation, an enhanced coagulation system, and advanced atherosclerotic lesions. These results suggest that vasospastic angina with exercise-induced ischemia puts patients at increased risk for thrombus formation. (Jpn Circ J 1996; 60: 277 - 284)

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This study investigated the therapeutic efficacy of a new beta-blocker, nipradilol, a non-selective agent with vasodilating activity, for the treatment of idiopathic dilated cardiomyopathy (DCM). The New York Heart Association functional class improved in the nipradilol group (n=9, p<0.01), but not in the control group who received conventional therapy (n=9). The observation period was 19±7 months in the nipradilol group, and 20 ±9 months in the control group. Before therapy there was no difference in heart rate between the 2 groups (76±12 vs 79±15 beats/min). The end-diastolic and end-systolic left ventricular dimensions decreased in the nipradilol group (p<0.05), but not in the control group. Radionuclide ventriculography revealed that the left ventricular ejection fraction increased in the nipradilol group (27±8 to 41±18%, p<0.05), but not in the control group (27±11 to 27±8%). Plasma norepinephrine tended to be lowered, although not significantly, whereas plasma alpha-atrial natriuretic peptide significantly decreased after the therapy (p<0.01) in the treatment group. Lymphocyte beta-adrenoceptors were up-regulated in the nipradilol group (p<0.05). None of these parameters changed during the observation period in the control group. Thus, nipradilol improved symptoms and cardiac function with a favorable effect on neurohumoral factors in patients with DCM. (Jpn Circ J 1996; 60: 285 - 292)

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The structure of the small pulmonary arteries was studied during autopsies performed on 38 patients with pulmonary atresia with intact ventricular septum. The thicknesses of the media of these small pulmonary arteries measured using a quantitative morphometric method varied widely. However, there was a notable tendency toward thinning of the media, especially in neonates. In cases in which the patient had undergone prostaglandin E₁ treatment, the media was thinner, which suggests that the longer the treatment, the thinner the media. Intimal lesions were observed in 18 of the 38 patients (47%), including 12 of the 22 neonates (55%). Intimal lesions were also found in the patients with thinner media. Based on these results, we propose that organized thrombus formation and intimal proliferation are more likely to develop in patients with reduced pulmonary blood flow, such as in those with pulmonary atresia and intact ventricular septum. In prostaglandin-treated patients, an imbalance between the markedly thinner median muscle and the relatively higher pulmonary blood flow and pressure may contribute to fibrous intimal proliferation. Small pulmonary arteries with a strikingly thinner media may be vulnerable to higher pressure, predisposing the patient to the development of intimal lesions. (Jpn Circ J 1996; 60: 293 - 299)

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To investigate the role that atrial natriuretic peptides (ANP) play in regulating coronary circulation in vivo, we examined the effects of intravenous (iv) ANP and/or HS-142-1 (HS), a specific ANP receptor antagonist, in chronically instrumented dogs on circumflex coronary artery diameter (CoD) and coronary blood flow (CBF). At ANP plasma levels of 366.7, 785.0, and 1850.0 pg/ml, which were induced by continuous iv infusion of ANP at 25, 50, and 100 ng/kg per min respectively, ANP increased CoD by 1.2±0.3%*, 2.2±0.5%* , and 2.9±0.5%*, and decreased mean systemic blood pressure by 2.3±1.0%, 4.3±1.5%* and 5.3±1.8%* (*p<0.05), respectively. A significant increase in the plasma cGMP level was also observed. However, neither CBF nor heart rate changed significantly. Pretreatment with HS (3 mg/kg) almost completely suppressed these hemodynamic effects of ANP along with inhibiting the increases in the plasma cGMP level. However, under control conditions, HS itself (3 mg/kg, iv) produced no significant changes in coronary parameters. Thus, ANP significantly increased CoD at plasma levels 10- to 20-fold higher than those in the control. These findings suggest that in patients under pathological conditions such as severe congestive heart failure increased endogenous ANP may contribute to the regulation of coronary circulation as a compensatory mechanism. It may also have direct vasodilatory effects on epicardial vessels, since HS suppressed both its coronary effects and the increase in plasma cGMP levels. However, in normal subjects, endogenous ANP may have little direct effect on coronary circulation. (Jpn Circ J 1996; 60: 300 - 310)

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An infant girl diagnosed with multiple peripheral pulmonary artery stenosis and Williams syndrome was followed-up for 17 years. Three cardiac catheterizations performed over the follow-up period showed that spontaneous gradual regression of the stenosis occurred with time. The initial systolic pressure gradient of 77-79 mmHg at the stenoses had decreased to 23-29 mmHg when measured at 17 years of age. Contrary to the progressive nature of systemic artery stenosis in Williams syndrome, peripheral pulmonary artery stenosis appears to have the capacity for spontaneous improvement. Careful consideration is required to determine the indications for interventional catheterization for the dilation of peripheral pulmonary artery stenosis in cases of Williams syndrome. (Jpn Circ J 1996; 60: 311 - 314)

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It has been reported that coronary diseases in patients with Fabry's disease are induced by deposits in endothelial cells and coronary smooth muscle cells. Most of those are ischemia due to stenosis. This report describes a case of a patient with Fabry's disease who showed severe vasospasms without coronary artery stenosis during acetylcholine loaded coronary angiography. In this case, a myocardial biopsy revealed that the deposits in the endothelial cells of the myocardial capillaries were lamellated appearance. Recently, it is reported that endothelial cell damage could be an important cause of coronary vasospasm. This case suggests that the some sort of functional disorder was induced by glycosphingolipid deposits in the coronary endothelial cells, and that this might have led to coronary artery spasms without the organic stenosis of coronary arteries. (Jpn Circ J 1996; 60: 315 - 318)

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