Risk factor analysis in coronary artery disease was conducted in 303 patients who underwent coronary arteriography to identify associations between personal characteristics and the prevalence of coronary heart disease. Age, sex, obesity, smoking, alcohol intake, hypertension, diabetes mellitus, serum uric acid, total cholesterol, LDL- and HDL-cholesterol, triglyceride, and atherogenic indices were statistically analyzed. All 13 variables were first compared between patients with positive and negative ergonovine tests. Only total cholesterol was significantly different, while significant differences in age, sex, history of diabetes, total cholesterol. LDL- and HDL-cholesterol, triglyceride and atherosclerotic indices were observed between patients with and without organic coronary artery stenosis. A multivariate analysis was performed, and the resulting equation was tested using the remaining patients. Logistic analysis of all 13 variables identified 5 (age, sex, diabetes mellitus, LDL- and HDL-cholesterol) which accounted for the differences between patients with and without significant coronary artery disease and that were validated in the test group. The sensitivity for prediction of coronary artery disease was 75.8%, specificity 68.5%, and predictive accuracy 71.5% in the test group. Thus, risk factor analysis appears to be very valuable in screening subjects with high-risk organic coronary stenosis and in optimizing the preventive and therapeutic modalities, but not in predicting vasospastic subjects.

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Concentrations of Manganese-containing superoxide dismutase (Mn-SOD) were measured perioperatively by enzyme immunoassay in serial samples of arterial and coronary sinus blood and urine taken from 18 patients undergoing mitral valve surgery. The mean Mn-SOD concentration in the arterial blood samples was 66.2 (SD 16.1 ng/ml) at induction of anesthesia, increased gradually after reperfusion and peaked on the 2nd post-operative day [150 (SD 58.3) ng/ml]. The mean concentration of Mn-SOD in the coronary sinus blood samples was significantly higher than in the arterial samples only at the 6th hour after reperfusion [97 (SD 21.8) ng/ml vs 90.3 (SD 20.9) ng/ml, p<0.05]. Although concentrations of Mn-SOD in blood did not increase in 8 patients who underwent midline sternotomy for a mediastinal tumor, they increased dramatically in 3 patients who sustained a perioperative myocardial infarction. During open heart surgery the peak values of plasma Mn-SOD concentrations were correlated to that of plasma creatine kinase-MB concentrations (r=0.5532, n=18, p<05) and cardiac ischemic period (r=0.5186, n=18, p<05). Although the meaning of an increase in plasma Mn-SOD concentrations during open heart surgery is not clarified, it may be released from the heart and anywhere also in the body damaged during cardiopulmonary bypass.

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We investigated changes in serum lipoprotein(a) (Lp(a)) and C4b-binding protein (C4bp) levels following acute myocardial infarction (AMI). Serum lipids, apolipoproteins, C-reactive protein (CRP), sialic acid and haptoglobin (Hp) were also measured and evaluated. The study involved 16 patients (11 men, 5 women, mean age 68.2±8.4 years) with AMI admitted within 12 h after the onset of illness. CRP rose sharply and immediately after the onset of AMI, reaching its maximum level on the 3rd day of illness. This was followed by temporary increases in sialic acid and Hp, both of which peaked on the 7th day of illness. The Apo A-I level was significantly lower on the 14th day, while the Apo B level was significantly lower on the 3rd day. Serum total cholesterol (T-Ch), HDL-Ch and LDL-Ch showed temporary decreases after the onset of illness. Serial examination of the serum of patients with AMI yielded the following findings; 1) Both Lp(a) and C4bp levels rose temporarily with similar pat-terns of variation, and 2) they took longer time to peak (around the 14th day) and lasted longer than the increases in the other acute reactive proteins.

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We devised a technique to record a greater number of leads (a 9-lead monitor) by connecting a lead-switching adaptor to a commercially available 3-channel Holter recorder (9-lead DCG). Anodes were attached from positions V1 to V6 (CMI to CM6), and to high lateral (HL), low lateral (LL) and low back (LB). A cathode was attached to the manubrium of the sternum. The CM5 lead was continuously recorded on channel 1. The device is able to switch continuously every 20 sec among leads CM6, LB, HL and LL on channel 2, and among leads CM1, CM4 CM2 and CM3 on channel 3. Electrocardiograms were simultaneously recorded with both the 9-lead DCG and the conventional 12-lead ECG systems during treadmill testing in 67 patients with coronary artery disease. In addition, 6 patients with acute myocardial infarction were studied with the 9-DCG to test ST elevation. The sensitivity and specificity of leads CM2 to CM6, HL, LL, and LB in detecting ST depressions that occurred in each corresponding lead of the 12-lead ECG lead were very high (p<0.0001). The LB lead in particular was noteworthy for its markedly high specificity (94%) and sensitivity (83%) in detecting ST depressions occurring in leads II and aVF. Our lead-switching technique is useful when an increase in the number of leads is required in the DCG method. The LB lead, an anode on the low back, may be specific to detect inferior myocardial ischemia.

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HA1077 is a newly synthesized vasodilator with unique intracellular calcium antagonistic action. In this study, its effect on the growth of vascular smooth muscle cells (VSMC) stimulated by fetal calf serum was examined. Both the proliferation and [³H]thymidine incorporation into DNA of the growth-arrested VSMC was dose-dependently inhibited by HA1077. The expression of a protooncogene, c-fos, which reached the maximum 30 min after addition of serum, was similarly inhibited by this agent in a dose-dependent manner. Thus, HA1077 is expected to be a useful vasodilator agent capable of suppressing the growth of VSMC which is thought to be an important underlying mechanism of atherosclerosis or restenosis after angioplasty.

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In order to clarify the direct effects of high blood pressure on erythrocytic intracellular sodium concentration ([Na⁺]_i) and sodium transport systems, a static pressure of 2.5 atm was applied to whole blood in plastic syringes at room temperature for 5 and 24 h. In the control samples, 5 h incubation under atmospheric pressure produced a significant decrease in ouabain-sensitive Na⁺-k⁺ pump activity and plasma pH, but no change in other parameters. After 24 h incubation, [Na⁺]_i and mean corpuscular volume were significantly increased and intracellular potassium concentration, ouabain-sensitive Na⁺-k⁺ pump activity, and plasma pH were decreased. The change in [Na⁺]_i during incubation under atmospheric pressure may be due to the increased permeability of the cell membrane and the decrease in ouabain-sensitive Na⁺-k⁺ pump activity. The pressure load did not increase erythrocytic [Na⁺]_i but did decrease it relative to the control. The pressure load had no apparent effects on sodium transport systems, mean corpuscular volume and pH of plasma relative to the control. Although the mechanisms of the effect of pressure load on [Na⁺]_i Were not determined, we did find that high blood pressure alone was unable to increase erythrocytic [Na⁺]_i.

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A PGI₂ derivative, OP-41483, and a hyperosmotic agent, glycerol, were tested for possible beneficial effects on brain edema, metabolism and pathological changes in cerebral ischemia. Combination treatment with these agents was also tested. Cerebral ischemia was produced in spontaneously hypertensive rats, using bilateral common carotid artery ligation (BLCL). OP-41483 was administered four times, hourly (500 ng/kg×4, i.p.). Ten per-cent glycerol was administered intravenously (6.6ml/kg). And, for the combination treatment, OP-41483 was administered three times, hourly (500 ng/kg×3, i.p.), and 10% glycerol was administered intravenously (6.6 ml/kg) in the same manner as the glycerol treated group. In ischemic controls, saline was administered intravenously (6.6 ml/kg). After 3h of ischemia, brain water content and metabolites were determined and pathological observation was conducted using electron microscopy. OP-41483 treated animals maintained higher levels of ATP concentration and reduced accumulation of lactate, but showed no difference in brain water content compared to saline treated controls. Glycerol treated animals showed significance in terms of reduction of brain water content and accumulation of lactate. Glycerol abated the depletion of ATP concentration. OP-41483+glycerol treated animals showed the most significant effect on the reduction of brain water content and accumulation of lactate. The combination treatment also maintained higher levels of ATP concentration. Additionally, swelling of astrocytic foot processes and mitochondria with destroyed crista were not observed pathologically in the combination treated animals. These results show that OP-41483, glycerol and combination treatment are beneficial in the treatment of cerebral ischemia. They also indicate that the combination treatment significantly enhances the protective effects compared to individual treatment.

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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.

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A 53-year-old woman was admitted with a diagnosis of acute extensive anterior myocardial infarction. Pulmonary capillary wedge pressure was 17 mmHg, and cardiac index 2.4 1/min·m². The patient was successfully treated with diuretics and nitrates but on the fifth hospital day moist rales were noted over the entire lung field. A chest roentgenogram showed diffuse bilateral pulmonary infiltration with unchanged cardiac silhouette. Arterial oxygen partial pressure was reduced to 45 mmHg under 3 Iiters of nasal oxygen inhalation. Pulmonary capillary wedge pressure was 8 mmHg. Diffuse infiltration was not ameliorated by intravenous injection of diuretics. The diagnosis of adult respiratory distress syndrome was finally established by successful treatment with steroids.

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