To examine gender differences in the long-term prognosis of patients with myocardial infarction, 1000 patients with myocardial infarction were studied after coronay arteriography. Over a follow-up period of 3.3±2.0 years, 65 patients died from cardiac causes aNt 301 experienced cardiac events (death, reinfarction and revascularization). Overall, the 5-year cardiac mortality was 8% : that in females (12.4%) was significantly higher than that in males (6.6%) (p=0.0073). The overall 5-year cardiac event-rate was 35%, with no significant difference between females and males (41.1% vs 33.3%). Univariate analysis revealed that differences in age (57.8±9.8 years in males vs 64.8±8.9 years in females, p<0.0001), presence of smoking habit, obesity, hypercholesterolemia, hypertension, heart failure, right coronary artery disease, nicorandil administration, hypolipidemic, diuretic and anti-hypertensive treatment, and warfarin administration were present between men and women. The mortality rate in elderly females tended to be higher than that in their male counterparts. Multivariate analysis demonstrated that number of diseased vessels, post-infarction angina and left main trunk disease were significant predictors for cardiac death in both sexes, while gender was not. Therefore, gender did not appear to affect the long-term prognosis after ageadjustment among patients with myocardial infarction in the Western part of Japan.

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This study examined the relationship between the myocardial washout rate (WR) of thallium-201 (²⁰¹Tl) in dipyridamole scintiigraphy and both coronaryflow reserve (CFR) and mvocardial lactate extraction rate (LER) after dipyridamole infusion in 31 patneits with coronary artery disease (CAD) without myocardial infarction and 16 control patients. Patients with CAD demonstrated significantly lower WR (21±17 vs 43±10%, p<0.001), lower CFR (128±82 vs 242±89%, p<0.001) and lower LER (-2±20 vs 10±10%, p<0.05) than did the control patients. WR was significantly correlated with CFR (r=0.50, p<0.001) and LER (r=0.41, p<0.01) in all of the patients. CAD patients with dipyridamole-induced chest pain demonstrated significantly lower WR (14±20 vs 27±12%, p<0.05), lower CFR (97±71 vs 162±82%, p<0.05) and lower LER (-13±21 vs 11±9%, p<0.001) than did CAD patients without chest pain. CAD patients with dipyridamole-induced ST depression demonstrated significantly lower WR (14±20 vs 29±8%, p<0.05), lower CFR (105±79 vs 170±73%, p<0.05) and The First Department of Internal Medicine, and lower LER (-8±21 vs 11±10%, p<0.01) than did CAD patients without ST depression. These results suggest that the myocardial washout rate of ²⁰¹Tl after dipyridamole infusion reflects the severity of coronary artery disease as assessed by coronary hemodynamics, myocardial metabolism, symptoms and electrocardiography.

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It is widely accepted that perfusion defects in 3 to 4-h delayed images in exercise thallium-201 (²⁰¹Tl) myocardial scintigraphy underestimate the viability of myocardium in the infarct rezion. In the rresent study, to examine the contribution of the condition of myocardium which demonstrates reverse redistribution in resting scintigraphy to the insufficiency of redistribution in the 4-h delayed image in exercise scintigraphy, we performed exercise and resting ²⁰¹Tl myocardial single-photon emission computed tomogarphy in 58 ratients with acute myocardial infarction and a single diseased coronary artery. Twenty eight patients demonstrated reverse redistribution (group RR) and 28 showed a fixed defect (group FD) in resting scintigraphy. Redistribution in the 4-h delayed image in exercise scintigraphy was significantly more insufficient in group RR than in group FD (p<0.01), and the degree of the insufficiency of redistribution in exercise scintigraphy closely correlated with the degree of reverse redistribution in resting scintigraphy (r=0.79, p<0.001). We conclude that in patients With acute myocardial infarction, the condition of myocardium which demonstrates reverse redistribution in resting myocardial scintigraphy is related to the insufficiency of redistribution in the delayed image in exercise scintigraphy.

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The reproducibility of carotid sinus hypersensitivity to carotid sinus massage was studied in the long-term follow-up of 8 patients with carotid sinus syndrome. A cardioinhibitory response was induced in 7 patients, while a vasode-pressor response was found in the remaining patient. The 7 patients were treated with dual-chamber pacemaker implantation and the remaining patient was treated with propranolol. All of the patients remained asymptomatic during a follow-up period of 48±11 months. Carotid sinus massage during the follow-up period in patients with a cardioin-hibitory response revealed asystolic intervals of 3s or longer in 4 patients and in 3 patients at the second and third follow-up examinations, respectively, although there were no significant differences in the ventricular asystolic intervals between before, and 34±11months and 48±11months after treatment. However, each patient showed a wide variation in asystolic intervals. The differences in asystolic intervals between prior to treatment (first) and the third test were significantly greater than those between the first and the second test (2.4±1.2s vs 0.7±0.6s ; p<0.05). The one patient with a vasodepressor response had a decreased systolic blood pressure greater than 50 mmHg by carotid sinus massage at all three occasions. In conclusion, most patients with carotid sinus syndrome showed abnormal and variable responses to carotid sinus massage during long-term follow-up period although there was no recurrence of symptoms after treatments. The lack of symptoms in these patients was believed to have been due to effective treatment with dual-chamber pacing and β-blocker, rather than to spontaneous remission.

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Calpain activity was measured in the various subfractions of rat myocardia after global ischemia for 60 min or after ischemia followed by 30 min of reperfusion after the chromatographic separation of μ-and m-calpains. The activity of m-calpain after ischemia and that of μ-calpain after reperfusion were both higher than that in the control. The activity of the endogenous calpain inhibitor calpastatin in 10, 000×g supernatant was decreased after both ischemia and ischemia-reperfusion. The increase in m-and μ-calpain activities was suppressed by pre-ischemic perfusion with a synthetic calpain inhibitor, transepoxysuccinyl-L-leucylamido (4-guanidino) butane (E64d, 100 μg/ml). After reperfusion, the calpain activity in the 10, 000×g pellet was also increased, which was inhibited by pre-ischemic perfusion with E64d or dimethylsulfoxide (a solvent for E64d) or by reperfusion with 1 mmol/L ethyleneglycol bis (β-aminoethylether) -N, N, N', N'-tetraacetic acid. SDS-polyacrylamide gel electrophoresis revealed the proteolysis of several proteins, including fodrin, in the 10, 000×g and 100, 000×g pellet fractions after ischemia and reperfusion, some of which were confirmed to be in vitro substrates of calpain. The creatine kinase release during the reperfusion was also partially inhibited by E64d or dimethylsulfoxide. Thus, calpain activity in the soluble or particulate fractions was altered during ischemia or reperfusion, and appeared to be implicated in the proteolysis of the membrane proteins, which may contribute to myocardial injury.

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We present a patient who had a localized myocardial lesion of the left ventricle. Major clinical sequelae were left ventricular tachycardia and heart failure. This case appears to represent a left-sided counterpart of arrhythmogenic right ventricular dysplasia.

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We describe the complications of pericardiocentesis and their management in an 18 year-old man. This patient was admitted because of dyspnea and was found on echocardiogram to have cardiac tamponade with coexisting left ventricular dysfunction. He developed acute left ventricular failure with severe pulmonary edema immediately after pericardiocentesis. This complication may have been caused by an abrupt increase in venous return to the failing left ventricle following the release of the pericardial compression. Therefore, pericardial fluid must be drained with caution in pericardiocentesis, especially in cardiac tamponade patients with left ventricular dysfunction, and hemodynamics should be monitored both during and after this procedure.

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