SUMMARYThe 4 year prospective trial on the effectiveness of the antihypertensive treatment was performed in 100 mild hypertensive patients of the aged, the average age being 76.1 years. Dropouts during the drug-off control period were 9 cases. The matched pair group was selected by the age, sex, and blood pressure. Forty-four drug treated cases and 47 placebo treated cases were comparable in blood pressure as well as in laboratory data.Cerebrovascular and cardiac complications were observed in 4 cases or 10.5% in the drug group, and in 9 cases or 22.0% in the placebo group. When 8 cases of blood pressure elevation over 200/110mmHg in the placebo group were added to the cardiovascular complications, dropouts in placebo group reached 41.5%, and this showed the significant difference. Other complications were observed in 12 cases or 31.6% in the drug group and in 17 cases or 41.5% in the placebo group. Major complications were cancers, infections, and bone or joint diseases.Blood pressure was decreased from 171/87 to 151/80 in the drug group, and the average decrease was 20/7mmHg in 4 year period. No significant changes in hematocrit, serum protein, urea nitrogen, uric acid, sodium, and potassium were observed during the trial period. The present study suggested that antihypertensive treatment was effective in the aged with mild hypertension, and that careful follow up was needed not only for cardiovascular complications but also for general health condition.

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Diagnosis of disseminated intravascular coagulation (DIC) was made in 64 cases (16.2%) among a total of 395 autopsy cases. There were 31 men and 33 women. Their ages ranged from 31 to 91 years (mean 76.3). Underlying diseases were mainly malignancy and sepsis. Fresh cardiac lesions were found in 40 cases (62.5%). Coronary thrombosis was found in 13 cases (20.3%) and myocardial necrosis in 24 cases (37.5%), with acute myocardial infarction in 9 and focal necrosis in 15. Nonbacterial thrombotic endocarditis was found in 17 cases (26.6%), mural thrombi in 11 (17.2%), and bleeding of the heart in 11 (17.2%). Platelet count, fibrinogen and euglobulin lysis time were not correlated with myocardial necrosis nor coronary thrombosis. Increase of fibrin degradation products correlated with the presence of coronary thrombosis with or without myocardial necrosis. DIG was found with a high incidence in the aged, and many of them were complicated with fresh cardiac lesions. Development of acute myocardial infarction depends on the small thrombi in the severe stenosis of the main coronary arteries or on the multiple microthrombi in the peripheral coronary branches.

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Remuzzi G, et al: Hemolytic-uremic syndrome: deficiency of plasma factor(s) regulating prostacyclin activity(?) Lancet ii: 871, 1978. Stuart MJ and Sills RH: Deficiency of plasma prostacyclin or PGI2 regenerating ability in sickle cell anemia. BrJ Hematol 48: 545, 1981. SeidJM, et al: The presence in normal plasma, serum and platelets of factors that stimulate the production of prostacyclin (PGI2) by cultured endothelial cells. Clin Science 64: 387, 1983. Wu KK, et al: Serum prostacyclin binding defects in thrombotic thrombocytopenic purpura. J Clin Invest 75: 168, 1985. Yui Y, et al: Decreased serum levels of a factor stimulating prostacyclin synthesis in acute myocardial infarction.

SUMMARYSeven elderly cases with reversible electrocardiographic changes simulating acute myocardial infarction in the absence of gross myocardial infarction on postmortem examination were observed following the blood transfusion. The underlying diseases were cancer of gastrointestinal tract or gall bladder in 4, gastric ulcer in 2, and 1 of pseudomembranous enterocolitis. The electrocardiogram revealed the abnormal Q waves with monophasic ST elevation and following coronary T inversion. These findings lasted only for 2 to 7 days and returned to the previous normal tracings. The hematocrit was elevated from 28.9 to 47.7 after the blood transfusion of 800 to 1,800ml. The disseminated intravascular coagulation was shown in 5 cases. GOT levels were within normal ranges except 1 case.Pathological findings in cases with recent electrocardiographic changes were characterized by the mural thromboses, extending into the myocardium through the Thebesian vein. The focal small necroses of the adjacent myocardium or around the thrombosis of small vessels were also observed. In the later phase the fine interstitial fibrosis took place after the resorption of the thrombi and necrotic foci.From these clinical and pathological findings we proposed a new concept of reversible myocardial infarction induced from the hypercoagulability, disseminated intravascular coagulation, and elevated hematocrit. Additional Indexing Words: Transient abnormal Q wavesGastrointestinal bleeding, cancer, and operation Elevated hematocrit Disseminated intravascular coagulation Thebesian vein thrombosis A PPEARANCE of abnormal Q waves with monophasic ST elevation and T inversion is well known to be a definite electrocardiographic manifestation of acute myocardial infarction, and the abnormal Q remains persistently as a sign of old infarction. However, the abnormal Q waves disappeared in rapid sequences and no myocardial infarction was proved at autopsy on rare occasions.1)-6) The pathogenesis of this transitory abnormal Q wave had