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Chronic magnesium deficiency in pregnant women is frequently seen because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problem, but also pediatric consequences that might last throughout life. Many epidemiological studies have disclosed that restricted fetal growth, i.e., intrauterine growth retardation (IUGR) is associated with an increased risk of insulin resistance in adult life. We previously postulated that intracellular magnesium of cord blood platelets is lower in the small for gestational age than in the appropriate for gestational age group, suggesting chronic intrauterine magnesium deficiency may result in IUGR. Taken together, chronic intrauterine magnesium deficiency in the fetus may lead to or program the insulin resistance after birth. Prospective study whether the children born with magnesium induced IUGR are at high-risk for metabolic syndrome in childhood or adulthood is currently undertaken.

Azithromycin (AZM), 10% fine granules or 100 mg capsules, were given orally to 27 children with various pediatric infections. The results of the study are shown below. 1. Pharmacokinetic investigation. We studied plasma and urinary concentrations after 100 mg AZM capsules were given. One patient received 8.3 mg/kg of AZM once a day for 3 days, and AZM concentration in plasma was 0.033 microgram/ml 48 hours after the final dosing. Doses of 8.3 and 12.5 mg/kg body weight of AZM were respectively given to two patients once daily for 3 days. As a result, AZM concentrations in urine during a period between 96 and 120 hours post-dosing were 1.67 and 4.53 micrograms/ml, respectively, and urinary excretion rate in 120 hours after the first dosing was 10.54% in the patient that was given 12.5 mg/kg. 2. Clinical investigation. Clinical efficacies were examined in 24 patients. Excellent results were obtained in 7 patients, good results in 14 patients, hence the clinical efficacy rate was 87.5%. Bacteriologically, Haemophilus influenzae strains isolates from 2 patients were eradicated in 1 and decreased in the other. Safety was evaluated in 26 patients. An adverse reaction was observed in 1 patient (urticaria). Abnormal laboratory test results were observed in 2 patients, decreased WBC in 1 and elevation of eosinophils in the other. The above results suggest that AZM is a useful oral antibiotic for pediatric patients with infection with susceptible organisms.

Cefozopran (CZOP, SCE-2787), a new parenteral cephem, was evaluated for its antibacterial activity and clinical efficacy. CZOP, 24.0-78.0 mg/kg/day, was given to 11 pediatric patients in 3 dose a day via 30-minute drip infusion. Clinically evaluated were nine patients including 4 with acute pneumonia, 2 with urinary tract infections, 2 with lymphadenitis and 1 with sepsis. Two patients were excluded because of possible non-bacterial infections. Clinical efficacies were excellent in 5, good in 3 and fair in 1. Bacteriological responses were confirmed for 5 strains in 5 patients. Four strains were eradicated, but one strain was not. MICs of CZOP were equal to those of ceftazidime. Side effects or abnormal laboratory test results were observed in 3 patients; diarrhea in 1, elevated GPT in 1 and thrombocytosis in 1, but none of them was significant.

The effects of residual stenosis after intracoronary thrombolysis (ICT) on the hospital course and on left ventricular function were investigated in 94 patients with acute myocardial infarction. The in-patient hospital events including death, post-infarction angina, and re-infarction occurred in 6 of 24 (25%) patients with 100-99% residual stenosis (Group I), 18 of 55 (32.7%) patients with 95-90% stenosis (Group II) and one of 15 (7%) patients with 75% or less stenosis (Group III), suggesting that the presence of severe residual stenosis could be associated with the occurrence of in-patient hospital events. However, re-infarction occurred in only 3.6% of Group II patients. In an analysis of left ventricular function, global and regional wall motion was significantly improved in this group of patients, compared with patients who had no reperfusion (Group I). What is more, the degree of the improvement in wall motion in Group II, despite the severe stenosis, was the same as that in Group III with 75% or less stenosis. It was concluded that further intervention following thrombolysis may not be necessarily required for patients who underwent reperfusion without filling delay, even if the residual stenosis is greater than 90%.

The purpose of this study was to determine whether two-dimensional echocardiography (2DE) can differentiate ischemic myocardial disease (IMD) from dilated cardiomyopathy (DCM). The subjects consisted of six cases of IMD which showed left ventricular dilatation (LVDd greater than or equal to 60 mm) and diffuse abnormality of wall motion, but did not show obvious localized myocardial infarction or left ventricular aneurysm on 2DE, and 16 cases of DCM. Two cases of IMD had previous myocardial infarction, and five cases of DCM had cardiomegaly following myocarditis. A short-axis image of the left ventricle was recorded at the chordal and the papillary muscle levels. Each image was divided into 4 segments, which were comprised of the septum, anterior wall, lateral (posterolateral) wall, and posterior (posteromedial) wall. Regional wall motion abnormality with reference to systolic thickening was analyzed qualitatively in each segment. The results were as follows: In ECG findings in IMD group, only one case showed abnormal Q waves and five cases showed left ventricular hypertrophy (LVH) similar to intraventricular conduction defect. On the other hand, in DCM group seven cases showed abnormal Q waves and five cases showed LVH. Two cases of IMD had two-vessel disease and four three-vessel disease, respectively. Left ventricular ejection fraction by cine-angiography ranged from 0.10 to 0.39 (mean 0.24) in IMD group and from 0.22 to 0.42 (mean 0.36) in DCM group. Mean LVDd showed no significant difference between these two groups. Five cases of DCM showed marked left ventricular dilatation (LVDd greater than or equal to 75 mm), but there were no such cases in IMD group. B-B' step was recognized in only one case of IMD, though it was present in eight cases in DCM. In regional wall motion, incidence of asynergy such as akinesis or dyskinesis was higher in IMD group than in DCM group. Left ventricular asynergy was more serious in the posteromedial wall than the posterolateral wall at the same image in five cases of IMD. However, in 12 cases of DCM, the degree of asynergy was equal at the both walls. In conclusion, it is recommended to examine echocardiographically the extent of severe asynergy in the posteromedial and posterolateral walls in order to differentiate IMD from DCM.

A 25-year-old man was admitted to Juntendo University Hospital with chief complaints of nocturnal dyspnea and shortness of breath on Sept. 22, 1983. He had no history of rheumatic fever or bacterial endocarditis. He was violently kicked in the chest while practicing Shorinji-Kempo (Karate) in July 1977. His heart murmur was first noticed in April 1978, but he was asymptomatic for six years after the accident until transient nocturnal dyspnea developed January 1983. Physical examination on admission revealed a grade 4/6 apical holosystolic murmur, a markedly accentuated third sound, and hepatomegaly of two finger breadth in the right midclavicular line. An electrocardiogram revealed sinus tachycardia (100/min), left atrial overload and left ventricular hypertrophy. Chest radiography showed slight cardiac enlargement with a cardiothoracic ratio of 55%, and slightly increased pulmonary vascular markings. Two-dimensional echocardiography showed a markedly prolapsed posterior mitral leaflet and fluttering in diastole. Cardiac catheterization showed elevated pressure of pulmonary capillaries (a: 16, v: 30, mean: 19 mmHg), the pulmonary artery and the right ventricle. Left ventriculography revealed grade four (Sellers) mitral regurgitation. Mitral valve replacement was performed on October 13, 1983. A chorda tendinae supporting the posterior leaflet of the mitral valve was found to be ruptured just above its origin from the posterior papillary muscle. Histological examination of the resected valve showed increased spongiosa tissue which mimicked so-called myxomatous changes, but it seemed preferable to interpret this as a "secondary change due to increased hemodynamic stress" rather than the "primary change".

Among 144 patients with hypertrophic cardiomyopathy, eight (58.3 +/- 7.0 years, M:F = 7:1) had complicating myocardial infarction, which was diagnosed clinically and by elevated cardiac enzymes or new Q-waves on electrocardiography. Coronary occlusion or stenosis evidenced by coronary angiography and nuclear cardiological findings were investigated. In six of the eight patients, coronary atherosclerosis caused infarction. These patients had many coronary risk factors compared to the other two patients. Sixteen of the 144 patients (11%) with hypertrophic cardiomyopathy had coronary atherosclerosis, the rate of which is reportedly 10 to 20%. Two of the eight patients had no coronary atherosclerosis. One patient had a diffusely spastic diathesis provoked by the intravenous administration of ergonovine maleate during coronary angiography, suggesting that coronary spasm caused myocardial infarction. The other patient had recurrent episodes of supraventricular tachyarrhythmia and no evidence of spasm during coronary angiography, suggesting coronary embolism as a cause of myocardial infarction. Myocardial infarction in patients with hypertrophic cardiomyopathy and normal coronary arteries as advocated by Maron et al. may have such pathogenesis. We conclude that coronary angiography may be mandatory in patients with hypertrophic cardiomyopathy, especially those who have many coronary risk factors and anginal symptoms. In these patients, ST-T changes and abnormal Q-waves on electrocardiography sometimes may be misleading when diagnosing the occurrence of acute myocardial infarction by electrocardiography alone. In such cases, infarct-avid scintigraphy with 99 m-Tc pyrophosphate is preferable.