BACKGROUND:There has been no report to date on mass screening of passive smoking in children using biomarkers. METHOD:To identify children exposed to actual environmental tobacco smoke (ETS), 261 children were divided into the following 3 groups: (A) both parents smoke; (B) one parent smokes; and (C) no parent smokes. Child urinary cotinine measurement and a parent questionnaire were obtained. RESULTS:Urinary cotinine was positive (>10 ng/ml) in 92 (35.2%) of the 261 children. Of the 92 children, 29 were classified into group A, 47 into group B, and 16 into group C. The percentages of children who tested positive for urinary cotinine in groups A, B, and C were 56.9%, 31.1%, and 27.1%, respectively. However, in group B, the percentage of children who tested positive for urinary cotinine was significantly higher if only the mother smoked (47.1%) than if only the father smoked (29.1%) (P<0.05). The mean+SD urinary cotinine level in group A was 12.9+/-6.5 ng/ml, and that in group B was 10.4+/-3.8 ng/ml if the mother smoked and 5.4+/-2.6 ng/ml if the father smoked. CONCLUSIONS:This smoking screening program may be useful in identifying children with actual ETS exposure and motivating their parents to either quit smoking or modify their smoking behavior around children.

Although no-reflow phenomenon may occur in patients that experience reperfusion after ischemia, there have been no reports describing the postmortem findings in these patients. We describe the findings of an autopsy in a 56-year-old man who experienced acute coronary syndrome with no-reflow phenomenon after coronary intervention. Macroscopic study demonstrated myocardial infarction with diffuse hemorrhage, and microscopic analysis revealed vascular damage and microembolization in the no-reflow area. In conclusion, coronary microembolization and damage to the small coronary artery may contribute to the pathogenesis of no-reflow phenomenon following coronary intervention in humans.

Segmental wall motion abnormalities are common in patients with myocarditis. Left ventricular (LV) regional wall motion was assessed in six patients with myocarditis by two-dimensional echocardiography. Some of our patients demonstrated regional thinning of the wall, similar to myocardial infarction. Therefore, segmental wall motion abnormalities with or without regional wall thinning detected by two-dimensional echocardiography cannot be used to differentiate myocarditis from coronary artery disease.

Although early total corrective repair for cyanotic tetralogy of Fallot is now safely performed at many institutions, long-term complications after surgical repair have been demonstrated. Therefore, the optimal procedure and timing for surgical treatment remain controxersial. In the present study, we conducted a quantitative analysis of the hypertrophy of all four chambers of 87 autopsied hearts of cyanotic tetralogy of Fallot and 71 normal control hearts utilizing the myocardial mass index, and evaluated the progression of lesions with advancing age. In cyanotic tetralogy of Fallot, hypertrophy of the right ventricle progresses immediately after birth, with that of the right atrium developing soon after. The left side of the heart is normal or slightly atrophied which could be corrected by sufficient palliative intervention or total corrective repair. The growth curves of both ventricles were parallel to those of normal hearts for the period studied. Pulmonary atresia, palliative operation, and total corrective repair have been shown to have some influence on the morphological characteristics of hearts of cyanotic tetralogy of Fallot.

The clinicopathologic findings of reversible ampulla-like ventriculogram of the left ventricle were studied in 8 elderly women and one middle-aged man. Their coronary arteriograms were normal, even in the 7 patients who had ST elevation on electrocardiogram. Coronary spasm was positive in only 2 of the 7 patients who received provocation tests. Biopsy specimens revealed focal myocyte injury. Normal coronary arteriograms during ST elevation and the presence of pathologic myocardial lesions were not consistent with a concept of stunned myocardium. The presence of myocardial lesions suggested that focal and disseminated myocardial damage had occurred.

A case-control study was conducted to investigate how basic habits of life including dietary habit, physical activity, cigarette smoking, and drinking, are involved in the development of idiopathic dilated cardiomyopathy (DCM). Collection of cases was entrusted to the clinical research group of DCM, and national pooled controls established by sex and age category by the epidemiological research group of intractable diseases were used to ensure representativeness of the controls. Fifty-eight cases of DCM which developed in and after January 1991 were collected, and 5,912 controls matched with the cases by residential area, sex, and age were selected. Analysis of the results of the study showed that items in the questionnaire suggestive of viral infection, such as "susceptibility to common cold" and "susceptibility to diarrhea", items concerning dietary habit, including "taking no breakfast", "ingestion of salty food", and "ingestion of fatty food", and such items as "cigarette smoking" and "lack of sleep" tended to be observed in the case group at significantly higher frequencies. Since viral infection has been suspected as a causative factor of DCM, further research of this area is thought to be of particular importance for determining the etiology of DCM.

We report on a 37-year-old man with congestive heart failure caused by eosinophilic myocarditis associated with toxicodermia. He developed many annular skin eruptions and peripheral eosinophilia due to reactions against phenobarbital. Right ventricular endomyocardial biopsy revealed extensive infiltration of eosinophils in the myocardium. A drug lymphocyte-stimulating test (DLSt) for phenobarbital was positive, His symptoms, cardiomegaly, and cardiac function were improved by discontinuing phenobarbital followed by oral ahministration of prednisolone. We conclude that this eosinophilic myocarditis must have been induced by an allergic reaction to phenobarbital and that long-term eosinophilia contributed to the myocardial injury.

We previously reported a clinical study in which probucol reduced the restenosis rate. The mechanism of this effect is unclear. Restenosis is characterized by neointimal hyperplasia caused by proliferation of smooth muscle cells (SMCs), which increases the expression of Platelet-derived growth factor (PDGF)-A and SMemb. SMemb, a non–muscle-type myosin heavy chain most predominantly expressed in embryonic smooth muscle, can be used as a good molecular marker for dedifferentiated SMC. The aim of this study was to analyze the effect of probucol on neointimal proliferation and the level of expression of PDGF-A and SMemb after balloon injury in rabbits. Probucol was given orally 1.3 g/d from 2 weeks prior to carotid balloon injury to the time of killing (2 or 4 weeks after balloon injury). Intimal area was determined histologically using a computerized morphometry program. For quantification of SMC proliferation, alpha-actin–positive cells and proliferating cell nuclear antigen (PCNA)-labeled cells were counted. The expression of PDGF-A and SMemb mRNA was analyzed by the RNase protection assay. SMemb expression was also examined by immunohistochemistry. Probucol remarkably decreased intimal area by 70% and the number of SMC and PCNA-labeled cells in the intima. The expression of PDGF-A mRNA was significantly increased after balloon injury in untreated rabbits, whereas it was markedly suppressed with probucol treatment. The expression of SMemb was significantly increased in injured arteries at mRNA and protein levels. However, probucol did not suppress SMemb expression. Probucol is effective in preventing SMC proliferation, which is possibly due to a decrease in the expression of PDGF.

The objective of this study was to examine the suppressive effect of nifedipine on intramural coronary arterial lesions in cholesterol-fed rabbits. Each rabbit in Groups A (n=6) and B (n=5) was fed a 0.3% cholesterol diet and was orally administered nifedipine (40 mg/day) or placebo. Each rabbit in Groups C (n=5) and D (n=6) was fed a 0.5% cholesterol diet and was orally administered nifedipine (40 mg/day) or placebo. The serum concentrations of total cholesterol (TC) were determined at 1-week intervals to calculate the integrated values. The lesion induction ratio was defined as the ratio of intramural coronary arteries 50-150 microm in diameter with arterial lipoidosis to the total number of arteries of the same diameter. There were no significant differences between the nifedipine-treated and placebo groups in either the integrated TC or lesion induction ratio in either the 0.3% and 0.5% cholesterol-fed rabbits. This study demonstrates that nifedipine does not suppress atherogenesis in the intramural small coronary arteries of cholesterol-fed rabbits.

The aim of this study was to examine the suppressive effect of simvastatin on intramural coronary arterial lesions in cholesterol-fed rabbits. In one experiment, six groups of rabbits were fed laboratory chow alone or with added 0.1%, 0.2%, 0.3%, 0.5% or 1.0% cholesterol for 16 weeks. In another experiment, four groups of rabbits were fed a 0.5% cholesterol diet and treated with simvastatin at 1, 3, or 5 mg/kg/day or placebo. In each rabbit, the levels of serum total cholesterol (TC) were determined at 1-week intervals to calculate the integrated values. The lesion induction ratio was defined as the ratio of intramural coronary arteries 50-150 microm in diameter with arterial lipoidosis to the total number of arteries of the same diameter. In the two experiments, there were positive correlations between the lesion induction ratio and integrated TC (r=0.785, P<0.0001 and r=0.763, P<0.0001, respectively). The slopes of the regression lines for integrated TC obtained in the two experiments were similar, but the lesion induction ratio in the simvastatin-treated group was always lower, by about 14%, in comparison with that in the non-simvastatin-treated group. These findings suggest that simvastatin induces lesion reduction not only by reducing the levels of circulating cholesterol but also by directly suppressing the development of lipoidosis.

Idiopathic restrictive cardiomyopathy (RCM) is rare. Even today little is understood of its etiology or underlying mechanisms, and definitive diagnostic criteria are lacking. In this report, we describe a case of idiopathic RCM in a young Japanese woman who died while awaiting cardiac transplantation during the 5-year course of the disease. Rare pathologic findings of diffuse perimyocytic fibrosis were revealed at autopsy.