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Previously, we reported that when Salmonella typhimurium and Escherichia coli were treated with N-nitrosodimethylamine (NDMA) under irradiation with ultraviolet-A (UVA), mutagenesis of the bacteria took place without externally added activation enzymes. We also observed the formation of O(6)-methylguanine (O(6)-meG), N(7)-methylguanine (N(7)-meG) and 7,8-dihydro-8-oxodeoxyguanosine (8-oxodG) in calf thymus DNA treated with NDMA plus UVA. In this study, we observed the mutagenicity of NDMA under irradiation of natural sunlight in S. typhimurium. Furthermore, we detected the formation of O(6)-meG, N(7)-meG and 8-oxodG in calf thymus DNA treated with NDMA plus simulated sunlight. Regarding the mutagenesis of S. typhimurium by NDMA plus UVA, we have now identified and quantified O(6)-meG formed in the genomic DNA of the bacteria under conditions of the mutagenesis.

The appearance of a new coronary artery lesion is important in patients with acute myocardial infarction or late coronary artery bypass grafting surgery, which sometimes lead to cardiac death. We studied coronary angiograms of 1,098 patients with coronary artery disease (from 1985 to 1996) and found new lesions in 94 patients (male 74, female 20; mean age 61.6 years). Mean observation period of all 1,098 patients was 50.1 +/- 30.4 months, and that of patients with new lesions was 73.2 +/- 31.2 months. Clinical findings of the 94 patients were acute myocardial infarction (n = 28), recurrent angina (n = 56), and silent ischemia (n = 10). The appearance of a new coronary lesion was found in 2.4% (1992), 1.9% (1993), 2.3% (1994), 1.7% (1995) of all patients with ischemic heart disease per year. The new lesions were found more often in patients with non-significant stenotic lesions (n = 74) than in patients with lesions of > or = 50% stenosis (n = 20). Complex lesions were found in 56% of the recurrent angina group, and in 22% of the silent ischemia group. In our study, the rate of appearance of new coronary artery lesions was much lower than in Europe or the United States of America. These results require careful consideration for coronary revascularization procedures in Japanese patients.

To evaluate the effects of intracoronary injection of nitroglycerin (NTG) on the coronary circulation, we measured the flow velocity of the coronary artery using a Doppler catheter. The Doppler catheter was introduced into the region proximal to the left anterior descending artery (LAD) via an 8F guide catheter positioned at the orifice of the left coronary artery. We measured the flow velocity at a point of 3 mm distal to the catheter tip. One mg (2 ml) of NTG was injected via the 8F guide catheter for 10 sec, followed by injection of 3 ml of normal saline. Then the increasing rate of the diastolic coronary flow velocity in the LAD was calculated. Five ml of iopamidol (dye) was also injected for comparison. The subjects consisted of 14 normal persons (G-N), and 12 patients with angina pectoris accompanying critical stenoses of the LAD, who had no ECG changes or no abnormalities by left ventriculography. The subjects with angina pectoris were subclassified as 90% stenoses (G-A: 5 patients), and 99% stenoses (G-B: 7 patients) in the LAD. 1. After intracoronary injection of NTG, the aortic pressure dropped to various degrees in G-N. In 7 of the normal subjects, who had less than a 20% aortic pressure drop, the increased diastolic flow velocity was more rapid than the control diastolic flow velocity 30 sec after the peak velocity.(ABSTRACT TRUNCATED AT 250 WORDS)

A 30-year-old man with chronic sustained ventricular tachycardia (VT) lasting more than seven years was treated with propranolol, 30 mg/day. This resulted in controlled cardiac rates of 90 to 130/min during sleep, and 100 to 195/min while awake. However, he experienced Adams-Stokes attacks twice, in September and December, 1986. During the second attack, ambulatory heart monitoring showed his VT rate of 212/min. An electrophysiological study revealed that the VT focal point was in the lower-mid region of the interventricular septum in the right ventricle. The VT was characterized by abnormal enhanced automaticity. This VT could not be interrupted either by single or multiple combinations of antiarrhythmic drugs. Cardiac catheterization revealed a diffusely enlarged hypokinetic left ventricle, even at the rate of 120/min VT (EF 27%, C.I. 2.3 l/min/m2). Because of his severe hemodynamic state, we performed electrical catheter ablation successfully. After the ablation, his left ventricular wall motion gradually improved. Nine months after the ablation, his left ventricular diastolic dimension decreased from 64 to 48 mm and the left ventricular systolic dimension decreased from 57 to 28 mm on M-mode echocardiography, while ejection fraction increased from 27 to 73% on the left ventriculography. Bi-ventricular myocardial biopsy specimens obtained prior to the ablation revealed only cellular hypertrophy of varying degrees, and vacuole degeneration consistent with non-specific cardiomyopathy. However, nine months after the ablation, these findings were no longer present. Thus, this case was considered tachycardia-induced cardiomyopathy initiated by VT, lasting many years.