To clarify the circadian variation in sudden death (SD) in Japan, where the causes of sudden death differ from those in the USA, we examined all of the death certificates from 1984 to 1986 in Niigata Prefecture, Japan. We defined SD as death which occurred within 1 h from the onset of the underlying cause. A significant circadian variation, with a high incidence between 6 and 8 am and a secondary peak between 6 and 8 pm, was found in the occurrence of sudden cardiac death (SCD, n=2953). Although the proportion of SCD due to acute myocardial infarction (AMI) was as low as 28% of SCD cases, the circadian variation of SCD was similar to that previously reported in the USA. In SCD due to AMI in males (n=487), a significant circadian variation with 3 peaks, including a primary peak between 4 and 6 am, was evident. There was also a marked increase in the incidence of fatal stroke between 6 and 8 pm (n=529). We concluded that 1) a circadian variation with two peak incidences, one between 6 and 8 am, and one between 6 and 8 pm, was characteristic of SCD in general, 2) there was a primary peak between 4 and 6 am for SCD due to AMI in males, and 3) there was a peak between 6 and 8 pm in the incidence of fatal stroke for both men and women. (Jpn Circ J 1996; 60: 193 - 200)

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Thrombin-antithrombin III (TAT) and D-dimer were measured in 50 patients suspected of deep venous thrombosis (DVT) to assess the usefulness of these indicators in the diagnosis of DVT. DVT was diagnosed by ultrasonography (compression method and Doppler imaging). In patients who were negative for DVT (Group A), TAT was 3.8±2.36 μg/L (mean ±SD) and D-dimer was 0.7±0.69 μg/ml, whereas in patients diagnosed with DVT (Group B), TAT was 20.4±19.10 μg/L (p<0.001) and D-dimer was 9.0±9.21 μg/ml (p<0.001). Thus, Group B had significantly higher levels of both markers. Moreover, 19 of the 23 cases in Group B had acute DVT, with symptoms appearing within 2 weeks of onset. When the cutoff for a positive diagnosis of DVT was set at TAT of 7.0 μg/L or more and D-dimer of 3.0 μg/ml or more, sensitivity was 84%, specificity was 96%, and accuracy was 90%. Based on these results, we concluded that TAT and D-dimer are extremely useful in screening for acute DVT. (Jpn Circ J 1996; 60: 201 - 206)

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The possible preventive effect of cilostazol, a novel anti-platelet drug, on restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) was examined. One hundred and two consecutive patients, who underwent successful PTCA, were followed for 3 to 6 months. To prevent restenosis, 46 patients (60 PTCA sites) were treated with cilostazol alone (200 mg/day) (cilostazol group) and the remaining 56 (61 PTCA sites) were treated with other anti-platelet drugs and/or warfarin potassium (control group). Restenosis was defined as a more than 50% loss of the initial gain of the coronary diameter achieved by PTCA. Cilostazol did not significantly reduce the patient or lesion restenosis rate; the patient restenosis rate was 32% in the control group and 22% in the cilostazol group (P=0.24), and the lesion restenosis rate was 30% in the control group and 23% in the cilostazol group (P=0.44). However, the lesion non-progression rate, which was defined as the incidence of lesions with either no change or regression of coronary stenosis at the PTCA site, was significantly greater with cilostazol (37%) than in the control group (16%) (p<0.05). Although cilostazol failed to show a significant reduction in restenosis after PTCA, the present results suggest that a further trial with a larger number of patients is needed to confirm its usefulness. (Jpn Circ J 1996; 60: 207 - 215)

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The total stroke volume of the left ventricle (LV) is equal to the sum of the regional cavity shrinkage. Since nonuniformity of regional wall motion in LV has been well documented even in normal subjects, the extent of the contribution of each region to total stroke volume cannot be easily determined. To assess the left ventricular regional contributions to total stroke volume under normal conditions and in compensated chronic mitral or aortic regurgitation, LV cineangiograms were analyzed in 14 normal subjects (N), 8 patients with mitral regurgitation (MR) and 10 patients with aortic regurgitation (AR). We assumed that the LV cavity could be viewed as a stack of 30 half-cylindrical discs, 15 in the anterior and 15 in the inferior wall regions. LV chamber shape was more spherical in MR than in N, but was more conical in AR. Percent regional hemichordal shortening was significantly decreased in the anterobasal and anteroapical walls in AR, but was similar between N and MR. The regional contribution to total stroke volume showed a significant quadratic correlation with the end-diastolic regional shape index (N, r=0.87; MR, r=0.79; AR, r=0.90), which was defined as the regional hemiaxial length divided by the LV long-axis length, but was not correlated with percent regional hemichordal shortening. Therefore, stroke volume is generated mainly in the mid-ventricular portion in N and MR, but in the basal portion in AR due to the characteristic change in cavity shape. (Jpn Circ J 1996; 60: 216 - 227)

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We evaluated criteria for the diagnosis of ventricular abnormal signal-averaged electrocardiogram (SAE) in 205 healthy children classified by age, body surface area and height. The children were classified by age into 4 groups: under 3 months old, 3 months old or more but less than 1 year old, 1 year old or more but less than 12 year old and 12 year old or more. They were also divided by body surface area into 4 groups: under 0.3 m², 0.3 m² or more but less than 0.5 m², 0.5 m² or more but less than 1.2 m², and 1.2 m² or more. In terms of height, they were classified into 4 groups: under 60 cm, 60 cm or more but less than 80 cm, 80 cm or more but less than 140 cm, and 140 cm or more. The boundary points in these 3 classifications were statistically consistent. Criteria for abnormal SAE in children classified according to age were filtered QRS duration (f-QRSd) >95 msec, root mean square (RMS) <30 μv and duration of low amplitude signal (LAS) >25 msec in those under 3 months old; f-QRSd >110 msec, RMS <25 μv, LAS >30msec in those 3 months or more but less than 1 year old; f-QRSd >115 msec, RMS <20 μV, LAS >30msec in those 1 year old or more but less than 12 year old; and f-QRSd >125 msec, RMS <20 μv, LAS >30 msec in those 12 year old or more. The criteria for evaluating abnormal SAE were similar regardless of whether children were classified by age, body surface area or height. Using these values as criteria, the 205 children were evaluated for the presence of abnormal SAE. All of the children were negative for abnormal SAE using these criteria according to age, body surface area or height. In evaluating abnormal SAE in children, it is useful to classify children by age, body surface area and height and to identify the criteria in each group. In this study, the criteria based on height and age were particularly useful, since these are more convenient than body surface area. (Jpn Circ J 1996; 60: 228 - 238)

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The purpose of this study was to determine the roles of extracellular cations (Na⁺, Ca²⁺ and K⁺), membrane K⁺ channels and Na⁺/K ⁺ ATPase in the development of myogenic contraction (transmural pressure-induced contraction) in isolated rat skeletal muscle and mesenteric small arteries. The vessels were pressurized under no-flow conditions in a tissue bath. Lumen diameter was measured with a videomicroscopic system. Myogenic contraction was evoked by increasing the lumen pressure from 40 to 100 mmHg. The vessels demonstrated myogenic contraction in low-Na⁺ (Na⁺ 1.18 mmol/L) physiological salt solution (PSS), and this was abolished by removing Ca²⁺ or by applying nifedipine or nisoldipine (10 μmol/L). Neither tetraethylammonium (TEA, 1 mmol/L), Ba²⁺ (10 μmol/L) nor glibenclamide (1 μmol/L) affected the magnitude of the myogenic contraction. K⁺-free PSS and ouabain (0.1 mmol/L) partially depressed myogenic contraction. In conclusion, myogenic contraction was triggered by a cellular process that requires extracellular Ca²⁺, but not Na⁺ or K⁺. This triggering process is not affected by TEA, Ba²⁺ or glibenclamide. (Jpn Circ J 1996; 60: 239 - 246)

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The reduced reactive hyperemic response of the right coronary artery (RCA) to brief coronary occlusion was assessed in dogs with pressure-induced right ventricular hypertrophy (RVH). Right coronary reactive hyperemia was observed in normal dogs and in dogs with pressure-induced RVH. RVH was induced by chronic pulmonary artery banding in eight 3- to 6-month-old dogs, and reactive hyperemia responses to coronary occlusion lasting for 5, 10, 15, 20, 30, 45, and 60 sec were compared to those in normal dogs. In dogs with RVH, the peak reactive flow rate and excess blood flow debt repayment after the release of 5- to 60 sec RCA occlusion were markedly attenuated. The calculated minimum coronary resistance was higher in RVH dogs than in normal dogs (p<0.02). The occlusion time that produced one-half of the maximum %PRHc, T1/2, was significantly (p<0.01) shorter in RVH dogs than in normal dogs, where %PRHc=(peak reactive flow rate baseline flow rate)/(baseline flow rate). T1/2 in RVH dogs varied inversely with right ventricular systolic pressure. Therefore, blood flow in the RCA in RVH is characterized by an attenuated flow response to acute myocardial ischemia, suggesting inadequate development of the coronary vasculature supplying the hypertrophied ventricle. (Jpn Circ J 1996; 60: 247 - 253)

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A 74-year-old Japanese woman with subarachnoid hemorrhage was admitted to our hospital. During her hospitalization, serial electrocardiograms showed the combination of abnormal Q waves, ST-segment elevation, and T-wave inversion, which strongly suggested acute myocardial infarction. However, postmortem examination revealed widespread focal myocytolysis of the myocardium which was unrelated to vascular distribution. (Jpn Circ J 1996; 60: 254 - 257)

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A 60-year-Old man was admitted to our hospital for investigation of dyspnea and disorientation with right hemiplegia. Echocardiography showed thickened mitral valve leaflets with vegetations and severe mitral regurgitation. Blood cultures grew Staphylococcus aureus. During the operation, perforation and destruction of the mitral valve leaflets and vegetations were confirmed. Debridement of the infected tissues resulted in segmental disruption of the posterior mitral fibrous annulus. Reconstruction of the mitral annulus with porcine pericardium treated with glutaraldehyde and mitral valve replacement were successful. The patient's postoperative course was complicated with metastatic cerebral and splenic abscesses. After splenectomy on the 8th postoperative day, he gradually recovered without major neurologic sequelae. We believe that reconstruction of the mitral valve annulus with pericardium, especially autologous pericardium, is reliable and useful for the treatment of patients with disruption of the mitral valve annulus. (Jpn Circ J 1996; 60: 258 - 261)

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