Determinants of the electrocardiographic voltage are reviewed with formulation of certain parameters. The dipole moment of a single fiber and consequently, a possible maximal moment of the double layer of the activation wave front are estimated as 0.21 mA·cm per unit area (cm²). The longitudinal activation of parallel fibers produces much stronger double layer than the transverse activation across fibers. Without any loss of the electrical force of fibers, a normal ventricle of 200 g in weight would create a possible maximal QRS area of 350 μV·sec in a surface lead. The normal endo- to epicardial ventricular activation is predominantly transverse with respect to fiber orientation and rather inefficient in electrogenesis. It is implied that abnormalities in ventricular conduction may possibly improve the effectiveness of myocardial generator.

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A meta-analysis reported that nifedipine increased mortality dose-dependently in patients with coronary artery disease. However, there have been few studies (specifically in Asians) on the long-term prognosis of patients treated with calcium antagonists after successful coronary angioplasty (PTCA). The subjects consisted of 583 consecutive patients (461 males, aged 59 ± 10), who underwent successful elective PTCA between 1985 and 1990. First, they were divided into two groups; the calcium antagonist (+) group (n = 560) and the calcium antagonist (-) group (n = 23), and were evaluated in terms of total survival and cardiac events. Second, the calcium antagonist (+) group was further divided into 4 groups according to calcium antagonist type, i.e., short-acting nifedipine group (n = 156), long-acting nifedipine group (n = 203), diltiazem group (n = 184) and the other group (n = 17), and these groups were evaluated in the same way. The primary end-point was set as death from any cause. Secondary end-points were any cardiac events, including non-fatal acute myocardial infarction, coronary artery bypass surgery and repeat PTCA. The mean follow-up period was 4.5 ± 1.8 years. A multivariate analysis was performed with the Cox proportional-hazard model. The Kaplan-Meier analysis showed that the calcium antagonist (-) group had significantly worse prognoses than the calcium antagonist (+) group (p < 0.05), and that there was no significant difference among the prognoses of the four calcium antagonists groups. The multivariate analysis revealed that the use of a calcium antagonist was one of the independent factors positively contributing to the prognosis. The use of any type of calcium antagonist did not increase mortality in patients who underwent successful elective PTCA, rather, it contributed to a favorable outcome.

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Nocturnal oxygen desaturation and sleep apnea may provoke myocardial ischemia and arrhythmias in patients with coronary artery disease (CAD). Additionally, these factors may accelerate coronary atherosclerosis in the long term and they may play a role in the progression of the disease process. On the other hand, studies related to this subject are limited. This study was conducted to investigate the nocturnal oxygen desaturation and apneas during sleep in patients with CAD and to assess the possible association of these factors with CAD. We studied 22 male patients with CAD confirmed by coronary angiography who did not have symptomatic pulmonary disease and fourteen male healthy controls without known heart disease. Patients were randomly selected from men undergoing coronary angiography. Controls were age and sex matched and selected from the population registry. The normal controls were of similar body mass index to the patients. None of them were obese. The patients and controls underwent standard polysomnography. Men with CAD and controls had a similar apnea-hypopnea index (2.3±3.8 vs. 1.2±1.7). Mean oxygen desaturation index was higher among patients than controls (2.1 vs. 0.5, p<0.05). Patients with CAD spent 3.1% (9.7±13.6) of total sleep time desaturated, while the same proportion in controls were 0.5% (1.9±4.1) (p<0.05). Although both groups of patients were of similar heart rates at initial, the development of bradycardia during sleep was significantly higher in patients compared with controls (43.3% vs. 25.3%, p<0.05). The results demonstrate that sleep disordered breathing, in particular nocturnal oxygen desaturation, occurs more common in patients with CAD compared to controls. Additionally, patients are at higher risk of developing bradycardia during sleep. This findings suggest that oxygen desaturation during sleep might contribute to the progression of CAD.

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To clarify the mechanism and the predictors of the reduction in left ventricular mass (LVM) induced by antihypertensive drugs, forty hypertensive patients were classified according to the presence of left ventricular hypertrophy (LVH) as defined by echocardiographic LVM findings (LVH group: 27 patients, non-LVH group: 13 patients) and according to the presence of negative U-waves (NU) (NU group: 10 patients, non-NU group: 30 patients). Negative U-waves appeared in the LVH group only (10 of 27 patients). The hemodynamic determinants were investigated as a mechanism of LVM reduction in 38 of these patients who were treated for 2 years with antihypertensive drugs. In the LVH group, thickness of interventricular septum (IVST), posterior wall thickness (PWT) and LVM increased significantly compared to the non-LVH group. In the NU group, the left ventricular end-diastolic dimension (LVDD) was significantly larger and the relative wall thickness was significantly smaller compared to the non-NU group in the LVH group, with no difference in LVM between the two groups. Negative U-waves disappeared in all cases after treatment. Significant decreases in LVDD and LV wall thickness were observed in the NU group and significant decrease in LV wall thickness in the non-NU group. LVM index was reduced by 24.0% in the NU group and 9.5% in the non-NU group. The disappearance of negative U-waves was an independent predictor of the reduction of LVH.

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Twelve lead standard ECGs 35 healthy male volunteers, recorded from 08.00 H up to 01.00 H, were analysed retrospectively in order to investigate primarily the diurnal changes in vital sign measurements, ECG interval durations (PQ, QRS, QTc) and R wave as well as T wave amplitudes. Data were analysed descriptively and by means of ANOVA, spectral analysis and cosinor models. ANOVA revealed significant variations for vital sign parameters and the QTc interval, although remarkable variation in all ECG parameters was observed. T wave amplitudes in particular showed marked alterations, with changes up to 40%. Transient maxima of median T wave amplitudes and QTc interval duration were found at 12.00 H and 14.00 H, respectively. R wave amplitudes and PQ duration revealed lower values in the afternoon. Although there was remarkable interindividual variability, ultradian rhythmic activity of ECG parameters was confirmed by spectral analysis and cosinor models based on population data.

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To assess whether electrocardiographic variables are useful to detect the regression of left ventricular (LV) mass after long-term antihypertensive treatment, we related electrocardiographic voltages to echocardiographic variables before and after treatment with an ACE inhibitor, temocapril (TEM), or direct vasodilator, cadralazine (CAD). Twenty-one patients with essential hypertension were treated with either TEM (n = 11) or CAD (n = 10) for one year. LV mass index (LVMI) by echocardiography and Sokolow-Lyon voltage (SV₁ + RV₅), Cornell voltage (RaV_L + SV₃) and RV₅ + RV₆ by standard 12-lead electrocardiographic voltages were determined before and after treatment. Both drugs decreased blood pressure to the same extent. Both Sokolow-Lyon voltage and RV₅ + RV₆ tended to decrease in the ACE group (40.0 ± 9.4 to 37.2 ± 9.4 mm and 44.7 ± 13.5 to 41.7 ± 11.7 mm, respectively, N.S.), but not in the CAD group (38.4 ± 6.8 to 39.7 ± 7.7 mm and 42.9 ± 10.4 to 46.8 ± 11.2 mm, respectively, N.S.). LVMI decreased in the ACE group (-24 ± 22 g/m²), whereas it increased in the CAD group (37 ±27 g/m², p < 0.01). Change in LVMI was correlated with the changes in RV₅ + RV₆ and Sokolow-Lyon voltage (r = 0.73, p < 0.01 and r = 0.70, p<0.01, respectively), but not with that in Cornell voltage. These results indicated that the changes in voltage criteria of RV₅ + RV₆ and Sokolow-Lyon are useful to assess the change in LVM after antihypertensive treatment in patients with essential hypertension although voltage variables in electrocardiogram were not sensitive to detect changes in LVMI.

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Previous studies have shown that serum concentrations of lipoprotein(a) [Lp(a)]are markedly different among different ethnic groups. We examined the serum levels of total cholesterol, high density lipoprotein (HDL) cholesterol and Lp(a) in apparently healthy subjects aged 20-69 years in Japan (n=865) and the Dominican Republic (n=1, 893). Dominicans had significantly lower levels of total cholesterol and HDL cholesterol than Japanese. The distribution of Lp(a) concentrations were markedly skewed towards low levels in both Japanese and Dominicans. However, the mean Lp (a) concentration in Dominicans was approximately 2 times higher than in Japanese (21.7 ± 23.7 vs 12.3 ± 15.9mg/dl, p<0.001). This is possibly because the majority of Dominicans are of mixed Negroid and European blood.

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Positive responses to head-up tilt testing occur in healthy subjects. However, the reproducibility of “false-positive” tilt testing results has not been clarified. To study the reproducibility of “false-positive” responses, we prospectively performed 2 tilt tests separated by 1 to 10 (mean 3.2) weeks in 20 healthy males aged 23 to 40 years (mean 30 years). The baseline tilt test (80° for 30 minutes) ended positive in 4 (20%) subejects on the initial test and 2 (10%) on the second test with only 1 (5%) who had consecutive positive responses. No additional positive responses were noted during the isoproterenol (0.01 μg/kg/min)-tilt test for 10 minutes. We demonstrated that a false-positive response occurred in 5 (25%) of 20 young males who underwent 2 tilt tests, however, only 1 (5%) subject had consecutive positive responses. Poor reproducibility may be characteristic of false-positive responses in head-up tilt testing.

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Experiments were performed in rat models to study the effectiveness of various antiplatelet agents in the prevention of ventricular tachyarrhythmias during acute myocardial ischemia. The time to the onset of ST-segment elevation and initiating ventricular arrhythmias, frequency and incidence of ventricular arrhythmias, and mortality rates were observed during acute myocardial ischemia (20 minutes) induced by ligation of the proximal left anterior descending coronary artery (LAD) in anesthetized rats. Four groups were studied: Control group (n=10, not pretreated); Aspirin pretreated group (n=10, 300 mg/kg po for 1 wk); Ticlopidine pretreated group (n=10, 200 mg/kg po for 1 wk); and Abciximab (Platelet glycoprotein IIb/IIIa receptor antagonist) pretreated group (n=10, 2 mg/kg iv 10-20 minutes before an experiment). No significant difference was observed in the time to the onset of ST-segment elevation and ventricular arrhythmias between the groups. The incidence of ventricular tachycardia (VT) in the abciximab group was significantly lower than in the control group (p<0.05) and ventricular fibrillation (VF) in the aspirin and ticlopidine group was significantly lower than in the control group (p<0.05). The mortality rate in the ticlopidine group was significantly lower than in the control group (p<0.01). This study suggests aspirin, ticlopidine, and abciximab can effectively prevent VT or VF during acute myocardial ischemia induced by nonthrombotic occlusion and its antiarrhythmic effect may lead to prolonged survival.

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An implantable cardioverter defibrillator (ICD) was implanted in a patient with ventricular fibrillation (VF) related to old myocardial infarction. During VF, amplitude of ventricular activation was small, and the ventricular sensitivity at 1.2 mV failed to detect several small ventricular activations. When the sensitivity was changed to 0.3 mV, both under- and oversensed beats occurred during VF, and at the ventricular sensitivity of 0.15 mV, the undersensed beats disappeared while oversensed beats markedly increased. Defibrillation test was repeated one and four weeks after the implantation, and these inappropriate beats were minimized at the ventricular sensitivity of 0.3 mV. We should pay attention to the amplitude of ventricular activation to avoid possible trouble in ICD therapy.

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A 59-year-old man receiving hemodialysis was hospitalized due to severe hypoglycemic attack. The patient had been treated with disopyramide (50 mg/day) because of paroxysmal atrial fibrillation. Hypoglycemia occurred after taking clarithromycin (CAM, 600 mg/day), a macrolide antibiotic. The serum disopyramide concentration reached 8.0 μg/ml (23.6 μM) in the presence of CAM, while it was 1.5 μg/ml before the addition of CAM. A 75 g oral glucose tolerance test and daily profiles of blood glucose value showed that blood glucose levels were significantly lower in the presence of CAM and disopyramide compared to that in the absence of these drugs. The Turner index in the presence of CAM and disopyramide was significantly higher than that in the absence of these drugs, suggesting that a toxic concentration of disopyramide enhanced insulin secretion, resulting in the induction of hypoglycemic attacks, in which the inhibitory effects of CAM on the hepatic chytochrome P-450 might be involved. QT and QTc intervals were prolonged in the presence of CAM and disopyramide, but torsades de pointes were not observed in this patient receiving nicorandil (15 mg/day). Thus, it should be taken into account that life-threatening hypoglycemia may result from the interaction between clarithromycin and disopyramide.

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