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The difference between the maximum and minimum QT interval measured from a 12-lead electrocardiogram was defined as an index of spatial inhomogeneous repolarization of the ventricular myocardium. The causal relationship between QT dispersion and incidence of ventricular arrhythmias has been pointed out in various heart diseases, but until now it was discussed mainly related to sinus rhythm. QT dispersion in extrasystole may be more important in the development of arrhythmias. We examined 5 cases (mean age 34 +/- 12 years) with a history of paroxysmal supraventricular tachycardia, who underwent electrophysiologic study. Both atrial and ventricular premature stimuli were given at a basic cycle length of 600 msec respectively. The QT interval and the ventricular activation time (VAT) (period from premature test stimulus to the summit of QRS) of the premature beats were measured in a simultaneously recorded 12-lead electrocardiogram. QT dispersion (the difference between the longest QT interval and the shortest QT interval) and VAT dispersion (the difference between the longest VAT and the shortest VAT) were measured. In atrial premature beats, there were no significant changes in the QT dispersion or VAT dispersion when the coupling interval of the premature beats was shortened. In the ventricular premature beats, however, both the QT dispersion and the VAT dispersion tended to increase with the shortening of the coupling interval. We concluded that only a short coupled ventricular premature beat induces greater QT and VAT dispersion. A ventricular couplet with short coupling interval may contribute to the development of ventricular tachyarrhythmias.

Background: Syncope of patients with bradyarrhythmia is perceived as severe sign of low cardiac output caused by bradycardia and as a major criteria for pacemaker implantation (PMI). However, it has been reported that PMI can not always prevent syncope; it has been suggested that not bradycardia but an abnormality of the autonomic nervous system plays a part in syncope., Purpose: To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB)., Subjects: Thirty-nine patients with SB were divided into two groups according to the presence (group S, n = 16, 46.9 +/- 20.0 years) or absence (group N, n = 23, 40.4 +/- 17.6 years) of syncope or presyncope., Methods: Corrected sinus node recovery time (CSNRT) was measured by electrophysiologic study. Pharmacologic autonomic nervous tests were performed as follows in a quiet room. Increased HR by application of 0.04 mg/kg atropine (para-tone), and by 0.004 microgram/kg/min isoproterenol divided by 0.004 (beta-sens) were evaluated, beta-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal beta-sympathetic activity was evaluated by beta-sec that was obtained by beta-tone/beta-sens. Increased SBP by application of 0.4 microgram/kg/min phenylephrine divided by 0.4 (alpha-sens) was evaluated. alpha-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol. Basal alpha-sympathetic activity was evaluated by alpha-sec, that was obtained by alpha-tone/alpha-sens., Result: There were no significant differences in basal clinical characteristics (age, sex, cardiac function) between the groups. The parameters of the functions of parasympathetic and beta-sympathetic receptors (para-tone, beta-sens, beta-tone, beta-sec) showed no significant differences between the groups, alpha-sens was attenuated (P < 0.01) and alpha-sec was augmented (P < 0.0001) significantly in group S., Conclusion: It was suggested that syncope or presyncope in SB patients could be attributed to failure of vasoconstriction mediated by alpha-sympathetic receptor but to severity of sinus node dysfunction.

Stimulation of receptors for alpha 1-adrenergic agonist, endothelin (ET) and angiotensin II (AT) activates the cardiac sarcolemmal Na+/H+ exchanger (NHE), perhaps via protein kinase C(PKC)-mediated pathway(s). We tested for the ability of these extracellular stimuli to exacerbate reperfusion arrhythmias and for the possible role of NHE activation and PKC in such phenomena. Isolated rat hearts (n = 12/group) were subjected to dual coronary perfusion. After 15 min of aerobic perfusion, flow to the left coronary bed was reduced to 5% of basal values for 12 min, and the same bed was then reperfused for 5 min. An alpha 1-adrenergic agonist phenylephrine (PE) at 1 or 10 mumol/L, ET at 0.5 or 5nmol/L or AT at 1 or 10mumol/L was infused selectively into the left coronary bed during 12 min of regional low flow ischemia. The incidence of reperfusion-induced ventricular fibrillation (VF) was increased from 17% in control to 33% and 75%* with 1 and 10 mumol/L PE(*p < 0.05 vs control) from 8% in control to 8% and 12% with 0.5 and 5 nmol/L of ET. However, AT had no effect. The selective NHE inhibitor NOE642 at 1 mumol/L, infused concomitantly with 10 mumol/L PE, reversed the proarrhythmic effects of PE; VF incidence was reduced from 67% to 8%*. However, glibenclamide (a blocker for the ATP-sensitive K+ channel) at 1 mumol/L did not affect the proarrhythmic effects of PE. Infusion of a specific PKC inhibitor GF109203X(GF) at 30 or 300 nmol/L, starting from 5 min before ischemia and maintained throughout ischemia concomitantly with 10 mumol/L of PE, was partially effective in reducing VF incidence; which reduced from 75% in control to 42% with 300 nmol/L of GF. These results suggest that, in rat hearts subjected to regional low-flow ischemia and reperfusion, stimulation of alpha 1-adrenergic receptor can exacerbate reperfusion-induced VF, whose mechanism(s) may involve NHE activation. Moreover, PKC activation does not appear to be the sole signaling mechanism for this phenomenon.

Closed-chest transcatheter electrical ablation (catheter ablation) has been applied to various supraventricular and ventricular tachyarrhythmias as a radical therapeutic technique since its introduction in 1982. Currently, it has become a first line therapy for supraventricular tachyarrhythmias except atrial fibrillation and uncommon types of atrial flutter. We first carried out the ablation procedure in 1991 for the treatment of ventricular tachycardia. Up to February 1997, a total of 187 patients underwent catheter ablation in our institution. The aims of this study are to demonstrate our results of catheter ablation in the early 5 years and to show the usefulness of this new curative method. Successful results were obtained in 168 of 187 patients (overall final success rate: 89.8%). The success rates of each category of tachyarrhythmias were 100/105 patients (95%) with WPW syndrome, 41/46 (89%) with atrioventricular nodal reentrant tachycardia, 7/10 (70%) with atrial flutter, 4/4 (100%) with atrial tachycardia, 2/2 (100%) with medically refractory atrial fibrillation, 13/15 (85%) with idiopathic ventricular tachycardia and 3/7 (43%) with sustained ventricular tachycardia associated with structural heart disease, respectively. Complications that required invasive treatments were observed in 3 patients (2 hemopericardium and 1 complete atrioventricular block). Our results indicate that catheter ablation is highly effective in most categories of tachyarrhythmias and can be applied safely without lethal complications.

To examine whether endothelial nitric oxide formation contributes to the vascular tone of resistance coronary vessels in vivo, we administered NG-nitro-L-arginine methyl ester (L-NAME) (10 and 100 micrograms/kg/min), a nitric oxide synthase inhibitor, as well as D-enantiomer into the left circumflex artery in normal dogs. Intracoronary L-NAME, which was associated with dose-related reductions in acetylcholine-induced coronary vasodilation, significantly reduced the baseline left circumflex blood flow by 6% and increased coronary vascular resistance of the left circumflex artery by 6%. D-enantiomer was ineffective in altering baseline coronary blood flow and vascular resistance of the left circumflex artery. These results indicate that continuous nitric oxide formation in the vasculature is important in the regulation of the coronary vascular tone of resistance vessels in vivo, and serves to maintain the vessels in a dilated state.

Non-invasive recording of the late potential (LP) by signal-averaging technique is useful in predicting ventricular tachycardia (VT), especially in patients with myocardial infarction (MI). However, the rate of positive LP is LOW in anterior or anteroseptal MI, since the LP is masked by QRS complex. The purpose of the present study is first, to detect local conduction delay in initial portion of QRS complex and secondly, to evaluate the clinical significance of the initial delay in patients with MI. Eighty patients with MI were analyzed; AS: anteroseptal, n = 18, including 6 VT, A: anterior, n = 22, 7 VT, I: inferior, n = 28, 9 VT, and P: posterior, n = 12, no VT. Twenty non-MI patients were used as normal controls (N). A signal processor (NEC 7 T 18) was used to record signal-averaged electrocardiograms and each 10 msec integral value of filtered QRS complex from the initial upstroke to the 60 msec point was automatically measured. The integral values of groups AS and A were lower than those of groups I, P, and N. AS with VT showed a lower integral value than AS without VT, but no differences were observed between A with VT and A without VT. We conclude that there is a much lower upstroke of signal-averaged initial QRS complex in patients with anteroseptal MI with VT, suggesting that the local conduction delay at the ventricular septum plays an important role in the mechanism of VT in these patients.

In order to clarify the relationship between thyroid function and left ventricular function in acute myocardial infarction (AMI), 52 patients (63.3 +/- 11.0 years old) admitted to the coronary care unit within 24 hours after the onset were studied. Both FT3 and FT4 levels measured at 48-72 h after the onset (1.66 +/- 0.59 pg/ml, 1.02 +/- 0.37 ng/dl) were significantly lower than those on admission (2.99 +/- 0.76 pg/ml; p < 0.01, 1.14 +/- 0.25 ng/dl; p < 0.05) and controls (3.27 +/- 0.66 pg/ml; p < 0.01, 1.22 +/- 0.23 ng/dl; p < 0.05). The decline of these thyroid hormone levels correlated well with the severity of AMI (Killip's classification), hemodynamic deterioration and liver function (low levels of albumin and cholinesterase). Low thyroid hormone levels were also associated with the elevation of catecholamine and alpha-hANP levels on admission. Low cortisol and impaired renal function were recognized as factors which might prolong the condition of low thyroid hormones. Non-survivors showed significantly lower levels of FT3 and FT4 48 hours after onset, and a lower level of FT4 in aged patients was consistent with a poor prognosis. In conclusion, the measurement of thyroid hormones in AMI is important in evaluating the severity of the condition and waking a prognosis.

An association between dermatomyositis-polymyositis and malignancy has been reported. However, controversy exists regarding a direct causal relationship between the two diseases. We describe a patient who had the concurrent onset and parallel clinical course of dermatomyositis and malignancy, and discuss the possible mechanisms for the association of the two disorders.

In order to evaluate the radioactive microsphere technique used in our laboratory for measuring regional myocardial blood flow (RMBF) in dogs with myocardial ischemia, simultaneous blood flow measurements with three different nuclide (141Ce, 51Cr or 113Sn)-labeled microspheres were performed after coronary artery occlusion. There were excellent correlations between all paired RMBF values in 80 samples. The linear regression lines were expressed as: 51Cr = 1.09x 141Ce-0.02 (r = 0.996, SEE = 0.06); 113Sn = 0.99x 141Ce + 0.01 (r = 0.997, SEE = 0.05); 113Sn = 0.90x 51Cr + 0.03 (r = 0.991, SEE = 0.08). The duplicate variability ranged from 5.5 +/- 0.7 to 9.9 +/- 1.1%. When RMBF was measured before and after intravenous administration of nipradilol (0.2 mg/kg), a new beta-blocker, in a dog with myocardial ischemia, RMBF fell in the normal zone (23.6 +/- 1.6%), and did not change in the severely ischemic zone. Thus, this study demonstrated that RMBF can be measured accurately and repeatedly with radioactive microspheres in dogs with regional myocardial ischemia.