We studied the effects of vigorous rowing training on left ventricular structure and function using M-mode, two-dimensional and Doppler echocardiography in 10 female college rowers. Echocardiographic measurements were performed before and after 20 weeks of rowing training. Diastolic function was also estimated by measuring the isovolumetric relaxation time (IRT), deceleration time (DcT), peak velocity of early diastolic rapid filling flow (Ep), peak velocity of atrial filling flow (Ap) and the Ep/Ap ratio on left ventricular inflow Doppler wave form. The relative contribution of atrial systole to stroke volume was also calculated as the area under the flow velocity profile during atrial systole using the total area of the flow velocity profile. After training there was a significant increase in the left ventricular diastolic dimension (LVDd), posterior wall thickness, left atrial dimension, left ventriculer mass (LVM), LVM index and stroke volume (SV). No significant change in IRT, or DcT was detected after training. Although there was an increase in mean values of Ep, no statistical significance was observed. Training also induced a significant decrease in Ap and the percent of SV contributed by atrial systole, while the ratio of Ep/Ap increased (p<0.01). These results indicate that rowing training increases the LVDd and LVM index without impairment of left ventricular diastolic function in college female rowers.

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The long-term relative benefits of thrombolysis and mechanical reperfusion therapy following acute myocardial infarction (AMI) have not been established. The purpose of this study was to compare left ventricular function, left ventricular remodeling and late outcome after AMI for different reperfusion therapies. Thirty consecutive patients suffering their first anterior wall myocardial infarction with coronary stenoses limited to the left anterior descending coronary artery were studied. They included 10 patients who underwent intracoronary thrombolysis (ICT), 10 who underwent PICA and 10 who underwent noninterventional medical treatment. All patients underwent coronary angiography (CAG) during the acute phase of AMI and also during the follow-up period, and left ventriculography during the follow-up period and clinical follow-up was performed (mean clinical follow-up period: 53±31 months). No significant difference in global ejection fraction was noted among the groups, although the end-diastolic volume index (EDVI) in the PTCA group (79.4±17.5ml/m²) was significantly smaller than in the noninterventional (106.1±25.1ml/m²) and ICT (107.9±28.3ml/m²) groups (p<0.05). The regional wall motion index (RWMI) for the anterior region in the PICA group (-2.7±0.8) was greater (p<0.05) than in the noninterventional (-3, 4±0.6) and ICT (-3.3±0.6) groups. A significant linear correlation was found between EDVI and % diameter stenosis and also between RWMI and % diameter stenosis following reperfusion (p=0.01). There was no difference in the incidence of cardiac death, nonfatal reinfarction, bypass surgery or congestive heart failure among the groups. Disturbed left ventricular regional wall motion and remodeling benefit most from angioplasty because of prompt restoration of adequate blood flow. However, there was no difference in late outcomes following AMI among the three groups.

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In Taiwan over the past decades there has been enormous economic growth and rapid westernization of people's life style, as well as a concomitant rise in coronary heart disease (CHD) mortality and morbidity. Studying the effects of such a degree of socioeconomic development on the coronary risk factors of the Chinese population, an ethnic group long regarded as having a low incidence of CHD, may provide some insight into the etiology of coronary atherosclerosis. Coronary risk factors among 1, 449 patients (759 with CHD) were retrospectively studied. Diagnosis was established by angiography or a definite history of myocardial infarction in approximately 60% of the patients, and for the remainder, at least by noninvasive testing. The frequencies of dyslipidemia and nonlipid risk factors in patients with and without CHD were determined and compared. The lipid levels of subjects with or without CHD were close to or approaching those reported from the United States. Socioeconomic development and changes in dietary patterns seem influential in this regard. Among risk factors, high-density lipoprotein cholesterol (HDL-C), smoking, diabetes mellitus, hypertension and family history in males and, in females, total cholesterol, HDL-C, diabetes mellitus and hypertension, were significantly and independently correlated with CHD. These risk factors are similar to those found in the West; however, there is an important association of serum HDL-C concentrations with CHD, irrespective of gender. This issue requires further study in Chinese populations in other Asian countries.

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The body surface potential map (BSPM) may reflect regional myocardial electrical activity. This technique can thus provide information regarding the excitation of ventricles. This study is an attempt to evaluate the usefulness of BSPM in determining the sites of the atrioventricular (AV) accessory pathway (AP) in patients with Wolff-Parkinson-White (W-P-W) syndrome.
The BSPMs were obtained from 40 consecutive patients with W-P-W syndrome in a fasting state, using the heart potential map system designed by Toyama et al. Unipolar electrocardiograms were recorded simultaneously from 87 lead points on the chest surface, including 59 lead points on the anterior chest and 28 on the back. Wilson's central terminal was used as a voltage reference and BSPMs in an isopotential distribution pattern were made every millisecond throughout ventricular activation from these unipolar ECGs with the use of a microcomputer system.
All patients underwent an electrophysiologic study (EPS) at cardiac catheterization. We analyzed the potential distribution during ventricular depolarization and compared the results between EPS and BSPM findings.
The following results were obtained: (1) seven types of BSPM pattern were identified in accordance with the sites of the AV AP confirmed by EPS; (2) the location of the potential minimum of ventricular depolarization and the direction of the excitation wavefront during early ventricular depolarization, the reversal pattern of ventricular potential distribution, the epicardial right ventricular breakthrough and the dynamic change of ventricular potential distribution were useful for the detection of the ventricular pre-excitation site; (3) epicardial right ventricular breakthrough occurred in nearly all patients with left ventricular free wall accessory AV connections; (4) the abnormal early reversal pattern of ventricular potential distribution did not occur in patients with left ventricular AV connections but did appear in most patients with right ventricular free wall AV connections. Accordingly, BSPM is a reliable noninvasive procedure to determine the ventricular pre-excitation sites of patients with W-P-W syndrome.

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Electrophysiologic effects of intravenous E-4031 and MS-551, novel class III antiarrhythmic agents, were evaluated in 5 and 6 patients with ventricular tachyarrhythmia, respectively. Six patients had sustained ventricular tachycardia (VT) and 5 had ventricular fibrillation (VF).
Electrophysiologic study was performed before and after administration of E-4031 and MS-551 [E-4031; loading infusion 9μg/kg for 5min+0.15μg/kg/min, MS-551; loading infusion 0.3mg/kg for 5min+0.01mg/kg/min].
The QT intervals were significantly prolonged after administration of E-4031 and MS-551 from 409±37 to 455±49 msec (11%), and from 359±52 to 411±63 msec (14%), respectively. The QTc intervals were significantly prolonged from 457±17 to 494±24 msec (8%), and from 410±36 to 452±47 (10%), respectively. There were no significant differences in the QT and QTc intervals between these two agents.
The right ventricular effective refractory period (VERP) with E-4031 was prolonged at 600 (from 244±27 to 270±31 msec, 11±2%), 400 (from 222±23 to 242±24 msec, 9±3%), and 300 msec (from 206±19 to 218±25 msec, 6±4%), and those with MS-551 were prolonged at 600 (from 240±23 to 268±23 msec, 12±2%), 400 (from 225±22 to 250±24 msec, 11±4%), and 300 msec (from 213±14 to 228±18 msec, 7±4%). Both E-4031 and MS-551 prolonged VERP in a "reverse" use-dependent manner without changing the conduction velocity.
E-4031 prevented the induction of VT in one patient. MS-551 prevented the induction of VT and VF in one patient each. Further evaluation of these selective class III agents may be needed to determine if higher doses are required to achieve the pharmacological effects in patients with ventricular tachyarrhythmias.

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We report on four elderly women in whom carbamazepine was suspected of inducing sinus node dysfunction (3 patients) and atrioventricular block (1 patient). Patients were treated with carbamazepine, 200 to 600mg a day, for trigeminal neuralgia (n=3) or epilepsy (n=1). After 1 to 16 months of carbamazepine therapy, these patients were admitted to our emergency room because of bradyarrhythmia. Their conduction disturbances on electrocardiographic monitoring disappeared immediately after the cessation of carbamazepine intake. Provocation tests were performed on three patients. Because of renal insufficiency, one patient could not undergo the provocation test. Her carbamazepine clearance was markedly decreased. Carbamazepine induced sinus arrest in two patients within 48 hours after intake, but did not induce atrioventricular block in the remaining patient. In two patients, computer simulation of carbamazepine pharmacokinetics was performed and disclosed a clear-cut relationship between the plasma concentration of carbamazepine and the frequency of sinus arrest. During the test, the maximum plasma carbamazepine concentration in these two patients did not exceed the therapeutic range. However, it did exceed the range in the one with a negative test. Our results suggest that careful monitoring of ECG and plasma drug concentration is required with carbamazepine therapy, especially in elderly women.

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Facial immersion testing in cold water (<4deg:C) was performed to study the responses of sinus cycle length to increased parasympathetic tone before and 5min after exercise testing in 27 children. There were no episodes of sinus arrest or extrasystole during the facial immersion testing. The resting sinus cycle lengths were significantly shorter after (539±68msec) than before (597±96msec) exercise testing (p<0.001).
The maximal sinus cycle lengths before and after exercise testing during cold water facial immersion testing did not differ significantly (928±167msec and 909±128msec, respectively). Vagal chronotropic responses were calculated from the control sinus cycle lengths and the maximal sinus cycle lengths during facial immersion testing. Facial immersion caused greater prolongation of sinus cyclc length after than before exercisc(73±27% and 54±26%, respectively; p<0.005). We speculate that this augmentation of vagal activity represents accentuated antagonism in these children, i. e., the same parasympathetic stimulus causes a greater response in the presence of a stronger background sympathetic activity.

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We devised a pulsed Doppler echocardiographic method of separately calculating early diastolic filling volume (EDFV) and late diastolic filling volume during atrial contraction (LDFV) and observed a relationship between diastolic filling volume and velocity in thirty patients with coronary artery disease. By analysing the transmitral flow velocity curve and mitral valve motion, EDFV and LDFV were measured on the basis of the equality of left ventricular inflow and outflow volumes. The Doppler-determined EDFV and LDFV correlated well with those obtained from the left ventricular filling curve produced by left ventriculography. Angiographic EDFV and LDFV were measured from the time (t)-volume (V) curve, using the t-dV/dt curve to define early and late diastolic phases. A good correlation was found between Doppler and angiographic EDFV (y=-3.0+1.0 x, r=0.98, p=0.0001, n=20), Doppler and angiographic LDFV (y=1.6+1.0 x, r=0.86, p=0.0001), and also between Doppler and angiographic EDFV/LDFV (y=0.05+0.9 x, r=0.93, p=0.0001). EDFV and the peak early diastolic filling velocity were significantly correlated (E velocity; y=25+0.51 x, r=0.48, p=0.0068), while LDFV and the peak late diastolic filling velocity during atrial contraction (A velocity) were not. Our results validate the method of calculating EDFV and LDFV separately and suggest that early diastole in the left ventricle has flow volume dependency, but that the late diastole filling velocity during atrial contraction may be regulated by other factors such as increased left atrial contraction.

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Previous evidence has shown that vagal nerve activity modulates ventricular arrhythmias in patients and in animal models. However, the effects of direct vagus nerve stimulation on ventricular tachyarrhythmias brought by direct sympathetic nerve stimulation have not been elucidated. In the present study, the effects of electrical stimulation of the left cervical vagus nerve on ventricular tachycardia (VT) which was induced by electrical stimulation of the left ansae subclaviae (LAS) in rabbits were assessed. Monophasic action potentials (MAPs) of the left ventricular endocardium were recorded simultaneously with surface ECG. In 27 rabbits tested, the stimulation of LAS induced VT in 19 rabbits. Polymorphic VT (PVT) was induced in 14 rabbits (PVT group), whereas monomorphic VT (MVT) was induced in 5 rabbits (MVT group). Vagus nerve stimulation during the sympathetically-induced PVT led to a restoration of sinus rhythm in 10 of 14 rabbits, while that during the sympathetically-induced MVT did not restore sinus rhythm in any of the 5 rabbits. Vagus nerve stimulation during the stimulation of LAS, which was of subthreshold intensity for the induction in VT, did not result in an induction of PVT in any of the 14 rabbits in the PVT group, while it induced slow MVT in 3 of 5 rabbits in the MVT group. These results indicate that vagus nerve stimulation preferentially exerts protective antiarrhythmic effects against PVT induced by sympathetic neural stimulation in this model, while it occasionally induces slow MVT under conditions in which sympathetic nerve activity is potentially elevated.

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Since the mechanism of creatine kinase (CK) leakage induced by β-adrenoceptor activation remains unclear, we studied the effects of incremental application (10^-9 to 10⁴M) of isoproterenol (ISP) on the CK efflux from Langendorff-perfused isolated rat hearts under aerobic conditions. Tissue water content was estimated after the perfusion experiment. ISP-induced dose-dependent CK leakage was noted in a sigmoidal fashion, which showed low temperature-dependency (Q₁₀ of 2.41), sensitivity to cepharantine (10^-6M) and propranolol (10^-7 to 10^-6M) without any signs of demand ischemia or oxidant stress. CK liberation was not replicated at all by maneuvers activating cAMP-dependent protein kinase (A-kinase). Myocardial edema noted in the control ISP application was ameliorated by exposure to 10^-6M propranolol or cepharantine (i. e., significant fall in tissue water content; p<0.05). Histological study revealed nonspecific myocardial fiber swelling and separation without any myocyte necrosis for all the perfusion groups. These results suggest that ISP-induced CK leakage in this model is not mediated by β-adrenoceptor stimulation, subsequent A-kinase activation or related demand ischemia, but is attributed most to the direct effects of ISP augmenting sarcolemmal CK and water permeability.

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