Monomorphic sustained ventricular tachycardia (MSVT) was revisited in relation to the electrophysiologic findings and their relation to the drug efficacy. Old myocardial infarction is less common cause of MSVT in Japan, and the majority (about 2/3) of MSVT is unrelated to coronary artery disease but, the mechanism shared a common mechanism: reentry with an excitable gap as others. The reentrant mechanism was supported from the inducibility, the terminability of VT by electrical stimulation, and by the ability to entrain with rapid pacing. In MSVT associated with underlying heart diseases, diseased myocardium showed low amplitude and fragmented electrograms and the area was considered to participate as the central common pathway of reentrant circuit. The area of slow pathway showed a decremental conduction or all-or-nothing conductive property. The width of the excitable gap seemed to be determined by the maximal conductive frequency but not by the duration of action potential: effective refractory period. As to the drug efficacy, there was no baseline characteristics in predicting the efficacy. However, the significant narrowing of the width of the excitable gap was associated with the drug efficacy and VT became non-inducible after addition of the same drug. The response pattern of the excitable gap to specific drug including class III, was not predictable. Further electropharmacological studies will be warranted.

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The use of the serum troponin T (TnT) level as a means of assessing minor myocardial injury, which affects the long-term prognosis, has not been fully clarified in patients with coronary artery disease in whom a coronary stent has been implanted. We measured the TnT level to determine the incidence of myocardial damage associated with stent implantation. A total of 29 patients who underwent successful stent implantation (stenting group) were studied and compared with 45 patients who underwent successful coronary balloon angioplasty during the same period (balloon angioplasty group). The serum TnT level was measured by enzyme immunoassay 36 hours after the stenting or balloon angioplasty. The activities of serum creatine kinase (CK) and its isoenzyme MB (CK-MB) were measured by a modified Rosalski method and an immunoinhibition method, respectively, before, immediately after, and 6, 12, and 24 hours after the procedure. Elevation of the TnT level was found in 3.4% (1/29; 0.35ng/ml) of the patients in the stenting group and in 8.9% (4/45; 0.75±0.21ng/ml) of those in the balloon angioplasty group. Elevation of the CK and CK-MB activities was found in 3.4% (1/29; 163IU/l) and 0%, respectively in the stenting group, and 15.5% (7/45; 375±143IU/l) and 4.4%(2/45; 24 and 49 IU/l), respectively, in the balloon angioplasty group. TnT elevation was not invariably accompanied by CK or CK-MB elevation, or by angiographically visible side branch occlusion. For TnT, CK-MB activity and CK activity, there was no significant difference between in the incidence of elevation in the balloon angioplasty group and that in the stenting group. In summary, the incidence of myocardial damage associated with stent implantation seems to be low and comparable to that associated with balloon angioplasty. Despite the low incidence, measurement of the serum TnT level in addition to CK-MB measurement is essential in assessing minor myocardial damage.

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It has not been determined if signal-averaged electrocardiograms (SAECGs) have a diurnal variation. We recorded 3-channel 24-hour ECGs in 30 healthy volunteers and calculated the following parameters for the first 500sec of every hour over the 24-hour period: the mean heart rate, the filtered QRS duration (f-QRS), the root-mean-square voltage of the signals in the last 40msec of the QRS (RMS40), and the duration of low-amplitude signals (<40μV) in the terminal portion of the QRS (LAS40). Heart rate and RMS40 increased in the daytime compared with the nighttime; f-QRS and LAS40 increased during the nighttime hours. The f-QRS and LAS40 were negatively correlated with heart rate in all and 22 (73%) of 30 subjects, respectively, and RMS40 was positively correlated with heart rate in 21 subjects (70%). In conclusion, SAECGs exhibit a clear diurnal variation in healthy subjects, which is closely related to changes in heart rate.

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The interaction between dl-sotalol and isoproterenol on the ventricular effective refractory period (VERP) and conduction were examined in an electrophysiologic study of 9 patients at drug-free baseline, after 14 days of dlsotalol administration (320mg/day), and after the administration of isoproterenol. In all 9 patients, ventricular tachyarrhythmia could not be induced after dl-sotalol treatment. Isoproterenol was administered as a loading dosage of 0.025μg/kg for 5min with a maintenance dosage of 0.0025μg/kg/min. The VERP and the QRS duration were determined at paced cycle lengths of 600, 400 and 300msec. DL-sotalol and dl-sotalol+isoproterenol had no effect on ventricular conduction at the three cycle lengths. The VERP was significantly prolonged after dl-sotalol treatment at paced cycle lengths of 600 (241±16 to 302±28msec, p<0.001), 400 (223±21 to 280±23msec, p<0.001) and 300msec (202±16 to 256±24msec, p<0.005), but there was a parallel shift of the VERP, suggesting the absence of use-dependent effects on the VERP. The dl-sotalol-induced VERP prolongation was partially reversed by isoproterenol, but it remained significantly prolonged above baseline values at paced cycle lengths of 600 (241±16 to 281±18msec, p<0.01), 400 (223±21 to 258±20msec, p<0.01) and 300msec (202±16 to 247±22msec, p<0.01). The shortening of the VERP was greater at longer basic cycle lengths (600 and 400msec) than at the shorter paced cycle length (300msec, p<.05), but the percentage increase of the VERP was similar at the three basic cycle lengths of 600 (16%), 400 (15%) and 300 (20%)msec, indicating the lack of reverse use-dependency. The absence of reverse use-dependency of dl-sotalol on the VERP, even after isoproterenol administration, may be beneficial in the therapy of ventricular tachyarrhythmias and may account in part for the high efficacy of this drug.

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The left ventricular (LV) posterior wall in patients with asymmetric septal hypertrophy or prior anteroseptal myocardial infarction (A-MI) frequently demonstrates normal or supernormal motion to compensate for hypokinesis of the interventricular septum. This study evaluated the systolic motion velocity of the posterior wall in these conditions using a pulsed tissue Doppler imaging system. The study population consisted of 30 patients with hypertrophic cardiomyopathy (HC) and asymmetric septal hypertrophy, 25 with prior A-MI and 30 normal controls. The systolic excursion of the posterior wall was obtained by M-mode echocardiography. The endocardial motion velocities of the posterior wall were obtained by pulsed tissue Doppler imaging. The systolic excursion of the posterior wall was significantly greater in the A-MI and HC groups than in the control group, and was significantly greater in the A-MI group than in the HC group. The peak systolic velocity of the posterior wall was significantly lower in the HC group than in the control and A-MI groups, and the time from the electrocardiographic Q wave to the peak of the systolic wave of the posterior wall was significantly longer in the HC group than in the other groups. There were rough negative and positive correlations between the LV end-diastolic pressure and the peak systolic velocity and time from the Q wave to the peak of the systolic wave, respectively. In conclusion, LV myocardial contractility in HC patients was impaired when compared to A-MI patients despite similar posterior wall motion on the M-mode echocardiogram. Pulsed tissue Doppler imaging method may provide new insights and allow further evaluation of myocardial dysfunction.

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Hypertrophic obstructive cardiomyopathy (HOCM), the cause of which is unknown, is a heart disease characterized by obstruction of the left ventricular outflow tract and an increase in interventricular septum thickness. Octreotide, a synthetic analogue of somatostatin, was administered subcutaneously to 15 patients for 6 months in order to determine its efficacy in HOCM. Echocardiographic examination was performed in each patient before we had initiated treatment and after treatment. Interventricular septum thickness, interventricular septum thickness/left ventricular posterior wall thickness, and subaortic gradient decreased significantly at the end of treatment. The ratio of the mitral valve E to A waves increased significantly. We observed that octreotide treatment caused a significant decrease in interventricular septum thickness and subaortic pressure gradient. Before and after therapy left ventricular enddiastolic diameter, left ventricular endsystolic diameter, ejection fraction and fractional shortening were not changed. No adverse effect was observed during the therapy. According to our results, octreotide has some beneficial effects on HOCM and it seems to be a new therapeutic approach for HOCM.

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The delayed outward rectifier K⁺ channel has a role in the increase in automaticity of myocytes under pathophysiological conditions. The purpose of the present study was to clarify the effect of blockade of outward recitifier K⁺ channels by a class III antiarrhythmic drug, E4031, on ischemia- and reperfusion-induced arrhythmias. Ion fluxes, energy metabolites and cardiac function were measured and the epicardial electrocardiograms of Langendorffperfused rat hearts were recorded during initial perfusion, global or regional ischemia and reperfusion. 10^-7M of E4031 administered during the initial perfusion did not prolong the QT interval, but slowed the heart rate (Control: 222, E4031: 183bpm, p<0.05), increased myocardial ⁴⁵Ca²⁺ uptake (Control: 2.1, E4031: 2.9μmol/g dwt, p<0.05) and attenuated the loss of intracellular K⁺ during ischemia (Control: 238, E4031: 248μmol/g dwt, p<0.05). E4031 tended to reduce ischemia-induced ventricular tachyarrhythmias (Control: 60, E4031: 30%, n. s.), but reperfusion-induced ventricular tachyarrhythmias were sustained longer by the administration of E4031 (Control: 255, E4031: 623sec, p<0.05). Prior exposure to E4031 decreased the depletion of high energy phosphates during ischemia, but suppressed their recovery during reperfusion. These results suggest that the attenuated loss of K⁺ from the ischemic myocardium and the decrease in heart rate by E4031 contributed to the reduction of ischemia-induced arrhythmias. However, the increase in myocardial Ca²⁺ uptake and altered energy metabolism may be responsible for the increase in reperfusion-induced arrhythmias.(Jpn HeartJ 1998; 39: 183-197)

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During postnatal brain development, the function of Na⁺ channels undergoes changes. We investigated at the single channel level whether the lidocaine sensitivity of the open state of brain Na⁺ channels changed during development and the underlying kinetic differences of the lidocaine-induced open channel block between brain and muscle Na⁺ channels. The lidocaine affinity for the open channel state was found to be about 30% higher in 15 day old than in newborn channels and reflected a higher binding rate constant in 15 day old channels. When compared with reported values from adult muscle Na⁺ channels, lidocaine blocked the open state of brain channels with about ten times higher potency and reflected a lower unbinding rate constant in brain channels. These results indicate that the conformations of the channel structures defining the lidocaine accessibility to its binding site must undergo changes during brain development and that the conformations of the channel structures interacting with lidocaine must be different in brain and muscle channels.

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The type XVII collagen α1 chain has been identified as a component of the type I hemidesmosome, and is thus thought to play a role in extracellular matrix (ECM) maintenance and signal transduction between the cell and the ECM. We examined the expression of type XVII collagen α1 chain mRNA in the mouse heart by Northern blot analysis and determined the sequential changes of its expression in different developmental stages of the heart using the reverse transcriptase-polymerase chain reaction (RT-PCR) method. Northern blotting: Total RNA was extracted from 10 adult mouse hearts by the guanidine/cesium method. Hybridization was performed with mouse cDNA for α1 (XVII) collagen. RT-PCR: Total RNA was extracted from 7 embryos, 4 neonates and 8 adult mice. Reverse transcription was performed using oligo-dT primer and MMLV. Amplification was carried out in α1 (XVII) collagen and glyceraldehyde 3-phosphate dehydrogenase (GAPDH). GAPDH served as an internal control. Northern blotting revealed a 5.6kb signal that was identical to that of the α1 (XVII) of skin and transformed keratinocyte reported previously. The sequences of the PCR products were also identical to those reported. The normalized expression ratios of α1 (XVII) were 0.91±0.20 in the embryonic heart, 0.36±0.20 in the neonatal heart and 0.96±0.21 in the adult heart. In conclusion, we identified the expression of type XVII collagen α1 chain mRNA in the mouse heart, suggesting that the type I hemidesmosome is located in the heart. The results of the RT-PCR at different developmental stages of the heart suggest that type XVII collagen contributes not only to cardiogenesis in the embryonic stage but also to maintenance of architecture and function in the adult heart.

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ST-segment alternans has been described in experimental coronary artery occlusion and in patients with variant angina. It is also seen during coronary angioplasty. This report describes a patient who on balloon inflation during coronary angioplasty demonstrated ST-segment alternans only on intracoronary electrocardiogram but did not on surface 12 lead electrocardiogram. Hemodynamic pulsus alternans of the aortic pressure tracing was not observed during electrical alternans.

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Two patients with long QT syndrome, who had episodes of syncope, underwent recordings of the monophasic action potential (MAP) from the right ventricle. Intracoronary administration of acetylcholine (ACh) induced prolongation of MAP duration and caused Torsade de Pointes (Tdp) in both patients. In one patient, intravenous atropine administration did not induce any change in MAP duration. In the other patient, ACh was administered after atropine. According to the results of the present study, abnormal regulation of the muscarinic receptor-mediated K-channel may be involved in the mechanism causing prolongation of MAP duration caused by ACh administration.

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We evaluated a 68-year-old male patient with isolated levocardia without intracardiac anomaly. The patient's condition was complicated by the absence of the inferior vena cava, a lobulated spleen and sick sinus syndrome. Isolated levocardia without intracardiac anomaly is very rare and only 25 cases of this disease have been reported, to our knowledge. In general, it is accepted that cardiac rhythm disorder is frequently observed in cases of isolated levocardia and/or absence of inferior vena cava. However, there are few cases of isolated levocardia without intracardiac anomaly complicated by the absence of the inferior vena cava, a lobulated spleen and apparent sick sinus syndrome.

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We report a rare case of hemolysis after coil occlusion of a patent ductus arteriosus (PDA), which was treated by surgical removal of the coil and closure of PDA. A 65-year-old woman was admitted to our hospital with congestive heart failure due to severe aortic regurgitation associated with PDA. Before undergoing open heart surgery she underwent closure of the PDA using a Jackson coil as an adjunct of treatment to improve her hemodynamic state. However, a small residual shunt resulted in severe hemolysis. Two weeks after the intervention she underwent aortic valve replacement and PDA closure after removal of the coil through the main pulmonary artery under moderate hypothermia and temporary circulatory arrest. Hemolysis is always secondary to a residual leak and several methods have been reported to manage this complication. Our report suggests that early surgical retrieval of the coil before the organized thrombus is formed, can be safely performed even in an elderly patient whose ductus is usually fragile.

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A 49-year-old male was admitted to our hospital because of chest pain. The pain occurred simultaneously with tachycardia-dependent left bundle branch block (LBBB) during exercise-stress and atropine-stress electrocardiogram (ECG) and on 24-h ambulatory ECG monitoring. Myocardial perfusion and metabolic scintigraphy with T1-201 and I-123 BMIPP, respectively, showed no evidence of ischemia. Coronary arteriography revealed no atherosclerotic lesions, but did show a fistula between three major coronary arteries and the main pulmonary artery. The left-to-right shunt was undetectably small. Administration of diltiazem and metoprolol suppressed LBBB by attenuating the heart rate response to exercise, and reduced the chest pain. Therefore we presume that the exertional chest pain was not caused by myocardial ischemia but by the tachycardia-dependent LBBB. Coronary artery-pulmonary artery fistula is the most common type of coronary artery fistulae found incidentally in adulthood. Involvement of three major coronary branches is, however, rare. The case is discussed with a review of the literature.

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We describe a successful delivery by prophylactic cesarean section in a patient with Takayasu's disease who had a previous history of intrapartum cerebral hemorrhage during vaginal delivery. Aortography showed occlusion of the common carotid, subclavian and vertebral arteries on the left side, severe narrowing of the right subclavian artery, and moderate narrowing of the entire abdominal aorta. Blood pressure was managed by monitoring central aortic pressure at the thoracic aorta. During the peripartum course, we recommend monitoring the central aortic pressure in patients with Takayasu's disease in whom accurate blood pressure readings can not be obtained in any extremity.

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