The usefulness of normalization of negative T waves in exercise ECG was investigated as an index of myocardial viability in patients with previous myocardial infarction with no symptoms or ischemic ST-segment change during exercise test. A total of 39 patients, 20 with T-wave normalization (POS group) and 19 without T-wave normalization (NEG group) on exercise ECG, were studied. Myocardial viability was evaluated by thallium-201 single-photon emission computed tomography (SPECT) during exercise or at rest. We also assessed left ventricular ejection fraction (LVEF) by contrast ventriculography before (n=39) and after percutaneous transluminal coronary angioplasty (PTCA) (n=17). SPECT detected myocardial viability in 16 (80%) of the 20 patients in the POS group and in 4 (21%) of the 19 patients in the NEG group (p<0.01). LVEF increased after successful PTCA in the POS group (from 53±13% to 63±8%, p<0.025), but fell in the NEG group (from 57±10% to 51±8%). It is concluded that normalization of negative T waves on exercise ECG is a useful, simple index of myocardial viability in patients with previous myocardial infarction with no symptoms or ischemic ST-segment change during exercise testing. (Jpn Circ J 1998; 62: 153 - 159)

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To evaluate the clinical significance of reversible perfusion defects that were observed soon after the successful deployment of a coronary stent, 47 patients underwent thallium-201 myocardial scintigraphy and radionuclide angiography in conjunction with adenosine-induced coronary hyperemia before and after complete revascularization. Coronary angiography showed a significant decrease in the percent diameter stenosis (from 87±11% before stenting to -1±5% after stenting, p<0.01) with no major dissection, residual stenosis, or intra-stent formation of thrombus. Even after the angiographically successful procedure, reversible perfusion defects were present in 17 (36%) of the 47 patients, none of whom showed any wall motion abnormalities during the infusion of adenosine. Disease duration was significantly longer and collateral vessels were more common in the patients with than in those without thallium redistribution, whereas the other clinical, pre- and post-stent angiographic and hemodynamic factors were similar. In conclusion, reversible perfusion defects without wall motion abnormalities were demonstrated during the infusion of adenosine in approximately one-third of patients soon after coronary stenting, and were not consistently related to acute unfavorable outcomes of stent placement. (Jpn Circ J 1998; 62: 160 - 166)

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Reversible thallium-201 (²⁰¹Tl) abnormalities during exercise stress have been used as markers of myocardial ischemia in hypertrophic cardiomyopathy (HCM) and are most likely to identify relatively underperfused myocardium. Although metabolic abnormalities in HCM were reported, the relationship between impaired energy metabolism and exercise-induced ischemia has not been fully elucidated as yet. To assess the relationship between myocardial perfusion abnormalities and fatty acid metabolic abnormalities, 28 patients with HCM underwent exercise ²⁰¹Tl and rest ¹²³I-15-(p-iodophenyl)-3-methyl pentadecanoic acid (BMIPP) scintigraphy. Perfusion abnormalities were observed by exercise ²⁰¹Tl in 19/28 patients with HCM. ¹²³IBMIPP uptake was decreased compared with delayed ²⁰¹Tl in 106/364 (29%) of the total myocardial segments (p<0.01, McNemar symmetry test). Such disparity between ¹²³I-BMIPP and ²⁰¹Tl was observed more often in the 49/75 (65%) segments with reversible exercise ²⁰¹Tl defects (p<0.001). Our results indicate that exercise-induced myocardial ischemia exists in HCM, resulting in metabolic abnormalities. The combination of 123I BMIPP and ²⁰¹Tl suggests that myocardial ischemia may play an important role in metabolic abnormalities in HCM. (Jpn Circ J 1998; 62: 167 - 172)

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Mental stress is an important factor affecting cardiac function. We evaluated the effect of a mental calculation stress (MS) test on hemodynamics and left ventricular (LV) diastolic function in patients with ischemic heart disease, and compared the hemodynamic responses with a treadmill exercise test. Fifteen patients were studied. Seven had old myocardial infarction with significant coronary artery stenosis (group I) and 8 had chest pain syndrome with non-significant coronary artery stenosis (group II) . The MS test was performed as follows: after memorizing 6 random numeral digits, patients repeated these numbers in reverse order for 5 min followed by serial subtraction of 1000 minus 17 for 5 min. Blood pressure (BP) and heart rate (HR) were measured every 1-5 min. Doppler mitral flow velocity (MFV) was recorded every 2-5 min. During the MS test, BP, HR, and rate pressure product increased by 38.3%, 17.3%, and 62.1% on average, respectively. Early diastolic MFV decreased by 10.0% in group I and 3.3% in group II. First third filling rate of MFV decreased by 32.3% in group I and 22.8% in group II. A/E ratio increased by 39.3% in group I and 25.8% in group II. These data indicate that the MS test led to a deterioration in LV diastolic function. The MS test induced LV diastolic dysfunction to a greater extent in patients with significant coronary artery stenosis than in those without significant coronary stenosis. Myocardial ischemia may be induced by increased left ventricular afterload and/or vasoconstrictive reflex of coronary microcirculation. (Jpn Circ J 1998; 62: 173 - 177)

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Thallium-201 (²⁰¹Tl) late reinjection after stress-redistribution imaging improves the detection of viable myocardium. Recently, early reinjection of ²⁰¹Tl immediately after stress imaging was proposed as a new method for distinguishing ischemic myocardium, hibernating myocardium, and myocardial scar. However, there are no data on the influence of the timing of reinjection on "fill-in." This study was designed to assess whether the reinjection time influences "fill-in" in chronic coronary artery disease. Thirty-three patients with chronic coronary artery disease were studied. All patients underwent exercise ²⁰¹Tl tomography. Immediately after stress imaging, 37 MBq of thallium was reinjected earlier than usual and early reinjection delayed image (ERDI) was acquired 3 h later. With the same protocol, all patients also underwent a second study involving late reinjection of ²⁰¹Tl within 1 week. An additional 37 MBq of thallium was reinjected 3 h after stress imaging, and late reinjection delayed image (LRDI) was obtained 10 min later. All images were analyzed qualitatively using a 4-point grading uptake score. Of the 72 hypoperfused segments on stress images, 66 segments showed fill-in and 6 showed persistent defects on ERDI, and of the same 72 segments 55 segments displayed fill-in and the remaining 17 showed persistent defects on LRDI (p<0.05). The delta uptake score (the uptake score of the delayed image minus that of stress image) in early reinjection was 1.60±0.80, which was significantly higher than that in late reinjection (1.24 ±0.94, p<0.01). A small dose of thallium reinjected immediately after stress imaging with delayed images obtained 3 h later is convenient and might provide another technique for determining myocardial viability. (Jpn Circ J 1998; 62: 178 - 182)

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This study was designed to assess the cardioprotective effect of intravenous nicorandil, a potassium channel opener, in preventing reperfusion injury in acute myocardial infarction. Seventy patients were treated with placebo or nicorandil concomitant with reperfusion therapy in a prospective, randomized, double-blind fashion within 6 h after the onset of acute myocardial infarction. Nicorandil was administered before reperfusion as a 2-mg boIus iv injection followed by continuous infusion of 2-6 mg/h for the next 3 h. Thirty-six patients (17 in the placebo group, 19 in the nicorandil group) who demonstrated both complete occlusion of an infarct-related vessel before treatment and successful reperfusion were included in the final analysis. No significant changes in left ventricular ejection fraction were observed between the immediate and chronic phases in each group. In the analysis of regional ventricular function, the placebo group did not show any significant change in regional chord shortening (26.8±8.2 vs 24.3±7.3%, NS) or hypocontractile perimeter (36.4±28.2% vs 28.3±24.8%, NS) between immediate and chronic phase left ventriculograms. In contrast, in the nicorandil group, a significant increase in regional chord shortening (21.5±11.0% vs 25.8±11.3%, p<0.05) and a significant decrease in hypocontractile perimeter (33.3±19.6% vs 25.6 ±24.3%, p<0.05) were observed in the chronic phase left ventriculogram. Thus, nicorandil may be a useful adjunctive therapy for preserving myocardial contractile function in patients with acute myocardial infarction undergoing reperfusion therapy. (Jpn Circ J 1998; 62: 183 - 189)

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To investigate whether circadian or any other temporal pattern(s) exist in the occurrence of acute myocardial infarction (AMI) in a Chinese population, we analyzed 428 patients with confirmed AMI for temporal patterns of AMI occurrence. The patients admitted to the Affiliated Hospital of Shandong Medical University during 1991-95 were from Jinan, the capital city of Shandong Province of China, which has a population of 2.5 million. The chi-square test for goodness of fit was used to test the difference among the frequencies of AMI occurrence in 4 equal intervals (O1.00-07.00 h, 07.00-13.00 h, 13.00-19.00 h, 19.00-01.00 h) during the day and among those on 7 days during the week. The results showed that AMI occurrence exhibited significant circadian (p<0.001) and septadian (day of the week) (p=0.046) periodicity, with a peak at O1.00-07.00 h and a trough at 13.00-19.00 h during the day, and a peak on Saturday and a trough on Wednesday during the week. The peak to trough ratio of risk was 2.7 during the day and 2.1 during the week. It is concluded that there were circadian and septadian biorhythms in AMI occurrence in the Chinese population and that these were different from those observed in Western populations. Further investigation of the underlying mechanisms may shed further light on the trigger mechanisms of AMI and thus be helpful in the prevention and treatment of AMI. (Jpn Circ J 1998; 62: 190 - 192)

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Plasma thromboxane B₂ (TXB₂)-a Stable metabolite of thromboxane A₂ (TXA₂)-conventional hemodynamic parameters, mean pulmonary input energy (input energy), and mean pulmonary output energy (output energy) were measured to assess platelet activation in 21 patients with pulmonary hypertension and a ventricular septal defect (VSD). The patients were divided into 2 groups: group A (normal range) and group B (high level). TXB₂ levels were measured by radioimmunoassay. There was no relationship between plasma TXB₂ concentrations and conventional hemodynamic parameters except the pulmonary-to-systemic pressure ratio. Output-to-input energy ratio was correlated logarithmically with the plasma TXB₂ concentration. We concluded that patients with output/input energy ratio >0.15 had a high TXB₂ concentration and activated platelets in pulmonary capillaries. (Jpn Circ J 1998; 62: 193 - 197)

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The purpose of this study was to apply virtual reality technology to spiral computed tomographic (CT) angiogram images in a rabbit model of atherosclerosis and to correlate the images with histopathologic evaluation of the aorta. Image data were transferred to the virtual endoscope system in a graphics workstation. "Virtualized angioscopy" includes an interactive graphic user interface, which controls the viewpoint, the direction of the observation, and rendering and navigation functions. The virtual angioscopy system demonstrated irregularities of the luminal surface of the ascending aorta and a smooth luminal surface in the descending aorta. These observations were correlated with histopathologic findings. The results of this study indicate that the potential and real benefits of virtualized angioscopy far outweigh several technical limitations. (Jpn Circ J 1998; 62: 198 - 200)

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The purpose of this study was to develop an animal model of atrial flutter (AFL) or fibrillation (AFB) and to determine precisely the pathway of atrial activation during arrhythmias induced by programmed stimulation. In 10 dogs, a shunt from the left subclavian artery to the left upper pulmonary vein was created to produce left atrial enlargement. Five months later, using programmed electrical stimulation, it was possible to induce 17 sustained atrial tachycardias in 9 of the 10 dogs, including 9 episodes of AFL caused by circus movement re-entry, 6 episodes of focal tachycardia, and 2 episodes of AFB. Short cycle length left atrial tachycardias caused by either circus movement or a focus did not propagate in a uniform 1:1 pattern to the right atrium (RA), resulting in RA dissociation. In these arrhythmias, complex wavefronts from both current and preceding left atrial cycles coexisted in the RA. Circus movement was associated with a spectrum of different re-entrant pathways with different path lengths. These differences in the path length were determined by various ways in which obstacles such as the superior vena cava and orifice of the right atrial appendage or pulmonary vein orifices were combined by contiguous areas of functional block. (Jpn Circ J 1998; 62: 201-210)

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Giant cell myocarditis (GCM) is a rapidly progressive disease that leads to ventricular tachycardia or highgrade atrioventricular (A-V) block, frequently requiring a pacemaker. A 64-year-old woman developed syncope as a result of idiopathic GCM with A-V block. She required both a temporary and a permanent pacemaker. Two-dimensional echocardiography showed severely reduced wall motion. There was no histologic or clinical evidence to suggest sarcoidosis. Despite treatment with diuretics and an angiotensinconverting enzyme inhibitor, exertional dyspnea persisted. She received prednisolone 4 months after the onset of complete A-V block in the late phase of GCM. Prednisolone improved A-V nodal conduction in spite of the fact that there was no influence from LV wall motion, and sinus rhythm has continued for more than 2 years. In this patient, prednisolone was effective in the treatment of GCM. (Jpn Circ J 1998; 62: 211 - 214)

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A case report of a 15-year-old girl who experienced syncope and torsades de pointes is presented. The girl had a normal QT interval (QTc=0.37 sec) on the resting electrocardiogram (ECG), Infusion of isoproterenol induced QT prolongation (QTc=0.62 sec) and frequent occurrence of multiform ventricular premature beats, Her Holter ECG showed a prolongation of the QTc interval with a shortening of the RR interval. Low-frequency power (LF) and high-frequency power (HF) of heart rate variability were evaluated from the Holter ECG. The patient showed a statistically significant negative QTc/HF and a significant positive QTc/(LF/HF) relationship, whereas none of the age- and sex-matched healthy subjects showed these relationships. The slope of the QT/RR relationship for the patient was below the lower limit of the normal range. This report describes the unusual relationship of QT interval to RR interval and heart rate variability in a long QT syndrome patient with a normal QT interval on resting ECG. (Jpn Circ J 1998; 62: 215 - 218)

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Selective right coronary angiography in a 22-year-old woman demonstrated an enormous right coronary artery, with the contrast medium opacifying to the left coronary artery through a well-developed collateral circulation and draining into the pulmonary artery. The diagnosis of anomalous origin of the left coronary artery from the pulmonary trunk [also known as Bland-White-Garland (BWG) syndrome] was thus established. Magnetic resonance imaging (MRI) showed a dilated right coronary artery arising from the aorta, the left coronary artery from the pulmonary trunk but not from the aorta, and well-developed channels in the interventricular septum. MRI could be a useful tool for diagnosing anomalous origin of the left coronary artery from the pulmonary trunk. (Jpn Circ J 1998; 62: 219 - 221)

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Hypertrophic cardiomyopathy (HCM) is a rare cardiac complication in patients with Klinefelter syndrome. We report the case of a 67-year-old Japanese man with Klinefelter syndrome, HCM, sick sinus syndrome, and coronary arteriovenous fistula, in whom the 47XXY/46XY mosaic pattern was revealed by chromosomal study. Echocardiography revealed HCM with an interventricular septum thickness of 17 mm and a left ventricular posterior wall thickness of 10 mm. Sick sinus syndrome type III was diagnosed by paroxysmal atrial fibrillation (longest sinus arrest 9.0 sec) on 24-h Holter ECG recording. Coronary arteriovenous fistula was detected from the left anterior descending artery to the right ventricle by coronary arteriography. To our knowledge, this is the first case report of Klinefelter syndrome with HCM. As there have been a few reports of patients with Klinefelter syndrome in association with skeletal muscular diseases such as Becker-type muscular dystrophy or myotonic dystrophy, the gene mutation that causes Klinefelter syndrome may occur in the cardiac muscle. HCM may represent another variable expression of this chromosomal abnormality. (Jpn Circ J 1998; 62: 222 - 224)

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Astemizole (Hismanal^®), an antihistamine agent, has been reported to be associated with ventricular arrhythmias. In this paper we present a case of QT prolongation and torsades de pointes (TdP) in a 77-year-old woman who had been taking astemizole (10 mg/day) for 6 months because of allergic skin disease. At the time of admission, the serum concentration of astemizole and its metabolites was markedly elevated at 15.85 ng/ml, approximately 3 times the normal level. The patient was also taking cimetidine, a known inhibitor of cytochrome P-450 enzymatic activity, and during her admission was diagnosed as having vasospastic angina. To the best of our knowledge, this is the first report of astemizole-induced QT prolongation and TdP in Japan. (Jpn Circ J 1998; 62: 225 - 227)

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We present the case of a 39-year-old woman with aortic regurgitation that may have been induced by primary antiphospholipid syndrome. The patient had suffered recurrent miscarriages, thrombocytopenia, and deep-vein thrombosis for the previous 16 years, and had been diagnosed as having primary antiphospholipid syndrome 9 years previously because of a high titer of anticardiolipin antibody. She had been receiving medication for moderate hypertension for 7 years. The patient was admitted to Tenri Hospital because of heart failure, which was thought to be caused by moderate aortic regurgitation, moderate hypertension, and mild chronic renal failure. Echocardiography revealed thickened aortic and mitral valves. Primary antiphospholipid syndrome might have induced valve regurgitation as a result of valvular thickening. (Jpn Circ J 1998; 62: 228 - 230)

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