Heart rate variability (HRV) reflects the autonomic tone of the heart, and QT dispersion reflects the regional inhomogeneity of ventricular repolarization. The purpose of the present study was to determine the effects of early exercise training on HRV and QT dispersion in patients with acute myocardial infarction (AMI). Forty patients (mean age: 59 years) with AMI were randomized to training rehabilitation (group Tr, n=20) or conventional rehabilitation (group C, n=20). Two weeks after AMI, group Tr underwent 10 min of exercise using a bicycle ergometer (80% of anaerobic threshold) twice a day. At the end of the second and fourth weeks, 12-lead and 24-h Holter ECGs were recorded. QT intervals were measured and corrected using Bazett's formula (QTc), and QTc dispersion (QTcd) was defined as the difference between maximum and minimum QTc. HRV was accessed by the high-frequency component (HF: 0.15-0.40 Hz) of the HRV power spectrum (parasympathetic activity) and the ratio of low frequency (0.04-0.15 Hz) to HF (L/H ratio: sympathetic activity). In group Tr, HF increased (82.5 to 131.1 ms²), the L/H ratio decreased (3.9 to 2.6), and QTcd decreased (77.2 to 57.2 ms). In group C, none of the indices changed. It was concluded that early exercise training improves sympathovagal balance and decreases QTcd, and may reduce the arrhythmogenic substrate following AMI. (Jpn Circ J 1999; 63: 577 - 582)

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The present study examined whether or not hepatocyte growth factor (HGF), an endothelium-specific growth factor that stimulates regeneration of the endothelium, is increased or has a prognostic significance in patients with acute coronary syndromes. HGF was measured in 106 patients with coronary artery disease (20 stable effort angina, 12 unstable angina without adverse events, 24 unstable angina with adverse events and 50 acute myocardial infarction) on admission and 21 normal volunteers. The measurements in all patients were recorded before administration of heparin, and in acute myocardial infarction patients they were recorded from days 2 to 6 after heparin discontinuation on day 1. HGF levels (ng/ml) were 0.30±0.06 for the controls, 0.31±0.08 for stable effort angina patients, 0.31±0.08 for unstable angina patients without adverse events, 0.40±0.20 for unstable angina patients with adverse events and in acute myocardial infarction patients they were 0.45±0.18 on day 0, 0.57±0.45 on day 2, 0.50±0.35 on day 3, 0.48±0.32 on day 4, 0.44±0.20 on day 5, and 0.38±0.14 on day 6. HGF plays a crucial role in the restoration of injured endothelial cells and is a predictor of adverse events in patients with acute coronary syndromes. (Jpn Circ J 1999; 63: 583 -588)

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Attention has been paid to the relationship between insulin resistance and coronary artery disease. The present study investigated the relationship between insulin resistance and the endothelial vasomotor function of the coronary artery of nondiabetic patients with chest pain and a positive exercise tolerance test. Twenty-five nondiabetic patients with chest pain were included. Patients with a steady state plasma glucose (SSPG) level of greater than or equal to 135 mg/dl were placed in the insulin resistant (IR) group, and those with a SSPG level less than 135 mg/dl were placed in the noninsulin resistant (NIR) group. The effect of acetylcholine, papaverine, and isosorbide dinitrate on the vasomotor response of the coronary endothelium was studied. The percent change in diameter of the coronary artery after injection of acetylcholine (20 μg ml^-1 min^-1) was 84±17% in the IR group, and 109±18% in the NIR group. The difference in the degree of the vasodilative response is statistically significant (p<0.01). The percent change in coronary flow velocity after injection of acetylcholine (20 μg ml^-1 min ^-1) in the IR group was 120±67%, whereas that in the NIR group was 256±58%; the increase in coronary artery flow velocity of the IR group was significantly smaller than that of the NIR group (p<0.01). Nondiabetic patients with insulin resistance have endothelial vasomotor dysfunction, which raises an important question as to whether nondiabetic patients with insulin resistance should be treated to prevent the development of coronary heart disease. (Jpn Circ J 1999; 63: 589 - 592)

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The present study measured the minimal diameter of the ductus (minimal D), the stretched minimal diameter (stretched D), and the stretch index (SI) before coil occlusion in 25 patients with a patent arterial duct. The following factors were compared in the success group (22 cases, coil successfully placed after initial deployment) versus the failure group (3 cases): minimal D, stretched D, SI, the sum of the loop diameter of coils (the loop diameter), the sum of the product of the loop diameter and the number of loops (the loop diameter and number), the loop diameter/minimal D, the loop diameter/stretched D, the loop diameter and number/minimal D, and the loop diameter and number/stretched D. In the failure group, minimal D, stretched D, SI, the loop diameter, and the loop diameter and number were larger than in the success group. The loop diameter/stretched D, and the loop diameter and number/stretched D were smaller in the failure group. Although the loop diameter and number/minimal D was slightly smaller in the failure group, the loop diameter/minimal D was comparable. It is concluded that the stretched D is more reliable than minimal D to determine the appropriate size of coil for successful initial deployment. (Jpn Circ J 1999; 63: 593 - 596)

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Long-term follow-up after percutaneous transvenous mitral commissurotomy (PTMC) is limited. Ninety-four middle-aged (51±9 years) mitral stenosis patients who underwent successful PTMC were followed up with annual echocardigraphy for 6.1±1.4 years. PTMC success was defined as either mitral valve area (MVA) >1.5 cm² or a MVA of more than twice the pre-procedural value, together with no worsening of mitral regurgitation >grade 2+. Mitral valve replacement (MVR), worsening of congestive heart failure (CHF), and thromboembolism were sought for survival analysis. Restenosis was defined as loss of more than 50% of the initial procedural MVA gain. Functional limit of daily activities was assessed through a questionnaire. The study population was divided into group 1 (post-procedural MVA >2.0 cm²), group 2 (MVA >1.5 cm² and ≤2.0 cm ²) and group 3 (MVA ≤1.5 cm²). The 6-year survival with freedom from MVR, CHF, thromboembolism, and combined events (MVR + CHF) was 92%, 95%, 91%, and 88%, respectively. No group 1 patient experienced MVR or CHF. Restenosis was predominant in group 3. Deterioration of daily activities during follow-up was not observed in group 1; however, it was significant in group 2 (p<0.05) and group 3 (p<0.001). These results demonstrated that patients who attained a large MVA (>2.0 cm²) immediately after PTMC maintained their procedural benefit with less clinical complication and with less limitation of daily activity. (Jpn Circ J 1999; 63: 597 - 604)

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The effects of phosphodiesterase III (PDE III) inhibitors administered after aortic declamping during cardiopulmonary bypass (CPB) for open heart surgery were investigated. Ten patients (group M) were administered milrinone (50 μg/kg) after aortic declamping during CPB, 10 patients were administered amrinone (1 mg/kg) at the same time during their surgery (group A), and 10 patients served as controls with no drug administered (group C). Soon after bolus infusion of the PDE III inhibitor, perfusion pressure dropped significantly in groups M and A. However, after release of CPB and at the end of surgery, there was no difference in aortic pressure between the 3 groups. There were also no differences between the groups in heart rate, pulmonary artery pressure, and pulmonary capillary wedge pressure. After weaning from CPB, the cardiac index was high and systemic vascular resistance index was low in groups M and A. There were no significant differences in the need for additional catecholamines and time for rewarming between groups. No adverse reactions were observed. A single administration of a PDE III inhibitor during CPB was useful for post-CPB management of patients undergoing open heart surgery. Amrinone reduced perfusion pressures more than milrinone, but cardiac indices and aortic pressures after weaning from CPB showed no differences between group M and group A patients. (Jpn Circ J 1999; 63: 605 - 609)

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The present study investigated whether regional ventricular dyskinesia (ie, systolic bulging) is a direct cause of ST-segment elevation in canine hearts in vivo. Regional ventricular dyskinesia was induced in 33 anesthetized open-chest dogs by injection of negative inotropic agents into the left anterior descending coronary artery (LAD) without disruption of coronary blood flow. Regional myocardial contraction was assessed in terms of the percent systolic shortening (%SS) and percent systolic bulging (%bulging), which were measured using ultrasonic crystals. The ST-segment elevation of the LAD-perfused area was measured with a unipolar electrode. Lidocaine, a sodium channel blocker, nicorandil, a potassium channel opener, propranolol, a beta-adrenergic blocker, or verapamil, a calcium channel blocker, was administered by intracoronary injection during maximal vasodilation induced by adenosine. All drugs induced dose-dependent ST-segment elevation in association with a parallel reduction in %SS and a parallel increase in %bulging. The absence of myocardial ischemia was confirmed by the absence of NADH fluorescence. It was concluded that regional ventricular dyskinesia had an important role in ST-segment elevation not associated with myocardial ischemia. (Jpn Circ J 1999; 63: 610 - 616)

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The plasma level of endothelin-1 (ET-1) increases in several cardiovascular disorders. The present study examined whether threshold doses of ET-1 affect vascular tone and autoregulatory vasodilation during a reduction in perfusion pressure in the coronary microcirculation in vivo. In anesthetized open-chest dogs, arterial microvessels in the epimyocardium were observed through a microscope equipped with a floating objective. In 6 dogs, ET-1 (10^-13 to 10^-8 mol/L) was superfused onto the epimyocardium in a cumulative fashion. In another set of dogs (n=16), the perfusion pressure of the observed vascular bed was reduced to 60 mmHg (mild stenosis) and to 40 mmHg (severe stenosis) by a hydraulic occluder, and the microvascular responses were observed in the presence (n=9) or absence (n=7) of ET-1 (10^-12 or 10^-11 mol/L). ET-1 ≥10^-11 mol/L constricted coronary arterioles (≤100 μm in diameter) and small arteries (>100 μm in diameter) in a dose-dependent fashion. ET-1 of 10^-12 mol/L affected neither the basal diameters nor the dilation of vessels during the pressure reduction. ET-1 of 10^-11 mol/L decreased the diameters of arterioles and small arteries before and during the mild and severe stenosis. However, ET-1 did not attenuate the percentage dilation of arterioles from the baseline in response to the mild and severe stenosis. The data indicates the following: (1) ET-1 at doses ≥10 ^-11 mol/L similarly constricts coronary arterioles and small arteries; (2) ET-1 at 10^-11 mol/L, which is slightly higher than the pathophysiological plasma level, increases the basal vascular tone, but does not attenuate the autoregulatory vasodilation of the coronary microcirculation. (Jpn Circ J 1999; 63: 617 - 623)

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Regional transmural ischemia causes both ST-segment elevation and systolic elongation (bulging) of the myocardium. Mechanical stretch might alter the transmembrane potentioal via stretch-activated ion channels (SAC); however, the role of SAC on ischemic ST-segment elevation has not yet fully studied. The present study investigated the role of SAC in the genesis of ischemic ST-segment elevation in the in-vivo canine heart. In 6 anesthetized dogs, an extracorporeal conduit connected to the left anterior descending coronary artery was occluded for 5 min before and after the intracoronary infusion of gadolinium (Gd, 500 μmol/min). To eliminate the effect of ischemic preconditioning, the bypass was occluded for 5 min before the experiment. Percent systolic shortening (%SS) and percent systolic elongation (%bulging) were measured using a pair of ultrasonic dimension crystals. A unipolar epicardial ECG was monitored at the center of the ischemic area for the measurement of the ST-segment level. At the end of coronary occlusion, there was no difference in the reduction of %SS or the increase of %bulging between before and after infusion of Gd. ST-segment elevation, however, was significantly attenuated by the infusion of Gd. These data demonstrated that the activation of SAC is one cause of ischemic ST-segment elevation. (Jpn Circ J 1999; 63: 624 - 628)

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There have been several reports with respect to idiopathic ventricular tachycardias (VTs) originating from the left ventricular outflow tract (LVOT). A previous report suggested that triggered activity plays a partial role in idiopathic LVOT tachycardia from the electrophysiological as well as the electropharmacological viewpoint. However, the exact role of triggered activity in this type of VT remains unknown. In the present study the relationship of the frequency of premature ventricular contractions (PVCs) and heart rate was examined and heart rate variability (HRV) was analyzed in 2 cases of LVOT tachycardia using 24-h Holter electrocardiographic (ECG) monitoring. The relation between the PVCs frequency and heart rate showed a persistently positive correlation, indicating frequent PVCs as heart rate increased. In HRV analysis, NN₅₀ (%), a time-domain variable of parasympathetic activity, showed no change prior to ventricular arrhythmias. In frequency-domain analysis of HRV, the high frequency (HF) component tended to fall prior to repetitive PVCs and VTs. The ratio of the low frequency to high frequency (LF/HF) components increased prior to single PVCs, repetitive PVCs and VTs. Sympathetic predominance predisposes the genesis of these kinds of arrhythmias originating from the LVOT and it is suggested that triggered activity plays an important role in LVOT tachycardia, at least in its initiation. (Jpn Circ J 1999; 63: 629 - 635)

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An 83-year-old man was admitted with refractory unstable angina and severe anemia. Colonofiberscopy revealed hemorrhagic colon cancer in the transverse colon. Coronary angiography showed total occlusion of the right coronary artery (RCA), diffuse, calcified 90% stenosis of the middle portion of the left anterior descending artery (LAD); and fair collaterals from the LAD to the RCA. Coronary revascularization was considered prior to colectomy, but because of the patient's advanced age and hemorrhagic cancer, conventional coronary aorta bypass grafting (CABG) using extracorporeal circulation, as well as coronary stenting requiring antiplatelet therapy, were regarded as inadvisable. Percutaneous transluminal coronary angioplasty (PTCA) for the LAD carried the risk of suboptimal coronary stenting. Thus, the patient was first treated with PTCA for the occluded RCA, followed 7 days later by a left internal thoracic artery graft to the LAD on the beating heart without extracorporeal circulation. The patient was stable thereafter. This approach to coronary revascularization may be suitable for patients for whom anticoagulation or antiplatelet therapy are contraindicated, or when complete revascularization would be difficult with CABG or PTCA alone. (Jpn Circ J 1999; 63: 636 - 639)

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A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left venticular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations. (Jpn Circ J 1999; 63: 640 - 643)

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Myocardial infarction is very rare in young female patients with systemic vascular disorders. Moyamoya disease is a cerebrovascular disease associated with an abnormal vascular network. This report presents a 19-year-old female patient who suffered from chest pain and exertional dyspnea for 2 months prior to admission. She had a history of Moyamoya disease and pituitary gigantism since childhood. Her ejection fraction on echocardiogram was 20% and a perfusion defect with partial reversibility in the anterior wall was demonstrated on stress single photon emission computed tomography (SPECT). Diagnostic coronary angiogram revealed critical stenosis in the middle left anterior descending artery, which was treated by coronary stenting. Her subjective symptoms were relieved and the perfusion defect seen on SPECT decreased after coronary intervention. (Jpn Circ J 1999; 63: 644 - 648)

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Exercise seldom provokes tachycardia in patients with paroxysmal supraventricular tachycardia (PSVT). This report presents a case of exercise-induced uncommon atrioventricular nodal reentrant tachycardia (AVNRT) with sick sinus syndrome. Treadmill exercise testing provoked AVNRT of long RP' with good reproducibility. Uncommon AVNRT was confirmed by the lack of atrial pre-excitation during PSVT and para-Hisian pacing. The patient has been successfully treated with verapamil and DDD pacing for 5 years. (Jpn Circ J 1999; 63: 649 - 651)

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This report presents 2 patients with thrombosed dissection of the ascending aorta complicating extravasation. The first case was an 85-year-old male admitted with shock due to cardiac tamponade. Plain computed tomography (CT) demonstrated a dilated ascending aorta without clear evidence of aortic dissection. The second case was a 77-year-old female presenting with shock, in whom an enhanced CT scan demonstrated a dilated ascending aorta and periaortic effusion. However, dissection of the distal ascending aorta was not identified in either case before emergency surgery. In case 1, soon after the bloody pericardial effusion was decompressed during the operation, bleeding from the ascending aorta occurred. A small intimal tear was found in the distal ascending aorta, and in each case the pseudolumen was filled with fresh thrombus. The ascending aorta was replaced. Each patient had an uneventful postoperative recovery. Based on this experience, it is suggested that patients with thrombosed ascending aortic dissection complicating extravasation should undergo early graft replacement. (Jpn Circ J 1999; 63: 652 - 654)

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