The elevation of aortic pressure increases myocardial oxygen consumption and increases the blood supply to the myocardium. It is not obvious whether elevated systemic arterial pressure would enhance or diminish myocardial protection during acute myocardial ischemia. This report reviews previously published data on the effects of aortic pressure elevation on the coronary pressureflow relationship, and on the ischemic myocardium in the dog. The shift of the maximallydilated coronary pressureflow line to the right on the pressureflow diagram is an indication of the deterioration of the oxygen supply/demand ratio caused by aortic pressure elevation. The only maneuver recognized for protecting the ischemic myocardium is early reperfusion. In patients with de novo acute myocardial ischemia, we propose that myocardial protection can be enhanced by reduction of systemic blood pressure until coronary reperfusion therapy is initiated.

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Although nicorandil, N-(2-hydroxyethyl) nicotinamide dinitrate, is a nitrate ester, its cardiovascular action differs from that of nitrate compounds in several aspects. In this quantitative angiographic study, the acute coronary dilating effect of intracoronary nicorandil (0.25, 0.50, 1.0mg) was compared with that of isosorbide dinitrate (ISDN; 1.0mg) in 46 patients with or without ischemic heart disease (IHD). Dosedependent right coronary dilating action was observed by intracoronary administration of nicorandil without any adverse effects. The same degree of right coronary dilation was achieved by the intracoronary application of equivalent doses of ISDN. We conclude that intracoronary administration of nicorandil is beneficial for the supportive treatment of IHD during coronary artery investigation and intervention without the risk of severe systemic hypotension.

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The longterm results of medical therapy and coronary artery bypass grafting (CABG) were compared in patients with multivessel disease. All patients were confirmed to have≥75% luminal narrowing of major coronary arteries by coronary arteriogram. When multivessel disease was stratified into double and triple vessel disease, the outcomes varied. In triplevessel disease, the outcome with CABG was good, but the outcome was unfavorable in those employing medical therapy, particularly in patients with decreased left ventricular (LV) function. In patients with doublevessel disease with good LV function, the longterm results with medical therapy were just as favorable as those with CABG. However, doublevessel disease complicated by reduced LV function (ejection fraction≤40%) had a clearly less favorable outcome when treated with medical therapy than with CABG. Thus, it is important for patients with multivessel disease to undergo revascularization if indicated, to improve their prognosis. On the other hand, the incidence of cardiac events arising from vein graft occlusions tended to increase in CABG patients after 5 years or more following surgery.

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Reevaluation of repeated balloon angioplasty as a model of ischemic preconditioning and of the role of collateral circulation and highfrequency electrocardiograms in repeated inflations was carried out. There have been few studies using angioplasty as a model of ischemic preconditioning of the collateral circulation during repeated inflations or of the use of highfrequency electrocardiograms during angioplasty. Twenty patients underwent 3 repeated balloon inflations, each with a duration of more than 138 seconds. During inflation, ipsilateral and contralateral coronary angiography and signalaveraged electrocardiography were performed.
At the 1st inflation, the ST segment gradually increased as the inflation time elapsed. During the 2nd and 3rd inflations, in which ST elevation was nearly equal, the ST segment gradually increased, but it was not as prominent as that at the 1st inflation; thus, the concept that ischemia is gradually ameliorated (adaptation to ischemia) was not documented. Comparison of the maximal ST elevation and ipsilateral and contralateral circulation at each inflation revealed that the ST segment became elevated and the contralateral collateral circulation increased significantly at the 1st inflation compared with those in the control. ST elevation, however decreased significantly and collateral circulation remained unchanged at the 2nd inflation; thus, collateral circulation did not cause the ST elevation decrease. The total root mean square voltage detected by signal averaging decreased significantly only at the 1st inflation. Balloon angioplasty is not always suitable as a model of ischemic preconditioning and collateral circulation is not the cause of ischemic preconditioning.

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Reevaluation of repeated balloon angioplasty as a model of ischemic preconditioning and of the role of collateral circulation and highfrequency electrocardiograms in repeated inflations was carried out. There have been few studies using angioplasty as a model of ischemic preconditioning of the collateral circulation during repeated inflations or of the use of highfrequency electrocardiograms during angioplasty. Twenty patients underwent 3 repeated balloon inflations, each with a duration of more than 138 seconds. During inflation, ipsilateral and contralateral coronary angiography and signalaveraged electrocardiography were performed.At the 1st inflation, the ST segment gradually increased as the inflation time elapsed. During the 2nd and 3rd inflations, in which ST elevation was nearly equal, the ST segment gradually increased, but it was not as prominent as that at the 1st inflation; thus, the concept that ischemia is gradually ameliorated (adaptation to ischemia) was not documented. Comparison of the maximal ST elevation and ipsilateral and contralateral circulation at each inflation revealed that the ST segment became elevated and the contralateral collateral circulation increased significantly at the 1st inflation compared with those in the control. ST elevation, however decreased significantly and collateral circulation remained unchanged at the 2nd inflation; thus, collateral circulation did not cause the ST elevation decrease. The total root mean square voltage detected by signal averaging decreased significantly only at the 1st inflation. Balloon angioplasty is not always suitable as a model of ischemic preconditioning and collateral circulation is not the cause of ischemic preconditioning.

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We investigated the significance of notched T waves on the ECG in 30 patients with Duchenne progressive muscular dystrophy (DMD) and 50 agematched controls using noninvasive cardiovascular examinations and measurement of urinary catecholamines. Notched T waves were more frequently observed in patients with DMD than in control subjects (46.7% vs. 20.0%, p<0.05). Moreover, their frequency was ageindependent in DMD, whereas they decreased with age in controls. Patients with notched T waves showed significantly increased heart rate, prolonged QTc and augmented excretion of urinary adrenaline compared with patients without them. There were no significant differences in casual BP or incidences of characteristic UCG abnormalities, such as mitral valve prolapse, and ECG abnormalities, such as tall R waves in the right precordial leads, between DMD patients with and without notched T waves. These findings suggest that notched T waves are associated with accelerated sympathetic nervous activity rather than progressive cardiac involvement in DMD.

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Percutaneous balloon pulmonary dilatation of the right ventricular tract was performed on 16 children with tetralogy of Fallot for palliative purposes after routine cardiac catheterization. Immediate improvement in aortic saturation from 73.4±6.8 to 84.0±4.8% (mean±SD=10.6±2.7%, p<0.001) and clinical symptoms were achieved in all 16 cases. The pressures in the right ventricle, pulmonary artery, left ventricle and aorta showed no remarkable changes after percutaneous balloon dilatation. The diameters of the proximal end and at the first branching of the right and left pulmonary arteries, pulmonary arterial index and the diameter of the descending aorta at the diaphragm increased significantly after balloon dilatation (p value 0.0004-0.006). One child suffered from repeated cyanotic spells in spite of the immediate improvement of aortic saturation. She received a left side BlalockTaussig shunt 2 months after the balloon dilatation. None of the children had a significant complication. Eight had followup cardiac catheterization one year later and demonstrated much improvement in the diameters of the proximal end and at the first branching of the right and left pulmonary arteries, pulmonary arterial index and the diameter of the descending aorta at the diaphragm (p value 0.005-0.04). All 8 patients had their cardiac lesions successfully corrected. Percutaneous balloon dilatation is an alternative palliative therapy for children with tetralogy of Fallot.

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To clarify the characteristics of the first heart sound in atrial septal defect (ASD) and its pathophysiological basis, 17 patients with ASD associated with incomplete right bundle branch block (IRBBB) and 7 with isolated IRBBB were studied using phonoechocardiography and Doppler echocardiography. Fifteen of the 17 ASD patients also were studied following surgical closure of the defect. Indices were compared among the preoperative ASD, postoperative ASD, and IRBBB groups including: P-Q intervals, loudness of the mitral and tricuspid component of the first heart sound (IM, IT), enddiastolic closing excursions of the mitral and tricuspid valves (MX, TX), and mitral and tricuspid inflow velocities during early diastole and atrial contraction. There were no significant differences in the P-Q intervals among these 3 groups. IM was attenuated, and IT was accentuated in ASD compared with IRBBB. Postoperatively, IM was augmented in all but l patient and IT was attenuated in all patients. MX was significantly smaller, and TX was significantly larger in ASD than in IRBBB. Postoperatively, MX was significantly increased and TX was significantly reduced; the maximal mitral inflow velocity during atrial contraction was increased while the maximal tricuspid inflow velocity was significantly reduced. Thus, the first heart sound in ASD is characterized by an attenuated mitral component and an accentuated tricuspid component. Hemodynamic alterations and consequent changes in closing energies of the atrioventricular valves probably account for these features.

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Transient prolongation of the action potential duration was observed in canine ventricular muscle during the reoxygenation period following metabolic inhibition. We investigated the effects of verapamil, lanthanum (La³⁺), and hexamethyleneamiloride (HMA) on the recovery time course of the action potential and its rebound prolongation. The time course of the intracellular resistivity was estimated from the conduction velocity and electrograms.
The action potentials of canine left ventricular trabeculae were recorded by the conventional microelectrode technique. After a control tracing was obtained, the preparation was perfused with a hypoxic, acidic solution for 20min and then reoxygenated with regular Tyrode's solution. After reoxygenation, action potential prolongation exceeding the control value by 21.0±7.3% was observed depending on the degree of metabolic inhibition. Verapamil depressed the rebound prolongation when it was added before the start of metabolic inhibition, but not when added after reoxygenation was started. La³⁺ and HMA depressed the rebound phenomenon. Intracellular resistivity was increased during metabolic inhibition, but showed no significant changes during the period of action potential prolongation. It was concluded that the rebound action potential prolongation was related to the accumulation of intracellular Ca²⁺ during metabolic inhibition. Other ions such as Na⁺ and H⁺ may also contribute to the phenomenon by modulating outward currents.

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The effect of alloxan monohydrateinduced diabetes on the resting plasma atrial natriuretic peptide (ANP) level was investigated in 22 male New Zealand white rabbits. Alloxan monohydrate (100mg/kg) dissolved in saline at a concentration of 50mg/ml was administered by a single intravenous injection 3 months before the experimental analysis. The diabetic state was examined 72h later by quantitative determination of blood glucose levels of >350mg/dl. Beginning on day 3, 14 animals (Group 1) received a daily subcutaneous injection of 1U insulin having moderate hyperglycemia (blood glucose concentration [BGC] between 300 and 400mg/dl ). Eight animals (Group 2; normoglycemic controls) received 3.2U of insulin daily to maintain the BGC below 100mg/dl. Eight healthy rabbits were included in the study as controls (Group 3). Blood samples for ANP analysis were obtained three months after administration of alloxan monohydrate.
The plasma ANP levels in moderately diabetic rabbits (328±43pg/ml) were significantly higher than those in normoglycemic (98.5±20pg/ml) and healthy (76.6±18pg/ml) controls (p<0.001 for both). In addition, we found a significant correlation between plasma levels of glucose and levels of ANP (r=0.665, p<0.001).Our data indicate that further experiments need to be performed to investigate what is responsible for the elevation of plasma ANP levels in diabetic rabbits.

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In the present study, we investigated the change in renal hemodynamics induced by a calcium antagonist in young (6 weekold) spontaneously hypertensive rats (SHR), a saltsensitive hypertensive model. In acute experiments, SHR were fed either a 0.66% or 8.0% NaCl diet for 4 weeks. In acute experiments, manidipine, a calcium antagonist, was administered in a bolus dose of 10μg/kg. In chronic experiments, SHR were fed a 0.66% NaCl, 0.66% NaCl plus 0.05% manidipine, 8.0% NaCl or 8.0% NaCl plus 0.05% manidipine diet for 4 weeks. Mean arterial pressure (MAP), glomerular filtration rate (GFR), and renal blood flow (RBF) were measured. Salt loading increased MAP in young SHR. Acute administration of manidipine decreased MAP more in saltloaded SHR compared to nonsaltloaded SHR (-43.3±3.1 vs. -18.6±2.1mm Hg: p<0.01). Moreover, chronic administration of manidipine attenuated the rise in MAP in saltloaded SHR (155±3mm Hg vs. 196±5mm Hg: p<0.01) and less so in nonsaltloaded SHR (150±2mm Hg vs. 160±3mm Hg: p<0.01). Salt loading elevated renal vascular resistance (RVR) but changed neither RBF nor GFR. The acuteand chronicadministration of manidipine increased RBF (Acute; +0.77±0.22ml/min/g kidney: p<0.05, Chronic; 4.32±0.29 vs. 5.50±0.90ml/min/g kidney: p<0.01) in nonsaltloaded SHR, which was greater in saltloaded SHR (Acute; +2.19±0.52ml/min/g kidney: p<0.05 vs. nonsaltloaded SHR, Chronic; 4.29±0.53 vs. 6.09±1.41ml/min/g kidney: p<0.01) Manidipine also decreased RVR (Acute; -10.2±2.2mm Hg/ml/min/g kidney: p<0.01, Chronic; 35.3±1.6 vs. 27.3±4.1mm Hg/ml/min/g kidney: p<0.01) in nonsaltloaded SHR, which was greater in saltloaded SHR (Acute; -21.1±3.1mm Hg/ml/min/g kidney: p<0.01 vs. nonsaltloaded SHR, Chronic; 44.9±2.6 vs. 27.6±4.1mm Hg/ml/min/g kidney: p<0.01). GFR did not change significantly following manidipine. It is suggested that the antihypertensive effect of the calcium antagonist, manidipine, was greater in saltloaded SHR and was accompanied by profound amelioration of the abnormal renal hemodynamics.

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Anomalous origin of the right coronary artery may lead to myocardial ischemia despite the absence of atherosclerosis. We report the case of a 52-yearold man who was admitted to our hospital with exertional chest discomfort and palpitations. An anomalous origin of the right coronary artery was demonstrated by coronary angiography. There was no evidence of atherosclerosis in either the left or right coronary arteries. However, detailed information regarding the proximal portion of the anomalous artery was not acquired by coronary angiography. In this patient, ultrafast computed tomography (UFT) revealed an acute angle takeoff of the anomalous right coronary artery from the aorta. Furthermore, the proximal portion of the right coronary artery traversed the aorta and pulmonary trunk. This case illustrates that UFT is useful for detecting an anomalous origin of the coronary arteries and evaluating the mechanism of myocardial ischemia in patients with anomalous origin of the coronary arteries.

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A persistent fifth aortic arch was recognized in a 4-yearold boy by echocardiography, magnetic resonance imaging and angiocardiography. The case was unique in at least two respects: right-sided aortic arch, and systemic-topulmonary connection without intracardiac lesion. This rare type of anomaly was correctly diagnosed and successfully repaired by patch closure of the arch. This is the first report of this combination of lesions in the Orient.

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Today, an increasing incidence of severe complications of cardiac malformations in adult patients must be expected since the life expectancy of such individuals is prolonged due to improved management. A 32-yearold woman with corrected transposition of the great arteries (CTGA) was admitted to the intensive care unit because of cardiac decompensation. Information provided by multiplane twodimensional transesophageal echocardiography was not sufficient for an unequivocal explanation of the cardiac decompensation. In CTGA uncommon complications may cause pulmonary edema. Using dynamic threedimensional echocardiography to reveal function, volume parameters and the morphology of both ventricles and to exclude additional complications may be considered an adequate diagnostic tool for responding to this challenge.

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A surgically-treated case of left atrial myxoma complicating congenital coronary artery fistula is reported. A review of the literature indicates that this complication has not been reported previously.

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We have experienced a case of left atrial (LA) myxoma with rapid progression of congestive heart failure and ensuing multiple organ insufficiency. After the tumor excision, the hemodynamic derangement was totally corrected and the patient dramatically recovered from kidney, liver, and lung insufficiency. Specifically, pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), and central venous pressure (CVP) significantly decreased in the intensive care unit. Administration of prostaglandin E1 (PGE1) was effective in treating residual pulmonary hypertension.

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