This paper discusses the brief history of Kawasaki disease, its main clinical features, diagnosis, main laboratory findings, cardiovascular complications in brief, treatment, epidemiology mainly in Japan, a summary of the pathology and concludes with five major problems which must be solved.

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Doppler echocardiography accurately identifies diastolic dysfunction through the assessment of transmitral flow patterns during the application of the handgrip (HG) maneuver. In this study, 45 normal control patients (mean age 46±9, group A) and 13 patients with coronary artery disease (CAD) (mean age 51±6, group B) were involved. The effects of handgrip maneuver on transmitral flow patterns were studied by Doppler echocardiography. Group B patients had higher peak late diastolic filling velocities (A), lower peak early (E) to late diastolic filling velocity ratios (E/A) and longer isovolumic relaxation times (IVRT) compared to group A. On the other hand, systolic blood pressure (SBP), heart rate (HR) and peak E velocity (E) did not change significantly (p>0.05) in either group, at rest. During the supine handgrip maneuver, NR (mean±standard error of mean, +21±13%, p<0.05) and SBP (+21±9%, p<0.05) increased significantly in both group A and group B (+20±13%, p<0.05, +22±15%, p<0.05, respectively). In group B, E/A ratio (-28±7%) decreased significantly (p<0.05) compared to group A (-20±6%), as a consequence of significantly increased peak A velocity in group B (+7±5%) compared to group A (+6±3%, p<0.05). Deceleration time decreased significantly in both groups (-10±6% vs -9±6%, p<0.05). Isovolumic relaxation time (IVRT) significantly increased in both groups (+18±7% vs +16±6%, p<0.001). Peak E/A ratios were>1.0 in all patients of both groups in the supine position. This parameter remained greater than 1.0 only in group A during the HG maneuver. Therefore HG was effective in identifying diastolic function abnormalities in patients with CAD.

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Although the pathophysiology of heart failure progression is important to survival it is not fully understood. In 92 patients with acute heart failure due to myocardial infarction or dilated cardiomyopathy, secondary organ dysfunction was evaluated to determine whether this factor contributed to heart failure progression and death. Forty-one patients had renal dysfunction, hepatic disease or loss of consciousness after the onset of the acute heart failure, and 26 of them (63%) died of progressive heart failure during the follow-up period of 20 months on average. The one-year survival rate was 22%. Although 51 other patients showed the same initial clinical features and cardiac function, they did not develop concurrent organ dysfunction during the course and only 11 (22%, p<0.001) died of progressive heart failure. The one-year survival rate was 67%. The survival rate decreased in the order of renal dysfunction, hepatic disease and loss of consciousness. Transient low cardiac output of less than 2.2l/min/m² was more frequent in patients with organ dysfunction.
It is suggested that heart failure progresses, in part, due to organ dysfunction secondary to heart failure and careful treatment to prevent organ dysfunction is important to long term survival.

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We assessed the changes in arterial potassium concentration during exercise and recovery in relation to exercise tolerance in patients with impaired exercise tolerance. Sixteen patients with cardiac disease were subjected to a cardiopulmonary exercise test on a cycle ergometer. Arterial potassium and lactate concentrations were measured every minute during and after exercise, and ventilatory threshold (VT) and lactate threshold (LT) were identified. Before exercise, arterial potassium concentration was 3.8±0.3mEq/l. It in-creased to 4.1±0.3mEq/l at LT (p<0.002 versus at rest), to 4.2±0.3mEq/l at VT, and to 4.8±0.5mEq/l at peak exercise (p<0.001 versus at LT, p<0.001 versus at VT). At an exercise intensity equivalent to 30, 40, 50 or 60% of predicted maximum oxygen uptake, the increase in arterial potassium showed a negative and significant correlation with %LT (r=-0.62∼-0.72, p<0.01∼0.05) and %VT (r=-0.62∼-0.75, p<0.001∼0.05), where %LT and %VT represent the ratios of LT and VT to the predicted maximum oxygen uptake, respectively. There was a good correlation between the rate of fall in potassium concentration during recovery and its increase during exercise. It was concluded that in patients with impaired exercise tolerance, the greater the degree of exercise intolerance, the greater the increase in arterial potassium concentration during exercise, and the steeper the fall in potassium concentration during recovery. Because the rise in potassium concentration during exercise and its fall during recovery were greater when the exercise level exceeded the anaerobic threshold, exercise levels below the anaerobic threshold are recommended for patients with cardiac diseases.

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In congenital heart disease (CHD) with pulmonary hypertension (PH) resulting from high pulmonary flow, we sometimes experience patients whose PH continues even after the normalization of flow following surgery. Preoperative identification of these patients is difficult even using direct hemodynamic measurements at cardiac catheterization. The purpose of this study is to interpret the state of the pulmonary vascular bed more precisely using a new theoretical approach and to present the criteria available for avoiding residual PH.
During preoperative routine catheter examination in CHD patients with PH we applied the Windkessel model to the pulmonary circulation and calculated the diastolic time constant (Td) of the pulmonary circulation. Td of Group 1 (0.50±0.03 sec), 6 patients who manifested residual PH after surgery, was higher than that of group 2 (0.23±0.14 sec), 42 patients with normalized pulmonary artery pressure after surgery. Furthermore, the relationships between Td and pulmonary blood flow (Qp) or pulmonary to systemic flow ratio (Qp/Qs) were very sensitive for distinguishing between these two groups. Group 1 was located in the left-upper quadrant of the graph of Td vs Qp or Td vs Qp/Qs relationships, whereas group 2 was located in the right-lower quadrant.
The relationships between Td and Qp or Qp/Qs were considered to reflect the pathological change in the pulmonary vasculature more precisely. As a consequence, they would be very useful in understanding the state of the pulmonary vascular bed and avoiding residual PH.

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An examination was made of the coronary thrombolytic effects of nasaruplase in a canine model of acute myocardial infarction. The model was produced by selective injection of an artificial thrombus into the coronary artery stenosed by laser ablation. Intravenous nasaruplase (8U/kg/min) showed an equivalent thrombolytic effect to a recombinant tissue-type plasminogen activator (rt-PA, 10, 000IU/kg/min) as assessed by reperfusion rate (78.6 versus 79.2%) and reperfusion time (37.4±5.2 versus 37.0±2.5min). Nasaruplase decreased the plasma α₂-plasmin inhibitor (α₂-PI) level by 28% immediately after reperfusion, but hardly altered fibrinogen or plasmin-α₂-plasmin inhibitor complex (PIC) levels. By contrast, rt-PA significantly decreased plasma α₂-PI and fibrinogen levels, by 84% and 92% respectively, and, increased PIC level more than 70-fold. Hemorrhagic infarction occurred in 2 of 14 animals in the nasaruplase group and in 9 of 19 animals in the rt-PA group. In these animals, significant correlations were found between the ratio of the hemorrhagic infarction area to total infarct area and the plasma α₂-PI (r=-0.740, p<0.05) or fibrinogen (r=-0.798, p<0.05) concentrations, as well as between the recovery rate of left ventricular regional wall motion and the plasma α₂-PI (r=0.924, p<0.01) or fibrinogen (r=0.864, p<0.01) concentrations. It is concluded that nasaruplase is a potent thrombolytic agent which preserves left ventricular function with a lesser rate of hemorrhagic infarction than rt-PA. Further, nasaruplase administration results in recovery of left ventricular regional wall motion and systolic function, such as Vmax.

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Beta-adrenergic receptor blockade reduces the mortality rate after acute myocardial infarction (AMI) in humans. However, the effects of beta blockade on left ventricular remodeling remain unknown. Therefore, in the present study we investigated the effect of prolonged beta-adrenergic receptor blockade with atenolol on left ventricular remodeling following AMI in rats. Myocardial infarction (MI) was produced in Wistar-Kyoto rats by ligating the coronary artery. Four groups of rats were studied: sham-operated (n=10); atenolol (1g/l in drinking water) treated sham-operated (n=8); untreated MI (n=11); atenolol treated MI (n=10). Hemodynamic measurements were made about 3 weeks after the operation. Infarct size was similar in treated and untreated MI rats (31.2±2.5% cf. 33.5±2.0%). MI rats were characterized by increases in left ventricular end-diastolic pressure (LVEDP), right atrial pressure (RAP), right ventricular systolic pressure (RVSP), and left ventricular end-diastolic volume index (LVEDVI), as compared with sham-operated rats. In sham-operated rats, prolonged beta-adrenergic receptor blockade produced only a reduced HR. Atenolol-treated MI rats had a significantly higher LVEDP, RAP and LVEDVI than did rats with untreated MI. Prolonged beta-adrenergic receptor blockade with atenolol appeared to promote left ventricular remodeling after AMI. Thus, the treatment of AMI with beta-adrenergic receptor blockade in the clinical setting should be evaluated with respect to ventricular remodeling during prolonged therapy.

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This study was performed to determine the effects of the angiotensinconverting enzyme inhibitor alacepril on hemodynamic variables and betaadrenoceptor number in rabbits with heart failure induced by aortic regurgitation. Aortic regurgitation was induced by perforation of the aortic valve in 12 rabbits. Sixty mg/kg of alacepril was administered by gastric tube for 7 days after manifestation of aortic regurgitation to 6 rabbits (group AR+A). The other 6 rabbits with aortic regurgitation were administered vehicle in the same fashion (group AR+C). Seven rabbits underwent sham operation (group S). One week after induction of aortic regurgitation left ventricular end-diastolic pressure was higher and cardiac output was lower in AR+C than in S. Enddiastolic and end-systolic left ventricular diameter were larger and left ventricular weight was also higher in AR+C than in S. For each of these parameters, the opposite findings were obtained from a comparison of AR+A and S. Myocardial beta-adrenoceptor density and norepinephrine content were reduced in AR+C, but were restored in AR+A. These findings indicate that alacepril has beneficial effects on ventricular remodeling and function, and on sympatho-neuronal regulation in the volume-overloaded myocardium.

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We attempted to determine the effects of transforming growth factor beta-1 on intracellular Ca²⁺ concentration changes in the presence of isoproterenol in cardiac fibroblasts.
Transforming growth factor beta-1 inhibited the increase of intracellular Ca²⁺ concentration in the presence of isoproterenol in fibroblasts. It also inhibited the production of cyclic-AMP in fibroblasts in the presence of isoproterenol. Islet-activating protein did not block these reactions of transforming growth factor beta-1. Forskolin did not affect the intracellular calcium concentration change resulting from treatment with transforming growth factor beta-1. Binding of [³H]CGP-12177 was decreased to 47% of control preincubated for 24 hours with transforming growth factor beta-1 in fibroblasts. Scatchard plots suggested a decrease in beta-adrenergic receptor number without specific change in receptor affinity.
These results suggested that transforming growth factor beta-1 modulates the signal transduction through beta-adrenergic receptor and intracellular Ca²⁺ concentration by regulating the number of receptors in fibroblasts.

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This report describes a 45-year-old Japanese man who had episodes of anginal chest pain on effort. Coronary arteriography in the baseline state revealed subtotal occlusion in the mid-portion of the left anterior descending coronary artery. After intracoronary infusion of an endothelium-dependent vasodilator, substance P, the subtotal occlusion was immediately abolished. We concluded that endothelium-dependent vasodilation evoked with substance P was present at the site where coronary vasospasm occurred spontaneously in our case.

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A 64-year-old woman was referred to cardiac surgery because of aortic stenosis. At surgery, it was confirmed that the right coronary artery arose from the pars membranacea of the left ventricle 5 mm beneath the commissure between the right coronary and noncoronary cusps.

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We report an unusual congenital cardiac anomaly consisting of a downward displacement of all leaflets of both atrio-ventricular valves. In addition to these changes, an atrial septal defect of the secundum type was noted. In light of the extreme rarity of this interesting anomaly complex, we reviewed the literature and compare the morphologic features of the present case with classic Ebstein's anomaly.

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