The underlying pathophysiology of hypertrophic cardiomyopathy (HCM) is still unclear. Positron emission tomography is a suitable and promising technique for the detection of possible metabolic consequences of the disease. To assess regional myocardial blood flow and metabolism, 19 asymptomatic or only mildly symptomatic patients with HCM and 10 normal control subjects were studied using carbon-11 acetate and fluorine-18-labelled deoxyglucose (FDG) as tracers of myocardial blood flow (Ao), oxygen consumption (k), and exogenous glucose utilization. In the patients, regional Ao in the hypertrophied septum and apex (H) was similar to that in the nonhypertrophied free wall (N) (91.3±3.9% vs 92.9±3.1%; p=NS). However, the k values were significantly lower in H than in N (0.044±0.012 vs 0.060±0.016/min, p<0.0001). The k value in N and normal control subjects (0.062 ±0.013) was similar. Postprandial FDG uptake was lower in H than in N (70±16 vs 91±7%; p<0.0001) in 16 patients and slightly higher in 3 patients, Fasting FDG study showed increased FDG uptake in H in 3 out of 13 patients, suggesting a disorder of the myocardial microvascular circulation. A relative decrease in hypertrophied septal and apical oxidative metabolism and glucose utilization without any corresponding perfusion defect could reflect abnormal regional aerobic metabolism in the disproportionately thickened myocardium in patients with HCM. This suggests that a primary myocardial metabolic defect might be present in patients with HCM. (Jpn Circ J 1997; 61: 201 -210)

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In general, anginal symptoms diminish with time in patients with vasospastic angina. We assessed changes in coronary vascular tone (CVT) in patients with vasospastic angina over a 4-year period to evaluate the time course of spastic activity. Vasospastic angina was evaluated in 39 patients in whom occlusive spasm was evoked by selective intracoronary injection of ergonovine maleate (ERG-S) 48 h after stopping all coronary vasodilator drugs. These patients had no organic coronary stenosis and developed no stenosis during follow-up. ERG-S was repeated 3 times at 2-year intervals. CVT was determined at each ERG-S study using the equation: CVT=1-(coronary artery diameter before ERG-S/coronary artery diameter after intracoronary injection of isosorbide dinitrate). Thirty-four patients (87%) had no angina pectoris at the second ERG-S study and 28 (72%) had none at the third. Coronary spasm was induced in 25 patients at the second ERG-S study and in 20 at the third. The overall CVT was shown to decrease at each successive ERG-S study (p<0.01). There was no correlation between changes in CVT and anginal symptoms or the coronary spasm induction rate. These results demonstrate that CVT decreases over time in patients with vasospastic angina, suggesting that myocardial ischemia may improve spontaneously. (Jpn Circ J 1997; 61: 211 - 217)

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This study compared the immediate and long-term outcome of percutaneous transvenous mitral commissurotomy (PTMC) in patients who had (restenosis group, n=9) or had not (de novo group, n=27) previously undergone surgical mitral commissurotomy. The baseline echocardiographic score, which is an index of deformity of the mitral valve apparatus, was significantly higher in the restenosis group than in the de novo group (11±3 vs 7±2, p<0.01), although age, Ieft atrial diameter, and the prevalence of atrial fibrillation were similar. PTMC was performed by the Inoue technique, and was abandoned in 1 patient from the restenosis group because of failed trans-septal puncture. Including this patient, 3 patients (33%) in the restenosis group had a thickened atrial septum compared with only 1 (4%) in the de novo group. One patient in the de novo group developed cardiac tamponade during this procedure. In both groups, the mitral valve area increased significantly, but the success rate of PTMC was lower in the restenosis group (4/9 patients, 44%) than in the de novo group (22/27 patients, 81%) (p<0.05). Twenty-six patients who had successful PTMC were followed up over 51±14 months. After 4 years of follow-up, 3 out of 4 patients (75%) in the restenosis group and 3 out of 22 patients (14%) in the de novo group demonstrated echocardiographic restenosis (p<0.01). Stepwise multivariate analysis revealed that the echocardiographic score was the only significant predictor of both the immediate and long-term outcome. In conclusion, the immediate and long-term outcome of PTMC were worse in patients who had undergone previous surgical mitral commissurotomy than in those who had not. This was mainly attributable to the difference in the severity of the valvular lesions. In addition, our data suggested that a thickened atrial septum, possibly related to surgery as well as chronic rheumatic disease, may affect the performance of PTMC. (Jpn Circ J 1997; 61: 218 - 222)

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We have shown that myocardial glucose metabolism is heterogeneous in patients with hypertrophic cardiomyopathy. It is not known, however, whether glucose metabolism is impaired in patients with apical hypertrophic cardiomyopathy, which is fairly common in Japan. We studied 7 patients with apical hypertrophic cardiomyopathy and 5 normal subjects using nuoro-18 2-deoxyglucose (FDG) and positron emission tomography (PET). We calculated regional FDG fractional uptake and the inter-regional coefficient of variation (CV) of FDG fractional uptake in the interventricular septal, anteroapical, and posterolateral regions. The regional FDG fractional uptake was similar in the 2 groups and among the 3 different segments within each group. However, the inter-regional CV of FDG fractional uptake was increased in the anteroapical wall segment of the patient group compared with the control group and also with the other 2 regions in the patient group. The results did not differ when we studied another 5 patients and 6 normal control subjects with a PET scanner with higher spatial resolution. These data suggest that myocardial glucose metabolism may be impaired in the anteroapical wall segment of patients with apical hypertrophic cardiomyopathy. (Jpn Circ J 1997; 61: 223 - 230)

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A total of 274 patients with abdominal aortic aneurysms due to atherosclerosis (AAA) and 16 patients with inflammatory abdominal aortic aneurysms (IAAA) were reviewed to compare and contrast the clinical characteristics of the 2 groups. The AAA group comprised 243 men and 31 women with a mean age of 69.2±0.4 (range 51-86) years. The IAAA group comprised 15 men and 1 woman with a mean age of 67.4±2.0 (range 53-81) years. Most patients with IAAA (12/16; 75.0%) had pain at presentation, whereas only 37 out of 274 patients (13.5%) with AAA had pain (p<0.001). Fifty out of 274 patients (18.2%) with AAA were asymp-tomatic, the most common principal complaint being a pulsatile tumor, which was found in 150 out of 274 patients (54.7%; p<0.005 vs IAAA). Regarding laboratory findings of inflammation, preoperative erythrocyte sedimentation rate values were elevated in 15 out of 16 (93.8%) patients, and C-reactive protein values were elevated in 13 out of 16 (81.3%) patients with IAAA. The incidence of perioperative complications was similar in the 2 groups. The 30-day postoperative mortality among AAA patients was 6.2% (17/274 cases), including 12 cases of non-ruptured and 5 cases of ruptured AAA; in contrast, no early deaths occurred among patients with IAAA. The cumulative 5-year survival rate was 80.2% for IAAA patients and 74.6% for AAA patients (NS). The results of our review suggest that careful diagnosis and intra- and postoperative management could lead to patients with IAAA having a similar survival rate to those with AAA. (Jpn Circ J 1997; 61: 231 - 235)

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An increased awareness of the adverse effects of homologous blood transfusion prompted us to initiate a blood conservation program consisting of preoperative autologous blood donation and platelet-rich plasma-pheresis. We studied 120 patients who underwent elective cardiac surgery at Aomori General Hospital between January 1991 and September 1994. If their hemoglobin values exceeded 12 g/ml, 400 g of whole blood was drawn 3 times before the operation. Platelet-poor plasma was collected 10 days before the operation and platelet-rich plasma was collected the day before the operation. However, despite participation in this program, 42 of 120 patients (35%) required homologous blood transfusion perioperatively. Factors that influenced the need for homologous blood transfusion were identified retrospectively, with the following found to be significant by univariate analysis: operative procedures performed, cardiopulmonary bypass time, and the amount of autologous blood and autologous plasma donated. Although the effectiveness of our blood conservation procedure remains to be verified, it reduced the need for the transfusion of homologous blood. Thus, additional units of autologous blood are required to obviate the need for homologous transfusion in patients undergoing long cardiopulmonary bypass procedures. (Jpn Circ J 1997; 61: 236 - 240)

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We investigated the involvement of circulating platelets in myocardial ischemia-reperfusion injury in canine autoperfused heart-lung preparations using filters to deplete platelets and/or leukocytes. The left anterior descending (LAD) coronary artery was occluded for 40 min, followed by 40 min reperfusion, in 3 groups: a leukocyte-platelet-depleted (LPD) group, in which both leukocytes and platelets were depleted; a leukocyte-depleted (LD) group, in which leukocytes alone were depleted; and a control group. There were no differences in hemodynamics or arrhythmias among groups before or during coronary occlusion. After reperfusion, the maximum rate of change in left ventricular pressure during systole and diastole was significantly higher in the LPD group than in the control and LD groups. The LPD group also showed gradual recovery of regional myocardial function and a decrease in the frequency of premature ventricular contractions. The LD group showed a slight improvement in cardiac function and arrhythmias compared with the control group. Although there was no significant difference in the pulmonary arterial plasma level of thromboxane B₂ at any stage among groups, the control group showed an increase after reperfusion. These results suggest that platelets are important in reperfusion injury and that the depletion of both leukocytes and platelets effectively protects against reperfusion injury. (Jpn Circ J 1997; 61: 241 - 248)

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We investigated alterations in the β-adrenergic receptor-adenylate cyclase system in rabbits with congestive heart failure induced by adriamycin cardiotoxicity. A dose of 24 mg/kg adriamycin was administered over 16 weeks in 16 rabbits. Five of them died and 4 of them could not tolerate the full dose of adriamycin. Complete data were obtained in the remaining 7 rabbits. Another 7 rabbits received physiological saline for the same period and served as controls. Plasma norepinephrine concentration increased in adriamycin-treated rabbits, but not in the control rabbits. Cardiac output was lower in the adriamycin-treated group than in the control groups. Both the left and right ventricular end-diastolic pressure were higher in the adriamycin-treated group. The density of myocardial β-adrenergic receptors and the norepinephrine content were reduced in both ventricles in the adriamycin-treated group. Basal and isoproterenol-, sodium fluoride- and forskolin-stimulated adenylate cyclase activities were lower in the adriamycin-treated group. Thus, alterations in β-adrenergic signaling occurred in both ventricles in animals with chronic biventricular failure induced by adriamycin. These may be the result of post-receptor abnormalities, including abnormalities of guanine nucleotide-binding proteins or of the catalytic unit of adenylate cyclase. (Jpn Circ J 1997; 61: 249 - 255)

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The purpose of this study was to evaluate the inhibitory effects of locally delivered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on intimal proliferation after balloon injury. A hydrogel-coated balloon catheter was immersed 3 times in an argatroban/saline solution (1, 0.1, or 0.01 mg/ml) for 60 s and inflated at 6 atm pressure for 1 min in the rabbit common carotid artery. Immersion in a saline solution without drug followed by the same procedure served as a control. Accumulation of argatroban in the vascular wall was confirmed by chemical determination using high-performance liquid chromatography (HPLC) . The concentration of argatroban in the vessel wall immediately after deflation after balloon immersion in solutions of 1 and 0.1 mg/ml was 14.8±10.9 and 5.5±4.6 nmol/g wet weight of artery, respectively. Argatroban was not detected in arteries treated with a balloon that had been immersed in the 0.01 mg/ml argatroban/saline solution. Intima-media area ratios 20 days after balloon injury in the groups treated with 1 mg/ml (n=8) and 0.1 mg/ml (n=6) agratoban were significantly smaller than that in the groups treated with 0.01 mg/ml (n=7) argatroban or saline (n=8) (0.35±0.11, 0.50±0.17, 1.24±0.39, and 1.35±0.43, respectively; p<0.001). These data suggest that locally administered argatroban dose-dependently inhibits intimal thickening in a rabbit model of carotid artery injury. (Jpn Circ J 1997; 61: 256 - 262)

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We present the case of a 44-year-old man with abnormal myocardial fatty acid metabolism who exhibited no myocardial uptake of ¹²³I-β-methyl- iodophenyl pentadecanoic acid (¹²³I-BMIPP). This patient presented to our hospital with an ECG abnormality detected during a medical check-up. He felt no chest discomfort, but a 12-lead ECG at rest showed flat T-waves in leads I, V5, and V6 with no marked ischemic changes during exercise. A left ventriculogram and coronary angiograms were normal. Thallium-201 single photon emission computed tomography imaging revealed a normal myocardial uptake, but ¹²³I-BMIPP imaging showed no such uptake. However, ¹⁸F-labelled fluorodeoxyglucose positron emission tomography imaging after an over-night fast showed a marked increase in myocardial uptake. It appears that myocardial uptake of ¹²³I-BMIPP was totally lacking and that energy production by the myocardium during fasting depended on the metabolism of glucose rather than of fatty acids. (Jpn Circ J 1997; 61: 263-267)

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In this report we describe 2 patients with exercise-induced, second-degree atrioventricular (AV) block. Case 1 was a 49-year-old man with normal AV conduction at rest but who developed dyspnea on exertion. Treadmill testing showed an exercise-induced 2:1 AV block. Electrophysiologic study (EPS) demonstrated rate-dependent, presumably intrahissian, AV block. Case 2 was a 31-year-old woman with first-degree AV block and complete right bundle branch block with dyspnea on exertion and occasional syncope. She had twice undergone surgical patch closure of an ostium primum atrial septal defect. Exercise testing induced type II second-degree AV block. Atrial pacing during EPS did not disclose rate-dependent type II AV block, but disopyramide induced second-degree AV block. (Jpn Circ J 1997; 61: 268 - 271)

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Idiopathic restrictive cardiomyopathy (RCM) is rare. Even today little is understood of its etiology or under-lying mechanisms , and definitive diagnostic criteria are lacking. In this report, we describe a case of idiopathic RCM in a young Japanese woman who died while awaiting cardiac transplantation during the 5-year course of the disease. Rare pathologic findings of diffuse perimyocytic fibrosis were revealed at autopsy. (Jpn Circ J 1997; 61: 272 - 274)

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