Survival of patients with heart failure has improved over the past decade due to advances in medical therapy. Sudden death continues to cause 20 to 50% of deaths. Ventricular arrhythmias are common in patients with heart failure. Ventricular hypertrophy, scars from prior myocardial infarction, sympathetic activation, and electrolyte abnormalities contribute. Some sudden deaths are due to bradyarrhythmias and electomechanical dissociation rather than ventricular arrhythmias. The risks and benefits of antiarrhythmic therapies continue to be defined, Class I antiarrhythmic drugs should be avoided due to proarrhythmic and negative inotropic effects that may increase mortality. For patients resuscitated from sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) amiodarone or an implantable cardioverter defibrillator (ICD) should be considered. ICDs markedly reduce sudden death in VT/VF survivors, but in advanced heart failure, this may not markedly extend survival. Catheter or surgical ablation can be considered for selected patients with bundle branch reentry VT or difficult to control monomorphic VT. For patients who have not had sustained VT/VF antiarrhythmic therapy should generally be avoided, but may benefit some high risk patients. Amiodarone may be beneficial in patients with advanced heart failure and rapid resting heart rates. ICDs may improve survival in selected survivors of myocardial infarction who have inducible VT. (Jpn Circ J 1997; 61: 727 - 740)

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Intercellular adhesion molecule-1 (ICAM-1) is a major ligand for 2 members of the CD18 family of leukocyte integrin adhesion molecules and mediates adhesion between leukocytes and stimulated endothelial cells. We examined plasma soluble ICAM-1 (sICAM-1) levels in 30 patients with acute myocardial infarction (AMI) within 6 h of symptom onset, 21 patients with unstable angina (UA) , 35 patients with stable exertional angina (SEA) and 21 control subjects. Plasma sICAM-1 Ievels (ng/ml) were significantly higher in both the acute and chronic phases of AMI and in the UA group than in the SEA and the control groups (195±14, 198±16 in the acute and chronic phases of AMI, 188±11 in the UA group vs 142±7 in the SEA group, 141±10 in the control group, p<0.01). Plasma sICAM-1 levels were significantly higher in AMI patients when preceded by unstable angina than when not preceded by unstable angina at any point over the time course except 1 week after admission (p<0.01 vs admission, 12 h, 2 days, 3 days, 5 days, 2 weeks, 3 weeks. p<0.05 vs 24 h). These results suggest that the increase in sICAM-1 is associated with repeated episodes of myocardial ischemia and reperfusion not leading to myocardial necrosis. The increase in sICAM-1 may play an important role as an inflammatory component in the pathogenesis of the ischemic myocardium. (Jpn Circ J 1997; 61: 741 - 748)

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Cytokines are proteins with pleiotropic biological effects, but the pathophysiologic role of cytokine inhibitors in advanced cardiac disease remains unclear. We assessed the levels of tumor necrosis factor (TNF)-α and its soluble receptors I (sTNF-RI) and II (sTNF-RII), soluble interleukin-1 receptor antagonist (sIL-1 Ra), and interleukin-6 soluble receptor (IL-6 sR) in sera from 11 patients with severe chronic congestive heart failure (mean left ventricular ejection fraction 19±6%; mean symptom-limited oxygen consumption 13±4 ml/min per kg) and 11 healthy volunteers. The serum concentrations of TNF, sTNF-RI, and sIL-1 Ra, but not of sTNF-RII and IL-6 sR, were significantly increased in heart failure patients. Importantly, their symptom-limited oxygen consumption was strongly associated with both sTNF-RI (R= -0.68, p=0.04) and sIL-1 Ra (R= -0.77, p=0.01). These results suggest that cytokine inhibitors from different receptor families may be involved in functional disability, a characteristic feature in patients with severe congestive heart failure. Understanding the response of cytokine inhibitors to heart failure might have therapeutic value as interventions against cytokines become available. (Jpn Circ J 1997; 61: 749 - 754)

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To investigate the vasodilatory effect of various doses of intracoronary verapamil on coronary resistance vessels, we studied 13 patients with normal angiograms. A coronary Doppler guide wire was inserted into the left anterior descending coronary artery, and coronary blood flow velocity (CBFV) was measured. Verapamil was injected into the left coronary artery at doses of 0.1 mg, 0.5 mg, 1.0 mg, and 2.0 mg at 10-min intervals. Nitroglycerin was also injected into the same artery to avoid changes in cross-sectional area. As a measure of coronary vascular resistance, coronary vascular resistance index (CVRI) was calculated as the quotient of mean aortic pressure/CBFV. An injection of verapamil produced a dose-dependent increase in CBFV: 79±38% with 0.1 mg, 131±56% with 0.5 mg, 143±46% with 1.0 mg, and 128±47% with 2.0 mg of verap-amil. The percent peak decreases in CVRI were dose dependent: -42±13% with 0.1 mg, -50±17% with 0.5 mg, -62±14% with 1.0 mg, and -60±9% with 2.0 mg of verapamil. Thus, intracoronary verapamil produces a dose-dependent dilation of coronary resistance vessels, and the optimal effect is produced with an injection of verapamil at a dose of 1.0 mg into the left coronary artery. At this dose, verapamil did not affect atrioventricular conduction. (Jpn Circ J 1997; 61: 755 - 761)

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The purpose of this study was to determine the influence of preoperative renal dysfunction on the outcome of patients undergoing elective, infrarenal abdominal aortic aneurysm (AAA) repair. Patients undergoing AAA repair from 1984 to 1996 (n=250) were divided into 2 groups, according to their preoperative serum creatinine levels: ≥1.5 mg/dl (group A, n=33) and <1.5 mg/dl (group B, n=217). There was no apparent difference in the incidences of preoperative risk factors, excluding ischemic heart disease, between the groups. The mortality rates of the 2 groups did not differ (9.9% vs 3.2% in groups A and B, respectively, p=0.13), but the morbidity rate of group A (30.3%) was significantly higher than that of group B (12.9%, p=0.0095). The 5-year cumulative survival rate of group A patients was 60%, which was significantly lower (p<0.0001) than that of group B patients (84%). Five group A patients underwent simultaneous renal artery reconstruction, which relieved postoperative renal deterioration in 4, although 2 of them developed chronic renal failure requiring hemodialysis over 5 years after the operation. These findings suggest that morbidity and long-term survival in patients with renal dysfunction can be severe after AAA repair and that simultaneous renal artery reconstruction may delay renal function decline. (Jpn Circ J 1997; 61: 762 - 766)

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We retrospectively reviewed all of the patients who were treated for cardiac tamponade at Linkou Chang Gung Memorial Hospital between January 1991 and December 1995. There were a total of 112 patients (57 males, 55 females) with a mean age of 51±14 years (53±15, 49±13, respectively). Dyspnea was the most common complaint (85%). The mean blood pressure was 129±24/78±17 mmHg, and only 8% had a systolic blood pressure of less than 90 mmHg. Sinus tachycardia was the most frequent electrocardiographic finding (72%, 62/86). Diffuse low voltage was noted in 35% (30/86) of the patients and electrical alternans was seen in 17% (15/86). The mean volume of pericardial effusion was 610±263 ml. Sixty-five percent of the pericardial effusions were bloody, 31% were serosanguineous, 2% were purulent and 2% were chylous. Overall, 54.5% of the patients had malignant diseases. Of the 61 patients who died, 79% had malignancies. Thirty-five (57%) of these 48 patients had lung cancer. The mean survival time from emergent pericardiocentesis was 3.4 months. In conclusion, non-traumatic cardiac tamponade had a poor prognosis because most patients had malignant etiologies. There is still no definitive treatment for recurrent malignant pericardial effusion-induced cardiac tamponade. Percutaneous pericardiocentesis as clinically required may be the most appropriate treatment, since it is questionable whether such subjects should be subjected to the unnecessary pain and suffering associated with an operative procedure, considering their short mean survival time. (Jpn Circ J 1997; 61: 767 - 771)

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Arterial conduit vessels dilate in response to increased blood flow stimuli. Our objective was to determine precisely how a change in large arterial diameter results in a change in peripheral tissue blood flow. Using high-resolution ultrasound Doppler echography, we measured the diameter of the right femoral artery at rest, during reactive hyperemia, and after administration of 2.5 mg of sublingual isosorbide dinitrate in 10 healthy young men. Reactive hyperemia was induced by distal circulatory arrest followed by reperfusion of the leg ipsilateral (right) or contralateral (left) to the side of arterial diameter measurements. Femoral arterial blood flow was calculated by simultaneous measurement of femoral arterial diameter and blood velocity. The change in skin blood flow was also analyzed simultaneously by laser Doppler flowmetry, Reactive hyperemia induced a 2-fold increase in femoral arterial blood velocity 30 sec after cuff release. During this flow augmentation, the femoral artery dilated. The peak of skin blood flow was coincident with the peak of femoral arterial vasodilation. The time required for the return of arterial diameter to baseline was longer than that for blood flow in both the conduit artery and the peripheral skin tissue. Equivalent cuff occlusion and release of the contralateral limb had no effect on ipsilateral arterial diameter. Isosorbide dinitrate induced dilation in all subjects, despite the absence of a significant increase in blood velocity. These results indicate that the human femoral artery dilates in response to increased blood velocity, and that the flow-mediated vasodilation of a large conduit artery is involved in the adjustments of blood flow in the downstream peripheral tissue. (Jpn Circ J 1997; 61: 772 - 780)

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We investigated the reliability and reproducibility of an image-analyzing system run on a personal computer for measurement of myocardial interstitial fibrosis. Measurements of myocardial interstitial fibrosis in right ventricular endomyocardial biopsies obtained from patients with hypertrophic cardiomyopathy determined by this image-analyzing system were compared with measurements determined by the point-counting method. We also investigated the correlation between measurements of interstitial fibrosis obtained by image analysis and biochemical measurements of myocardial levels of hydrozyproline in normal and cardiomyopathic hamsters. The intra- and interobserver variability were significantly lower for measurements obtained by the image-analyzing system than for measurements obtained by the point-counting system. Reproducibility was superior with the image-analyzing method. The rate of myocardial interstitial fibrosis determined by the computer image-analyzing method was positively correlated with the hydroxyproline measurement (r=0.89). Our results suggest that an image-analyzing system using a personal computer provides reproducible results with a high level of reliability. (Jpn Circ J 1997; 61: 781 - 786)

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To elucidate the role of bronchial hyperresponsiveness (BHR) in pulmonary congestion, an inhaled histamine provocation test was performed in dogs with acute pulmonary congestion, and the role of vagal nerve activity and arachidonic acid metabolites on bronchial responsiveness was evaluated. We assessed BHR with the provocation concentration of histamine causing a 100% increase in pulmonary resistance (PC₁₀₀) in an open-chest anesthetized and tracheotomized canine model before and after left atrial balloon inflation. Twenty-two mongrel dogs (8-14 kg) were anesthetized with sodium thiopental (15-20 mg/kg) and mechanically ventilated with positive end-expiratory pressure at 3 cmH₂O. A Foley catheter was inserted into the left atrium to cause pulmonary congestion, in which mean left atrial pressure was increased to 18 mmHg. In 6 dogs, histamine provocation was examined before and after pulmonary congestion was effected. Intravenous indomethacin (1 mg/kg) administration and vagotomy were performed in 5 dogs. In pulmonary congestion, PC₁₀₀ Was significantly decreased both before and after vagotomy and after indomethacin administration. We conclude that pulmonary congestion augments bronchial responsiveness to inhaled histamine and that neither vagotomy nor indomethacin administration prevents bronchial hyperresponsiveness in pulmonary congestion. These findings suggest that bronchial hyperresponsiveness in pulmonary congestion is related to another factor such as bronchial edema. (Jpn Circ J 1997; 61: 787 - 794)

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We report a case of chondrosarcoma of the heart that was managed surgically. As chondrosarcoma of cardiac origin is extremely rare, this case is described with a brief comment. (Jpn Circ J 1997; 61: 795 - 797)

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A 47-year-old woman was admitted with fever, hypotension, an elevated serum creatinine kinase level, and electrocardiographic abnormalities, which led to the diagnosis of acute myocarditis. She was placed on percutaneous cardiopulmonary support because of hemodynamic collapse on the third hospital day. Serial echocardiography showed gradual recovery of profound hypokinesis and edematous thickening of the left ventricle, but she died of sepsis on the 17th day without overt renal insufficiency or electrolytic abnormalities. Autopsy revealed myocardial necrosis with lymphocytic infiltrates and extensive myocardial calcification. Calcification was dense in the area of severe myocardial necrosis, and the distribution of calcium deposits suggested that the calcification was a consequence of significant inflammation of the myocardium. Recovery of regional wall motion was prominent in the area of severe inflammatory change. Dissociation between the pathologic and echocardiographic findings suggested the possibility of functional reversibility of severely damaged myocardium and possible mechanisms of abnormal contractile function other than inflammatory change. (Jpn Circ J 1997; 61: 798 - 802)

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The case of a 20-year-old man with acute myocardial infarction is described. He developed acute myocardial infarction on 11 July 1995. An emergency coronary arteriogram revealed total occlusion of the proximal left anterior descending coronary artery. Reperfusion was achieved by intracoronary injection of 6.4×10 ⁶ units of native tissue plasminogen activator, which left multiple, angiographically identifiable, thrombi in the left anterior descending coronary artery. As a coronary angiogram 28 days after the onset showed no organic stenosis or wall irregularity, we conducted an ergonovine provocation test. The infusion of 32 μg of ergonovine into the left coronary artery provoked diffuse, high-grade vasospasm. The patient's medical history showed that he had been diagnosed as having Kimura's disease when he was 19 year-old. Additionally, he had exhibited persistent eosinophilia of unknown origin for 10 months or more. Thus, his condition was consistent with a diagnosis of hypereosinophilic syndrome (HES). This is the first report to document angiographically the presence of acute coronary obstruction in a patient with HES. The acute coronary occlusion was thought to be related to coronary artery vasospasm. (Jpn Circ J 1997; 61: 803 - 806)

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