Constrictive pericarditis (CP) is an unusual sequela of cardiac surgery, so the present study evaluated the clinical characteristics of patients with CP after coronary artery bypass grafting (CABG). Four hundred and sixty-three patients who underwent isolated CABG between January 1989 and March 1999 were examined retrospectively. The first choice of treatment for postoperative pericardial effusion was non-steroid anti-inflammatory agents, and an increased dose of diuretics. The second treatment choice was corticosteroids or pericardial drainage. When CP was suspected during the follow-up period (mean, 54±31 months), cardiac catheterization was carried out to establish the diagnosis. Of the 463 patients undergoing CABG, there were 11 (2.4%) who developed CP after surgery. The median time to the onset of symptoms after CABG was 4 weeks (range, 3-96 weeks). On univariate and multivariate analysis, normal left ventricular ejection fraction, warfarin administration, and early postoperative pericardial effusion were significantly associated with a greater potential of postoperative CP. The effusion was bloody in all cases of pericardial drainage despite warfarin therapy. Not draining the postoperative effusive pericardial effusion was a risk factor for the development of CP. Pericardial drainage for patients with significant effusion after CABG is important for the prevention of subsequent CP, especially in those patients being treated with warfarin or with normal left ventricular function. (Jpn Circ J 2001; 65: 480 - 482)

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Brugada syndrome is characterized by marked ST-segment elevation in the right precordial leads (Bru-ECG) and is associated with a high risk for sudden death. However, it is unclear whether the arrhythmogenesis is caused by the mechanisms responsible for Bru-ECG. The present study investigated the risk of arrhythmias in patients with Bru-ECG by retrospectively analyzing 30 patients (28 men; mean age, 51±14 years) with Bru-ECG. Aborted sudden cardiac death (ventricular fibrillation or syncope) occurred in 9 patients (30%); paroxysmal atrial fibrillation was present in 9 (30%) patients in addition to malignant ventricular arrhythmias, and some type of arrhythmic event (aborted sudden cardiac death or paroxysmal atrial fibrillation) occurred in 15 patients (50%). Of all the arrhythmic events, 93% occurred at night or early in the morning, and 92% had pronounced ST-segment elevation. These results suggest that Bru-ECG may be associated not only with an increased risk of ventricular tachyarrhythmias but also with an increased risk of paroxysmal atrial fibrillation, and that the arrhythmogenesis may be related to the pronounced ST-segment elevation. (Jpn Circ J 2001; 65: 483 - 486)

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Evidence is increasing for small vessel remodeling and disturbance of endothelium-dependent vasodilation in diabetic patients. Insulin increases vascular wall thickening and produces endothelial dysfunction. Troglitazone, a new insulin-sensitizer antidiabetic agent, is considered to reduce plasma insulin level and the present study assessed its effect on the coronary circulation of the patients with non-insulin-dependent diabetes mellitus (NIDDM). Analysis of the myocardial washout rate with adenosine triphosphate-stress thallium-201 scintigraphy was used to estimate coronary circulation, and for estimation of insulin sensitivity, the homeostasis model insulin resistance index (HOMA-R) was calculated. Patients were treated with monotherapy of either troglitazone (200 mg bid, n=12) or glibenclamide (2.5 mg daily, n=12) for 3 months. Age-, sex- and risk factors-matched subjects without NIDDM were employed as a control. Fasting plasma glucose and hemoglobin A_1c were similarly decreased by troglitazone or glibenclamide. Plasma insulin level (pmol/L) decreased from 66.6±10.8 to 39.0±7.2 with troglitazone, but was unchanged by glibenclamide (58.8±7.2 to 66.0±10.8). The diabetic groups had a significantly lower washout rate than controls, which was improved by troglitazone, but not by glibenclamide. In addition, the increase in washout rate correlated significantly with the decrease in HOMA-R in the troglitazone group. In conclusion, troglitazone can restore coronary circulation by improving insulin resistance in patients with NIDDM. (Jpn Circ J 2001; 65: 487 - 490)

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An increase in oxidative stress is thought to be involved in the progression of heart disease, but the serum level of thioredoxin (TRX), which regulates the cellular redox state, has not been investigated in patients with heart diseases. The present study determined serum TRX levels with a sandwich enzyme-linked immunosorbent assay in a total of 39 patients with dilated cardiomyopathy (DCM) (n=5), acute coronary syndrome (ACS) (n=7) or stable angina (n=18), including effort angina (n=7) and vasospastic angina (n=11), and in control subjects (n=7). The serum TRX level in patients with New York Heart Association (NYHA) functional classes III and IV (n=8, 33.3±8.6 ng/ml) was significantly higher than in the control subjects (n=7, 14.0±4.6 ng/ml). In addition, the serum TRX levels correlated positively with the severity of NYHA class, and negatively with the left ventricular ejection fraction. The serum TRX levels were elevated in patients with ACS and DCM compared with the controls. These results indicate a possible association between TRX concentration and the severity of heart failure. (Jpn Circ J 2001; 65: 491 - 494)

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The present study assessed whether lipid peroxidation in plasma might predict restenosis after coronary balloon angioplasty. A total of 87 patients, who had undergone successful coronary balloon angioplasty using standard techniques, were enrolled. Fasting blood samples before the intervention were measured for plasma levels of thiobarbituric acid reactive substances (TBARS, an indicator of lipid peroxidation). Angiography was carried out before and 15 min after angioplasty, and at follow-up (4 months after angioplasty), and evaluated using a quantitative approach. There were 23 patients with restenosis (group R) and 64 patients without restenosis (group N) after coronary balloon angioplasty. The plasma TBARS level (mean ± SEM) of 4.3±0.1 μmol/L in group R was significantly higher than that of 3.2±0.1 μmol/L in group N (p<0.01). There were no significant differences in other parameters, including plasma lipid levels, between the 2 groups. The plasma level of TBARS positively correlated with lumen loss of the coronary artery at the time of follow-up angiography (r=0.57, p<0.01). Our results suggest that oxidative stress contributes to restenosis and indicate that an elevated plasma level of TBARS may be a reliable predictor of restenosis. (Jpn Circ J 2001; 65: 495 - 499)

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The Doppler echocardiograms of the aortic valve and associated aortic regurgitation (AR) were reviewed in 72 patients with a ventricular septal defect (VSD). Group 1 comprised 13 patients without any deformity of the aortic cusp for ≥10 years, group 2 included 35 patients who did not develop AR for ≥10 years after right coronary cusp prolapse (RCCP) was first detected, group 3 comprised 11 patients with RCCP and AR in whom the AR remained subclinical for ≥10 years, and group 4 was 13 patients who underwent surgical treatment because of moderate to severe AR. The cusp imbalance index [width of right (R) or non- (N) coronary cusp/width of left coronary cusp (L)] was compared among the 4 groups. R/L or N/L was larger in group 4 than in groups 1-3; R/L exceeded 1.30 in all the patients in group 4, whereas it was less than 1.30 in all the atients in groups 1-3. Two patients in group 4 with non-coronary cusp prolapse had an N/L greater than 1.50. No other patients in any group had an N/L larger than 1.20. An imbalance of cusp width may predict possible progressive deterioration of AR. (Jpn Circ J 2001; 65: 500 - 504)

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The pathogenesis of unstable angina pectoris (UAP) following percutaneous transluminal coronary angioplasty (PTCA) or directional coronary atherectomy (DCA) has not been adequately investigated, so the present study aimed to determine whether thrombi are present in restenotic lesions. The study group comprised 14 patients (16 arterial branches) with angina pectoris in whom either PTCA or DCA was performed and who had developed UAP associated with restenosis, and who then underwent DCA of the restenosed lesion (R-UAP group). The control groups comprised individuals with UAP undergoing DCA with no prior history of PTCA or DCA (P-UAP group; n=29, 29 branches), patients with acute myocardial infarction (AMI group; n=34, 34 branches), and patients with stable angina pectoris (SAP group; n=31, 33 branches). The presence of thrombi was determined by light microscopy of histologic specimens. Thrombus was present in only 1 of the 16 (6.3%) branches in the R-UAP group, 21 of the 29 (72.4%) branches in the P-UAP group, and in 25 of the 34 (73.5%) in the AMI group. In the SAP group, it was detected in only 2 of the 33 (7.1%) branches. The incidence of thrombus was significantly lower in the R-UAP group than in the P-UAP group. In conclusion, the role of thrombus is limited in causing post-interventional UAP at restenosed sites. (Jpn Circ J 2001; 65: 505 - 508)

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Using data from a survey of a white-collar working population in Taiwan (438 women, 526 men), the relation between job strain status and cardiovascular risk factors (high serum total cholesterol, low serum high-density lipoprotein (HDL) cholesterol, and high plasma fibrinogen) was examined. Job strain indicators, defined by Karasek's model, included psychological demand and decision latitude. Blood pressure, cholesterol and fibrinogen were analyzed as continuous variables, whereas psychological demand and decision latitude were dichotomized into 2 levels and job strain into 4 exposure categories. Plasma fibrinogen was significantly and positively associated with job strain status in both male and female workers and also with decision latitude in female workers only. No consistent association between job strain status and total serum and HDL cholesterol was detectable. In conclusion, plasma fibrinogen is a possible intermediate factor linking occupational stress to elevated cardiovascular risk. (Jpn Circ J 2001; 65: 509 - 513)

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Trials have demonstrated that carvedilol can produce hemodynamic, symptomatic, and prognostic improvements in dilated cardiomyopathy (DCM), but some DCM patients have deteriorated after carvedilol, developing congestive heart failure. The present study investigated the use of isoproterenol (ISP) stress echocardiography to select those patients with DCM who would respond to carvedilol. ISP was infused intravenously in 22 patients with DCM and they were classified into 2 groups based on the left ventricular systolic response: good response to ISP [change in fractional shortening (FS) with ISP >0.05, n=13] and poor response to ISP (change ≤0.05, n=9). In the good response group, FS significantly increased from 0.12±0.04 to 0.17±0.08 (mean±SD, p<0.05) with carvedilol, and 7 patients improved symptomatically (New York Heart Association class). However, in the poor response group, no significant difference was observed between FS at baseline and that at the end of follow-up. Moreover, only 1 patient in the poor response group improved symptomatically. ISP stress echocardiography can assist in selecting patients with DCM who will respond positively to carvedilol. (Jpn Circ J 2001; 65: 514 - 518)

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There have been few clinical studies exploring the characteristics of spontaneous polymorphic ventricular tachycardia (VT) during a vasospastic angina attack. During a 4-year recruitment period, Holter ECG recordings were monitored for 42±24 h during a drug-free period in 60 consecutive patients with vasospastic angina (VSA) and of these, 8 patients had at least one episode of polymorphic VT during monitoring. Ischemic ST segment elevation was immediately preceded the spontaneous polymorphic VT in all 8 patients, 4 of whom had silent coronary vasospasm. Immediately before the onset of polymorphic VT, both R-on-T and long - short sequences were observed in 4 of the 8 patients and ST wave alternans were recorded in 2 patients. VT exhibited a pattern of torsade de pointes in 4 of the 8 patients. Five patients underwent electrophysiologic testing during a drug-free asymptomatic phase, and polymorphic VT was induced in 2 of the 5 patients, with one developing ventricular fibrillation. During a follow-up period of 73±17 months, there was a significant difference in the incidence of sudden death between patients with and without VT (2/8 cases [25%] vs 0/52 [0%]; p<0.01). Thus, vasospastic attacks, even if asymptomatic, that immediately precede the development of polymorphic VT may be associated with a repolarization abnormality and an increased risk of sudden death. (Jpn Circ J 2001; 65: 519 - 525)

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The human heart progressively becomes more tolerant to ischemia after repeated balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). The present study investigated whether nicorandil, a hybrid between nitrate and an ATP-sensitive potassium channel opener, affects this ischemic preconditioning. Sixteen patients with stable angina pectoris caused by left anterior descending artery lesions were subjected to 2 balloon inflations of 2-min duration with a 3-min reperfusion period. Seven of these patients served as the control group and in the remaining 9 patients, nicorandil was administered intravenously (6 mg/h) throughout the PTCA procedure (nicorandil group). The lactate extraction ratio (LER) was obtained at 30 s after each ischemic event (LER_post-1 and LER_post-2) in both groups. In the control group, LER_post-1 was more negative than LER_post-2 (-185.7±74.2 vs -98.0±37.3%, p<0.01). The ratio of the sum of the ST elevation in the precordial leads during the second inflation (ΣST-2, 0.94±0.66 mV) to that during the first inflation (ΣST-1, 1.43±1.17 mV) was 0.72±0.16 in the control group, which was less than the ratio in the nicorandil group (1.06±0.13, p<0.01). Nicorandil abolished the difference between the 2 ischemic events (LER_post-1, -45.1±41.6 vs LER_post-2, -43.5±51.1%; ΣST-1, 1.38±0.80 vs ΣST-2, 1.46±0.90 mV). LER was less negative in the nicorandil group than that in the control group (LER_post-1, -45.1±41.6 vs -185.7±74.2%, p<0.01; LER_post-2, -43.5±51.1 vs -98.0±37.3%, p<0.05). Thus, nicorandil improved lactate metabolism during PTCA without significantly influencing ST-elevation. In conclusion, intravenous pre-administration of nicorandil appears to precondition the human heart during PTCA. (Jpn Circ J 2001; 65: 526 - 530)

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The effect of cibenzoline on left ventricular diastolic function was investigated in patients with hypertrophic cardiomyopathy (HCM). Before and 2 h after an oral administration of 200 mg of cibenzoline, echocardiographic, apexcardiographic and gated radionuclide angiographic studies were performed in 12 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 7 with hypertrophic nonobstructive cardiomyopathy (HNCM). After administration of cibenzoline, the left ventricular pressure gradient decreased from 96±33 mmHg to 29±22 mmHg (<0.0001). Fractional shortening decreased from 53.3±7.5 to 45.4±6.2% (p=0.0008) in patients with HOCM and from 49.9±8.7 to 40.9±7.5% (p=0.0039) in patients with HNCM. On the other hand, E-wave velocity increased and A-wave velocity decreased in both groups. The time between the second heart sound and O point was shortened from 253±53 to 176±21 ms (p<0.0001) in patients with HOCM and from 245±54 to 185±44 ms (p=0.0050) in patients with HNCM. The time to peak filling rate was shortened from 248±79 to 190±40 ms (p=0.0072) in patients with HOCM and from 218±33 to 163±26 ms (p=0.0052) in patients with HNCM. These results indicate that in patients with HCM, cibenzoline suppresses left ventricular systolic function, but can markedly improve left ventricular diastolic dysfunction through its direct action. (Jpn Circ J 2001; 65: 531 - 538)

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The present study investigated the clinical significance of preheparin serum lipoprotein lipase (LPL) mass in coronary vasospasm by examining its relationship with the acetylcholine-induced coronary artery response in patients without angiographically demonstrable atherosclerotic coronary artery disease (CAD). The subjects were 39 men who had suspected CAD and who underwent coronary angiography. Coronary vasospasm was defined as a marked luminal narrowing or total occlusion provoked by the intracoronary administration of acetylcholine. Preheparin LPL mass was lower (p<0.05) in 25 subjects in whom vasospasm was induced by the acetylcholine provocation test than in the 14 subjects with a negative response. As regards preheparin LPL mass, the subjects with multiple vessel spasm had significantly low concentrations (p<0.05) compared with single vessel spasm, although serum lipid levels were not significantly different. Multiple regression analysis revealed only preheparin LPL mass had a significant absolute t-value (2.016) among the coronary risk factors. Low preheparin LPL mass is interpreted as reflecting an impaired acetylcholine-induced coronary relaxation in coronary vasospasm and preheparin LPL mass may be useful as a marker of early stage coronary atherosclerosis that is not detectable by angiography. (Jpn Circ J 2001; 65: 539 - 544)

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When heart rate (HR) increases, mitral flow can become monophasic. Prolonged isovolumic contraction and relaxation time (ICT and IRT), directly related to left ventricular (LV) function, can potentially influence the HR with monophasic mitral flow. The present study investigated the relation between HR that causes monophasic flow and LV function. During diagnostic catheterization, HR was increased using right atrial pacing by 2 beats/min every 2 min in a stepwise manner until the development of monophasic mitral flow in 17 patients with normal sinus rhythm. ICT, IRT, end-diastolic and end-systolic LV volumes, LV ejection fraction, LV peak + and -dP/dt, peak (+dP/dt)/P, and the relaxation time constant (tau) were measured by Doppler echocardiography or catheterization when monophasic mitral flow developed. The monophasic HR varied from 74 to 106 beats/min. By univariate analysis, ICT (p<0.01, r²=0.73), LV peak +dP/dt (p<0.05, r²=0.37), peak (+dP/dt)/P (p<0.01, r²=0.71), peak -dP/dt (p<0.05, r²=0.25), and tau (p<0.05, r²=0.33) had a significant correlation with monophasic HR. By multivariate analysis, prolonged ICT and reduced LV peak -dP/dt independently contributed to monophasic mitral flow with less increase in HR. Monophasic mitral flow with less increase in HR indicates impaired LV systolic and diastolic function during isovolumic contraction and relaxation. (Jpn Circ J 2001; 65: 545 - 549)

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The effects of exercise training on metabolic and functional recovery after myocardial transient ischemia were investigated in a rat model. Male Wistar Kyoto rats were subjected either to a 30-min left coronary artery occlusion followed by reperfusion or to a sham operation. At 4 weeks after operation, the rats were randomly assigned either to sedentary conditions or to exercise training for 6 weeks. In the ischemic rats, pinhole SPECT (single photon emission computed tomography) imaging with thallium-201 (²⁰¹Tl) and ¹²³I-(ρ-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) showed a reduction of both myocardial perfusion and fatty acid metabolism in the risk zone of the left ventricle (LV). The LV was dilated and the ejection fraction was decreased after ischemic injury. The severity score showed a significant decrease on both ²⁰¹Tl and BMIPP (²⁰¹Tl, from 19.9±2.7 to 17.0±2.2, p<0.05; BMIPP, from 21.5±2.4 to 18.6±1.9, p<0.05) after exercise training in the ischemic trained rats, but did not change significantly in their sedentary counterparts. Plasma levels of free fatty acids normalized in the ischemic trained rats, but elevated in the ischemic sedentary rats (0.53±0.05 vs 0.73±0.06 mmol/L, p<0.05). Furthermore, the trained rats had a significant increase in LV stroke volume (0.25±0.02 vs 0.21±0.01 ml/beat, p<0.05) and adaptive cardiac hypertrophy. These findings demonstrate that adaptive improvements in myocardial perfusion, fatty-acid metabolism and LV function were induced by exercise training after transient ischemia. (Jpn Circ J 2001; 65: 550 - 555)

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Although Fas-mediated cell death may play a role in atherogenesis, causal data in support of this hypothesis are lacking. The present study investigated the possibility that endothelial cells are involved in vascular smooth muscle cell (VSMC) apoptosis via the Fas - FasL pathway, and hence in atherogenesis. FACS analysis detected FasL on the surface of human umbilical vein endothelial cells (HUVECs) and immunofluorescence staining of the HUVECs demonstrated high levels of FasL in the intracellular compartment. FasL was down-regulated 4 h after tumor necrosis factor (TNF_α) treatment, coinciding with maximal surface expression of the adhesion molecules vascular cell adhesion molecule-1 and E-selectin. However, the down-regulation of FasL expression was transient, as surface expression returned within 24 h of TNF_α treatment. When cocultured with VSMCs, the FasL-expressing EC could kill the VSMCs in a manner that could be blocked by recombinant Fas-Fc, deployed as a soluble receptor for Fas. Moreover, when human coronary arteries were studied with immunohistochemistry using G247-4 monoclonal antibody for the detection of FasL, few FasL positive EC were observed in diffuse intimal thickening. In contrast, endothelium overlying the plaque showed prominent and uniform expression of FasL. These findings suggest that the Fas/FasL pathway can be used by EC to induce VSMC apoptosis in the atherosclerotic lesion. (Jpn Circ J 2001; 65: 556 - 560)

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Redox regulating mechanisms may be involved in the pathogenesis of viral myocarditis and thioredoxin (TRX) is a small multifunctional protein that contains a redox active sequence. The present study investigated the histopathology and characteristics of TRX expression in acute coxsackievirus B3 myocarditis in inbred strains of mice (severe myocarditis in DBA/2 mice, moderate myocarditis in BALB/c mice and mild myocarditis in C57BL/6 mice). Thioredoxin was upregulated and its expression correlated with the severity of the disease. In addition, 8-hydroxy-2'-deoxyguanosine, which is an established marker for oxidative stress, was concominantly positive in damaged myocytes. Thus, TRX may be specifically induced by the acute inflammatory stimuli in murine viral myocarditis, and the severity and development of acute viral myocarditis may be regulated by the cellular redox state. (Jpn Circ J 2001; 65: 561 - 564)

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Although the mechanisms of the clinical benefits of transmyocardial laser revascularization (TMLR) are considered to be angiogenesis with increased perfusion, denervation and placebo effect, it is unknown whether laser energy is a prerequisite in obtaining these beneficial effects. The present study investigated whether it is possible to create transmyocardial channels and induce angiogenesis by ultrasound. Myocardium was penetrated with an ultrasonically activated surgical blade by advancing the blade tip perpendicularly to the left ventricular free wall of the beating heart of 6 mongrel dogs. The power of ultrasound was set at either the lowest or highest of the system. The animals were killed 30 min (acute; n=3) and 2 weeks (chronic; n=3) after channel creation. Holmium:YAG laser, which is currently used for clinical TMLR, was used to create myocardial channels in 4 other dogs, which were also killed 30 min (n=2) and 2 weeks (n=2) after channel creation. The areas of acute channel core, acute thermal damage and chronic fibrosis were compared between the laser and ultrasound channels by Masson's trichrome stain. Factor VIII and proliferating cell nuclear antigen (PCNA) immunostaining were carried out on the samples obtained from chronic animals. The density of vessels and that of proliferating vascular endothelial cells and vascular smooth muscle cells around the channels were measured. The area of acute core was larger in the lowest and highest outputs of ultrasound than in laser channels (0.78±0.09, 1.0±0.12 vs 0.38±0.04 mm²; p<0.01). The area of acute damage in both laser and the highest output of ultrasound channels was greater than in the channels produced by the lowest output of ultrasound (4.43±0.28, 4.63±0.44 vs 2.90±0.29 mm²; p<0.01). The ratio of acute damage area to acute core area was greater in laser channels than in either type of ultrasound channel (16.86±1.66 vs 6.04±0.67, 7.86 ±1.07; p<0.01) and the area of chronic fibrosis was greater (3.23±0.20 vs 1.59±0.18, 2.24±0.20 mm²; p<0.01). Factor VIII and PCNA immunostaining revealed new vessels not only inside the areas of chronic fibrosis, but also in the surrounding myocardium, in both laser and ultrasound channels. Ultrasound created transmyocardial channels histologically similar to laser channels and angiogenesis was induced in the normal myocardium surrounding ultrasound channels. (Jpn Circ J 2001; 65: 565 - 571)

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A 52-year-old woman suffered from acute massive myocardial infarction in association with a large thrombus in the ascending aorta. She was a moderate smoker and was taking hormone supplement therapy for menopausal hormone insufficiency and the contraceptive pill for endometriosis. Cardiac angiography revealed a large mobile filling defect close to the orifice of the left coronary artery, but the left coronary artery could not be visualized. Her hemodynamic condition was impaired so greatly that intraarterial counterpulsation and intravenous thrombolysis was immediately performed. The thrombus dissolved in 1 h and recanalization of the left coronary artery was achieved without serious systemic thromboembolism. She has been doing well with no cardiac events for 7 years. This is the second report of a large thrombus in ascending aorta being the cause of acute myocardial infarction in the whole territory of the left coronary artery, and the first to diagnose such a thrombus antemortem and treat it successfully. (Jpn Circ J 2001; 65: 572 - 574)

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The present study evaluated the usefulness of 3-dimensional volume rendering (VR) images using electron-beam computed tomography (EBCT) in determining the possible causes of ischemia resulting from the anomalous origin of the right coronary artery (RCA) from the left sinus of Valsalva, which coursed between the ascending aorta and pulmonary trunk. Such anomalies could cause ischemia or sudden death without obstructive coronary artery disease. The suggested mechanism is either compression causing closure of the slit-like orifice of the anomalous artery as the aorta dilates with exertion or compression of the anomalous artery by the aorta and pulmonary trunk as it courses between these 2 arteries, which dilate with exercise. A 17-year-old male underwent EBCT coupled with a 100-ml intravenous injection of iodinated contrast medium. Data were reconstructed into 3-dimensional images through VR to evaluate the shape of the orifice and the spatial relationship of the RCA, ascending aorta and pulmonary trunk. Perspective VR showed the shape of the orifice of the left main trunk, which was not slit-like, and cut-plane VR showed the spatial relationship of both the lumen and the surface of the RCA, ascending aorta and pulmonary trunk, providing information on whether the ascending aorta or pulmonary trunk would compress the RCA and cause ischemia. (Jpn Circ J 2001; 65: 575 - 578)

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A 51-year-old woman with acute myocardial infarction underwent emergency coronary angiography. The patient had an episode of idiopathic thrombocytopenic purpura, and underwent splenectomy at the age of 36. On admission, platelet count in the peripheral blood was 43.2×10⁴/μl. During the initial emergency left coronary angiography, a thrombus was detected in the left main trunk. The thrombus was drawn back to the orifice of the left coronary artery, and finally disappeared into the aorta by injecting contrast media. After the thrombus disappeared, no stenotic lesion was detected in the left coronary artery. One month later, when acetylcholine-provocation coronary angiography was performed, marked vasospasm was detected in the left coronary arteries. Coronary thrombosis in the patient might have been induced by a coronary spasm, and the presence of thrombocytosis might also have affected the development of a coronary thrombus. However, it was spontaneously drawn back to the aorta by back flow of contrast media, which was injected via the entrance of the left coronary artery. A case of acute myocardial infarction whose thrombus occluded the left main coronary artery and was removed at first injection of contrast media is presented. (Jpn Circ J 2001; 65: 579 - 580)

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Rupture of the posterior wall of the left ventricle after mitral valve replacement is a dire complication associated with a very high mortality. This study reports a successful repair of type 1 left ventricular rupture, which occurred after mitral valve replacement concomitant with a left atrial reduction procedure, by combination of an intracardiac patch and an extracardiac buttress suture. In a case such as this, in which hemostasis is quite difficult to establish, this combination technique is particularly effective. (Jpn Circ J 2001; 65: 581 - 583)

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Although an increased expression of proinflammatory cytokines has been reported in cardiac tissue samples from patients with congestive heart failure (CHF) and in various animal models of CHF, the role of these cytokines in the disease remains to be determined. Dahl salt-sensitive (DS) rats fed a high salt diet develop hypertension, cardiac hypertrophy and eventually CHF. In the present study, DS rats were treated with FR167653 (1-[7-(4-fluorophenyl)-1,2,3,4-tetrahydro-8-(4-pyridyl)pyrazolo[5,1-c][1,2,4]triazin-2-yl]-2-phenylethanedione sulfate monohydrate), a new low molecular weight inflammatory cytokine inhibitor. Treatment with 10 mg/kg per day of FR167653 significantly prolonged the survival of the animals and also prevented the bodyweight loss associated with heart failure. In conclusion, a non-peptide proinflammatory cytokine inhibitor improved the survival of animals with heart failure. (Jpn Circ J 2001; 65: 584 - 585)

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