Restenosis after coronary artery stent implantation is attributed chiefly to intimal hyperplasia, which is prevented experimentally by angiotensin-converting enzyme (ACE) inhibitors. Therefore, the present study investigated whether the effect of quinapril, a tissue-specific ACE inhibitor, on the prevention of coronary restenosis differs according to ACE polymorphism. One hundred consecutive patients with successful stent implantation were randomly assigned to quinapril and control groups. Both follow-up angiography and ACE polymorphism analysis were obtained from 92 patients (control, 46; quinapril treatment, 46). The prevalence of risk factors did not differ statistically according to quinapril treatment or ACE genotypes. There was no statistically significant difference in the occurrence of restenosis 6 months after stenting between the groups. Quantitative coronary angiography revealed that quinapril treatment resulted in significantly higher minimal lumen diameter and significantly lower percent diameter stenosis (22.9±22.6 vs 37.1±19.7% in the control group, p<0.05) in patients with the D allele although there was no difference in those with the II genotype. In addition, intravascular ultrasound revealed that quinapril treatment significantly prevented the loss of minimal lumen cross-sectional area and the increase in percent area stenosis (34.5±14.0 vs 53.3±16.4% in the control group, p<0.05) in patients with the D allele compared to those with the II genotype. These results suggest that the administration of ACE inhibitors for the attenuation of lumen loss after coronary stent implantation is best for subjects with the D allele of the ACE genotype. (Circ J 2002; 66: 311 - 316)

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Nicorandil, a hybrid nitrate and ATP-sensitive potassium channel opener, has had a preconditioning effect in some coronary angioplasty studies. The present study investigated whether the cardioprotective effects of nicorandil involve coronary collateral function. Thirty-two patients with stable angina pectoris were randomized to receive a 1-min intravenous infusion of nicorandil (100 μg/kg) or normal saline. Five minutes later they underwent three 2-min balloon inflations 5-min apart. The maximum ST-segment elevation (ΔSTmax), the sum of ST-segment elevations in all leads (ΣST), and the chest pain score were determined at the end of each balloon inflation. The collateral flow index (CFI) was derived from simultaneous measurement of the mean aortic pressure and the coronary wedge pressure obtained from a pressure guidewire during balloon inflation. The ΔSTmax, ΣST, and chest pain score decreased progressively during the 3 sequential balloon inflations in both groups, and the ΔSTmax and ΣST were less in the nicorandil group than in the control group during each inflation. The CFI did not change during the 3 inflations in either group and was similar in the 2 groups during each inflation. In conclusion, pretreatment with intravenous nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty. (Circ J 2002; 66: 317 - 322)

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Nationwide clinico-epidemiological surveys of cardiomyopathies in Japan were carried out. Disorders surveyed included idiopathic dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restrictive cardiomyopathy (RCM), arrhythmogenic right ventricular dysplasia (ARVD), mitochondrial disease, Fabry's disease of the heart and prolonged Q-T interval syndrome. The total number of patients was estimated at 17,700 for DCM, 21,900 for HCM, 300 for RCM, 520 for ARVD, 640 for mitochondrial disease, 150 for Fabry's disease of the heart, and 1,000 for prolonged Q-T interval syndrome. The prevalence of both DCM and HCM was higher in men than women: the male-to-female ratios were 2.6 and 2.3 for DCM and HCM, respectively. Detailed data on patients with DCM or HCM were collected by a follow-up survey. In 1 year more patients with DCM (5.6%) died than with HCM (2.8%): congestive heart failure (CHF) and arrhythmias were the leading causes of death for DCM and HCM, respectively. Angiotensin converting enzyme inhibitors (64.6%) and β-adrenergic blockers (40.9%) are commonly used to treat the CHF complicating DCM and may be associated with the clinical improvement in a significant number of DCM patients. Thus, the nationwide surveys of Japanese patients have yielded important current epidemiological and clinical information on the characteristics of cardiomyopathies in Japan. (Circ J 2002; 66: 323 - 336)

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The purpose of this study was to define the role and indications of partial left ventriculectomy (PLV) in children with end-stage dilated cardiomyopathy (DCM). Clinical data were collected by retrospective chart review of children with DCM who were treated from 1997 to 2000. Four patients underwent PLV (PLV group) and 5 patients were managed without PLV (non-PLV group). In the PLV group, 2 patients are well 18 and 35 months postoperatively. One infant survived 6 months and then successfully underwent heart transplantation, and the other child died of hemoptysis 2 weeks postoperatively. Factors affecting outcome were preoperative status, in particular whether surgery was performed urgently or electively. In the non-PLV group, 4 patients were well controlled by medical treatment and 1 infant underwent mitral valve replacement for severe mitral regurgitation. The cardiothoracic ratio ranged from 72% to 76% in the PLV group and from 45% to 60% in the non-PLV group. The percentage of the expected left ventricular diastolic dimension ranged from 184% to 218% in the PLV group and from 109% to 163% in the non-PLV group. Ejection fractions in the PLV group were from 10% to 22% and from 36% to 56% in the non-PLV group. The serum brain natriuretic peptide concentration was above 1,200 pg/ml in the PLV group and below 168 pg/ml in the non-PLV group. In conclusion, PLV is indicated for selected children with end-stage DCM, and is most appropriate when medical therapy is not effective and heart transplantation is unavailable. (Circ J 2002; 66: 337 - 340)

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In areas of severe asynergy, the clinically important task is to identify functionally recoverable myocardium. Fourteen patients with asynergy were investigated by H₂ ¹⁵O dynamic positron emission tomography imaging before revascularization. Regional myocardial blood flow (MBF) was determined and the water-perfusable tissue fraction (PTF) for each region of interest and the total anatomical tissue fraction (ATF) were estimated. The PTF/ATF was analyzed as the water perfusable tissue index (PTI). Asynergy was defined as segments with wall motion more than 2 SD below than that of a normal population. An increase of >0.8 SD in anterior wall segments with asynergy and an increase of >0.6 SD in inferior wall asynergy were defined as significant improvements of wall motion indicative of viable myocardium. Fifteen segments with wall motion abnormalities less than -2 SD and 10 control segments were identified; 7 segments recovered and 8 segments did not. MBF was similar in both groups of segments before revascularization (0.78 ±0.27 vs 0.73±0.18 ml · min ^-1 · g^-1, NS). The PTI in the recovered segments was significantly higher than that in the unimproved segments (0.734±0.058 vs 0.592 ±0.038, p<0.0001) and was similar to that of the control segments. After revascularization, the PTI correlated with the SD of wall motion (p<0.05, r=0.58). PTI may be a good predictor of contractile recovery after revascularization. (Circ J 2002; 66: 341 - 344)

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The peripheral pulmonary artery stenosis (PPS) that complicates congenital heart anomalies can improve after percutaneous transluminal balloon angioplasty (PTA), despite an initial poor response, but there is little information concerning the factors that determine such remodeling. The present study reviewed the hemodynamic and angiographic data before, immediately after, and at late follow-up after PTA for 17 lesions in 14 patients. Lesions were classified into either the (+) group (with pulmonary artery remodeling) or the (-) group (without remodeling). Remodeling was defined as an increase of more than 30% in the predictive percent of normal (%N) of the peripheral pulmonary artery diameter at late follow-up compared with the diameter immediately after PTA. Remodeling occurred in 6 of 17 lesions (35%), and the pressure gradient immediately after PTA was significantly smaller (<10 mmHg) in the (+) group than in the (-) group. Late expansion of the lesion (remodeling) occurs after PTA in some children with PPS and an adequate initial reduction in the pressure gradient favors subsequent remodeling. (Circ J 2002; 66: 345 - 348)

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Coronary perforation is a rare but serious complication that occurs during percutaneous coronary intervention (PCI). This study examines the frequency of coronary perforation during PCI, evaluates the management strategies used to treat perforations, and describes the long-term prognosis of patients who have developed coronary perforation during PCI. Coronary perforations were found in 69 (0.93%) of 7,443 consecutive PCI procedures, occurring more often after use of a new device (0.86%) than after use of balloon angioplasty (0.41%) (p<0.05). Coronary perforation was attributable solely to the coronary guidewire in 27 (0.36%) cases. Coronary perforations were divided into 2 types: (1) Those with epicardial staining without a jet of contrast extravasation (type I, n=51), and (2) those with a jet of contrast extravasation (type II, n=18). Patients with type I and type II perforations were managed by observation only (35% and 0%, respectively), reversal of anticoagulation (57% and 94%), pericardiocentesis and drainage (27% and 61%), and prolonged perfusion balloon angioplasty (16% and 100%). Two patients with type II perforations required emergency coronary artery bypass surgery. There were no in-hospital deaths. Late pseudoaneurysms developed in 18 (28.6%) patients during the 13.4±11.3 months' follow-up period, and were more common in patients with type II perforations (72.2% vs 11.1% with type I perforations; p<0.001). During the follow-up period, no patient had evidence of coronary rupture. The results suggest that coronary perforation is uncommon after PCI, and can be managed without cardiac surgery in the majority of cases. Late pseudoaneurysms developed in some patients, particularly in patients with type II perforations, but there were no late consequences of coronary perforation after PCI. (Circ J 2002; 66: 349 - 356)

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Endoscopic transthoracic sympathicotomy (ETS) is a minimal invasive procedure of thoracic sympathetic block and has been used successfully in the treatment of primary palmar hyperhidrosis. To examine the effect of Th 2-3 ETS on hemodynamic responses to submaximal upright treadmill exercise in humans, cardiac output, plasma noradrenaline and adrenaline at rest and during the last 40 s of stage 2 in a modified Bruce protocol were measured before and after ETS in 21 patients with primary palmar hyperhidrosis. Heart rate, mean arterial pressure, rate - pressure product, and noradrenaline decreased at rest and at submaximal exercise after ETS. Cardiac index at rest did not change either before or after ETS, but decreased (8.9±0.6 vs 6.8±0.4 L · min^-1 · m^-2; p<0.01, mean ± SEM) at submaximal exercise after ETS. Stroke index and systemic vascular resistance were similar both at rest and at submaximal exercise before and after ETS. Thus, ETS reduces myocardial oxygen demand and plasma noradrenaline levels both at rest and during exercise without significantly depressing cardiac function in terms of stroke volume. (Circ J 2002; 66: 357 - 361)

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Previous reports suggest that vessel remodeling is the most important factor in late lumen loss in non-stented lesions, but because results of directional coronary atherectomy (DCA) show that increased plaque area (PA) is also important, the aim of this study was to redefine the mechanism of late lumen loss after DCA. One hundred and twenty lesions that underwent DCA with intravascular ultrasound (IVUS) guidance and serial IVUS analysis were studied, and vessel area (VA), lumen area (LA), PA (VA-LA) and corrected values (each value divided by the value of VA pre procedure to correct the vessel size) were analyzed. During follow-up, corrected VA (cVA) decreased by 0.058±0.191, whereas corrected PA (cPA) increased by 0.087±0.159. Though the %PA (PA/VA) after the procedure showed significant negative correlation with the subsequent change in cPA, it did not correlate with the subsequent change in cVA. In conclusions, the mechanism of late lumen loss after DCA consists of both arterial remodeling and plaque proliferation, and the residual %PA after the procedure determines the subsequent lumen loss. With a lower %PA, a change in the PA contributes more to late lumen loss than do changes in VA. With a high %PA, a change in the VA contributes more to late lumen loss. (Circ J 2002; 66: 362 - 366)

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The efficacy of empirical chronic oral amiodarone therapy in 129 patients with sustained ventricular tachyarrhythmia (VT/VF) and structural heart disease is evaluated. Twenty-nine patients were treated with class I drugs and monitored by electrophysiological study (EPS) and Holter electrocardiogram (ECG) (class I). The remaining 100 non-responders to the class I drugs were treated with oral amiodarone, of whom 70 were tolerant (AMD⁺) and 30 were intolerant (AMD^-). Patients were followed up to 36 months. The primary and secondary end-points were recurrence of VT/VF and hypothetical death, respectively; whereby, hypothetical death was defined as actual death and the event of rapid VT/VF (heart rate >240 beats/min) in patients with an implantable cardioverter defibrillator. Class I and AMD+ patients showed a better prognosis than AMD- patients. The VT/VF event free at 36 months in class I (64.8%) and AMD⁺ (56.1%) patients were significantly higher than that in AMD^- (27.2%) (p<0.01) patients. Hypothetical survival rates in class I (92.0%) and AMD⁺ (83.6%) patients were significantly higher than that in AMD^- (57.0%) (p<0.001) patients, but there were no significant differences in the actual survival rate among the 3 patient groups. The independent clinical factors suppressing the recurrence of VT/VF (Cox hazard) were treatment with amiodarone (p=0.02, 95% confidence interval (CI) =0.19-0.86) and EPS/Holter ECG-guided Class I drugs (p=0.04, 95% CI=0.14-0.94). The results demonstrate that empirical amiodarone has a substantial long-term benefit that is comparable to EPS/Holter ECG-guided class I drugs in the treatment of high-risk patients with VT/VF and structural heart disease. (Circ J 2002; 66: 367 - 371)

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The effect of colforsin daropate hydrochloride (colforsin), a water-soluble forskolin derivative, on blood flow in internal mammary artery (IMA) grafts was evaluated in a prospective randomized study of 26 patients undergoing coronary artery bypass grafting. Patients were randomized to receive either colforsin treatment (colforsin; n=14) or no colforsin treatment (control; n=14). Administration of colforsin (0.5 mg · kg^-1 · min ^-1) was started after induction of anesthesia and was continued for 6 h. IMA blood flow and hemodynamic measurements were assessed perioperatively. During cardiopoulmonary bypass (CPB), perfusion flow was adjusted to 2.5 L/m2 and IMA free blood flow was measured. IMA blood flow was also measured 1 h after CPB by an ultrasonic flow meter. Systemic vascular resistance was significantly lower in the colforsin group during and after CPB. IMA blood flow was significantly greater in the colforsin group than in the control group during (44±2 vs 33±3 ml · min^-1 · m^-2, p=0.02) and after CPB (38±6 vs 20±3 ml · min^-1 · m^-2, p=0.01). IMA blood flow 1 h after CPB correlated inversely with concurrent systemic vascular resistance (r=-0.61, p=0.001). Intraoperative administration of colforsin daropate hydrochloride caused potent vasodilation, resulting in an increase in IMA blood flow. The results indicate that the regimen can be used perioperatively in patients undergoing coronary artery bypass grafting. (Circ J 2002; 66: 372 - 376)

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The Cardiac Arrhythmia Suppression Trial has shown that treatment with flecainide is associated with an increased incidence of cardiac death in patients following myocardial infarction. It is believed that there is a complex mechanism involving an interaction between flecainide, sympathetic activation, and acute ischemia that is responsible for the increased risk of sudden death. The purpose of this study was to determine the effects of flecainide on muscle sympathetic nerve activity (MSNA) in humans. We measured MSNA using microneurography and cardiac output using the dye dilution method in 30 healthy individuals. Measurements were made at rest and after the oral administration of flecainide (200 mg, n=12) or placebo (n=9), or intravenous administration of propranolol (0.2 mg/kg, n=9). Flecainide significantly increased heart rate and decreased the cardiac index (both p<0.01). Flecainide increased the burst rate from 16.7±3.5 to 23.3±4.1 bursts/min and the burst incidence from 26.6±5.1 to 34.7±5.6 bursts/100 heartbeats (both p<0.01). For all of the hemodynamic parameters except heart rate, the effects of propranolol were similar to those of flecainide. Propranolol also increased the burst rate by 52±34% and the burst incidence by 106±39%. These results suggest that flecainide suppresses myocardial contractility and produces reflex-mediated increases in sympathetic nerve firing in humans. (Circ J 2002; 66: 377 - 381)

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To investigate whether microvascular lesions are present in the skin of patients with chronic congestive heart failure (CHF), skin biopsies were performed at the time of cardiac catheterization, and the results were compared with control subjects. The diagnosis of CHF was done by cardiac catheterization with reference to the elevation of plasma levels of brain natriuretic peptide (BNP). Although the severity of arteriolar hyalinosis did not correlate with the New York Heart Association functional class, increased hyalinosis was found in skin biopsies from 17 of 20 patients with CHF, but in none of the 6 control subjects. These results indicate that microangiopathic alterations in arterioles may exist in patients with CHF and therapy for peripheral vascular remodeling might be considered for such patients. (Circ J 2002; 66: 382 - 384)

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Autoimmune myocardial injuries are involved in the pathogenesis of myocarditis and dilated cardiomyopathy, but effective strategies for treating myocardial inflammation have not yet been established. The present study investigated the effects of suramin, a growth factor blocker, on experimental autoimmune myocarditis (EAM) in rats. Lewis rats were immunized with cardiac myosin and placed into one of 4 groups: every 72 h for 1 month the control group (C) was subcutaneously injected with saline; group L received 4 mg/kg of suramin; group M, 10 mg/kg; group H, 40 mg/kg. The heart weight/body weight ratios of the M and H groups were significantly lower than that of the C group. Macroscopic and microscopic scores for myocarditis were reduced in the M and H groups. The expression of transforming growth factor (TGF)-β1 mRNA in the heart was significantly decreased in the M and H groups compared with the C. In the next experiment, we investigated the effects of suramin on the cytokine milieu in EAM. The serum level of interleukin-10 on day 15 was significantly increased by suramin treatment. Furthermore, suramin increased the number of T cells with Th2 function in the popliteal lymph nodes. Suramin suppressed myocardial inflammation in EAM and was associated with modulation of the Th1/Th2 cytokine milieu and reduced TGF-β1 expression in the heart. (Circ J 2002; 66: 385 - 389)

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Ca²⁺ influx via the Na⁺/Ca ²⁺ exchanger (NCX) may lead to Ca²⁺ overload and myocardial injury in ischemia - reperfusion. Direct evidence that increased cytoplasmic Ca²⁺ concentration ([Ca ²⁺]_i) is mediated by the reverse mode of the NCX is limited, so in the present study the [Ca²⁺] _i dynamics and left ventricular pressure were monitored in perfused beating hearts. The effects of KB-R7943 (KBR), a selective inhibitor of the NCX in the reverse mode, were analyzed during low-Na ⁺ exposure and ischemia - reperfusion. Hearts from Sprague-Dawley rats were retrogradely perfused and loaded with 4 μmol/L fura-2 to measure the fluorescence ratio as an index of [Ca²⁺]_i. To evaluate KBR effects on the reverse mode exchanger, the increase in [Ca²⁺] _i induced by low-Na⁺ exposure (Na⁺: 30 mmol/L, 10 mmol/L caffeine pre-treatment) was measured with and without 10 μmol/L KBR (n=5). In another series, the hearts were subjected to 10 min of low-flow ischemia with pacing, followed by reperfusion in the absence (n=6) or in the presence of 10 μmol/L KBR (n=6). Background autofluorescence was subtracted to estimate the ratio in the ischemia - reperfusion protocol. KBR significantly suppressed the increase in [Ca²⁺] _i induced by low-Na⁺ (40.2±11.2% of control condition, p=0.014), as well as on increase in diastolic [Ca²⁺]_i during ischemia (% increase from pre-ischemia in [Ca²⁺]_i at 10 min: KBR, 17.9±6.4%; no KBR, 44.4±7.7%; p=0.024). After reperfusion, diastolic [Ca²⁺]_i normalized more rapidly in KBR-treated hearts (% increase at 1 min: KBR, 4.5 ±7.0%; no KBR, 39.8±12.2%; p=0.03). Treatment with KBR also accelerated recovery of the rate - pressure product on reperfusion (1 min: KBR, 8,944±1,554 min^-1 · mmHg; no KBR, 4,970±1,325; p<0.05). Thus, inhibition of the reverse mode exchanger by KBR reduced ischemic Ca2+ overload and possibly improved functional myocardial recovery during reperfusion in a whole heart model. (Circ J 2002; 66: 390 - 396)

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To determine whether acute pressure overload (POL) can stimulate adrenomedullin (AM) production, the response of ventricular AM gene expression and plasma AM concentration to aortic banding was investigated in the rat. Furthermore, any link between AM expression and the renin - angiotensin system (RAS) enhanced by acute POL was examined using: a Ca channel blocker (manidipine), an angiotensin II type 1 receptor antagonist (candesartan), and an angiotensin-converting enzyme inhibitor (quinapril). Rats with acute POL produced by suprarenal aortic banding were studied 1, 5 and 14 days after surgery. Plasma AM concentrations in banded rats at day 1 increased 1.49-fold (p<0.01), then gradually declined to near the control level at day 14. Plasma AM concentrations correlated with plasma renin activity (PRA) (p<0.001). Adrenomedullin mRNA expression in the left ventricle (LV) increased 1.35-fold (p<0.05) at day 1. This increase was not significant at either 5 or 14 days after surgery. Adrenomedullin mRNA expression in the right ventricle on days 1 and 5 increased by 1.46-fold (p<0.05) and 1.52-fold (p<0.05), respectively. Candesartan, quinapril and manidipine reduced systolic blood pressure equally and activated PRA at day 1. However, augmented LV AM gene expression was suppressed completely by candesartan and quinapril, but remained unaffected by manidipine. In conclusion, POL induces a rapid increase in cardiac AM gene expression and in plasma AM concentrations. Cardiac AM transcription could therefore be partly regulated by RAS in suprarenal aortic banding rats. (Circ J 2002; 66: 397 - 402)

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ATP-sensitive K⁺ (K_ATP) channel openers have a cardioprotective effect and so mexiletine (Mex), a class Ib anti-arrhythmic drug, may also be cardioprotective because of its K_ATP channel-opening effect. The present study examined the effect of Mex on acute myocardial ischemia in a closed-chest acute ischemia and reperfusion model in rabbits. The rabbits were divided into 3 groups: (1) control (n=8); (2) Mex (n=8), continuous infusion of mexiletine (24 mg · kg ^-1 · h^-1); and (3) Mex + Gli (n=8), pre-administration of glibenclamide (Gli; 0.5 mg/kg) followed by mexiletine infusion. The incidence of arrhythmia, the hemodynamics and left ventricular ejection fraction (LVEF), and the infarct size were evaluated and compared among the 3 groups. The incidence of fatal ventricular fibrillation (VF) was least in the Mex group. The LVEF at 30 min after reperfusion was least in the Mex group, but at 360 min after reperfusion, it was least in the Mex + Gli group. The area of myocardial infarction determined by 2,3-triphenyltetrazolium chloride (TTC) staining was smallest in the Mex group. In this model, Mex reduced infarct size and improved left ventricular function during the late phase after reperfusion, although the effect was totally negated by the addition of glibenclamide. (Circ J 2002; 66: 403 - 410)

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The influence of ischemic preconditioning (IP) and mitochondrial _ATP-sensitive potassium (mito-K_ATP) channel openers on chronic left ventricular (LV) remodeling remains unknown, so the effect of IP and mito-K_ATP channel openers on the LV pressure - volume curve was assessed in rats subjected to 30 min ischemia followed by a 3-week reperfusion. Infarct size was histologically determined at 3 weeks after reperfusion. The LV pressure - volume curve was significantly shifted left by IP, diazoxide and nicorandil compared with the controls. These effects were blocked by the selective mito-K_ATP channel blocker 5-hydroxydecanoate. The LV remodeling and the infarct size at 3 weeks after reperfusion correlated well, indicating that the reduction of LV remodeling in the ischemic - reperfused model was strongly influenced by attenuation of the ischemic injury. LV remodeling in the chronic phase is attenuated by IP and mito-KATP channel openers with concomitant reduction of infarct size. (Circ J 2002; 66: 411 - 415)

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A 25-year-old woman was admitted because of acute myocarditis. Echocardiogram revealed hypokinesis of the left ventricle with increased wall thickness, but on day 7, the wall motion normalized. Cyclic variation of myocardial integrated backscatter on day 1 was reduced to 1.8 dB (normal range, 2.9-5.3 dB) and normalized to 3.2 dB on day 3. The normalization of the cyclic variation of integrated backscatter in the myocardium preceded the recovery of the left ventricular wall contractility, suggesting the ability of tissue characterization to predict recovery of cardiac function. (Circ J 2002; 66: 416 - 418)

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A 73-year-old woman suffering from septic shock was given circulatory assistance by intra-aortic balloon pumping (IABP). Eleven hours later, pumping stopped abruptly and blood reflux was observed in the intra-aortic balloon catheter (IABC). We removed it and inserted another IABC; 3.5 h later, pumping stopped again and blood reflux was seen. Removal of the IABC was attempted, as the systolic aortic pressure remained above 100 mmHg, but there was resistance during the removal and as a result 7.5 cm of the catheter from the tip remained inside the vessel. Fluoroscopy indicated that the metal tube that formed the central lumen in the balloon was fractured, and that its edge had perforated the femoral artery. The balloon was then removed surgically. Fracture of the metal tube and balloon perforation were confirmed in both the damaged IABCs. Postoperative computed tomography and magnetic resonance imaging indicated a highly severe posterior - anterior bend in the patient's aorta. A vessel model similar to the aorta in this case was made and a reproducibility test was conducted; the central lumen fractured within 3 h and under a microscope the profile of the fractured test lumen was similar to the one in the clinical case. These findings suggest that placing a pumping IABC in a bending aorta causes fracture of the central lumen from fatigue failure because the central lumen is under excessive stress. (Circ J 2002; 66: 419 - 422)

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Perforation of the proximal descending aorta occurred in a patient on intra-aortic balloon pump (IABP) support after emergency coronary intervention for acute myocardial infarction. The IABP catheter was inserted under fluoroscopic guidance into the right femoral artery without difficulty, but after 8 h on IABP support the patient went into shock with a left hemothorax. Emergency surgery was performed with cardiopulmonary bypass and a perforation of the proximal descending aorta with active bleeding was found and successfully repaired. A distorted descending aorta in which the IABP catheter was kinked, as in the aortic arch, was discovered during surgery and confirmed postoperatively with 3-dimensional computed tomography scans, particularly in the lateral view. Not only the antero-posterior but also the lateral fluoroscopic view is recommended to prevent aortic perforation by a kinked IABP catheter. (Circ J 2002; 66: 423 - 424)

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A 62-year-old woman with a history of pulmonary embolism and primary antiphospholipid syndrome (PAPS) with positivity for lupus anticoagulant was admitted to hospital with shortness of breath. A filter had been implanted in her inferior vena cava (IVC) 5 years previously. Emergency echocardiography revealed a lobulated, mobile echogenic mass on the tricuspid valve, and on pulmonary perfusion scintigraphy several apparently new defects were noted. Fibrinolytic therapy improved her symptoms and the pulmonary perfusion, then intravenous heparinization was continued for a further week. Repeat echocardiography performed on the 7th day of the admission showed complete disappearance of the mass, which was retrospectively diagnosed as a thrombus based on its resolution with fibrinolytic and anticoagulant therapies. (Circ J 2002; 66: 425 - 427)

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