The mortality rate following rupture of an abdominal aortic aneurysm (AAA) is 80-90% and the main goal of treatment is to prevent rupture. Treatment of the aneurysm is generally recommended for patients with an aneurysm larger than 5 cm in diameter, and the only effective treatment has been to replace the aneurysm with a prosthetic graft. Traditionally, this is performed through a major laparotomy; that is, open surgical repair, which itself carries a mortality rate of 4-8% and requires a hospital stay of 7-10 days. In addition, some sick patients are deemed a prohibitive risk for such major surgery and, therefore, treatment may be deferred. Endovascular grafts (EVGs) that enable treatment of patients with AAA without the need for laparotomy were developed in the hope of improving on the shortcomings of the standard repair technique. In addition to the various industry-made EVGs the authors have been using a surgeon-made Montefiore Endovascular Grafting System (MEGS). The recent introduction of several industry-made devices has prompted some to postulate that MEGS is no longer required. The 60 patients with AAA treated from 1 July 1997 to 30 June 1998 were evaluated for the inclusion criteria for industry-made EVG protocols. Those excluded from these protocols were evaluated for the MEGS. Open surgical repair was reserved for those unsuitable for any EVG repair or those not consenting to EVG repair. Thirty-seven percent of all cases could be treated with an industry-made device. By using the MEGS, an additional 43% of the cases could be treated endovascularly. In total, 80% of AAAs were able to be treated endovascularly. The reasons for excluding patients from industry-made devices were a combination of the following factors: (1) Short (<1.5 cm) or angulated (>60) proximal necks, (2) iliac artery aneurysms, (3) small, diseased or tortuous access arteries, and (4) small distal aortas. The mean length of stay for those treated endovascularly was 2.3 days, whereas it was 9 days for those treated by open surgery. There was no difference in the morbidity and mortality rates. EVG repair is feasible and safe for the majority of patients with AAAs; however, long-term durability is yet to be shown. Despite the availability of industry-made devices, there appears to be a continuing role for MEGS, especially for difficult aneurysms including those patients with complex anatomy and those with ruptured AAAs. (Jpn Circ J 1999; 63: 829 - 837)

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Thrombolytic therapy improves survival after acute myocardial infarction (AMI) primarily by preserving left ventricular function. Its influence on the arrhythmogenic substrate remains uncertain. To investigate the electrophysiologic effects of thrombolytic therapy, signal-averaged electrocardiography, endocardial catheter mapping and programmed stimulation were performed in 93 consecutive patients with their first AMI who underwent thrombolytic therapy. Early reperfusion was achieved in 75 patients (group 1), but not in 18 patients (group 2). The incidence of the signal-averaged electrocardiogram abnormality was 11% in group 1 (8 of 75 patients) and 33% in group 2 (6 of 18 patients) (p<0.02). Catheter mapping detected delayed endocardial electrograms in 30 group 1 patients and 10 group 2 patients (p=NS). The spatial distribution of these electrograms was smaller, and the longest duration of endocardial electrograms was shorter in group 1 than in group 2 (p<0.01). Sustained monomorphic ventricular tachycardia was induced less commonly in group 1 (20%) than in group 2 (44%) (p<0.05). In conclusion, thrombolytic therapy can reduce the arrhythmogenic substrate and improve electrical stability after AMI. This antiarrhythmic effect may contribute, in part, to the improved survival of patients treated with thrombolytic drugs. (Jpn Circ J 1999; 63: 838 - 842)

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This study investigated the effects of aerobic exercise training on the early phase of the recovery process following acute myocardial infarction (AMI) in terms of the autonomic nervous system, cardiac function and exercise capacity. Twenty-eight patients in the first week after the onset of AMI were assigned randomly to either a training group or a control group. The training group performed aerobic exercise for 2 weeks. Cardiopulmonary exercise testing was performed 3 times during the 3 months after the onset. Heart rate variability, plasma norepinephrine (NE) levels, and cardiac index (CI) during exercise were measured. In the training group, plasma NE level and ΔCI (peak CI - rest CI) were significantly improved from 1 to 3 weeks after the onset, and the high frequency of heart rate variability and peak oxygen uptake were significantly increased up to 3 months after the onset. In the control group, the plasma NE level and the ΔCI during the 1-3 weeks post-AMI, the high frequency of heart rate variability and the peak oxygen uptake showed a tendency to improve up to 3 months after the onset. These results indicate that sympathetic nervous activity improves soon after the onset of AMI, in conjunction with improvement in cardiac function, and that this improvement is not affected by exercise training. In contrast, the recovery of parasympathetic nervous activity requires a longer period, along with the recovery of exercise capacity, which is facilitated by even short-term aerobic exercise training. (Jpn Circ J 1999; 63: 843 - 848)

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No flow is an unsolved issue in primary percutaneous transluminal coronary angioplasty (PTCA) for patients with acute myocardial infarction (AMI), and the pathophysiology of no-flow is undetermined. To evaluate the potential participation of coronary thromboembolism in no-flow during primary PTCA, the present study reviewed cinefilms of 256 consecutive patients who underwent primary PTCA for AMI within 24 h after the onset of chest pain between January 1992 and June 1998, focusing on the thrombus size. Angiographic no-flow was defined as the cessation of flow into the distal coronary circulation of the treated vessel with a to-and-fro contrast movement, not attributable to high-grade stenosis or spasm of the original target lesion. The coronary thrombus size was determined by using the 2-cm balloon catheter as a reference after crossing the infarct-related occluded artery with a guide wire. Angiographic no-flow was observed in 37 patients (37/256, 14%): 14 of 29 cases (48%) with a large thrombus (≥2 cm) versus 23 of 227 cases (9%) with a small thrombus (<2 cm, 14/29 vs 23/227, p<0.01). Among 37 patients who experienced angiographic no-flow, overt distal emboli were observed in 14 patients. A thrombolytic agent was used through a guiding catheter in 102 cases prior to or after balloon dilatation to prevent or attenuate distal embolism, particularly in all those cases with a large thrombus (29/29 100%), and angiographic no-flow was seen in 27 cases of this subgroup (27/102, 26%). It is suggested that distal thromboembolism plays an important role in the mechanism of angiographic no-flow during primary PTCA performed for AMI. (Jpn Circ J 1999; 63: 849 - 853)

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The effect of unilateral stellate ganglion block on cardiovascular regulation remains controversial, so the present study used power spectral analysis of heart rate variability to investigate its effect on the autonomic neural control of the heart. In 20 young healthy volunteers (mean age: 25 years), heart rate variability was determined before and after unilateral stellate ganglion block (right side 11, left side 9) using 8 ml of 1% mepivacaine during supine rest. Using autoregressive spectrum analysis, power spectra were quantified by measuring the area in 3 frequency bands: high-frequency power (lnHF, parasympathetic influence) from 0.15 to 0.40 Hz, low-frequency power (lnLF, predominantly sympathetic influence) from 0.04 to 0.15 Hz, and total-frequency power (lnTF) less than 0.40 Hz. Right stellate ganglion block decreased not only the lnLF component from 6.55±0.84 to 5.77±0.47 but also the lnHF component from 4.40 ±0.95 to 3.42±1.12 (p<0.05). In contrast, left stellate ganglion block changed neither the lnLF nor the lnHF component. The lnTF component was also decreased significantly by right stellate ganglion block from 7.80±0.95 to 7.01±0.36 (p<0.05), but was unchanged following left stellate ganglion block. Neither right nor left stellate ganglion block induced any significant change in both the RR and corrected QT intervals. However, changes in the RR interval induced by right stellate ganglion block showed significant positive correlation with changes in lnHF (p<0.005) and lnTF (p<0.05). These results suggest that (1) autonomic innervation to the sinus node is mainly through the right-sided stellate ganglion, (2) pharmacological right-sided stellate ganglion block may attenuate not only sympathetic but also parasympathetic activity and (3) following right stellate ganglion block the decrease in both the sympathetic and parasympathetic influence on the sinus node may inconsistently counterbalance and change the RR interval. (Jpn Circ J 1999; 63: 854 - 858)

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The present study investigated gender differences among adult patients with obstructive hypertrophic cardiomyopathy (OHCM) and resting gradient. Using outflow gradients >10 mmHg and the presence of asymmetrical septal hypertrophy of the left ventricle as inclusion criteria, 122 patients were identified among patients referred for echocardiographic examinations between May 1990 and October 1996. Clinical, echocardiographical and follow-up data were compared between male and female patients. The female patients were significantly older than male patients (mean age ± SD 66.7±10.5 vs 54.8±12.5 years). The female patients had a smaller interventricular septal wall thickness, less frequent systolic anterior movement of the mitral valve, more frequent association with hypertension, and less frequent association with ischemic heart disease (IHD) and giant T wave inversion. In this study population, adult female patients presented with OHCM 12 years later than males. Whether this represents female patients' reluctance to seek medical attention early, a different disease process that affects predominantly elderly females, or a gender-specific end organ response to aging, hypertension, IHD and other processes, or the protective effects of estrogen remains to be determined. (Jpn Circ J 1999; 63: 859 - 864)

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The aim of this study was to elucidate the electrophysiologic characteristics and clinical significance of the accelerated junctional rhythm (JR) that remains after termination of radiofrequency (RF) current delivery during catheter ablation (CA) for atrioventricular nodal reentrant tachycardia (AVNRT). Fifty consecutive patients with AVNRT (21M, 29F, age 48 years) underwent RF-CA targeting the slow pathway. JR occurred at 124 out of a total of 236 ablation sites (53%) during the RF delivery. With 15 RF deliveries (6.4%, n=10), JR remained after termination of the RF delivery (Post-JR). The mean cycle length of the Post-JR immediately after termination of the RF delivery was 639±124 ms and its duration was widely distributed from 3 s to more than 1 h. The Post-JR exhibited a spontaneous rate deceleration and overdrive suppression by rapid atrial pacing. The JR during the RF delivery followed by Post-JR had a greater time span in which the JR appeared, compared with that without Post-JR. The Post-JR had less sensitivity(18 vs 96%), but greater specificity (97 vs 59%) and a positive predictive value (60 vs 39%) in predicting successful ablation compared with JR seen only during the RF delivery. It is concluded that the presence of Post-JR might be a reflection of the intense effect of RF energy on the nodal or peri-nodal tissue. (Jpn Circ J 1999; 63: 865 - 872)

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This study aimed to clarify the significance of ST-segment depression in the lateral chest leads in anterior wall acute myocardial infarction (AMI) with ST-segment elevation. A total of 196 patients with their first anterior wall AMI (≤6 h) were divided into 2 groups according to the presence (group A, n=39) or absence (group B, n=157) of ST-segment depression ≥0.1 mV in V₅ and/or V₆ on the admission electrocardiogram. Patients with electrocardiographic confounding factors were excluded. No patients had persistent ST-segment depression in the lateral chest leads. Emergency coronary angiography revealed that group A had higher incidences of occlusion of the left anterior descending coronary artery (LAD) proximal to its first septal branch (77% vs 51%, p<0.01) and good collateral circulation than group B (46% vs 25%, p<0.05). Peak creatine kinase levels were significantly lower in group A than in group B (2060±1099 vs 2873±2077 IU/L, p<0.01). Left ventricular ejection fraction in the chronic phase was significantly greater in group A than in group B. Regional wall motion in the infarct region in the chronic phase was better in group A than in group B. These results indicate that patients with `transient' ST-segment depression in the lateral chest leads in anterior wall AMI had a relatively smaller infarct size, despite their higher incidence of occlusion of the LAD proximal to its first septal branch, because of their higher incidence of good collateral circulation. (Jpn Circ J 1999; 63: 873 - 876)

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An A-to-G transition at position 3243 of the mitochondrial DNA is known to be a pathogenic factor for mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS), diabetes and cardiomyopathy. This mutation causes dysfunction of the central nervous system in MELAS. Because the heart, as well as the brain and nervous system, is highly dependent on the energy produced by mitochondrial oxidation, these tissues are more vulnerable to mitochondrial defects. Cardiac abnormalities were assessed in 10 diabetic patients associated with this mutation using echocardiography and ¹²³I-metaiodobenzylguanidine (MIBG) scintigraphy, and compared with 19 diabetic patients without the mutation. Duration of diabetes, therapy, control of blood glucose and diabetic complications, such as diabetic retinopathy and nephropathy, were not different between the 2 groups. Diabetic patients with the mutation had a significantly thicker interventricular septum (16.8±3.7 vs 11.0 ±1.6 mm, p<0.001) than those without the mutation. Fractional shortening was lower in diabetic patients with the mutation than those without it (30.7±7.0 vs 42.5±6.6, p<0.001). MIBG uptake on the delayed MIBG image was significantly lower in diabetic patients with the mutation than in those without the mutation (mean value of the heart to mediastinum ratio: 1.6±0.2 vs 2.0±0.4, p>0.05). In conclusion, left ventricular hypertrophy with or without abnormal wall motion and severely reduced MIBG uptake may be characteristic in diabetic patients with a mutation in the mitochondrial tRNA^Leu(UUR) gene. (Jpn Circ J 1999; 63: 877 - 880)

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In hypertensive patients with left ventricular hypertrophy (LVH), the influence of exercise on the regional variations in ventricular repolarization is not well understood. The present study compared dispersions of QT and QT apex (QTD and QTaD), which are indices of regional variations in ventricular repolarization, between hypertensive patients with echocardiographic evidence of LVH and those without LVH. Seventy essential hypertensive patients underwent a modified Bruce protocol exercise test, and QTD and QTaD were measured at rest and at peak exercise level. All subjects had undergone coronary angiography and did not have coronary artery disease. None of them showed ST-segment depression during or after exercise. There were 20 patients with LVH and 50 patients without LVH. The QTD and QTaD at rest were not different between the patients with LVH and those without LVH (56±32 vs 57±28 ms, 52±20 vs 49±23 ms). At peak exercise level, QTaD was significantly decreased compared with the baseline in hypertensive patients without LVH (49±23 to 42±16 ms, p<0.05), whereas in patients with LVH QTaD increased (52±20 to 67±17 ms, p<0.05). QTaD at peak exercise level was positively correlated with the left ventricular mass index (r=0.357, p=0.0024). These data were unchanged after correction for heart rate using Bazett's equation. In conclusion, QTaD increased after exercise in hypertensive patients with LVH. Inhomogeneity of repolarization is induced by exercise stress in hypertensives with LVH. (Jpn Circ J 1999; 63: 881 - 884)

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Between January 1984 and December 1998, 19 patients (16 with Takayasu's arteritis, 3 with non-Takayasu's aortitis) underwent surgical treatment for aortic regurgitation resulting from the aortitis. Of the 19 patients, 14 had aortic valve replacement (AVR) and 5 had aortic root replacement. One patient (5.3%) died of graft infection during the hospital stay. During the follow-up period, 1 (5.6%) of the 18 postoperative patients died of paravalvular leakage due to valve detachment, which also required redo-operations in 2 patients with non-Takayasu's aortitis. Both patients were operated on during the active phase of the inflammation without perioperative steroid therapy. Although transmural pledgeted sutures were used for replacement of the detached prosthetic valve in 1 of these 2 patients, disruption of the aortic wall resulted in recurrence of valve detachment. In the other patient, aortic root replacement was successfully performed with the Cabrol technique in the second operation. Perioperaitve steroid therapy plays an important role in preventing complications after AVR when the valve replacement is carried out during the active phase of the inflammation, and for patients with non-Takayasu's aortitis, aortic root replacement should be considered to reduce the tension on the suture line and the native aortic valve annulus. (Jpn Circ J 1999; 63: 885 - 888)

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Complete atrioventricular septal defect (AVSD) associated with tetralogy of Fallot is a rare condition that still has problems in the postoperative period. The authors report their surgical experiences over the past 10 years. Nine children underwent total correction. The defect was repaired by the 2-patch technique and the atrioventricular valve was reconstructed by suturing the cleft and annuloplasty. A transannular right ventricular outflow patch was used in 5 patients. All patients had Down syndrome and a free-floating superior bridging leaflet. One patient died from cardiac failure. Although there was no reoperation or death in the late postoperative periods, mild mitral regurgitation occurred in 4 patients and there was moderate or severe pulmonary regurgitation in 2 patients. All survivors currently have no critical symptoms in their daily lives. With the standard of patient selection used, the optimal body weight was around 8 kg and PA index was 200 or more. Right ventriculotomy provided a better view for complete closure of the ventricular septal defect (VSD). In order to avoid re-regurgitation of the atrioventricular valve, the 2-patch technique is the most suitable procedure for total repair. (Jpn Circ J 1999; 63: 889 - 892)

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The aim of this study was to investigate the relationship between baroreflex sensitivity (BRS) and humoral factors in patients with congestive heart failure (CHF). BRS was assessed by the phenylephrine method in 16 patients with CHF and in 13 healthy controls. The CHF group was subdivided into 2 groups according to BRS (group A: <6 ms/mmHg, n=9; group B: ≥6 ms/mmHg, n=7). BRS was markedly depressed in CHF than in the controls (4.8±2.0 vs 8.3±3.6 ms/mmHg, p<0.01), and lower in group A than group B (3.3±1.3 vs 6.7 ±0.6 ms/mmHg, p<0.01). The plasma human atrial natriuretic peptide (h-ANP) level in group A was significantly higher than in group B (54.6±27.6 vs 18.0±7.4 pg/ml, p<0.01), and a significant inverse correlation was observed between plasma h-ANP and BRS (r=-0.635, p<0.01). However, there were no significant differences between the 2 groups in plasma catecholamine concentration, plasma renin activity and cardiac function by echocardiogram. These findings suggest that the elevation of endogenous ANP may also serve to compensate for impaired BRS in patients with CHF, in addition to its principal actions, such as diuresis and vasodilation. (Jpn Circ J 1999; 63: 893 - 899)

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A new canine myocardial infarction model using thrombi induced by closed-chest injection of thrombin and autogenous blood with fibrinogen into coronary arteries was developed. Occlusive thrombi were formed in all treated animals. Occluded vessels did not spontaneously reperfuse 1 day after occlusion, but did so within 3 days. Infarction was confirmed by increased levels of creatine kinase-MB, glutamate-oxaloacetate transaminase and α-hydroxybutyrate dehydrogenase. Additionally, the left ventricular ejection fraction (LVEF) decreased within 0.5 h after occlusion and had not improved 4 weeks later. After 1 week, extensive transmural anteroinferior myocardial infarction was observed and heart mass had increased. By 4 weeks after occlusion, pulmonary capillary wedge pressure and central venous pressure were increased, and oxygen pressure was decreased. Dropout of nuclei in cardiomyocytes and increased amount of collagen fiber were observed in myocardial infarct regions of hearts excised 4 weeks after occlusion. This canine model may be useful and convenient in evaluating treatment efficacy and the long-term outcome of acute myocardial infarction. (Jpn Circ J 1999; 63: 900 - 905)

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A 68-year-old male with acute myocardial infarction (AMI) was admitted to the hospital with chest pain that had started 1 day earlier. The serum levels (ng/ml) of hepatocyte growth factor (HGF) were 1.06, 1.22, 1.05, 0.72 and 0.64 on days 2, 3, 4, 5 and 6 postinfarction, respectively. He died suddenly due to cardiopulmonary arrest on day 6. At autopsy, approximately 400 ml of bloody pericardial fluid, caused by rupture of the left ventricle, was detected and the c-Met expression in the myocardium was immunohistochemically found to be most intense in the border zone of the infarcted and non-infarcted region. Although there was no c-Met expression in the infarcted myocardium, it was increased in the myocardial cells surrounding the blood vessels. This is the first report to show sequential changes of HGF in the serum, as well as c-Met expression in the myocardium, in a patient with AMI. (Jpn Circ J 1999; 63: 906 - 908)

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Right ventricular thrombus is a very rare manifestation of cardiovascular Behcet's disease. A 25-year-old man was admitted to hospital due to cough and fever of unknown origin. He experienced repetitive pulmonary embolism due to a right ventricular thrombus, which was surgically removed. A diagnosis of Behcet's disease was made based on his clinical course and the histological findings of the right ventricular wall and the skin lesion. He was quickly relieved of his symptoms after warfarinization and cyclosporine therapy. (Jpn Circ J 1999; 63: 909 - 911)

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A 65-year-old male with unstable angina underwent coronary angiography, which revealed a significant stenotic lesion in the right coronary artery. This narrowing was subsequently treated with the Multi-Link stent. During the balloon inflation associated with stent deployment, balloon rupture occurred and resulted in overdilatation of an elastic membrane in the stent delivery system. This, in turn, resulted in coronary dissection, which required treatment with further stenting. (Jpn Circ J 1999; 63: 912 -913)

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An unusual case of an inflammatory abdominal aortic aneurysm (IAAA) associated with coronary aneurysms and pathological fracture of the adjacent lumbar vertebrae. The associated coronary lesions in cases of IAAA are usually occlusions. In the present case, it was concluded that a possible cause of the coronary aneurysm was coronary arteritis and the etiology of the pathological fracture of the lumbar vertebrae was occlusion of the lumbar penetrating arteries due to vasculitis resulting in aseptic necrosis. Inflammatory AAA can be associated with aneurysms in addition to occlusive disease in systemic arteries. The preoperative evaluation of systemic arterial lesions and the function of systemic organs is essential. (Jpn Circ J 1999; 63: 914 - 916)

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