Coronary balloon angioplasty is now well accepted as an effective therapy for patients with significant coronary artery stenosis. However, a number of deficiencies, including short-term complications, long-term restenosis, and limited application to complex morphologic lesions, restrict the widespread use of this technique. The precise lesion measurement provided by quantitative coronary angiography and intracoronary ultrasonography is a prerequisite for the optimization of balloon dilation or stent implantation. The short-term outcome may be improved by stent implantation, as this can prevent acute closure by acting as a scaffold for the disrupted vessel wall. The indications for percutaneous revascularization have been extended to chronic total occlusion by using a special guidewire, a laser wire and a coronary stent. Local drug delivery techniques to distribute agents to target revascularization sites may play a role in reducing the restenosis rate. Although the limitations of balloon angioplasty have led to the introduction of new devices, it remains to be seen whether these new devices can demonstrate, in a scientific manner, their safety, feasibility and superiority over conventional balloon angioplasty. Percutaneous coronary revascularization therapy may be an acceptable alternative to coronary bypass surgery in the future. However, to confirm this, a large multicenter randomized study is necessary to compare new percutaneous coronary interventional devices with bypass surgery. Additionally, further studies are required to demonstrate the most effective device for treating specific lesions in each individual patient. (Jpn Circ J 1997; 61: 1 - 13)

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Patients with abdominal aortic aneurysm (AAA) associated with iliofemoral occlusive disease due to arteriosclerosis obliterans (ASO) are often encountered clinically, but their clinical characteristics remain poorly defined. We divided 275 patients undergoing aneurysmectomy into 2 groups: 58 patients with both AAA and ASO (Group A) and 217 patients with AAA only (Group B). General characteristics, morphological features of the aneurysms, surgical procedures and operative results were then compared between the groups. In Group A, ruptured aneurysms were significantly less common (p=0.005) and the aneurysms were smaller (p=0.0009). The most common cause of death in Group A was acute myocardial infarction (3/7), in contrast to aneurysmal rupture of another arterial segment and malignancy (6/27, each) in Group B. These findings indicate that patients with AAA and ASO represent a subgroup of patients with particular clinical features. (Jpn Circ J 1997; 61: 14 - 18)

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We evaluated the usefulness of left atrial appendage (LAA) flow velocity during atrial fibrillation as an objective measure for prediction of the outcome of electrical cardioversion. Left atrial appendage peak velocities were measured by transesophageal echocardiography before cardioversion in 56 patients. Left atrial thrombus was demonstrated in 6 (11%) of these patients. Cardioversion was then performed in the 50 patients who did not have a thrombus and in 1 patient whose left atrial thrombus disappeared after anticoagulant therapy (n=51). Thirty-eight patients converted to sinus rhythm which remained stable until discharge (initial success group). Of these, Iong-term (>6 months) maintenance of sinus rhythm was achieved in 31 patients (82%). Five patients with almost no detectable appendage contractions during atrial fibrillation were classified in the initial failure group. The peak LAA flow velocity was significantly higher in patients in the initial success group compared with the patients in the initial failure group (25.6±12.0 vs 15.3 ±10.7 cm/s, respectively; p<0.01). Left atrial appendage flow velocity during atrial fibrillation may be useful for identifying candidates for electrical cardioversion. (Jpn Circ J 1997; 61: 19 - 24)

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Blood pressure (BP) values (systolic BP=Ps, diastolic BP=Pd, heart rate=HR) fluctuate widely throughout the day, and are at their lowest levels during sleep (sleep-Ps=Ps₀, sleep-Pd=Pd₀, sleep-HR=HR₀). We analyzed the relationships among these values using the Windkessel model (logarithmic gradient of diastolic pressure decay A=E/R, E=elastic modulus, R=vascular resistance). Intra-arterial BP and ECG were recorded throughout 24 hours in 23 patients with mild essential hypertension (EH) by telemetry, and EEG was monitored during the night. The waveform of each BP pulse was analyzed by computer, The dye-dilution method was used to obtain the cardiac output while the subjects were awake, recumbent and during slow-wave sleep on the EEG. A high correlation coefficient (r) was observed between mean BP and √E ×√R during sleep (r=0.88, p<0.001). Sleep-HR was determined from the waveform that most effectively permitted peripheral blood flow. Furthermore, the simple algebraic relationships Pd=ø×Pd₀ and ø=FI+a₁(BI)+b₁ (a ₁, b₁=constant) were observed between Pd₀ and different 24 h Pd values [FI=e^A(RRo-RR); BI=baroreflex index=RR×Pd/(RR₀×Pd₀)-1, which was significantly correlated with the baroreflex sensitivity, r=0.79; RR₀ and RR are the RR intervals in Pd₀ and Pd waves]. The mean r between Pd₀×ø and the actual Pd over 24 h was 0.91±0.02 <SD> . We conclude that sleep-BP and sleep-HR depend mainly on √E ×√R, [m=log_e(Ps/Pd)] and E/R, whereas BP variability (ø) over a 24 h period is related to HR variation, the baroreflex index and E/R in mild EH patients. (Jpn Circ J 1997; 61: 25 - 37)

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The efficacy of combining antiplatelet agents with low doses of aspirin to prevent cardiac events in patients with myocardial infarction was examined. A total of 1,083 patients with prior myocardial infarction were randomly divided into those who were (618) and were not (465) treated with antiplatelet agents, and observed for 12.5±18.5 months. Those treated with antiplatelet agents included 113 patients treated with aspirin (50 mg) plus dipyridamole (150 mg/day), 253 treated with aspirin (50 mg) plus ticlopidine (200 mg /day), and 252 treated with only 1 of the 3 antiplatelet agents. Cardiac events, including fatal or nonfatal recurrent myocardial infarction, death by congestive heart failure, and sudden death, occurred in 34 patients (7.3%) in the nontreatment group and in 19 patients (3.1%: p<0.01) in the treatment group; odds ratio 0.40, 95% confidence interval 0.23-0.71. There were only 2 cardiac events (1.8%) in the aspirin+dipyridamole group (p<0.05 vs nontreatment group: odds ratio 0.28: 0.08-1.03), and 5 such events (2.0%) in the aspirin+ticlopidine group (p<0.01; odds ratio 0.28: 0.11-0.69). Subgroup analysis to exclude differences in the patients' background confirmed the efficacy of these antiplatelet agents. We conclude that combined treatment with low doses of aspirin plus either dipyridamole or ticlopidine is effective in preventing cardiac events in patients who have had prior myocardial infarction. (Jpn Circ J 1997; 61: 38 - 45)

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The electrographic features of successful sites of radiofrequency catheter ablation were analyzed in 33 cases of posteroseptal accessory pathways and compared with those from 155 cases of free wall accessory pathways. The atrioventricular intervals in the posteroseptal cases were significantly longer than in the free wall cases (posteroseptal vs left and right free wall; 38 vs 33 and 26 msec, respectively; p<0.05), and the incidences of continuous electrograms (42 vs 63 and 79%; p<0.01) and PQS-pattern unipolar electrograms (50 vs 76 and 78%; p<0.05) were significantly lower in the posteroseptal cases. The V-delta intervals in the posteroseptal cases were significantly longer than in the left free wall cases (17 vs 13 msec; p<0.05), but shorter than in the right free wall cases (17 vs 23 msec; p<0.05). No statistically significant difference in the incidence of Kent potentials among the 3 groups was observed. In radiofrequency ablation of posteroseptal pathways, the length of the atrioventricular interval and the incidences of continuous electrograms and PQS-pattern unipolar electrograms may be unsatisfactory even at the appropriate target site, but the V-delta interval and Kent potential are good indicators of suitable target sites. (Jpn Circ J 1997; 61: 46 - 54)

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We performed radiofrequency catheter ablation (RF ablation) for ventricular tachycardia (VT) in 2 patients with dilated cardiomyopathy (DCM) and 1 patient with arrhythmogenic right ventricular dysplasia (ARVD). Patient 1 had incessant VT associated with DCM. RF ablation was performed where diastolic potentials were recorded and concealed entrainment was demonstrated. VT was terminated by RF ablation. Patient 2 had drug-resistant VT associated with ARVD. RF ablation was performed where perfect pace-mapping was obtained during sinus rhythm, diastolic potentials were recorded and concealed entrainment was demonstrated. VT was terminated by RF ablation. Patient 3 had 2 morphologically distinct VTs associated with DCM. The target for RF ablation was 1 of the 2, which was a drug-resistant type. Perfect pace mapping was obtained where delayed potentials were recorded. As the current strength of pacing was reduced, the QRS complex configuration switched to the other type. This site was thought to be the common slow conduction zone for the re-entry circuit of the 2 types and RF ablation was performed at this site. In these 3 cases, VT did not recur after ablation. RF ablation is effective for the treatment of VT associated with cardiomyopathy. (Jpn Circ J 1997; 61: 55 - 63)

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Serial changes in cardiac norepinephrine content and the β-adrenergic system were investigated during the development of cardiomyopathy in spontaneously diabetic Chinese hamsters (CHAD strain), in comparison to age-matched control Chinese hamsters (CHA) or non-diabetic CHAD hamster littermates. Cardiac norepinephrine content and 1-adrenergic receptor density significantly increased in short-term diabetics. These changes preceded both the development of cardiac hypertrophy and the enhanced response of adenylyl cyclase to isoproterenol plus 5'-guanylylimidodiphosphate [Gpp (NH)p], sodium fluoride, or forskolin stimulation. However, as the diabetic state developed cardiac norepinephrine content, 1-adrenergic receptor density, and adenylyl cyclase activity returned to control levels. The amount of stimulatory or inhibitory guanine nucleo-tide binding proteins in the diabetic group was similar to those in the control groups. These data suggest that the cardiac 1-adrenergic system is enhanced by the alterations in cardiac sympathetic activity during early diabetes, which are associated with the duration of diabetes rather than with the degree of hypertrophy or strain differences. (Jpn Circ J 1997; 61: 64 - 73)

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A 52-year-old man with inflammatory disease of unknown origin but no specific laboratory abnormalities was referred to our hospital. He was subsequently diagnosed as having adult Still's disease. During an episode of severe inflammation he suffered reversible myocardial damage as revealed by electrocardiography, echocardiography and ²⁰¹Tl myocardial scintigraphy; this was ameliorated by treatment with steroids and immunosuppressive drugs. No significant stenosis of the coronary artery was observed on coronary angiography. Interstitial mononuclear infiltration was apparent in the right ventricle on endomyocardial biopsy. Myocardial injury with adult Still's disease, which may result in heart failure, has rarely been reported. We report a case of adult Still's disease with myocardial dysfunction that may have been caused by microangiopathy. (Jpn Circ J 1997; 61: 74 - 77)

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We present here a patient with the unusual combination of a newly developed right bundle branch block (RBBB) and an acute posterior myocardial infarction (MI). A dissecting MI with interventricular septal (IVS) rupture was initially thought to have caused RBBB. However, histologic examination revealed that the right bundle branch (RBB) had no ischemic involvement, but did show fibrosis, which suggests that this chronic damage of the RBB was a major contributor to the development of RBBB. This case confirms that the RBB is rarely involved by a posterior MI even in the presence of a dissecting IVS rupture. (Jpn Circ J 1997; 61: 78 - 81)

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We report a 67-year-old man who developed pulmonary hypertension as an initial clinical manifestation of occult gallbladder adenocarcinoma. He had a 6-week history of persistent dry cough followed by progressive dyspnea on exertion. Physical examination and chest roentgenogram revealed signs of precapillary pulmonary hypertension. He died of shock 1 h after pulmonary angiography, which failed to show any intravascular filling defects. Autopsy disclosed a mucin-producing small adenocarcinoma (2 cm diameter) and a gallstone in the gallbladder with a few small metastases to peri-aortic, peri-bronchial and mediastinal lymph nodes. Macroscopically, there was no gross thrombotic pulmonary embolism or pulmonary metastases. However, microscopically, more than 60% of the small pulmonary arteries less than 1 mm in diameter were occluded with pulmonary tumor microemboli. This case emphasizes the need to include tumor pulmonary embolism in the differential diagnosis of pulmonary hypertension whether or not there is evidence of an underlying malignant tumor. (Jpn Circ J 1997; 61: 82 - 86)

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A 66-year-old woman underwent elective cardiac catheterization for investigation of periodic attacks of chest pain at rest. During the examination, a chest pain attack occurred unexpectedly, resulting in ST elevation in the precordial leads on electrocardiography. Immediate coronary arteriography demonstrated no organic stenosis but markedly delayed contrast medium perfusion in the mid to distal portion of the left anterior descending artery. These phenomena spontaneously disappeared about 3 min later, and the patient was diagnosed as having angina pectoris due to microvascular spasm. The demonstration of angina pectoris due to microvascular spasm by coronary arteriography during a spontaneous attack is very rare. (Jpn Circ J 1997; 61: 87 - 89)

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