The aim of this study was to assess whether the incidence of early occlusion following angioplasty was greater among patients with unstable angina and whether the coronary lesions prone to early occlusion could be predicted from their angiographic appearance. Seventy-seven patients who had had a first angioplasty of a native vessel for stable or unstable angina in one twelve month period were included. The angiographic appearances of the angioplastied lesions were classified as either Type 1, which were smooth and unlikely to have thrombus or intimal rupture, or Type 2, which were irregular due to thrombus or intimal rupture. The lesion classification was compared to the patients' clinical features, i.e. stable or unstable angina, and the outcome of the angioplasty. Type 2 lesions occurred in 25% of patients with stable angina but 49% of patients with unstable angina (p<0.05). Early sudden occlusion of the angioplastied vessel occurred in 24% of patients with unstable angina but in only 3% of patients with stable angina (p<0.05) and in 6% of Type 1 lesions compared with 24% of Type 2 lesions (p<0.05). Thus it is possible to identify the clinical characteristics and angiographic appearances of those patients undergoing angioplasty who are most likely to experience early vessel occlusion.

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Fifty-one consecutive patients underwent modified catheter-mediated direct-current ablation of accessory pathways. Energy was delivered through the distal pair of electrodes (dual electrode configuration) of a 6F quadripolar catheter to the internal surface of the right or left atrioventricular (AV) annulus. In an attempt to prevent the later resumption of accessory pathway conduction, one additional shock was given after the initial successful interruption of accessory pathways. A mean of 2.7 shocks wth cumulative energy of 453±32 Joules/patient interrupted the accessory pathways in 47 patients and modified the accessory pathway conduction in 2 patients. Forty-eight patients were asymptomatic and free of any antiarrhythmic agents with a follow-up ranging from 3-20 months (mean 12±1 months), without early or late serious complications (AV block or tamponade). Conduction characteristics, concealed or manifest, and recording of accessory pathway activity did not affect the outcome. Mean cumulative energy and number of applications of energy to achieve a successful outcome were lower in patients with concealed (376±31 Joules, 2.4±0.2 shocks) than manifest accessory pathways (516±50 Joules, 2.9±0.2 shocks). At the successful ablation sites, the mean shortest retrograde ventriculoatrial interval during orthodromic reentrant tachycardia (VA') was 80±3msec (78% had VA' less than 90msec) and was not different between concealed and manifest accessory pathways; the mean shortest antegrade AV interval was 47±3msec in manifest preexcitation; the mean ratio of atrial to ventricular wave amplitude was not significantly different between left-sided (0.8±0.1) and right-sided (1.1±0.2) accessory pathways (p>0.05). A successful outcome was achieved in 94% of 51 patients. This procedure is relatively safe and effective, regardless of the location of the accessory pathway.

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This study evaluated diagnostic criteria, clinical observations, surgical indications and complications in 90 cases of fixed subvalvular aortic stenosis. Echocardiography, catheter angiography and surgical findings indicated that 60 (66.6%) patients had subvalvular membranous stenosis, 20 (22.2%) patients had fibromuscular stenosis, 4 (4.4%) patients had membranous and fibromuscular stenosis, and 6 (6.6%) had a tunnel-type obstruction. Forty-two patients had additional cardiac anomalies, such as PDA, valvular aortic stenosis and VSD. Fifty patients were treated surgically. Thirty-six patients were evaluated by two-dimensional and Doppler echocardiography at post-surgical intervals ranging from 7 days to 11 years (mean 3.6 years). There were pathological echo findings in 12 patients. The prognosis of this anomaly depends upon early diagnosis and treatment. The results of this study support the importance of the two-dimensional and Doppler echocardiography in early diagnosis and follow-up of the surgical results in treatment of this anomaly.

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Blade atrial septostomy has been applied in 3 patients with transposition of the great arteries under two-dimensional echocardiography instead of fluoroscopy. The blade at the tip of the catheter was seen on an echo screen when it was in the left atrium. The blade was then extended and pulled slowly across the atrial septum from the left into the right atrium, under echocardiographic monitoring. The procedure was successful in all 3 patients. Interatrial communication measured echocardiographically was sufficient in size. Since the interatrial septum is clearly seen by means of echocardiography during blade atrial septostomy, the method is thought to be superior to fluoroscopy in the prevention of complications.

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Peripartum cardiomyopathy is a relatively rare complication of pregnancy, characterized by heart failure of obscure etiology during the antepartal or postpartal period. During a 10-year period in our hospital, of 36, 882 women who delivered, 6 were diagnosed as having peripartum cardiomyopathy. The incidence in our hospital was estimated as 1: 6, 147 deliveries. Among these 6 patients, 2 cases with fulminating courses died 1 month after treatment. Two other cases had cardiomyopathy and multiple congestive heart failure and died after 3 years and 6 years. Only one case, whose cardiac size returned to normal within 4 months, completely recovered from this disease. Another survivor with persistent cardiomegaly was followed for 5 years and remained clinically stable. In addition to congestive heart failure, the occurrence of complications such as sepsis, hepatorenal failure, and arrhythmia were the major causes of death. According to the results of our study, return of cardiac chamber size to the normal range indicated a good prognosis. We concluded that the prognosis of peripartum cardiomyopathy depends upon the degree of cardiac dysfunction and the response to therapy.

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The t-PA/PAI-1 complex is a good indicator of the release of fibrinolysis activators and inhibitors from the vascular wall, but its clinical significance in chronic ischemic heart disease is unclear. The plasma levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), and the t-PA/PAI-1 complex (including various coagulation factors) were assayed in 72 patients with coronary artery disease (CAD) and 29 control (C) subjects. The CAD patients were subdivided into 3 groups: single-vessel disease (G1, n=30), double-vessel disease (G2, n=20), and triple-vessel disease (G3, n=22). The patients with triple-vessel disease had higher fibrinogen values (G3: 318±75mg/dl, C: 263±56), factor VII activity (G3: 143±36%, C: 123±14), and t-PA antigen levels (G3: 4.7±0.8ng/ml, C: 3.3±0.7) than controls. Patients with double- and triple-vessel disease also showed higher levels of factor VIII, vWF antigen, thrombin-antithrombin III complex (G1: 2.3±0.6ng/ml, G2: 2.7±0.5, G3: 3.1±0.5, C: 2.0±0.5), and t-PA/PAI-1 complex (G1: 13.9±6.1ng/ml, G2: 16.4±4.6, G3: 18.2±5.9, C: 10.7±4.9) than control subjects. The t-PA/PAI-1 complex levels were correlated significantly with the activities of factors VII and VIII and the thrombin-antithrombin III complex. These findings suggest that patients with CAD have greater blood coagulability than controls, and that this difference is related to the severity of the disease. Since there was a significant correlation between coagulation factors and t-PA/PAI-1 complexes, higher t-PA/PAI-1 complex levels may be a vascular endothelial response to higher blood coagulability in multivessel disease.

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We compared the effects of intravenous infusions of clonidine and placebo on heart rate variability in 10 healthy male controls. Clonidine produced a significant decrease in blood pressure and significantly decreased the heart rate variability during quiet standing.

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The antiarrhythmic properties of the opiate antagonist naloxone have been reported in a variety of models of arrhythmia. To determine the generality and the possible central involvement of its antiarrhythmic activity, the effects of naloxone were assessed against cardiac arrhythmias induced by intravenous bolus injections of picrotoxin. Naloxone at doses of 0.33 and 1mg/kg significantly reduced the incidence and severity of picrotoxin-induced arrhythmias in a dose-related manner, without alteration of blood pressure and heart rate. The results demonstrate the antiarrhythmic efficacy of naloxone in an additional animal model. They further suggest that the antiarrhythmic actions of naloxone may be mediated by the central nervous system via both the autonomic and GABAergic pathways.

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The formation of new blood capillaries (angiogenesis) occurs in response to angiogenic factors released by either normal or tumoral cells. In the present study, we cultured human umbilical vein endothelial cells (HUVEC) on collagen gels and aimed to clarify the effects of cyclic nucleotides on angiogenesis induced by endothelial cell growth factor (ECGF). HUVEC invaded the underlying collagen matrix and formed tube-like structures when ECGF was added. ECGF (9.4 to 75μg/ml) induced angiogenesis in a concentration-dependent manner; the effect reached a plateau at 75μg/ml. Cyclic AMP (10^-3M), dibutyryl cyclic AMP (10^-3M), 8-bromo cyclic AMP (10^-5M) and Sp-cAMPS (10^-3M), a stimulator of cyclic AMP-dependent protein kinase, each significantly inhibited ECGF-induced angiogenesis by 64.2, 86.1, 46.5, 74.7%, respectively. Forskolin and cholera toxin, which are activators of adenylate cyclase, did not inhibit ECGF-induced angiogenesis. Dibutyryl cyclic GMP (10^-4, 10^-3M) also did not affect the formation of capillary-like tubes induced by ECGF. In conclusion, cyclic AMP, but not cyclic GMP, inhibits angiogenesis in vitro. This antiangiogenic activity may be applicable to the treatment of such conditions as solid tumors, diabetic retinopathy and rheumatoid arthritis in which the suppression of angiogenesis is important.

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Acute and chronic experiments were performed in rats to examine whether atrial natriuretic peptide (ANP) has any beneficial effects on glycerol-induced acute renal failure (ARF). ANP infusion (Atriopeptin III, 1.0μg/kg+0.2μg/kg/min) improved the renal blood flow (RBF) and the glomerular filtration rate (GFR), and induced profound natriuresis in the early stage of ARF. By contrast, ANP decreased RBF in the control rats. In addition to these acute hemodynamic effects, long-term beneficial effects of ANP were also observed. A 75-min infusion of ANP significantly lessened the degree of azotemia as well as the extent of renal histologic damage assessed 24 hours after the glycerol injection. These results indicate that ANP can afford partial protection against both acute renal dysfunction and the chronic course of the glycerol-induced ARF, suggesting that ANP may be useful in the treatment of ARF.

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Right atrial thrombi are usually immobile. However, a mobile type mimicking a cardiac tumor, especially myxoma, has been described on rare occasions. We report here a case of atrial thrombus which was mobile in the cardiac chambers. A 29-year-old male was admitted because of exertional dyspnea. On admission, his echocardiogram showed an abnormal mass in the right atrium with a stalk attached to the interatrial septum. It decreased in size on the next day. On the fourth day of admission, it moved to the right ventricle. Multiple pulmonary emboli were revealed by the lung perfusion scintigram. Two days after the administration of intravenous urokinase, the abnormal mass in the cardiac chambers was no longer seen on the echocardiogram. This was a rare case of mobile atrial thrombus associated with multiple pulmonary emboli. Thrombolytic therapy appeared to be effective in this case.

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Low-energy electrical ablation at 100 joules was attempted via a catheter in a patient with sustained ventricular tachycardia (VT) refractory to drug therapy. The patient was a 17-year-old woman who had undergone complete surgical correction of a double outlet right ventricle at the age of 9. The first episode of VT appeared at the age of 17. It was refractory to procainamide and lidocaine and it was sustained until termination with direct countershock. Two different QRS morphologies of VT were documented in the electrophysiologic study and one was identical to the VT observed in the clinical course. Conventional drug therapy failed to prevent induction of VT and catheter electrical ablation was attempted. The earliest activation site during the clinical episode of VT was localized to the right ventricular side of the interventricular septum (site 14-15), but pacing from this site resulted in a slightly different QRS morphology from that of VT. At the left ventricular side of this site (site 2), pacing during VT resulted in a QRS morphology identical to that of VT but the electrogram of this site did not precede the onset of the surface QRS complex. From these findings, the origin of VT was considered to be in the muscular layer of the interventricular septum. The method of transeptal shock using two catheters was applied and direct countershock at 100 joules successfully ablated the VT.

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In immunocompromised patients, cytomegalovirus myocarditis leading to dilated cardiomyopathy is rare, and the duration of myocardial damage in such patients has not yet been determined. We report here one renal transplant recipient with cytomegalovirus myocarditis. This case shows that the myocardial damage secondary to cytomegalovirus may be insidious and persist for a relatively long period in the immunocompromised patient.

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