A new combined test, accelerated exercise following mild hyperventilation (HV), was examined to determine whether it is effective at detecting a positive response in patients with pharmacologically-induced coronary vasospasm and near normal coronary arteries.
Fifty-eight consecutive patients who underwent both triple non-invasive spasm provocation tests and diagnostic coronary angiography were enrolled. They all had pharmacologically-induced coronary vasospasms and no significant organic stenosis. In these patients, an HV test was performed first, followed by a treadmill exercise test (TET), and finally the new combined test under no medication within 3 days. Of the 58 patients, positive responses were observed in 9 patients to the HV, in 15 to the TET, and in 35 to the newly combined test. The remaining 21 patients had negative responses although the triple sequential tests were perfomed. Thus, the sensitivities of the HV test, TET, and newly combined test were 16% (9/58), 26% (15/58), and 63% (35/56), respectively. Forty-six subjects with near normal coronary arteries and no ACh-provoked spasm served as controls. None of these subjects had positive responses to any of these three tests, and thus their specificity was all 100%. No serious or irreversible complications were seen in this study.
We recommend this newly-combined protocol for the induction of coronary artery spasm in patients with vasospastic angina pectoris and without significant stenosis as a diagnostic tool.

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To evaluate the stabilizing effects of an antilipemic agent, bezafibrate, on coronary plaques, we carried out a prospective angioscopic and angiographic open trial. From April 1997 to December 1998, 24 patients underwent coronary angioscopy of plaques in non-targeted vessels during coronary interventions and then again 6 months later. The patients were divided into control (10 patients, 14 plaques) and bezafibrate (14 patients, 21 plaques) groups. Oral administration of bezafibrate (400 mg/day) was started immediately after the intervention and was continued for 6 months. The vulnerability score was determined based on the angioscopic characteristics of plaques and compared before and 6 months later. Six months later, the vulnerability score was reduced (from 1.6 to 0.8; P<0.05) in the bezafibrate group and unchanged (from 1.4 to 1.3; NS) in the control group. In the bezafibrate group, the changes in the vulnerability score were not correlated with those in % stenosis or minimal lumen diameter. The plasma total cholesterol level (T-C) was unchanged, triglyceride level (TG) was decreased, and high density lipoprotein cholesterol level (HDL-C) was increased in the bezafibrate group, but were unchanged in the control group. In the bezafibrate group, T-C and TG were decreased and HDL-C was increased in patients with a reduced vulnerability score but were unchanged in those with an unchanged score. These results indicate that 6 month administration of bezafibrate stabilizes coronary plaques and that the stabilization is not correlated with angiographic changes.

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The pathogenesis of dilated cardiomyopathy (DCM) is unknown, but clinical evidence suggests that coronary vasospasm is associated with the development of DCM in some cases. In the present study, we aimed to clarify the prevalence of coronary vasospasm in patients with DCM, the characteristics of patients with DCM and coronary vasospasm, and the effects of anti-vasospastic agents on patients with DCM and coronary vasospasm. This study included 18 consecutive patients with DCM who underwent cardiac catheterization with ergonovine provocation testing. The patient was diagnosed as having coronary vasospasm if ergonovine induced coronary vasoconstriction ≥75% diameter narrowing was observed compared to the diameter after nitroglycerin administration. Six (33%) patients were found to have coronary vasospasm and anti-vasospastic agents were added after the cardiac catheterization. The prevalence of atrial fibrillation in the patients with DCM and coronary vasospasm was greater than that in DCM without coronary vasospasm [67% vs 8% (P<0.05)]. The left ventricular end-diastolic dimension decreased from 61 mm (56/64) to 55 mm (53/56) (median, 25th/75th percentile, P<0.05) and the left ventricular ejection fraction increased from 36% (32/40) to 47% (46/48) (median, 25th/75th percentile, P<0.05) after the administration of anti-vasospastic agents and 4 of the 6 patients improved symptomatically. Therefore, ergonovine provocation testing is useful in identifying patients with DCM and coronary vasospasm, in whom cardiac performance is expected to be improved with anti-vasospastic agent therapy. DCM patients with atrial fibrillation may be a clue for identifying patients with coronary vasospasm.

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Coronary artery bypass grafting (CABG) in patients with poor left ventricular function remains a surgical challenge and is still controversial. The purposes of this study were to evaluate the effectiveness of CABG in such patients when performed without case selection on the basis of preoperative viability tests and to determine the predictors of postperative outcome.
The preoperative, perioperative, and postoperative early and mid-term follow-up data of 273 patients with ≤30% left ventricular ejection fraction (LVEF) who underwent isolated CABG between January 1995 and November 2000 were evaluated. Preoperative echocardiography and cardiac catheterization, and postoperative control echocardiography were performed in all patients. Follow-up was achieved via monthly periodical examinations in the first 6 months, and thereafter by either regular visits or phone contact. Preoperatively, 242 (88.65%) patients were in NYHA class III or IV, and the mean LVEF was 26.51±3.64%.
The overall hospital mortality total was 14 (5.13%) patients. There were 44 (16.12%) late mortalities. Postoperative morbidities were observed in 74 (27.1%) patients. Two-hundred and two (93.95%) of the surviving 215 (78.75%) patients were in NYHA class I or II at 49.55±14.84 months of follow-up. Postoperative follow-up echocardiographic examinations revealed a mean LVEF of 39.66%±5.43%. The improvements in functional capacity and LVEF were significant. Advanced age, diabetes, hypertension, cross-clamp time >60 min, bypass time>120 min, and severity of functional class (class III-IV of NYHA) were found to be the determinants of mortality. However, multivariate analyses revealed only older age and class III-IV of NYHA and CCS were predictors of mortality.
The low mortality and morbidity rates as well as satisfactory postoperative improvements in functional capacity and LVEF measurements support the use of CABG without the need for any viability assessment in patients with left ventricular dysfunction.

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Most focal atrial fibrillation (AF) is initiated by premature beats from the pulmonary veins (PV), and ablation of these foci can effectively cure AF. We investigated the efficacy of focal ablation and the role of rapid focal activation (RFA) in the maintenance of AF using simultaneous multisite catheter mapping in four PVs.
Forty-two patients with frequent attacks of paroxysmal AF were included in the study population. Bipolar electrograms were simultaneously recorded from all four PVs. RFA was determined at AF onset, during sustained AF, or just before the spontaneous termination of AF. RFA was continuously observed not only at a triggered PV, but also at all sites including an opposite non-triggered PV, coronary sinus and high right atrium in sustained AF (>10 minutes), whereas RFA was observed only in the triggered PV and not at the other sites in nonsustained AF. Once RFA ceased, AF terminated immediately. After a mean follow-up of 21 months, focal ablation had eliminated AF without drugs in 24 patients (57%).
The technique of simultaneous mapping of the PV using microcatheters is a feasible and effective method for mapping and ablation of focal AF originating from the PV. RFA arising from PVs is important not only as a trigger of onset, but also in the maintenance of AF.

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Right bundle branch block and ST segment elevation (RBBB-STE) in the right precordial leads have been reported as a distinct clinical and electrocardiographic syndrome in patients prone to ventricular fibrillation (VF) in the absence of structural heart disease (Brugada syndrome). The purpose of the study was to investigate the role of signal averaged electrocardiogram (SAECG) in identifying patients at high risk among asymptomatic RBBB-STE patients. Thirteen patients with the RBBB-STE ECG were identified. Symptoms were: syncope (n=3, cases 1, 3, and 11), atypical chest pain (n=3, cases 4, 10, and 12) and palpitations (n=2, cases 6, and 7). The other 5 patients were asymptomatic. SAECG and programmed electrical stimulation (PES) were conducted in all patients. Body surface late potentials (LPs) were present in 7 of 13 patients before PES. Vf was induced in 6 of 7 LP positive patients. Vf was induced in 3 of 6 LP negative patients, but LP became positive in 2 of 3 patients in whom Vf was induced. One patient with syncope due to VF (case 1), 1 patient without symptoms who died suddenly during follow up (case 2), and 1 asymptomatic patient (case 9) showed reproducibly positive LP. In a patient (case 9) with positive LP at baseline, LP transiently became negative during follow up. In RBBB-STE patients, reproducibly positive LP is at risk for malignant ventricular arrhythmias and sudden death. Repeated SAECG recording may be useful for screening high-risk patients who should receive electrophysiological study among asymptomatic RBBB-STE patients.

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Although surgical treatment of left ventricular aneurysms has been performed for a long time, it is still a point of debate. In this study, we investigated 159 patients who had undergone surgery for a left ventricular aneurysm in our clinic between 1985 and 1994. Perioperative mortality, long term survival rates, and parameters which probably affect these ratios were evaluated. All of the patients except one were followed by clinical records, mail or phone. Classic linear repair (111 cases), plication (46 cases), and Dor plasty (2 cases) were performed. Revascularisation procedure was also performed in 140 (88%) cases. The average number of distal anastomosis was 2.6. Twenty cases (12.6%) died in the perioperative period. The most important parameter which affected early mortality was the requirement for an intra-aortic balloon pump in the postoperative period. Mean follow-up duration was 47±35 months. Forty-two late deaths occurred in this period. The overall 5-year survival rate was 71%. Predictors for long term mortality were related to preoperative left ventricular function, presence of congestive heart failure, and poor functional capacity. The type of surgery did not affect short and long term survival. The functional capacity of the survivors was improved.
In conclusion, surgical treatment of left ventricular aneurysms with classic linear repair and plication had acceptable short and long term survival rates and improved functional capacity. The most important predictor of survival in either the early or late postoperative period was preoperative left ventricular function.

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The incidence and nature of cardiac involvement in Behçet's disease are not yet clearly documented. We first used transesophageal echocardiography in combination with resting and signal averaged electrocardiography to define cardiac involvement in Behçet's patients. Transthoracic and multiplane transesophageal echocardiography, and resting and signal averaged electrocardiography were performed in 35 Behçet's disease patients (9 women and 26 men, mean age: 38±12 years) and 30 normal subjects. Higher incidences of interatrial septum aneurysm (31% to 6%), mitral valve prolapse (25% to 3%), mitral regurgitation (40% to 6%) and aneurysmal dilatations of sinus valsalva and ascendan aorta were observed in the Behçet's disease patients than in the normal subjects. Mean QT dispersion and mean corrected QT dispersion values were significantly greater in the patients with Behçet's disease. Patients with interatrial septum aneurysm (and/or PFO), valvular dysfunction or proximal aorta dilatation had greater QT dispersion values than thase without these pathologies in the Behçet's group (63±11 vs 44±19 ms, 58±23 vs 41±24 and 60±27 vs 42±23 ms respectively, P<0.05). Positive signal averaged electrocardiography parameters were detected in 18 (51%) Behçet's disease patients compared with one (3%) in controls (P<0.001). Dilatation of the proximal aorta, interatrial septal aneurysm, mitral valve prolapse, and mitral regurgitation are the common findings of cardiac involvement in Behçet's disease. Increased dispersion of ventricular repolarisation and positive late potentials are also detected. QT dispersion is significantly higher in patients with these cardiac abnormalities. These findings suggest that cardiac involvement in this disorder is a diffuse process which involves both cardiac structure and vascular elements.

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The L-type Ca²⁺ current (I_Ca,L) plays an important role in the regulation of cardiac contractility. However, there is little data with regard to the significance of the I_Ca,L-independent mechanism of β-adrenoceptor mediated positive inotropy. The effects of isoproterenol (ISO) on I_Ca,L and contractility in the presence of Ca²⁺ channel blockers (nifedipine, verapamil) were examined in adult mouse ventricular myocytes. ISO increased contractility over the level before the administration of Ca²⁺ channel blocker, although it had a very limited effect on I_Ca,L. The positive inotropy of ISO disappeared after administration of Ni²⁺, an inhibitor of the Na⁺-Ca²⁺ exchanger. The addition of ISO after nifedipine pretreatment also increased the [Ca²⁺]i transient over the control level and the application of Ni²⁺ or KB-R7943, a selective Na⁺-Ca²⁺ exchange inhibitor (reverse mode), abolished the increase in [Ca²⁺]i transient. Therefore, an I_Ca,L-independent mechanism plays a significant role in β-adrenoceptor mediated positive inotropy. The Na⁺-Ca²⁺ exchanger is necessary for the development of this action.

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We examined the mechanism of action of lysophosphatidylcholine (lyso-PC), which is suggested to be involved in the pathogenesis of atherosclerosis and inflamatory disorders, and its interaction with well-known vasoactive compounds such as hydrogen peroxide (H₂O ₂), thromboxane A₂ (TX-A₂), serotonin (5-HT), angiotensin II (Ang-II), endothelin-1 (ET-1), or urotensin II (U-II) on VSMC proliferation. Growth-arrested rabbit VSMCs were incubated with given concentrations of lyso-PC with H₂O₂, TX-A₂, 5-HT, Ang-II, ET-1, or U-II. [³H]Thymidine incorporation into DNA was measured as an index of VSMC proliferation. Lyso-PC induced a maximal effect on [³H]thymidine incorporation at a concentration of 15 μM (156%), and its effect was significantly inhibited by the phospholipase C inhibitor U73122 (10 μM), the intracellular antioxidant NAC (400 μM), and the NADPH oxidase inhibitor diphenylene iodonium (1 μM), but not by the MAPK kinase inhibitor (10 μM). H₂O₂, TX-A₂, 5-HT, Ang-II, ET-1, or U-II also stimulated [³H]thymidine incorporation in a dose-dependent manner. A non-mitogenic concentration of lyso-PC (5 μM) significantly potentiated the effect of low concentrations of H₂O₂ (0.1 μM, 110 to 222%), TX-A₂ (5 μM, 120 to 202%), 5-HT (5 μM, 182 to 259%), Ang-II (0.5 μM, 167 to 304%), ET-1 (0.01 μM, 139 to 297%), or U-II (0.025 μM, 120 to 332%) on [³H]thymidine incorporation. The results suggest that lyso-PC acts synergistically with the vasoactive compounds H₂O₂, TX-A₂, 5-HT, Ang-II, ET-1, or U-II in inducing VSMC proliferation, which may play an important role in the progression of atherosclerosis.

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The case of a 43-year-old Taiwanese man who presented with spinal epidural hematoma following intravenous administration of recombinant tissue plasminogen activator (rTPA) and heparin therapy for acute myocardial infarction (AMI) is reported. Upper back pain and progressive neurological dysfunction ensued, secondary to spinal epidural hematoma with spinal cord compression. The patient did not recover neurologic function postsurgically, possibly because the operation was delayed. In conclusion, cardiologists should be alert to this rare, severe complication of rTPA and should perform early laminectomy (in ≤36 hours for those with complete deficit and in ≤48 hours for those with incomplete deficit) if possible.

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Myocardial bridging most frequently occurs on the left anterior descending coronary artery and may cause ischemia and related complications. Right coronary artery myocardial bridges (MB) are rare. We report a patient with an unusual coronary bridge, a left circumflex coronary artery bridge, who presented with exercise-induced angina pectoris that was relieved with medical therapy.

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Isolated left subclavian artery has been documented to be associated with several congenital cardiac defects, including tetralogy of Fallot and transposition of the great arteries. In some cases subclavian or pulmonary artery steal phenomenon may occur when the isolated left subclavian artery connects to the main pulmonary artery via a ductus arteriosus. The isolated left subclavian artery may be part of the cardiac manifestations in multiple congenital anomalies, such as VACTERL association. We describe subclavian and pulmonary steal phenomenon in a neonate with complex congenital heart disease, including an isolated left subclavian artery, and left lung agenesis. An isolated left subclavian artery is rare and its association with agenesis of the left lung has not been reported previously.

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