A 64-year-old man was admitted to hospital under the suspicion of unstable angina pectoris. Coronary angiography showed that he has a single coronary artery originating from the right coronary artery (RCA) without significant fixed stenosis. Acetylcholine was superselectively infused into the left main coronary artery (LMCA), and confirmed the coronary vasospastic occlusion associated with chest pain and elevation of the ST-segment in the precordial leads. This is the first report of the induction of a totally occlusive spasm of the LMCA of a patient with a RCA type single coronary artery, and this case suggests that spasm of the aberrant coronary artery is a potential mechanism for sudden death in patients with a single coronary artery.

The net effects of sympathetic and vagal activity on the QT interval and the mode of spontaneous onset of torsade de pointes (TdP) are still unclear in long-QT syndrome. Two patients with long-QT syndrome had syncope while undergoing Holter ECG investigation. The spontaneous onset of TdP in these patients was analyzed with respect to the relation between the RR and QT intervals. Both patients were high-school students (16- and 17-year-old boys) who had been diagnosed as long-QT syndrome and followed up without medical treatment because they had had neither a history of syncope nor arrhythmia induction by treadmill exercise tests. The first episode of syncope in both patients occurred during ordinary daily life and was not related to exercise or psychological stress. The dynamic changes between the RR and QT intervals associated with the spontaneous onset of TdP were analyzed by Holter ECG. Both patients showed sinus tachycardia followed by abrupt sinus bradycardia immediately before the onset of TdP. The enhanced rate of the adaptive response of the QT interval that occurred during the deceleration of the heart rate preceded the onset of TdP. These observations suggest that the complex situation that follows sympathovagal imbalance may have an important role in the dynamic change in the QT interval and initiation of TdP in patients with long-QT syndrome.

The present study reports a case of the successful surgical repair of a ruptured infra-renal mycotic abdominal aorta with Enterobactor cloacae in a 66-year-old man. During the operative procedure, an extra-anatomic bypass was installed before the laparotomy in order to avoid bacterial contamination. A complete resection of the infected aorta, tapering of the arterial stumps, wrapping of the omentum, and ligation of the aorta and arteries with Teflon tapes was carried out. The patient is alive and well 1 year postsurgery.

Cytokines have an important role in the pathogenesis and pathophysiology of myocarditis. In this study, subsets of peripheral helper T lymphocytes (Th) in a patient with acute viral myocarditis were analyzed by 3-color flow cytometry. During the clinical course of myocarditis, the Th1/Th2 ratio of peripheral lymphocytes changed. Th1 was dominant in the acute inflammatory phase during which levels of creatine kinase (CK) increased (day 6), then Th2 levels overtook those of Th1 in the recovery phase during which levels of CK decreased (day 13 and 20). At the time of discharge (day 35), Th1 and Th2 had normalized. Thus, it was speculated that the induction of lymphocytic myocarditis was associated with Th1 dominant status, and recovery was related to Th2 polarity. Th subset imbalances may play an important role in the pathogenesis of acute viral myocarditis and these analyses may be useful for understanding the disease activity of myocarditis.

Atrial electrical remodeling is thought to be the cause of the maintenance of atrial fibrillation (AF). Although the initiation and maintenance of AF is partially associated with autonomic nervous tone, vagally mediated AF does not tend to become permanent. Therefore, the effects of preceding vagal stimulation (VS) on the atrial effective refractory period (ERP) under electrical remodeling conditions were investigated in anesthetized dogs. Atrial ERPs were measured at 5 sites before and after a 7-h period of atrial rapid pacing in the control group. In the VS group, the vagus nerve was stimulated for 20 min before a period of atrial rapid pacing. Atrial rapid pacing shortened the ERP at each site in the control group (electrical remodeling). On the other hand, atrial rapid pacing after VS did not shorten the ERP at any site in the VS group. Tetrodotoxin, which was administered into the fatty tissue overlying the right atrial side of the right pulmonary vein junctions, blocked the protective effect of VS against the shortening of the ERP induced by atrial rapid pacing. In contrast, atropine did not interfere with such protective effects. These results suggest that VS prior to atrial rapid pacing protects the atrium from atrial electrical remodeling.

It is known that the tolerance against ischemia-reperfusion and the effects of preconditioning decrease in aged hearts, but the mechanisms responsible for this diminished ischemic tolerance and reduced efficacy of preconditioning remain unknown. To determine the age-related changes in these mechanisms, protein kinase C (PKC) isoform expression and its translocation by phorbol ester were analyzed because PKC is believed to be involved in preconditioning. Immunoblotting and immunostaining analysis were performed with isoform-specific PKC antibodies using cardiomyocytes isolated from young-adult (12-week-old: 12W) and middle-aged (50-week-old: 50W) Fischer 344 rats. There was significantly greater PKC-delta expression in both the cytosolic and membrane fractions of 12W cardiomyocytes than in 50W ones. Exposure of cardiomyocytes to 100 nmol/L 4-beta-phorbol 12-myristate 13-acetate (PMA) caused translocation of PKC-delta from the cytosol to the membrane in the 12W group, whereas in the 50W group, the translocation was attenuated. Immunostaining confirmed the PKC-delta translocation in the 12W cardiomyocytes. Oil pellet examination showed that the translocation of PKC-delta induced by preconditioning was associated with cell protection from ischemic injury in the 12W group only. Age-related changes in PKC isoform expression and activation in cardiomyocytes might be responsible for the reduced ischemic tolerance and less efficient preconditioning that accompanies aging.

The cellular mechanisms of abnormal calcium regulation and excitation-contraction coupling in relation to glucose metabolism in the hypertrophied heart are not well understood. The present study evaluated the myocardial mechanics of 6-7-week-old pressure overload hypertrophied rabbit hearts in response to dobutamine by (1) serial echocardiograms in vivo and (2) isolated Langendorff perfusion. Cytosolic Ca2+([Ca2+]i) and sarcoplasmic reticulum Ca2+-ATPase (SERCA2) expression were measured by fluorescence spectroscopy and Western immunoblotting, respectively. The effect of glycolytic inhibition by 2-deoxy-D-glucose +/- pyruvate was also evaluated. Both systolic and diastolic [Ca2+]i tended to be higher and diastolic calcium removal (tauCa) significantly slower in the hypertrophied heart. The myocardial response to dobutamine was blunted and dobutamine insignificantly improved tauCa. The SERCA2 protein level was higher in early hypertrophy, but was significantly reduced by 6 weeks of age, with progressive contractile failure. Inhibition of glycolysis or SERCA2 caused an increase in [Ca2+]i as well as a slower tauCa. Pyruvate completely preserved myocardial function and [Ca2+]i handling during glycolytic inhibition. It was concluded that in this model of advanced pressure overload hypertrophy, contractile failure and inotrope insensitivity are associated with increased [Ca2+]i, slower tauCa and reduced sensitivity of the contractile proteins to Ca2+. These changes occur in association with downregulation of the SERCA2, probably caused by impaired glucose metabolism.

The effects of subthreshold stimulation (STS) by direct current were investigated in 20 patients with atrioventricular nodal reentrant tachycardia (AVNRT), 27 with atrioventricular reentrant tachycardia (AVRT) and 3 with idiopathic atrial reentrant tachycardia (IART) STS was delivered to each eligible site for ablation prior to radiofrequency application. STS was defined as 'positive' if it could terminate the tachycardia or disrupt the conduction of accessory pathways without myocardial capture and defined as 'negative' if it could not. Radiofrequency ablation was performed irrespective of a positive or negative result from STS and was successful in all 50 patients. Among the 50 successful ablation sites, STS was positive at 26 sites (11 sites in AVNRT, 12 in AVRT and 3 in IART). STS was positive at 4 sites where ablation failed in 3 patients with AVRT and was negative at 8 sites where ablation was successful in 4 patients with AVNRT and 4 with AVRT. The positive and negative predictive value of STS for the detection of the optimal ablation site were, respectively, 100% and 74% in AVNRT, 73% and 72% in AVRT, and both 100% in IART STS-guided mapping is a specific method to predict the successful catheter ablation of reentrant supraventricular tachycardia.

It is unclear whether coronary endothelial function is linked to the pathogenesis of coronary spastic angina (CSA), so the present study examined the coronary vasomotor responses to acetylcholine (ACh) and bradykinin (BK) in 23 patients with CSA, 26 patients with CSA+coronary artery disease (CAD), and 21 control patients. Acetylcholine induced vasospasm of the left coronary artery in all of the patients with CSA, but not in any of the control patients. The changes in dilatation of the left coronary artery in response to bradykinin at doses of 0.2, 0.6 and 2.0 microg/min in the CSA group were significantly greater than those in the other 2 groups. The ratio of epicardial coronary vasodilations induced by BK to those induced by nitroglycerin did not differ among any of the groups. Bradykinin caused a similar increase in coronary blood flow in the control group and CSA group, but had less of an effect in the CSA+CAD group. In conclusion, the vasorelaxing effect of BK was preserved not only in epicardial spasm coronary arteries induced by ACh, but also in resistance coronary arteries distal to the spasm arteries in patients with CSA. The coronary vasodilation response induced by BK may not deteriorate until coronary atherosclerosis advances in patients with CSA.

The aim of this study was to use fast Fourier transform analysis to clarify the characteristics of human atrial fibrillation (AF) waves with respect to the duration of AF and the effect of class I antiarrhythmic drugs. Twenty-two patients (10 paroxysmal AF, 12 persistent AF) without organic heart disease were studied by conventional electrophysiological methods. Electrograms were recorded from the right atrial free wall during AF and spectral analysis was performed for 35s (16 consecutive 4096-ms epochs with 50% overlap) and the fibrillation cycle length (FCL) was calculated from the peak frequency. Mean FCL and SD were determined from 16-epoch data, and the temporal variability of FCL was defined as the SD of FCL. Paroxysmal AF had a longer mean FCL than persistent AF (178+/-26ms vs 139+/-16 ms, p<0.001) and AF duration had a significant inverse correlation with mean FCL (r=-0.79, p<0.001). The temporal variability of FCL was significantly greater in paroxysmal AF than in persistent AF (p<0.05) and there was a significant positive correlation between the mean FCL and the temporal variability of FCL (r=0.66, p<0.001). In 8 of 18 patients given a class I antiarrhythmic drug (cibenzoline or procainamide), AF was terminated and in those patients the mean FCLs before administration of class I drugs were significantly greater than in patients without AF termination. With respect to mean FCL before drug administration, conversion occurred in 100% of patients with FCL > or =168 ms and in 17% of those with FCL <168 ms. A longer duration of AF shortens the mean FCL, which is consistent with atrial electrical remodeling. Class I drugs prolong the mean FCL above a critical level and will terminate AF, which can be estimated from the mean FCL before drug administration.

Cardiac sympathetic nervous function is altered in congestive heart failure (CHF) and the uptake and washout rate of cardiac 123I-metaiodobenzylguanidine (MIBG) are useful markers for evaluating the severity of it. To assess what parameters predict decreased uptake or increased washout rate of MIBG, the concentrations of neurohumoral factor in both the aorta (Ao) and coronary sinus (CS) were measured, as well as hemodynamic parameters by catheterization, in patients with dilated cardiomyopathy (DCM). MIBG imaging was performed within 1 week of cardiac catheterization. Regarding MIBG parameters, the correlation with the transcardiac gradient of norepinephrine (NE), brain natriuretic peptide (BNP) and hemodynamics was investigated. Stepwise multivariate regression analysis was used to determine which variables closely correlated with cardiac MIBG parameters. There was a significant increase in the NE level between the Ao (446 pg/ml) and the CS (727 pg/ml). According to stepwise multivariate regression analysis, the heart/mediastinum (H/M) ratio independently correlated with the transcardiac gradient of BNP (r=-0.480, p<0.01), and the washout rate independently correlated with the transcardiac gradient of NE (r=0.481, p<0.01). These findings indicate that the H/M ratio may reflect the transcardiac gradient of BNP, which implies the degree of left ventricular dysfunction and/or damage and the washout rate may reflect altered cardiac sympathetic nerve terminal in DCM patients with CHF, suggesting that both the H/M ratio and washout rate provide important information about the failing ventricle.

The initiation of focal atrial tachycardia (AT) from the superior vena cava (SVC) remains unclear. In 3 patients (2 females, 1 male; aged 57, 66 and 50 years, respectively) with focal AT arising from different parts of the SVC, the AT occurred spontaneously, rather than being induced by electrical stimulation. The cycle length of the tachycardia was highly variable, ranging between 190 and 300 ms in patient 1, 180 and 320ms in patient 2, and 200 and 300ms in patient 3. The clinical or associated arrhythmias were atrial fibrillation (AF) (patients 1, 3) and atrial flutter (AFL) (patients 2, 3). A presumed SVC potential that was earlier than the activation of all the other mapping sites was recorded during AT at the lower anterior (15-mm above the atriocaval junction), the mid-anterior (25-mm above the atriocaval junction) and the lower posterior aspect of the SVC (17-mm above the atriocaval junction. Radiofrequency (RF) ablation targeting the SVC focus with the SVC potential promptly eliminated the focal AT in all 3 patients. The coexistent typical AFL was ablated, but the AF was not. The follow-up period was 6, 6, and 3 months, respectively, for each of the patients under no antiarrhythmic medication; there has not been a recurrence of symptomatic palpitation. In conclusion, focal electrical firing in the SVC can initiate AT and this type of focal AT is always associated with AFL or AF. RF ablation guided by the presumed SVC potential is safe and highly effective in eliminating the tachycardia.

Stress-induced ST-segment elevation following myocardial infarction (MI) has been correlated with myocardial ischemia, viability and wall motion abnormality, but its mechanism is still unclear, so the present study compared ST-segment elevation and wall motion response during exercise, dobutamine and dipyridamole stresses. Twenty-five patients with their first anterior MI underwent exercise, dobutamine and dipyridamole echocardiography on different days 4-6 weeks after MI. Left ventricular wall motion was analyzed using 5-grade/16-segment model and myocardial ischemia was considered as a worsening of the wall motion score index (WMSI) during the stress test; myocardial viability was defined as a reduction of WMSI during low dose dobutamine. Dyskinesis formation was defined by visual analysis as akinesis that became dyskinetic or if the dyskinesis worsened. Both exercise and dobutamine induced ST-segment elevation, but dipyridamole did not. There was no significant difference in the degree of ST-segment elevation between the patients with and without myocardial ischemia or dyskinesis formation. Exercise induced a higher ST-segment elevation in patients with myocardial viability than those without (0.17+/-0.09 mV vs 0.09+/-0.07 mV, p<0.05). Exercise-induced ST-segment elevations correlated with dobutamine-induced ST-segment elevations (p<0.01), changes in heart rate (p<0.05) and systolic blood pressure (p<0.05). In conclusions, stress-induced ST-segment elevation does not correlate with either myocardial ischemia or stress-induced dyskinesis, but may be associated with myocardial viability.

Spontaneous degeneration of rapid atrial fibrillation (AF) to ventricular fibrillation has been documented in patients with hypertrophic cardiomyopathy (HCM) and Wolff-Parkinson-White (WPW) syndrome. However, the importance of rap

The usefulness of glucose-insulin-thallium-201 (GI-Tl) infusion single photon emission computed tomography (SPECT) in predicting reversible dysfunction has not been evaluated, so the present study recruited 20 patients with regional ischemic dysfunction for investigation. All patients underwent GI-Tl SPECT, post-stress Tl reinjection imaging and low dose dobutamine echocardiography. The diagnostic accuracy of these 3 techniques in predicting functional recovery was evaluated by receiver operating characteristic (ROC) analysis. In segments with functional recovery, regional Tl activities of GI-Tl SPECT were significantly higher than those of reinjection imaging (p<0.05), although there were no significant differences in segments without recovery. The area under the ROC curve for GI-Tl SPECT (0.75+/-0.06) was greater than that for reinjection imaging (0.68+/-0.07). The optimal cutoff values to identify viable myocardium were considered to be 55% of peak activity for GI-Tl SPECT and 50% for reinjection imaging. At this cutoff point, the sensitivity and specificity for detection of functional recovery were, respectively, 85% and 61% for GI-Tl SPECT, and 73% and 61% for reinjection imaging. Dobutamine echocardiography had the same sensitivity (85%), but lower specificity (48%) than GI-Tl SPECT. Continuous infusion of GI-Tl solution enhances regional Tl uptake compared with conventional post-stress reinjection imaging. This study suggests that GI-Tl SPECT is superior to reinjection imaging and dobutamine echocardiography in predicting functional recovery after ischemic left ventricular dysfunction.