There are few district-based surveys to investigate the actual effects of thromobolytic therapy and percutaneous transluminal coronary angioplasty (PTCA) on short-term mortality in patients with acute myocardial infarction (AMI) in Japan. The study population comprised 974 patients (319 women and 655 men, aged 69 ± 12 years) admitted with confirmed AMI to 41 hospitals in Yamagata Prefecture from January 1, 1994 to December 31, 1996. Thrombolysis and PTCA were performed in 262 (27%) and 428 (44%) patients, respectively, and 161 patients died within 28 days after the onset of AMI (short-term mortality 16.5%). Thirteen variables, including risk factors and clinical manifestations, were examined by bivariate and multiple logistic regression analyses to identify the predictors of short-term mortality. Multiple logistic regression analysis, incorporating variables with a p value < 0.05 in a bivariate analysis, demonstrated that advanced age, history of myocardial infarction and Killip class III or IV independently correlated with increased short-term mortality and treatment with PTCA independently correlated with decreased short-term mortality (odds ratio 0.21, 95% confidence interval [CI] 0.11-0.39). Thrombolytic therapy was not an independent predictor of short-term mortality (odds ratio 0.67, 95% CI 0.37-1.20). Treatment with PTCA but not thrombolysis significantly improved the short-term mortality in patients with AMI in our area-based study.

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The objective of the present study was to investigate the characteristics of body surface potential map (BSPM) findings during ventricular repolarization in patients with coronary artery disease (CAD). A total of 108 consecutive patients, 99 men and 9 women with angina pectoris and positive treadmill exercise test results as well as angiographically documented CAD underwent BSPM study in a fasting state. Their ages ranged from 30 to 70 years. There were 13 patients with right coronary artery (RCA) lesions, 37 with left anterior descending artery (LAD) lesions, 5 with left circumflex artery (LCX) lesions, 17 with both RCA and LAD lesions, 12 with both LCX and LAD lesions, and 24 with 3-vessel disease. The BSPMs were obtained by using the heart potential map system designed by Toyama et al. There were 59 lead points on the anterior chest wall and 28 on the back. The BSPMs in isopotential distribution were made every one msec throughout the ventricular activation period. The distribution of positive and negative potentials, potential maximum and potential minimum, polarity of potential distribution, and the reversal of potential distribution during ventricular repolarization were analyzed. The following information on BSPMs was obtained: (1) In early ventricular repolarization, the negative potential and the potential minimum appeared abnormally on the anterior thorax. The potential abnormality displayed on the right portion or the inferior portion in patients with RCA lesions, on the middle portion or the left portion in patients with LAD lesions, and on the left-superior portion or the left-middle portion in patients with LCX lesions. In patients with multi-vessel disease, the abnormal potential distribution showed a combined pattern of individual vessel lesions. (2) In some cases, the multipolar potential distribution appeared abnormally during the initial stage and the peak of the T wave. (3) The reversal of potential distribution was observed in about half of the patients. The characteristic findings of the BSPM during ventricular repolarization, including abnormal potential distribution, multipolar potential distribution and reversal of potential distribution, will be of clinical value in patients with CAD.

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Electrocardiographic repolarization changes, comprising QT prolongation, are most commonly seen after intracerebral hemorrhage. In this study in patients with intracerebral hemorrhage (ICH), QT dispersion and its daily changes were examined and the relation between QT dispersion and in-hospital mortality assessed. In 28 patients with intracerebral hemorrhage, diagnosed by computerized tomographic scanning, an ECG was obtained on the day of admission to hospital and then serial ECGs were recorded on the following four consecutive days. Blood electrolytes (K, Ca, Mg) were also analysed. The patients with intracerebral hemorrhage were followed until discharge or death (mean 14±4 days). QT, QT peak, and QT-QTpeak dispersion were measured on simultaneous twelve lead electrocardiograms. Also, in 29 healthy subjects as a control group, five consecutive day serial electrocardiograms were recorded. There were no statistically significant differences between the study and control groups in terms of gender and age. During the five days, QT, QT peak, and QT-QTpeak dispersion values were significantly higher in patients with intracerebral hemorrhage than in the control subjects (p<0.001). There were no statistically significant differences in two patient groups with intracerebral hemorrhage who died and who were discharged in terms of mean QT, QT peak, and QT-QTpeak dispersion values. In conclusion, QT, QT peak, and QT-QTpeak dispersion values were significantly greater in patients with intracerebral hemorrhage than in the control subjects, but QT, QT peak, and QT-QTpeak dispersions were not independent risk factors for in-hospital mortality in patients with intracerebral hemorrhage.

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Three-dimensional (3D) radionuclear myocardial imaging has improved the evaluation of left ventricular wall motion. However, there have been no studies evaluating left ventricular function using 3D-perfusion/motion map techniques. We hypothesized that the 3D-perfusion/motion map could accurately evaluate left ventricular wall motion even in patients with a history of myocardial infarction. Electrocardiogram (ECG)-gated single photon emission computed tomography (SPECT) using ^99mTc-methoxy isobutyl isonitrile (MIBI) was performed in 20 patients with a history of myocardial infarction who underwent left ventriculography. Myocardial imaging data were collected during ECG-gated SPECT using a 3-headed gamma camera. Reconstructed 3D SPECT images were oriented to correspond to standard left ventriculography views (right anterior oblique and left anterior oblique projections), and the shortening fraction (SF) was calculated using the center line method. The SF and left ventricular ejection fraction from 3D SPECT images were compared with those determined by left ventriculography. There was a significant correlation between left ventriculography and the 3D-perfusion/motion map procedure in determining SF for all regions of the left ventricle except the anterobasal and posterior segments by using the Bland and Altman method. The 3D-perfusion/motion map procedure offers the advantage that the influences of contraction-related myocardial torsion and three-dimensional compression are minimized. In addition, this method facilitates evaluation of images from nonstandard projections. We conclude that this method may be useful for evaluating left ventricular function.

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Lipids, lipoproteins and apolipoproteins are among the risk factors for the most serious health problem of the age-coronary artery disease (CAD). They vary from country to country, from area to area within a country, depending on genetic, environmental, dietary and many other factors. Our aim was to determine the levels of lipids, lipoproteins and apolipoproteins in healthy people in the central Black Sea region of Turkey. Subjects included 1348 volunteers (682 women, 666 men) referred to the Medical Faculty hospital from the study area. The population consisted of healthy people or those whose disease was not affecting the metabolism of lipids. Cholesterol, triglyceride and HDL-cholesterol levels in the obtained serum samples were measured spectrophotometrically, while apolipoprotein A-I, apolipoprotein B, apolipoprotein E and lipoprotein(a) levels were measured nephelometrically. The levels of lipid parameters were as follows: total cholesterol for men was 4.22±1.00mmol/l (mean arithmetic±SD), triglyceride 1.20 mmol/l (0.30-4.44) [geometric mean (range)], HDL-cholesterol 0.88±0.22 mmol/l, LDL-cholesterol 2.69±0.85 mmol/l, apolipoprotein A-I 1.26±0.22 mmol/l apolipoprotein B 1.12±0.32 mmol/l, apolipoprotein E 0.037±0.012 mmol/l and lipoprotein(a) 0.25 g/l (0.03-2.75); total cholesterol for women was 4.53±1.00 mmol/l, triglyceride 1.05 mmol/l (0.28-4.50), HDL-cholesterol 1.08±0.26 mmol/l, LDL-cholesterol 2.87±0.88 mmol/l, apolipoprotein A-I 1.45±0.25 mmol/l, apolipoprotein B 1.11±0.31 mmol/l, apolipoprotein E 0.039±0.011 mmol/l and lipoprotein(a) 0.22 g/l (0.03-2.16). In conclusion, our study in four different regions in Turkey reflected that the people living in the central Black Sea region are less vulnerable to the risk of CAD, although at a relatively higher risk compared to some other countries.

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Familial hypercholesterolemia (FH) is a monogenic disorder associated with primary hypercholesterolemia. FH is characterized by autosomal co-dominant inheritance with strikingly elevated LDL-cholesterol, the presence of xanthoma and premature atherosclerosis. In the course of investigations of coronary artery disease in Utah, we identified a family whose proband showed elevated plasma levels of LDL cholesterol. To determine the genetic etiology of the lipoprotein abnormalities, we screened DNA samples from the family for mutations in all 18 exons and the exon- intron boundaries of the low-density lipoprotein receptor (LDLR) gene. Novel point mutations were identified in the proband: a one-base insertion of G to a five-G stretch at nucleotides 2412-6 (codons 783-785), causing a frameshift in exon 17 of the LDL receptor gene. The direct sequencing method was used to examine six members of the family recruited for the diagnosis. This method helped to unequivocally diagnose the five individuals as heterozygous for this particular LDL receptor mutation. This method also helped us to diagnose with FH, or to exclude from carrier status, three children between ages 6 and 11.

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Heterozygous familial hypercholesterolemia (FH) is a serious disorder causing twice normal low-density lipoprotein cholesterol levels early in childhood and very early coronary disease in both men and women. Previously published blood cholesterol criteria greatly under-diagnosed new cases of FH among members of known famillies with FH and over-diagnosed FH among participants of general population screening. Thus, there is a need for accurate and genetically validated criteria for the early diagnosis of heterozygous FH. In the course of investigations of coronary artery disease in Utah, we identified a family whose proband showed elevated plasma levels of LDL cholesterol. To carry out molecular genetic diagnosis of the disease, we screened DNA samples for mutations in all 18 exons and the exon- intron boundaries of the low-density lipoprotein (LDL) receptor gene. Novel point mutations were identified in the proband: a C-to-T transversion at nucleotide position 369, causing substitution of Tryptophan for Arginine at codon 103 in exon 4 of the LDL receptor gene. The SSCP method was used to examine seven members of the family recruited for the diagnosis. This method helped to unequivocally diagnose only the proband as heterozygous for this particular LDL receptor mutation while excluding the remaining six individuals from carrier status with FH.

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An electrocardiographic computer simulation was conducted to study the feasibility of predicting accessory pathway locations in Wolff-Parkinson-White (WPW) syndrome with body surface potential Laplacian maps. Three-dimensional, realistically-shaped heart and torso models were used. Ten accessory pathways (APs) around the atrioventricular ring corresponding to Gallagher et al. were set in the heart model, and body surface Lapacian and potential maps of WPW syndrome with single or multiple APs were simulated and compared to each other. In simulations with a single AP in the anterior walls, the maximum-minimum pairs in Laplacian maps appeared to be similar to those in potential maps with respect to their locations and orientations, but the maximum-minimum pairs in Laplacian maps were sharper and more localized than in potential maps. In simulations with a posterior AP or multiple APs, the maximum-minimum pairs in the Laplacian maps showed features correlative to the AP locations, but no such features were found in potential maps. These results suggest the possibility of using Laplacian maps, as a non-invasive method for predicting accessory pathways locations in WPW syndrome.

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Remodeling is a fundamental cardiac response to injury and involves cardiac fibroblast proliferation and extracellular matrix (ECM) production. Angiotensin II (Ang II) directly promotes these changes in cardiac fibroblasts and thus, plays critical roles in cardiac hypertrophy and wound healing. Osteopontin, fibronectin and laminin mRNA were detected in total RNA harvested from cultured adult rat cardiac fibroblasts. Immunocytochemistry staining of cultured adult rat cardiac fibroblasts grown on coverslips revealed the presence of β3 integrins on the surfaces of the cells. In the present study, we investigated the role of Ang II in a model of wound repair using floating collagen gels harboring adult rat cardiac fibroblasts, and we determined which members of the integrin family existed on these cells. The presence of either MPIIIB 10, a monoclonal antibody against osteopontin (7.2μg/ml) or RGD (arginine-glycine-aspartate) peptide (10^-4 M) had no effect on gel contraction. Osteopontin itself induced gel contraction; however this effect was completely neutralized by MPIIIB 10 (7.2μg/ml), RGD peptide (10^-4 M) and a monoclonal antibody against rat β3 integrin (25μg/ml). We identified αv, β3 and β5 integrins on adult rat cardiac fibroblasts by fluorescence-activated cell sorting and confirmed that RGD peptide and an antibody against β3 integrin completely blocked osteopontin-induced gel contraction. These results suggest that Ang II promotes cardiac wound healing and remodeling processes by inducing expression of osteopontin and β3 integrin by cardiac fibroblasts.

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A 33 year-old woman was referred to our hospital for further treatment of ventricular tachycardia (VT). During treatment with amiodarone (200 mg/day), clinical VT at the cycle length of 510 ms was induced. During the VT, rapid ventricular pacing was repeated at progressively shorter cycle lengths after a decrement of 10 ms steps. The VT was entrained by the rapid pacing and reproducibly terminated at a paced cycle length of 380 ms. Four weeks after reducing the amiodarone to 100 mg/day, programmed stimulation was repeated. The VT with the same morphology but with a slightly shorter cycle length of 480 ms was again induced. However, at this time, rapid pacing from the same site could not terminate VT and transient acceleration developed at a shorter paced cycle length of 260 ms. The QT (QTc) interval, effective refractory period at the pacing site and width of the paced QRS complex were similar before and after changing the amiodarone treatment. The most characteristic change of VT in the second study was a widening of the entrainment zone, which was calculated as the difference between VT cycle length and the longest pacing cycle length which interrupts VT during the entrainment (from 130 to > 220 ms), and it may be explained by the preferential shortening of the action potential duration and/or facilitation of the depressed cell to cell conduction within the reentry circuit. Amiodarone must exert a preferential action in the reentry circuit and modulate the conduction property as well as the effective refractory period. We should pay close attention to the efficacy of antitachycardia pacing during the modification of amiodarone treatment.

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Venous thrombosis induced by a transvenous permanent pacemaker is a common complication. However, superior vena cava (SVC) syndrome caused by pacemaker leads is only occasionally seen and its prevalence has been estimated to be less than 1 in 1000 pacemaker patients. Herein, we report a Taiwanese patient of high grade AV block, who presented with SVC syndrome 2 years after transvenous permanent pacemaker implantation. This case features fibrotic stenosis of the junction of right brachiocephalic trunk and SVC, and an extensive thrombus formation resulting in complete obliteration of the left brachiocephalic vein. The collateral circulation was so delicate that he still could lead a rather normal life, even if anticoagulant therapy proved to be ineffective from an angiographic point of view.

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We report a rare combination of a right atriofascicular Mahaim fiber and two left-sided atrioventricular accessory pathways in a 57-year-old female presenting with an antidromic atrioventricular reciprocating tachycardia. Radiofrequency ablation was first targeted at the left lateral accessory pathway that served as the retrograde limb of the tachycardia. After elimination of the left lateral pathway, a bystander left posterolateral pathway was detected, and it too was successfully ablated. Although no tachycardia was reinducible, the Mahaim pathway was ablated because of its short effective refractory period. A discrete Mahaim potential recorded at the right atrial free-wall successfully guided the ablation.

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We present a 57-year-old man with Wolff-Parkinson-White syndrome who exhibited a wide “gap” in retrograde conduction through a concealed atrioventricular accessory pathway. The appearance of the wide “gap” depended on the ventricular pacing sites. While ventricular extrastimuli at a basic cycle length of 600 msec from the right ventricular outflow tract consistently conducted to the atria, retrogradely through the accessory pathway, those from the right ventricular apex repeatedly revealed disappearance of the retrograde conduction at the wide coupling intervals from 550 to 380 msec. The mechanisms of this rare “gap”-like phenomenon are discussed in this paper.

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Aneurysm formation after aortic coarctation repair is not a rare complication of post-coarctation of aorta repair. We describe the case of a 43-year-old woman who had undergone repair of an isolated interruption of the aortic arch 30 years earlier, who came to our hospital with progressive chest pain, cough and dyspnea. A giant aortic aneurysm was revealed in the distal aortic arch by CT study. The patient underwent aneurysmectomy with total aortic arch replacement using a Dacron graft through redo median sternotomy. An embryologic explanation of this patient's anomaly and the previous surgical procedure are discussed for defining this rare clinical condition.

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Uhl's anomaly is a rare congenital hypoplasia of the right ventricular (RV) myocardium. It can be seen together with some other congenital anomalies. Here we first report a 16-year-old male patient with Uhl's anomaly which appears with cardiac tamponade.

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A 61-year-old female who had shown Raynaud's phenomenon and articular swelling for 10 years, was admitted to hospital because of fever of unknown origin (FUO) and dry cough. She was diagnosed by skin biopsy to have a collagen disease or overlap syndrome. Anemia developed rapidly and FUO persisted, but blood culture was negative. Although indomethacin and prednisolone were administered for the progression of clinical signs and symptoms, severe dyspnea developed, resulting in bradycardia, followed by recurrent episodes of ventricular tachycardia. In spite of extensive treatment for her arrhythmia she died on the 9th hospital day. An autopsy revealed generalized Wegener's granulomatosis with extensive cardiac involvement. Necrotizing angitis and severe granulomatous inflammatory foci affected characteristically the common bundle of His and right bundle branch in addition to the ordinary myocardium.

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We report a 50-year-old man with a right ventricular structure causing an intraventricular pressure gradient. He had been diagnosed as vasculo-Behçet with a history of aphthous stomatitis and thrombophlebitis. He had also been suffering from atrial flutter and mild right-side heart failure. Echocardiography showed that there was an abnormal structure attached to the right ventricular free wall and protruding into the cavity, and that it caused the pressure gradient estimated to be approximately 19 mmHg. Chest X-ray computed tomography demonstrated that the structure was partially calcified. Magnetic resonance imaging depicted the structure separating the right ventricle into two chambers. Angiographic study revealed a markedly enlarged right atrium and a filling defect at the mid-portion of the right ventricle, which divided the right ventricular cavity into two parts. Hemodynamic study showed a slightly elevated right atrial pressure (mean 7 mmHg) and a peak-to-peak intraventricular pressure difference of 18 mmHg in the right ventricle. The diastolic pressure tracing of the right ventricular low pressure chamber showed a ‹dip and plateau' pattern. Although the pathological features of the abnormal right ventricular structure in this case were not fully clarified, abnormal muscle bundle and/or endocardial fibrosis, which were reported to be associated with Behçet's disease, may have contributed to its generation.

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