The outcome of stent implantation and redilatation was investigated in 4 pediatric patients with 7 stenotic lesions of the pulmonary vein (PV), paying particular attention to late neointimal proliferation. The minimal diameter of the lesions increased from 0.8-3.6 (2.3±1.1) mm to 3.6-8.4 (5.1±1.6) mm immediately after stent implantation. Although the pressure gradient across the lesion was not measured in patient 4, in patients 1-3, it decreased from 4-34 (18±13) mmHg to 3-15 (7±4) mmHg. Except for case 4, who achieved a lesion diameter of 8.4 mm after initial stent dilatation, the other 6 lesions all restenosed within a few months, with an increasing pressure gradient. One patient with multiple PV stenoses associated with persistent severe pulmonary hypertension died suddenly. However, repeat dilatations were effective in all other lesions. Furthermore, in one lesion in patient 1, no serious restenosis developed for 20 months after the lesion was dilated up to 5.6 mm. Although further follow-up is mandatory, the final stent diameter within a vessel may determine long-term patency, and aggressive redilatation may be crucial for successful therapy of such a difficult disease. (Circ J 2003; 67: 187 - 190)

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Sudden cardiac death is a well-documented complication of hypertrophic cardiomyopathy and additionally, failure to raise blood pressure (BP) during exercise has been associated with a poor outcome. The present study group comprised 58 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) who were receiving β-blocker therapy. All patients underwent submaximal exercise radionuclide ventriculography (RNVG) to evaluate left ventricular (LV) function at both rest and peak exercise. Patients were divided into 2 groups based on the increase in systolic BP during exercise (ie, group A <30% or group N ≥30% of resting systolic BP) and were involved in long-term follow-up (10.4±4.0 years). Group A comprised 29% of the subjects. Age and workload at peak exercise were similar in the 2 groups. LV end-diastolic dimension was smaller and the interventricular septum was thicker in group A. LV ejection fraction on RNVG was similar in the 2 groups at rest and at peak exercise. During the follow-up period, more patients in group A than group N suffered syncopal attack (29% vs 5%, p<0.05) and cardiac sudden death (24% vs 2%, p<0.05). Patients with HNCM whose BP fails to rise during exercise have a poor prognosis. (Circ J 2003; 67: 191 - 194)

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Antiarrhythmic therapy requires monitoring of serum drug concentrations to determine a patient's optimal oral dose of medication. Repeated examination of blood samples, however, is costly and time-consuming, so the present study evaluated whether changes in serum concentrations could be estimated from changes in electrocardiographic (ECG) parameters. Of 36 patients receiving antiarrhythmic drugs for supraventricular or ventricular arrhythmias, 12 were treated with flecainide, 12 with pilsicainide, and 12 with pirmenol. Signal-averaged ECG (SAECG) were recorded before starting drug administration, 1 month later, and twice during ongoing therapy. At the time of the 2nd to the 4th recordings, serum concentrations of the drugs were also measured. As previously reported, all agents, but especially flecainide and pilsicainide, prolonged the filtered QRS (f-QRS) and the duration of low-amplitude signals at the terminal portion of the QRS complex. The SAECG parameters varied between the recordings made during therapy. Differences in the duration of the f-QRS between 2 recordings correlated significantly with differences in serum drug concentrations (r=0.91 for flecainide, r=0.70 for pilsicainide, and r=0.61 for pirmenol). No significant correlation between drug concentration and other SAECG parameters was found. Changes in the serum concentration of flecainide, pilsicainide and pirmenol can be estimated from changes in the duration of the f-QRS on the SAECG and periodic monitoring of such could help reduce the number of repeat measurements of drug concentrations in blood samples. (Circ J 2003; 67: 195 - 198)

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This study compared the outcomes of combined coronary artery bypass grafting (CABG)/aortic valve replacement (AVR) and CABG alone in patients with moderate aortic stenosis and determined the possible indications for AVR at the time of CABG. Between December 1988 and January 2001, in Tenri Hospital, 41 patients with aortic stenosis underwent CABG: 26 patients underwent the combined procedure and 15 patients underwent CABG alone. The patients who underwent CABG alone were separated them into 2 groups on the basis of the results of annual echocardiography: the rapid progression group, defined by an increase of ΔP by ≥10 mmHg/year, and the slow progression group. Of the 15 patients who underwent CABG alone, the probability of survival at the end of the study in 2001 was 92% at 5 years and 74% at 10 years, and the respective event-free rates were 65% and 50%. Patients less than 70 years old and who were in the rapid progression group had a greater risk for re-operation. The study suggests that patients younger than 70 years old with risk factors for rapid progression should undergo CABG/AVR, and conversely, those older than 70 years old without the risk factors can undergo CABG only. (Circ J 2003; 67: 199 - 202)

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It is very important to prevent embolisms from left atrial thrombi (LAT). The present study was a trial for the management of patients with AT using 122 patients with atrial fibrillation and LAT who were followed for 1 year after transesophageal echocardiography. LAT were classified by their shape and mobility into the mobile ball type (MB, n=28), fixed ball type (FB, n=32) and mountain type (MO, n=42). The patients were given warfarin (INR: 1.5-2.0, n=43), aspirin 81 mg (n=74) and/or ticlopidine 200 mg/day (n=31). The embolic rate (ER) in the MB group was significantly higher than in the other groups [ie, MB 39.3% vs FB 15.6% (p<0.05), vs MO 2.4% (p<0.05)]. The ER in the FB group was significantly higher than in the MO group (p<0.05). Therapy with a combination of ticlopidine and aspirin reduced the ER in the patients with ball thrombi. The ER of the ball thrombus type group, especially the MB group, was very high in spite of therapy with anti-coagulants and/or anti-platelet agents, and such patients should be treated by early surgical intervention. However, the combination of ticlopidine and aspirin may be useful for preventing embolism. (Circ J 2003; 67: 203 - 208)

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The current reperfusion strategy in Japan for acute myocardial infarction (AMI) is that the majority of early arrival patients are treated with primary percutaneous coronary intervention (PCI). However, the efficacy of primary PCI, intravenous thrombolysis (IV-T), intracoronary thrombolysis (IC-T) and rescue PCI has not been compared in the clinical situation. In the present study, 3,258 cases of AMI in 1992-2000 from the data base of the Miyagi Study Group for AMI were analyzed. These patients were hospitalized within 6 h of the onset of symptoms. IV-T and IC-T were initially performed in 120 and 441 patients, respectively, and 41 and 199 rescue PCI procedures, respectively, were needed. Primary PCI was performed in 1,822 cases, and no reperfusion therapy was done in 875 patients. The crude 30-day in-hospital mortality was 12.7% for IV-T, 3.7% for IC-T, 4.8% for primary PCI, 7.9% for rescue PCI, and 14.1% in patients who did not undergo reperfusion therapy. The covariate-adjusted odds ratio (95% confidence interval) was 0.38 (0.28-0.52) for primary PCI, 0.30 (0.15-0.60) for IC-T, 1.04 (0.51-2.10) for IV-T and 0.77 (0.46-1.30) for rescue PCI. The present data verify that primary PCI is superior to other reperfusion strategies in the real clinical situation and justifies the current unique strategy of reperfusion therapy for AMI used in Japan. (Circ J 2003; 67: 209 - 214)

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Chronic heart failure is characterized by impaired cardiac function, but the relationship between clinical indices and subjective perception is not clear. This study was undertaken to investigate the relationship between cardiac function, exercise capacity and clinical classification, and the health-related quality of life (HRQOL) in 91 outpatients with an left ventricular ejection fraction (LVEF) less than 40%. Exercise capacity was evaluated by the Specific Activity Scale, and HRQOL by the Medical Outcome Study Short Form 36. Exercise capacity and the cardiothoracic ratio were correlated with the HRQOL related to physical functioning, although the correlation between exercise capacity and mental health was not significant. LVEF was not related to HRQOL. Factor analysis revealed (1) LVEF was independent of physical functioning; (2) physical function and exercise capacity comprise a factor reflecting physical HRQOL; and (3) socio-emotional functioning is the third factor independent of LVEF and physical function. Physical and socio-mental HRQOL measurement included information independent of the widely used clinical indices such as LVEF and New York Heart Association classification. The evaluation of HRQOL should be included in the assessment of patient status. (Circ J 2003; 67: 215 - 220)

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Exercise training improves the endothelial function of arteries in skeletal muscle, but few studies have examined its clinical effect on human coronary endothelial function. Non-infarct-related coronary arteries in 41 patients with a recent myocardial infarction who underwent successful percutaneous transluminal coronary angioplasty were studied. Patients were divided into 2 groups: regular exercisers (n=24, 17 males, mean age: 58 years), and non-exercisers (n=17, 12 males, mean age: 58 years). Acetylcholine (ACh) was infused into the non-infarct-related coronary artery and its diameter was measured by quantitative angiography at baseline and at 6 months after angioplasty. ACh, given in doses of 1, 3, 10, 30 μg/min, increased the coronary artery diameter in a dose-dependent manner in both groups. The mean percent change in the diameter at the site of stenosis change (%DS) was less in the regular exercisers than in the non-exercisers (11%±12 vs 41%±36, p<0.05). Multivariate analysis showed that regular exercise was the only significant determinant of improvement in endothelial function (p=0.01). These findings suggest that regular exercise improves endothelial function in the coronary arteries following myocardial infarction. (Circ J 2003; 67: 221 - 224)

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The aim of the present study was to test the hypothesis that inadequate improvement in heart rate variability (HRV) in the healing stage of acute myocardial infarction (AMI) is associated with left ventricular (LV) remodeling. The study group comprised 20 patients (14 men, 6 women; mean age, 61±12 years) with a reperfused first anterior AMI (≤24 h). The standard deviation of normal RR intervals (SDNN) was calculated from the 24-h ambulatory electrocardiogram recorded on day 3 of admission and at predischarge from the hospital. Left ventriculography was performed immediately after primary angioplasty and at predischarge. The change in SDNN (ΔSDNN) was compared with the change in the LV end-systolic volume index (ΔLVESVI), a parameter of LV remodeling. SDNN increased from 73±19 ms on day 3 to 109±35 ms at predischarge (p=0.0003). SDNN at predicharge and ΔSDNN correlated negatively with ΔLVESVI (r=-0.52, p=0.02, and r=-0.61, p=0.004, respectively), whereas SDNN on day 3 did not correlate with ΔLVESVI. Multiple regression analysis selected ΔLVESVI (p=0.02) as an independent factor of ΔSDNN. This study indicates that ΔSDNN and SDNN at predicharge are associated with ΔLVESVI in patients with a reperfused first anterior wall AMI, indicating that persistently reduced HRV is associated with postinfarction LV remodeling. (Circ J 2003; 67: 225 - 228)

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Pulmonary thromboembolism (PTE) is associated with various electrocardiogram (ECG) abnormalities, but the utility of evaluating the severity of PTE based on ECG abnormalities alone has not been investigated in Japanese patients previously. The purpose of this study was to examine the relationship between ECG abnormalities and the mean pulmonary artery pressure (MPAP) in patients with acute massive PTE (AMPTE). ECG examination of 21 patients, who were diagnosed with AMPTE by pulmonary arteriography, found that S₁Q₃T ₃ was the most frequently observed abnormality (in 67% of the patients), followed by negative T (62%), clockwise rotation (57%), and ST elevation (48%). When these patients were divided into 2 groups based on the level of MPAP, 8 of the 11 ECG findings, which were associated with PTE in a previous report, were more frequently observed in Group H (MPAP ≥40 mmHg) than in Group L (MPAP <40 mmHg). MPAP correlated significantly with the total number of ECG abnormalities (r=0.82, p<0.001). In particular, at least 5 ECG abnormalities were noted in patients with MPAP ≥45 mmHg. These results suggested that the total number of ECG abnormalities in patients with AMPTE can be used to evaluate the severity of APTE, including PAP level. (Circ J 2003; 67: 229 - 232)

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A growing body of evidence suggests that walking reduces the incidence of coronary events, so the present study investigated whether walking influences left ventricular function in 30 patients with acute myocardial infarction (AMI) who had undergone successful percutaneous coronary intervention (PCI). The patients were randomly assigned to either a 3-month exercise training program of walking (group W, n=15) or a control group (group C, n=15). At both the beginning and end of the study, patients underwent exercise stress echocardiography to determine left ventricular ejection fraction (LVEF) at rest and during exercise. At baseline, there was no difference in LVEF at rest or during exercise between the two groups. After 3 months, LVEF during exercise was significantly improved compared with at rest in group W (61±3% during exercise vs 57±5% at rest, p<0.01), whereas no difference was observed between the LVEF at rest and that during exercise in group C (54±5% at rest vs 52±7% during exercise, NS). Walking may be beneficial for improving left ventricular function during exercise in patients with AMI. (Circ J 2003; 67: 233 - 237)

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Although pre-interventional thrombolysis has recently been shown to restore early patency and preserve left ventricular function in patients with acute myocardial infarction, the significance of Thrombolysis in Myocardial Infarction (TIMI) grade flow early after thrombolysis remains unclear. Patients were classified into 3 groups according to TIMI grade flow 45 min after thrombolysis; 38 patients with TIMI grade 0 or 1 flow (group T0) and 46 with TIMI grade 2 flow (group T2) additionally received immediate percutaneous coronary intervention (PCI) and 50 patients with TIMI grade 3 flow (group T3) were treated conservatively after thrombolysis. Although the door-to-balloon times did not differ in groups T0 and T2, group T2 had lower peak creatine kinase, a higher rate of complete (≥70%) ST resolution and better regional wall motion at discharge as compared with group T0, similar to group T3 (group T2, group T3 vs group T0; 2,857±1,756, 2,314±1,948 vs 3,779 ±2,214 mU/ml; 57, 72 vs 34%; -1.5±1.6, -1.2±1.6 vs -2.2±1.6; all p<0.01, respectively). These results suggest TIMI grade 2 flow at 45 min after thrombolysis followed by immediate PCI, as well as TIMI grade 3 flow, is associated with greater myocardial salvage than TIMI grade 0 or 1 flow. (Circ J 2003; 67: 238 - 242)

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This study was designed to examine whether the cross-sectional area of vena contracta measured by color Doppler flow mapping (CFM) could be used for assessing aortic regurgitation (AR) and developing an index for grading AR. The 75 study patients with AR were classified into quadrant grades according to New York Heart Association functional class, regurgitant fraction, left ventricular (LV) end-diastolic dimension and LV end-systolic dimension. Using CFM, the cross-sectional area of the vena contracta was measured and it could distinguish all grades without significant overlap. An area of less than 0.10 cm² corresponded to Grade 1, 0.10-0.19 cm² corresponded to Grade 2, 0.20-0.29 cm² corresponded to Grade 3 and an area of more than 0.30 cm² corresponded to Grade 4. An area of vena contracta of more than 0.30 cm² identified high-scoring AR (Grade 4) in 11 of 11 (sensitivity 100%) and correctly predicted the absence of high-scoring AR in 60 of 64 (specificity 94%). Conversely, there was considerable overlap between the jet distances with the clinical grades. The cross-sectional area of the vena contracta measured by CFM can provide a simple quantitative assessment of AR that correlates well with the clinical grade of AR. (Circ J 2003; 67: 243 - 247)

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This experimental study was designed to determine if caspase-3-like protease is activated during a short period of ischemia - reperfusion (I-R) that did not induce apoptosis, and whether protease-3-protease inhibitor could prevent myocardial I-R injury, especially necrotic cell death. The subjects were 20 isolated rat hearts; 10 were pretreated for 20 min with 100 μmol/L of the protease-3-protease inhibitor, peptide antagonist Asp-Glu-Val-Asp-CHO (DEVD) (Group D), and compared with the 10 no-pretreated hearts (Group C). The hearts were then subjected to 20, 30, 45, and 60 min of normothermic global ischemia followed by 30 min of reperfusion. Caspase-3-like protease was significantly elevated after 45 min and 60 min in ischemic hearts. Group D had reduced levels of caspase-3-like protease activity after 45 min and 60 min (302±58%, 378±69% of pre-ischemic control, respectively), as compared with Group C (542±74%, 689±85%, respectively) (p<0.05, p<0.05, respectively). Histological analysis also demonstrated a decrease in cellular damage in Group D, as the count ratio of necrotic cells with total cardiomyocytes was 38%, as compared with 78% in the control group (p<0.05). Caspase-3-like protease participated in I-R injury in rat hearts and inhibition of this protease resulted in a reduction of necrotic cell death. (Circ J 2003; 67: 248 - 252)

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Among the several mechanisms proposed for ischemic preconditioning (IPC), generation of reactive oxygen species (ROS) is reported to be involved in the cardioprotective effects of IPC. The present study was designed to investigate whether repetitive exposure to hydrogen peroxide (H₂O₂) can protect the myocardium against subsequent ischemia/reperfusion injury, and whether the H₂O₂-induced cardioprotection is related to the preservation of energy metabolism. Langendorff-perfused rat hearts were exposed to two, 5 min episodes of IPC or to various concentrations of H₂O₂ twice and then to 35 min global ischemia and 40 min reperfusion. Using ³¹P nuclear magnetic resonance (³¹P-NMR) spectroscopy, cardiac phosphocreatine (PCr) and ATP and intracellular pH (pH_i) were monitored. IPC and the treatment with 2 μmol/L H₂O₂ significantly improved the post-ischemic recovery of left ventricular developed pressure (LVDP) and the PCr and ATP compared with those of the control ischemia/reperfusion (LVDP: 36.9 ±7.4% of baseline in control hearts, 84.0±3.5% in IPC, 65.4±3.8% in H₂O₂; PCr: 51.1±5.3% in control hearts, 81.4±5.5% in IPC, 81.7±5.2% in H₂O₂; ATP: 12.3±1.6% in control hearts; 30.0±2.8% in IPC, 28.6±2.3% in H₂O₂, mean ± SE, p<0.05). However, lower (0.5 μmol/L) or higher (10 μmol/L) concentration of H₂O ₂ had no effect. There were significant linear correlations between mean LVDP and high-energy metabolites after 40 min reperfusion in H₂O₂-treated hearts. In IPC-treated hearts, the mean LVDP was greater than that in the 2 μmol/L H₂O₂-treated hearts under similar levels of high-energy metabolites. IPC also ameliorated intracellular acidification (6.38±0.03 in control hearts, 6.65±0.04 in IPC, p<0.05), but treatment with H₂O₂ did not affect pH_i during ischemia (6.40±0.05 in H₂O₂). In conclusion, H₂O₂ had protective effects against ischemia/reperfusion injury and the effects were related to the preservation of energy metabolism. IPC could have additional protective mechanisms that are associated with the amelioration of intracelluar acidosis during ischemia. (Circ J 2003; 67: 253 - 258)

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Establishing the existence of α-adrenoceptor subtypes in isolated human gastroepiploic and omental arteries was the goal of the present study. Functional vascular reactivity of selective α₁- and α₂-adrenoceptor agonists and antagonists was studied, using a cannula inserting technique. Intraluminal administration of norepinephrine (NE), phenylephrine (PE) or BHT-933 caused a vasoconstrictive response in a dose-related manner. The relative potencies of the 3 agonists were almost the same in both arteries. NE-induced vasoconstrictions were significantly antagonized by either prazosin or rauwolscine. PE-induced responses were strongly inhibited by prazosin. BHT-933-induced constrictions were inhibited by rauwolscine. These results indicate that both α₁- and α₂-adrenoceptors exist in the human gastroepiploic and omental arteries. (Circ J 2003; 67: 259 - 262)

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The ventricular tachyarrhythmias associated with the LQT3 syndrome are typically bradycardia-dependent. However, some episodes can be associated with exercise or emotional stress, suggesting a different arrhythmogenic mechanism when sympathetic activity predominates. This study examined the potential arrhythmogenic mechanisms during periods of autonomically mediated transient heart rate acceleration in a canine anthopleurin-A model of LQT3 syndrome. Using plunge needle electrodes, transmural unipolar electrograms of the left ventricle were recorded from endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) sites. The activation - recovery interval (ARI) was measured to estimate local refractoriness. The cardiac cycle length was gradually shortened by cessation of vagal stimulation (vagal stimulation protocol (VSP)), and intramural electrograms and onset mode of ventricular tachyarrhythmias were analyzed in 7 experiments. The VSP was performed 8 times before and 5 times after administration of mexiletine in each experiment. Before mexiletine, vagal stimulation slowed the heart rate and created large transmural ARI dispersion because of a greater ARI prolongation at Mid rather than Epi/Endo sites. After cessation of vagal stimulation, unipolar electrograms started to show ARI alternans and ventricular premature beats developed sporadically. Sustained ventricular tachyarrhythmias were induced in 12 of the 56 trials of the VSP. Initiation of ventricular tachyarrhythmias was associated with delayed conduction at Mid/Endo sites. Mexiletine attenuated transmural ARI dispersion, and neither ARI alternans nor ventricular tachyarrhythmias was observed during all 35 trials of the VSP after mexiletine administration. Heart rate acceleration induced by an abrupt shift to a state of predominant sympathetic activity enhances arrhythmias in this LQT3 model. Mexiletine homogenizes ventricular repolarization, suppresses premature complexes and was antiarrhythmic during ventricular tachyarrhythmias induced by the VSP. (Circ J 2003; 67: 263 - 268)

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A 52-year-old woman, a hemodialysis patient, was admitted because of exertional dyspnea. Echocardiography showed left ventricular (LV) dilatation and reduced contraction. Coronary angiography showed no fixed stenosis. She had elevated levels of parathyroid hormone (PTH) as a result of secondary hyperparathyroidism with advanced renal failure. After parathyroidectomy, marked improvement of LV function following immediate decrease of blood levels of PTH was observed. It is suggested that PTH might have a significant role in the pathogenesis of LV dysfunction and that parathyroidectomy might be effective as a therapy for heart failure in some patients with secondary hyperparathyroidism and LV dysfunction. (Circ J 2003; 67: 269 - 272)

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A 21-year-old woman without any known coronary risk factors was found at coronary catheterization to have normal coronary angiograms, but demonstrated acethylcholine (ACh)-induced coronary spasm. She had a history of Kawasaki disease (KD) at 19 months of age and, although coronary angiography was not performed at that time, no coronary aneurysms were detected by echocardiography. To the best of our knowledge, this is the first case report of ACh-induced coronary spasm associated with normal coronary angiograms in a young person with a history of KD. The findings suggest that subclinical, persistent coronary endothelial dysfunction may exist in this patient; furthermore, the dysfunction appears diffuse and might be unrelated to coronary aneurysm formation. The long-term significance of coronary endothelial dysfunction in patients with KD, as suspected by coronary spasm, remains unknown but may be an important risk factor for future atherosclerosis. (Circ J 2003; 67: 273 - 274)

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A 62-year-old woman was referred to hospital to be treated for complete heart block with syncope. A quadricuspid aortic valve without vegetation and aortic valve regurgitation (AR) were observed by transesophageal echocardiography. Blood culture showed penicillin-resistant Streptococcus pneumoniae. The patient received a permanent pacemaker implantation (VDD type) and was given antibiotics. Although infection improved, heart failure was not improved because AR hemodynamic changes became worse. An aortic valve replacement was performed using a prosthesis on the 26th day of hospitalization. The patient recovered and was discharged. (Circ J 2003; 67: 275 - 276)

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Although pharmacological agents are frequently used to control ventricular rate or restore sinus rhythm of patients with atrial fibrillation (AF), there are no reports of the relationship between those agents and left atrial appendage (LAA) function. Two cases of a decrease in LAA blood flow velocity caused by negative inotropic agents are presented as an indication that negative inotropic agents are a risk factor for systemic thromboembolism with AF. (Circ J 2003; 67: 277 - 278)

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