We assessed the relationship between right atrial (RA) function and obstructive lesions of the coronary arteries in 29 patients with recent or old myocardial infarction (MI). Patients were divided into 3 groups according to the location of obstructions as follows: obstruction at the proximal right coronary artery (segments 1 and 2) (RCA proximal group, n=9); obstruction at the distal RCA (segments 3 and 4) (RCA distal group, n=6); and obstruction at the left anterior descending coronary artery (LCA group, n=14). The RA volume and the fractional change in the RA area during atrial contraction (RA %AC) were evaluated by apical 2-dimensional echocardiography. The right ventricular (RV) end-diastolic pressure (RVEDP) was measured in 4 patients in the RCA proximal group and 4 patients in the LCA group. The ejection fraction of the right ventricle (RVEF) was measured by radionuclide angiography or 2-dimensional echocardiography in 7 patients in the RCA proximal group, 5 patients in the RCA distal group, and 7 patients in the LCA group. The RVEF tended to be lower in the RCA proximal group the in the RCA distal and LCA groups. The RA volume was significantly greater in the RCA proximal group than in the LCA group. The RA %AC was significantly smaller in the RCA proximal group than in the RCA distal and LCA groups. There were no significant differences in the early diastolic RV inflow velocity among groups, but the late diastolic RV inflow velocity was significantly lower in the RCA proximal group than in the RCA distal and LCA groups. There was no significant difference in the RVEDP between the RCA proximal and LCA groups. Thus, RA dysfunction in the RCA proximal group appeared to be due to myocardial damage rather than no afterload mismatch. These findings suggest that RA dysfunction may occur in patients with an inferior MI who have an obstructive lesion of the proximal RCA. (Jpn Circ J 1998: 62: 393 - 398)

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Optimal pace mapping is a good predictor of the appropriate ablation site for idiopathic right ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT). We studied the relationship between the RVOT pacing site and QRS morphology in the 12-lead ECG during pacing to find the optimal site more quickly. In 13 patients with idiopathie VT, pacing at 8 sites in the RVOT (free wall, septum, and anterior and posterior regions of upper and lower sites) was performed while 12-lead ECGs were recorded. The R-wave amplitude minus the S-wave amplitude in lead I (R_I-S_I) and aV_F (R_aVF-S _aVF) and the transitional zone index (TZI) were compared in different pacing site; TZI was defined to examine the transitional zone as a value. The R_I-S_I was smaller in the anterior region than in the other regions, and the negative R_I-S_I predicted that the pacing site was in the upper or lower anterior regions. The R_aVF-S_aVF was larger in the septum and anterior regions than in the free wall and posterior regions. The TZI was larger in the free wall region than in the septum. From the results, we constructed a flow chart that differentiates the origin of the arrhythmia in the RVOT and a directional guide that indicates the direction from the current mapping site for optimal pace mapping. The results provided an ECG guide for locating the focus of VT originating from the RVOT. These findings may systematically improve the mapping procedure. (Jpn Circ J 1998; 62: 399 - 404)

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To evaluate the prognostic value of the simultaneous assessment of perfusion and reft ventricular wall motion, exercise non-gated/rest electrocardiogram (ECG)-gated ^99mTc methoxy-isbutyl isonitrile (MIBI) single-photon emission computed tomography (SPECT) was preformed in 182 patients suspected of having coronary artery disease. After injection of 250 MBq of ^99mTc-MIBI at peak exercise, stress perfusion images were classified into 3 groups: normal, equivocal, and abnormal. Normal subjects completed the 1-day protocol but not the resting study, whereas patients with abnormal or equivocal perfusion images underwent ECG-gated SPECT study with injection of 750MBq of ^99mTc-MIBI 3 h later. Patients with normal perfusion during this protocol had a benign prognosis. Only 4 soft events occurred in the normal group (4.8%). In contrast, patients with both myocardial infarction and abnormal wall motion at rest experienced more cardiac events (7 cardiac events including 1 cardiac death among a total of 45 patients; 15.6%, p<0.05 compared with normal subjects). In addition, ischemic patients also experienced more cardiac events (7 events including 2 cardiac deaths among a total of 25 subjects; 28.0%, p<0.01 compared with normal patients). Our data suggest that the simultaneous assessment of perfusion and wall motion by stress/rest ECG-gated ^99mTc-MIBI SPECT is a reliable indicator of prognosis in patients suspected of having coronary artery disease. (Jpn Circ J 1998; 62: 405 - 408

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The aim of this study was to assess whether the psychobehavioral pattern alexithymia is related to coronary artery spasm. Alexithymia, deficient psychological awareness, was examined using the Minnesota Multiphasic Personality Inventory Alexithymia Scale in 100 patients with angina pectoris in whom coronary spasm, defined as ≥99% coronary narrowing, was documented upon ergonovine provocation, and in 109 patients with chest pain syndrome who were shown to have almost normal coronaries without inducible coronary spasm on coronary angiogram (control group). Alexithymia was approximately twice as prevalent in the coronary spasm group (31%) as in the control group (14%) (p<0.01). Among various conventional risk factors including hyperlipidemia, obesity, diabetes mellitus, hypertension, hyperuricemia, or family history of ischemic heart disease, only male sex and smoking were more prevalent in the coronary spasm group than in the control group (p<0.001). The odds ratios of coronary spasm adjusted for all the other risk parameters including sex and age were 4.14 [95% confidence interval (CI) 1.81-9.47] for alexithymia and 2.38 (95% CI 1.18-4.82) for smoking . A psychobehavioral pattern, alexithymia, relates to coronary spasm. This relationship is independent of the conventional coronary risk factors. (Jpn Circ J 1998; 62: 409 - 413)

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Although considerable information is available regarding the prognosis after acute myocardial infarction (AMI) in Western populations, little is known about the fate of Japanese subjects after AMI. The purpose of this study was to assess short-term mortality and factors influencing it after AMI in Japan. From April 1993 to December 1995, 1,014 patients with AMI from 41 hospitals in Yamagata Prefecture were registered by cardiologists for the prospective survey. Among patients who died within 28 days after the onset of AMI, immediate causes of death were examined and the clinical profiles of these subjects were compared with those of patients that survived. Early death occurred in 184 patients (short-term mortality 18%). Patients who died were significantly older than survivors (76.1±9.4 vs 67.6±11.8 years, p<0.01). They were also more likely to be women (50% vs 31%, p<0.01), to have had hypertension (64% vs 54%, p<0.05), diabetes mellitus (29% vs 20%, p<0.02), prior MI (17% vs 12%, p<0.05), or Killip class III or IV disease (63% vs 15%, p<0.01), and were significantly less likely to be current smokers (26% vs 45%, p<0.01) or to have been treated with reperfusion therapy (27% vs 63%, p<0.01). Multivariate logistic analysis demonstrated that independent predictors of early death were Killip class III or IV and advanced age. Reperfusion therapy was a negative predictor of death. Patients who died had arrived at hospital earlier than patients who survived. Mortality as a result of heart failure, cardiac rupture, or arrhythmia fell exponentially after the onset of AMI. Thus, the predictors of short-term mortality were similar to those reported in Western populafions. More deaths occurred just after the onset of disease, suggesting that early therapy is important in reducing short-term mortality. (Jpn Circ J 1998; 62: 414-418)

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Tissue factor pathway inhibitor (TFPI) is known to inhibit the initial reaction in the tissue factor-mediated coagulation pathway. We measured plasma free-form TFPI antigen levels and monitored 24-h Holter recordings at 06.00, 14.00 and 22.00 h in 15 patients with coronary spastic angina, 13 patients with stable exertional angina, and 11 control subjects. There was a significant circadian variation in plasma free-form TFPI antigen levels in patients with coronary spastic angina (25.8±2.0 ng/ml at 06.00 h, 21.1 ±1.6 ng/ml at 14.00 h, 20.2±1.4 ng/ml at 22.00 h; p<0.01). Furthermore, free-form TFPI antigen levels at 06.00 h were significantly higher in coronary spastic angina patients than in patients with stable exertional angina or control subjects (p<0.01). Free-form TFPI antigen levels increased after the ischemic attacks in coronary spastic angina (p<0.01). This circadian variation correlated with the frequency of attacks, with the peak level occurring between midnight to early morning in patients with coronary spastic angina. (Jpn Circ J 1998; 62: 419 - 424)

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We examined the relationship between flow-mediated dilation (FMD) of the brachial artery and the extent and severity of coronary artery disease (CAD). Using high-resolution ultrasonography, we measured FMD and nitroglycerin-induced brachial artery dilation. We studied 121 patients (77 men, 44 women; mean age 64±11 years, range 25-79 years) who underwent coronary arteriography. The extent and severity of CAD were assessed by the coronary stenosis index (CSI). The adjusted FMD correlated inversely with CSI (r_s=-0.63, p<0.0001). Multivariate analysis demonstrated that the adjusted FMD was an independent predictor of CSI. The adjusted FMD was 10.2 ±4.8% in patients without CAD (n=32), 7.7±6.0% in patients with single-vessel disease (n=31), 5.2±5.5% in patients with double-vessel disease (n=29), and 2.0±3.9% in patients with triple-vessel disease (n=29). The adjusted FMD was significantly lower in the double- (p<0.01) and triple-vessel (p<0.0001) disease groups than in patients without CAD. The adjusted FMD was significantly lower in the triple-vessel disease group than in the single-vessel disease group (p<0.001). Based on our results, as coronary atherosclerosis becomes more severe, the adjusted brachial artery FMD becomes more severely impaired. (Jpn Circ J 1998; 62: 425 - 430)

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We developed a self-administered diet history questionnaire (DHQ) for use in prevention and control of cardiovascular diseases and cancer, and validated it by comparison with single 24-h urinary excretion of sodium (Na) and potassium (K). The subjects were 154 male and 69 female freshmen university students. Mean intakes (mmol/day) assessed by DHQ and the urinary excretion of Na were 196 and 165 respectively for men and 179 and 136 respectively for women. Those of K were 61.5 and 43.9 respectively for men and 56.8 and 41.6 respectively for women. The ratios of urinary excretion to dietary intake of Na were 0.97 in men and 0.84 in women. Those of K were 0.78 in men and 0.80 in women. The results for both Na and K were reasonable, except for Na in men. When Pearson correlation was examined between dietary and urinary Na and K, no significant correlations for Na in men (r=0.14) or women (r=0.23, p=0.06), or significant correlations for K in men (r=0.34, p<0.001) or women (r=0.40, p<0.001) were observed. The results suggest a reasonable ability to estimate a subject mean for Na in women, K in both sexes, and individual level for K for both sexes. The validity for individual level for Na intake is not conclusive because the duration of urine collection was too short. (Jpn Circ J 1998; 62: 431-435)

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The purpose of this study was to examine cardiac geometry and function by Doppler echocardiography and to analyze mRNA expression of cardiac phenotype and extracellular matrix in myocardial infarcted rats. Doppler echocardiograms and hemodynamics were measured 2 weeks after myocardial infarction (MI). mRNA levels in the non-infarcted left ventricle (LV) and infarct site were measured by Northern blot analysis. LV internal diastolic dimension was greater in infarcted (MI) than in sham-operated rats (control) (MI 7.2±0.3mm vs control 4.6±0.3mm, p<0.01). The fractional shortening decreased in MI rats (MI 32±4% vs control 61±3%, p<0.01). Peak early filling velocity increased in MI rats (MI 91±5cm/see vs control 72±4cm/see, p<0.05), and deceleration rate of the early filling wave was more rapid in rats with MI (MI 25.1 ±2.8m/sec² vs control 12.4±1.7m/sec ², p<0.01). Late filling velocity decreased (MI 16±3cm/see vs control 35±6cm/see, p<0.05), resulting in a marked increase in the ratio of early filling to late filling (MI 7.1±1.2 vs control 2.5±0.4, p<0.01). mRNA levels for β-myosin heavy chain (β-MHC), α-skeletal actin, atrial natriuretic polypeptide (ANP), collagen types I and III, and matrix metalloproteinase 2 (MMP-2) in the non-infarcted LV increased significantly by 1.8-, 2.4-, 4.7-, 2.6-, 2.1- (all p<0.01) and 1.4-fold (p<0.05), respectively, compared with sham-operated myocardium. In the infarct site, mRNA levels for transforming growth factor (TGF)-β₁, collagen types I and III, and MMP-2 significantly increased by 3.2-, 11.0-, 9.7-, and 6.3-fold (all p <0.01), respectively, compared with sham-operated myocardium. Myocardial infarcted rat was characterized by cavity dilation and marked abnormalities of systolic and diastolic function, accompanied by a shift of myocytes to fetal phenotype and activation of collagen genes in the non-infarcted myocardium. (Jpn Circ J 1998; 62: 436-442)

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Previous evidence has shown that the action potential duration of rabbit ventricular muscle cells shortens after a rest period (postrest shortening). However, there has not been much research on postrest shortening in the intact heart. We recorded transmembrane action potentials (TAPs) of isolated papillary muscle from rabbit ventricle with glass microelectrodes and monophasic action potentials (MAPs) of the rabbit left ventricular endocardium with contact electrodes. In the in vitro experiments, repetitive regular stimuli (S1) at a cycle length of I1sec were followed by a single extrastimulus (S2) at coupling intervals (S1S2) ranging between 0.5 sec and 8 sec. The increase in the S1S2 interval resulted in a progressive shortening of the duration of TAP elicited by the S2, which was abolished by the simultaneous application of 1 mmol/L 4-aminopyridine and 2 μmol/L ryanodine. In the in vivo experiments, regular right ventricular pacing (S1) at a cycle length of 0.35 sec was followed by a single extrastimulus (S2) with coupling intervals (S1S2) ranging between 0.25 sec and 3 sec. The increase in the S1S2 interval also resulted in a progressive shortening of the duration of MAP elicited by the S2. This is the first report to demonstrate postrest shortening in the intact heart, which probably occurs because of a mechanism analogous to that observed in the isolated ventricular muscle. (Jpn Circ J 1998; 62: 443-448)

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The purpose of this study was to investigate the function of sarcoplasmic reticulum (SR) and the role of angiotensin II type 1 receptor (AT1) in ventricular remodeling in non-infarcted areas after myocardial infarction (MI). MI was produced in anesthetized Sprague-Dawley rats (10-12 weeks old) by ligation of the left anterior descending coronary artery. Four weeks after MI, hemodynamic measurements were performed. SR Ca²⁺-ATPase activity and mRNA (SERCA2a) and AT1 mRNA (AT1a, AT1b) were analyzed. Left ventricular end-diastolic pressure was higher and left ventricular dp/dt was significantly lower in the MI group. In non-infarcted areas in the MI group, myocardial transverse diameter was significantly greater and both Ca²⁺-ATPase activity in the SR and SERCA2a level decreased. The AT1a level was higher in non-infarcted areas than in controls, where-as the AT1b mRNA expression level was unchanged. These results suggest that, in the ventricular remodeling after MI, alterations in SR protein and its mRNA in non-infarcted myocardium help initiate heart failure and that Ca overload caused by the up-regulation of AT1a mRNA is an important cause of alteration in SR function. (Jpn Circ J 1998; 62: 449 - 454)

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We compared the imaging capability of magnetic resonance angiography (MRA) with that of conventional coronary angiography in a patient with coronary-pulmonary fistulae. Using the latter procedure, it is difficult to measure abnormal tortuous blood vessels in one section. However, the course of blood vessels could be evaluated quite well by rearranging serial cross-sectional MRA images using multiplanar reconstruction (MPR). This procedure allowed us to determine the anatomic positional relationship of these vessels to the peripheral cardiac great vascular system. MPR may detect sites of influx and outflow of abnormal blood vessels. (Jpn Circ J 1998; 62: 455 - 457)

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A 65-year-old woman was admitted for assessment of recurrent tachycardia. Cross-sectional echocardiography showed that the anterobasal portion of the ventricular septum was thin and dyskinetic. An electrophysiologic study revealed ventricular tachycardia, during which marked fragmented potentials could be obtained from the anterior septal aspect of the right ventricle. The site of earliest activation was in the vicinity of the His bundle. A diagnosis of cardiac sarcoidosis was made by based on endomyocardial biopsy combined with the clinical manifestations. Ventricular tachycardia originating from the anterior septum may be an indicator of underlying cardiac sarcoidosis. (Jpn Circ J 1998; 62: 458 - 461)

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Acute pulmonary thromboembolism is a life-threatening disease and in almost all cases originates from deep venous thrombosis in the proximal deep venous system of the legs. In order to prevent further episodes of thromboembolism in 2 patients with acute pulmonary thromboembolism, we inserted an Antheor temporary vena cava filter after catheter-directed fragmentation and thrombolysis. No complications occurred during the insertion of the filters and our results suggest that this filter device may be clinically safe and effective for temporary protection against pulmonary thromboembolism. (Jpn Circ J 1998; 62: 462 - 464)

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A 62-year-old woman with skin sarcoidosis was admitted to our hospital to ascertain whether she had cardiac involvement. Although she displayed no cardiac signs or symptoms, the electrocardiogram showed first-degree atrioventricular block, right bundle branch block with left anterior fascicular block, and giant negative T waves in the V₃ lead. Echocardiography revealed marked hypertrophy localized in the basal portion of the interventricular septum (IVS) without systolic dysfunction, mimicking hypertrophic cardiomyopathy (HCM). Exercise thallium-201 myocardial imaging revealed redistribution in the anteroseptal region. Both gallium-67 (⁶⁷Ga) and technetium-99m pyrophosphate (^99mTc-PYP) scintigraphy revealed abnormal uptake in the myocardium. These findings disappeared after 2 months of steroid treatment. Reports of cardiac sarcoidosis mimicking HCM are rare. However, hypertrophy in the basal portion of the IVS is an important sign of early cardiac involvement in sarcoidosis. ⁶⁷Ga and ^99mTc-PYP scintigraphy were useful and necessary to differentiate this type of cardiac sarcoidosis from HCM. (Jpn Circ J 1998; 62: 465-468)

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Although left ventricular dP/dt_max can be accurately assessed using Doppler echocardiography, the fact that, Doppler-derived dP/dt_max depends both on preload and Doppler incident angle limits its clinical value. We investigated the clinical usefulness of Doppler-derived (dP/dt_max)/IP (IP, isovolumic pressure), which is known to be relatively insensitive to preload and theoretically independent of the incident angle in 9 subjects. We conclude that Doppler-derived (dP/dt_max)/IP is relatively insensitive to both the incident angle and preload. In addition to its noninvasiveness, these unique features makes it very attractive as a clinical index of ventricular contractility. (Jpn Circ J 1998; 62: 469 - 471)

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