A newly developed critical pathway has been applied to emergency medical care of patients with acute myocardial infarction (AMI) in the emergency department. The arrival-in-cath-lab interval (ACI) was selected as a clinical indicator of quality assurance, according to American Heart Association and American College of Cardiology guidelines. This report describes the first experience of applying the critical pathway to patients with AMI in an emergency department in Japan. The ACI of 35 AMI patients who underwent primary percutaneous transluminal coronary angioplasty during a 24-month period following application of the pathway were compared with those of 50 AMI patients during the 48 months before application of the pathway. The median ACI value was significantly reduced from 65.5 min to 50.0 min. Also, the proportion of patients with acceptably short ACI (<60 min) significantly improved from 42.0% to 68.6%. (Jpn Circ J 2001; 65: 849 - 852)

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Elevated levels of acute-phase proteins, a systemic marker for inflammation, predict coronary events; Chlamydia pneumoniae (C. pneumoniae) infection is associated with coronary atherosclerosis. The present study investigated whether inflammation or infection is involved in the pathogenesis of acute coronary syndrome (ACS) and which one has the more important role. The study group comprised 49 patients with angiographically diagnosed ACS, 48 cases of chronic coronary heart disease (CCHD), and 44 subjects with a normal coronary profile. The levels of serum C-reactive protein (CRP), fibrinogen and anti-C. pneumoniae IgG antibody were measured. The IgG antibody against C. pneumoniae was higher in the ACS and CCHD groups compared with the control group after adjusting for age and gender. The levels of CRP and fibrinogen were significantly increased in patients with ACS compared with controls and CCHD patients. Multiple stepwise logistic regression analysis revealed that C. pneumoniae IgG antibody is an independent risk factor for both ACS and CCHD (odds ratio 2.3 and 2.1, respectively), but the CRP level is a risk factor only for ACS (odds ratio 6.9). The inflammatory response, as indicated by acute-phase proteins, especially CRP, rather than C. pneumoniae infection, may contribute more to the clinical course of ACS. (Jpn Circ J 2001; 65: 853 - 857)

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Increased neurohormone and cytokine concentrations are associated with adverse outcome in patients with congestive heart failure, so minimizing these increases may improve outcome, even in the acute phase of decompensated heart failure. The present study was designed to test the hypothesis that phosphodiesterase inhibitors, but not catecholamines, could favorably affect neurohormone and cytokine profiles in patients with acutely decompensated heart failure. Twenty-nine patients underwent monitoring using a Swan-Ganz catheter and were randomly allocated to receive phosphodiesterase inhibitors (PDEI group, n=19) or catecholamines (CA group, n=10). Pulmonary capillary wedge pressure decreased significantly in both groups and cardiac output showed a slight, but not statistically significant increase, in both groups. There was a significant decrease in plasma brain natriuretic peptide concentration in the PDEI group, but not in the CA group, whereas plasma interleukin-6 concentration increased in the CA group, but not in the PDEI group. Phosphodiesterase inhibitors favorably affect neurohormone and cytokine concentrations in patients with acutely decompensated heart failure. (Jpn Circ J 2001; 65: 858 - 862)

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The present study was designed to determine whether the wall thickening seen in acute myocarditis is caused by interstitial edema. The study group comprised 25 patients (idiopathic myocarditis, 17; eosinophilic myocarditis, 8) in whom acute myocarditis was diagnosed histologically and who underwent echocardiography and endomyocardial biopsy during both the acute and convalescent phases. The following echocardiographic parameters were measured: interventricular septum and left ventricular posterior wall thickness, left ventricular end-diastolic dimension, and left ventricular ejection fraction. Based on the myocardial biopsy specimens, the degree of interstitial edema was classified into 3 grades [(-), 1(+), 2(+)] and the transverse diameter of cardiac myocytes was measured using light microscopy. The thickness of both the interventricular septum and left ventricular wall decreased from 14.3±3.7 mm and 13.3±2.4 mm in the acute phase to 9.7±1.7 mm (p<0.001) and 10.2±1.7 mm (p<0.0001), respectively, in the convalescent phase. Edema was present in 22 patients (88.0%) in the acute phase, but in the convalescent phase, edema was present in only 7 patients (28.0%), indicating a significant reduction in the degree of edema (p<0.0001). Cardiac myocyte diameter did not differ significantly between the acute (13.6±1.1 μm) and convalescent (13.8±1.8 μm) phases. (Jpn Circ J 2001; 65: 863 - 866)

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Few previous reports have comprehensively screened all the anti-myocardial autoantibodies (AMCA) in relation to other clinical profiles in patients with idiopathic dilated cardiomyopathy (IDC), so the present study used both immunohistochemistry (FITC) and immunoblotting (IB) for screening patients with IDC in order to characterize the clinical significance of AMCA. Sera were collected from 100 patients with IDC and age-matched 100 healthy control subjects (CTL). For FITC, an unfixed frozen section of human myocardium was used for the standard indirect immunofluorescence; for IB, total cardiac homogenates of the same myocardium were blotted to serum at 2 sets of dilution (1:200 and 1:10,000). The positive rates of AMCA detection for each method were as follows (IDC vs CTL); 39% vs 6% for FITC, 38% vs 4% for IB (1:200), and 10% vs 0% for IB (1:10,000). Fifty-nine patients with IDC and 8 CTL were positive for AMCA by either method, and 18 patients with IDC and 2 CTL were positive for AMCA by both methods. IB-positivity at 1:200 was an independent predictor by multiple logistic regression analysis of non-sustained ventricular tachycardias as well as left ventricular end-diastolic diameter and plasma norepinephrine concentration. (Jpn Circ J 2001; 65: 867 - 873)

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The purpose of this study was to determine whether parameters derived from transesophageal echocardiography (TEE) could predict thromboembolism in patients with chronic nonvalvular atrial fibrillation (AF). Eighty-nine patients, mean age 66±9 years, who underwent TEE in 1996 to 1999 were studied. The clinical endpoint was a thromboembolic event, including transient ischemic attack (TIA). Sixty-seven patients (75%) were anticoagulated with warfarin after TEE. After a follow-up period of 29±10 months, 1 patient died suddenly, 4 had a thromboembolism, and 3 had a TIA; the annual embolic event rate was 3.3%. Left atrial appendage (LAA) thrombus (86% vs 17%, p<0.001), LAA dysfunction (LAA velocity <20 cm/s; 71% vs 25%, p=0.009), and severe LA spontaneous echo contrast (29% vs 2%, p=0.002) were more prevalent in patients with an embolic event than in those without. In patients with LAA thrombus, the annual event rate was 11% as compared with 1.2% in those without (p=0.004). On the Cox proportional hazards model analysis, LAA thrombus (chi-square 7.0, p=0.008), severe LA spontaneous echo contrast (chi-square 7.0, p=0.008), and LAA dysfunction (chi-square 5.9, p=0.015) were significantly related to thromboembolism. Multivariate analysis revealed that LAA thrombus (chi-square 5.5, p=0.019) and LAA dysfunction (chi-square 4.0, p=0.045) were the independent predictors. In conclusion, TEE parameters, particularly the presence of LAA thrombus, can be used to assess thromboembolic potential in patients with chronic nonvalvular AF. (Jpn Circ J 2001; 65: 874 - 878)

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This study investigated the association between blood pressure (diastolic [DBP] and systolic [SBP]) and cardiac events in a total of 6,602 patients with a healed myocardial infarction (MI) (5,320 men, 1,282 women; mean age, 58.9±10.4 years), including in-patients and out-patients, from January 1986 to January 1999. The primary endpoints (cardiac events) were recurrent MI (fatal and non-fatal), death from congestive heart failure, or sudden death. The total number of cardiac events was 195 (3.0%) and the incidences of the 3 cardiac events were compared among the 3 DBP groups (DBP low group, <70 mmHg; DBP middle group, 70-89 mmHg; DBP high group, ≥90 mmHg). There were some significant differences in the characteristics of patients among the 3 groups, but no significant difference in cardiac death and total mortality was found among the 3 groups. Cardiac events occurred in 59 of 1,780 patients (3.3%, 33.9/1,000 person years) in the DBP low group, tended to be reduced in number in the DBP middle group (87 of 3,549 patients 2.5%, 21.4/1,000 person years) and were slightly increased in number in the DBP high group (24 of 642 patients 3.7%, 35.2/1,000 person years). Although this correlation between BP and cardiac events appears to be J-shaped, because there is no statistically significant difference in the rate of cardiac events among the 3 groups, we conclude that DBP does not influence the occurrence of cardiac events. The prevalence of cardiac events tended to be greater with a SBP less than 120 mmHg. (Jpn Circ J 2001; 65: 879 - 886)

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The levels of risk factors for coronary heart disease (CHD) in men in the post World War II (WWII) birth cohort are almost similar between Japan and the USA, except for the considerably higher prevalence of cigarette smoking in Japan and the much higher prevalence of obesity in the USA. The present study evaluated the CHD mortality among men in the post WWII birth cohort by prefecture in Japan in 1995-1999 and then compared the data with those for white men in different states in the USA. There was a greater than 2-fold difference in CHD mortality among men aged 35-44 by prefecture in Japan: 5.3/100,000 in Kumamoto vs 12.6/100,000 in Tochigi. CHD mortality among men aged 35-44 in the top 3 prefectures in Japan is about half that of white men in the USA and is similar to that of white men in the lowest 3 states. The much lower CHD mortality in Japan does not appear to be caused by differences in the classification of causes of death and the results suggest that there may be strong and important protective factors that reduce the risk of CHD in Japan. (Jpn Circ J 2001; 65: 887 - 892)

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To investigate the mechanism of atrial fibrillation (AF), monophasic action potentials (MAPs) from the atrial myocardium were studied in 7 patients with paroxysmal AF (PAF) and in 7 control individuals. The MAPs were recorded using a contact catheter during sinus rhythm and continuous pacing at the high right atrium (HRA) with pacing cycle lengths of 600, 500 and 400 ms. MAPs were obtained from 6 sites in each participant. The MAPD₉₀ was measured from onset to 90% of MAP repolarization. Average, maximal and minimal MAPD₉₀ (avMAPD₉₀, maxMAPD₉₀ and minMAPD ₉₀) were obtained from all participants. The dispersion of MAPD₉₀ (dispMAPD₉₀) was defined as the difference between maxMAPD₉₀ and minMAPD₉₀. The width of each atrial potential (WAP) and the wavelength index (WLI = MAPD₉₀ / WAP) were determined. Average, maximal and minimal WLI (avWLI, maxWLI and minWLI) were obtained from all participants. The avMAPD₉₀ and maxMAPD₉₀ did not significantly differ between the 2 groups. The minMAPD₉₀ in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (210±18 ms vs 245±14 ms, p<0.05; 207±23 ms vs 238±20 ms, p<0.05; respectively). The dispMAPD₉₀ was significantly longer in the PAF group than in the control group during sinus and HRA pacing. The WAP value did not differ between the 2 groups. The minWLI in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (3.3±0.5 vs 3.8±0.3, p<0.05; 3.2±0.4 vs 3.7±0.3, p<0.02). A shortened and widened dispersion of atrial refractoriness may play an important role in the genesis of AF. Furthermore, smaller wavelengths may form in the atrium of patients with PAF. (Jpn Circ J 2001; 65: 893 - 896)

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Stent implantation has decreased the incidence of restenosis after coronary intervention, but has not eliminated it. The contribution of the angiotensin-converting enzyme (ACE) genotype to the development of coronary artery disease and restenosis after coronary stenting was investigated in 67 Japanese patients in whom 103 lesions in which stents had been successfully implanted were assessed by quantitative coronary angiography, before, immediately after coronary stenting, and during follow-up. The distribution of the patients with the DD, ID, and II genotypes was 13%, 54%, and 33%, respectively. The prevalence of multivessel disease in the DD genotype was significantly higher (DD genotype: 78%; ID genotype: 58%; II genotype: 27%, χ²=8.13, p=0.016) and the late loss in the DD genotype (1.43±0.96 mm) was significantly greater (ID genotype: 0.78±0.98 mm and II genotype: 0.79±0.88 mm, p<0.05 vs DD genotype). However, there was no significant difference in the restenosis rate among the 3 genotypes. The present study in Japanese patients indicates that the DD genotype is associated with more extensive coronary artery disease and progression of the inward remodeling within the stented lesion, which is primarily caused by neointimal hyperplasia. (Jpn Circ J 2001; 65: 897 - 900)

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The time from admission to reperfusion in patients with acute myocardial infarction (AMI) was compared according to the type of hospital and treatment strategy. A total of 164 patients with a first AMI within 12 h of onset were enrolled at one tertiary emergency center (TEC) and 6 community hospitals (CHs). The subjects were randomly assigned to receive either primary percutaneous transluminal coronary angioplasty (PTCA) (TEC-primary PTCA and CHs-primary PTCA groups) or 800,000 units of intravenous monteplase, half the standard dose of a mutant tissue plasminogen activator (t-PA), followed by rescue PTCA if the Thrombolysis in Myocardial Infarction (TIMI) flow grade was 2 or less (TEC-monteplase and CHs-monteplase groups) on the first coronary angiogram. Sixty minutes after admission, TIMI flow grade 3 rates of the study groups were as follows, in descending order: TEC-monteplase group, CHs-monteplase group, TEC-primary PTCA group, and CHs-primary PTCA group (56%, 41%, 36%, and 8%, respectively; p<0.01). However, there was no significant difference in the final TIMI flow grade 3 rate among the 4 groups. In the CHs, the peak creatine kinase tended to be lower in the monteplase group than in the primary PTCA group. The results suggest that low-dose monteplase followed by rescue PTCA is an effective strategy for promoting early reperfusion in patients with AMI, especially those who are treated at CHs. (Jpn Circ J 2001; 65: 901 - 906)

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Some infarcted myocytes undergo caspase-dependent DNA fragmentation, but serine protease-dependent DNA fragmentation may also be involved. There is controversy regarding whether caspase inhibitors can reduce infarct size, so the present study investigated whether serine protease inhibitor can reduce the DNA fragmentation of infarcted myocytes and whether serine protease or caspase inhibitors attenuates myocardial infarct size in Japanese white rabbits without collateral circulation. Rabbits were subjected to 30-min coronary occlusion followed by 48-h reperfusion. A vehicle (dimethylsulfoxide, control group, n=8) or Z-Val-Ala-Asp(Ome)-CH₂F (ZVAD-fmk, a caspase inhibitor, ZVAD group, 0.8 mg/kg iv at 20 min before coronary occlusion and 0.8 mg/kg at 90 min after reperfusion, n=8) or 3,4-dichloroisocoumarin (DCI, a serine protease inhibitor, 2 mg/kg iv at 20 min before coronary occlusion, DCI group, n=8) was administered. Animals were killed at 48 h after reperfusion for the detection of myocardial infarct size and at 4 h after reperfusion for the detection of dUTP nick end-labeling (TUNEL)-positive myocytes, the electrophoretic pattern of DNA fragmentation and ultrastructural analysis. The left ventricle (LV) was excised and sliced. The myocardial infarct size as a percentage of the area at risk was assessed by triphenyltetrazolium chloride staining. DNA fragmentation was assessed by in situ TUNEL at the light microscopic level. ZVAD and DCI significantly reduced the mean blood pressure during reperfusion without affecting heart rate. There was no significant difference in the % area at risk (AAR) of LV among the 3 groups (control: 26.3±3.0%; ZVAD: 25.6±2.6%; DCI: 25.6±2.0%). The % infarct size as a percentage of the AAR in the ZVAD group (41.3 ±4.5%) and the DCI group (50.4±3.8%) was not significantly different from the control group (43.5±4.5%). However, the percent DNA fragmentation in the infarcted area in the ZVAD (3.5±0.8%) and DCI groups (4.2±0.9%) was significantly reduced compared with the control group (10.7±1.9%). The DNA ladder pattern observed in the control group was attenuated in both the ZVAD and DCI groups. There was no difference in electron microscopic changes among the 3 groups. Serine protease-dependent DNA fragmentation is present in infarcted myocytes, in addition to caspase-dependent DNA fragmentation, but an infarct-size reducing effect was not observed with either of these inhibitors. (Jpn Circ J 2001; 65: 907 - 911)

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Severe right-side heart failure developed in a 47-year-old Japanese woman who suffered from hypoalbuminemia and a massive right-side chylous pleural effusion. She had been diagnosed as having protein-losing enteropathy with right ventricular cardiomyopathy. Autopsy showed congenital anomalies of the lymph ducts and abnormal deposition of fibrous and fatty tissue in the right ventricular myocardium. The clinical and pathological findings are consistent with the nonarrythmogenic form of the arrythmogenic right ventricular dysplasia. (Jpn Circ J 2001; 65: 912 - 914)

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A 71-year-old woman had hypertrophic cardiomyopathy associated with midventricular obstruction and an apical aneurysm in the left ventricle. She had had abnormal electrocardiograms for more than 30 years and for the past year had been suffering from occasional attacks of dizziness and low systemic blood pressure. Holter 24-h electrocardiographic monitoring revealed ventricular paroxysmal contractions (676/day) with nonsustained ventricular tachycardia. Doppler echocardiography revealed paradoxical jet flow from the apical aneurysm to the left ventricular outflow during early diastole. Magnetic resonance imaging depicted midventricular hypertrophy and a dyskinetic thin apical wall, which were confirmed by angiography. Coronary angiograms showed no narrowing of the major extramural coronary arteries, but there was compression of aberrant coronary arteries apparently feeding the hypertrophic portion of the left ventricular wall. Stress thallium-201 myocardial imaging showed a persistent severe defect in the left ventricular apex. A hemodynamic study revealed low cardiac output and an intraventricular pressure gradient (approximately 90 mmHg) between the left ventricular apical high-pressure chamber and the subaortic low-pressure chamber. The present case represents a rare combination of hypertrophic cardiomyopathy, midventricular obstruction, and an apical aneurysm in an elderly woman. Myocardial ischemia may have played an important role in the genesis of the apical aneurysm. (Jpn Circ J 2001; 65: 915 - 919)

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A 36-year-old woman with effort thrombosis of the subclavian vein associated with multiple pulmonary emboli was successfully treated with local thrombolysis of the subclavian vein using a pulse-spray catheter and systemic anticoagulation. Balloon venoplasty of the residual stenosis of subclavian vein was carried out and in follow-up venography 6 months later, there was no restenosis, and the patient has been asymptomatic for 12 months. Pulmonary embolism is not a rare complication of upper extremity deep vein thrombosis and should be managed as aggressively as lower extremity deep vein thrombosis. (Jpn Circ J 2001; 65: 920 - 922)

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Acute necrotizing eosinophilic myocarditis is the most severe form of eosinophilic myocarditis, or hypersensitivity myocarditis, and is characterized by rapidly progressive congestive heart failure followed by fulminant clinical deterioration that is nearly always fatal. A 55-year-old previously healthy patient with acute necrotizing eosinophilic myocarditis was diagnosed by early myocardial biopsy and successfully treated with corticosteroids. Throughout his hospitalization, the eosinophil count in the peripheral blood remained normal (56-201/mm³). Early stage corticosteroid therapy can have dramatic effects in acute necrotizing eosinophilic myocarditis and early diagnosis by endomyocardial biopsy is recommended. (Jpn Circ J 2001; 65: 923 - 926)

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