Inflammation plays an important pathogenic role in the initiation and progression of atherosclerotic plaque lesions. C-reactive protein (CRP), which directly participates in plaque inflammation, induces vascular cell adhesion molecule-1 (VCAM-1) expression in endothelial cells. However, the levels and values of high-sensitivity (hs)-CRP, white blood cell (WBC) count, and VCAM-1 in both stable and unstable angina pectoris (AP) have not been fully investigated. This study examines the levels and values of these inflammatory markers in patients with stable or unstable AP.
From March 2003 to December 2003, a prospective cohort study was conducted in 128 consecutive patients, including unstable AP patients (class I: n = 59; combined class II and III: n = 16) and stable AP patients (n = 53) undergoing elective coronary stenting. Blood samples for hs-CRP, WBC count, and VCAM-1 were obtained in the catheterization laboratory before coronary angiography. The circulating levels of hs-CRP and VCAM-1 were also evaluated in 40 healthy volunteers. The circulating levels of these three inflammatory markers were substantially higher in patients than in healthy volunteers (all P values < 0.0001). Additionally, circulating levels of hs-CRP and the WBC count were significantly higher in patients with unstable AP than in patients with stable AP (all P value < 0.0001). However, only those patients with class II and III unstable AP had significantly higher circulating levels of VCAM-1 than patients with stable AP (P < 0.0001). On the other hand, the circulating levels of VCAM-1 did not differ between patients with class I unstable AP and patients with stable AP (P = 0.782). Multiple stepwise logistic regression analysis showed that only hs-CRP level was independently associated with unstable AP (P = 0.0002). In conclusion, circulating levels of hs-CRP, WBC count, and VCAM-1 were significantly increased in patients with AP. The circulating level of hs-CRP was strongly associated with the clinical setting of unstable AP.

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The relation between n-3 polyunsaturated fatty acid (PUFA) and nonfatal myocardial infarction is still controversial.
A multicenter case-control pilot study on n-3 PUFA as a negative risk factor for myocardial infarction was performed in Niigata prefecture. Seventy-three patients with acute myocardial infarction (AMI) and age and gender matched controls (n = 84) were recruited. Serum leptin levels were significantly higher in patients with AMI than the controls (8.1 ± 6.7 ng/mL versus 5.8 ± 3.7 ng/mL, P < 0.01), and serum high-density lipoprotein cholesterol (HDLc) levels were significantly lower in patients with AMI than the controls (46 ± 10.5 mg/dL versus 60 ± 15 mg/dL, P < 0.00001). Statistically significant differences were preserved in leptin and HDLc when the data were analyzed separately by gender. Serum levels (%weight) of linolenic acid (C18:3:n3), eicosapentaenoic acid (C20:5:n3), docosapentaenoic acid (C22:5:n3), and total n-3 PUFA were significantly lower in patients with AMI than the control group (P < 0.000001, < 0.05, < 0.05, < 0.05, respectively). The serum n-3 PUFA/saturated fatty acid (SF) ratio and n-3 PUFA/n-9 monounsaturated fatty acid (MUFA) ratio were significantly lower in patients with AMI than the controls (P < 0.05 and < 0.01, respectively). When the subjects were separated into two categories according to an n-3/n-6 PUFA ratio below 0.3 or above 0.3, patients with AMI were more frequently in the former while the controls were more frequently in the latter (P < 0.05).
N-3 PUFA may be a negative risk factor for AMI. The results suggest leptin is a risk factor for AMI irrespective of ethnicity and gender.

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High plasma HDL-cholesterol (HDL-c) is a well-established protective factor in coronary artery disease (CAD). One of its potential protective mechanisms is the inhibition of the cytokine-induced upregulation of expression of cellular adhesion molecules (CAMs). High sCAM levels were found to be associated with low HDL-c in some studies performed mostly in hyperlipidemic subjects, but this association has not yet been investigated in CAD patients. In addition, conflicting results were obtained from in vitro studies that explored the proposed HDL effect on cytokine-induced CAM expression. The aim of the present case-control study was to investigate whether low HDL-c values are associated with CAM overexpression in normolipidemic CAD patients and healthy individuals, matched according to age and gender. Plasma HDL-c, sICAM-1, sVCAM-1, and sE-selectin were measured in 37 normolipidemic patients with angiographically verified coronary artery disease and in 52 healthy normolipidemic subjects. The sCAM values obtained in the subjects (patients or controls) with low HDL-c levels (< 1.03 mmol/L) were compared with the values in the subjects with high HDL-c (≥ 1.03 mmol/L). No significant difference was found between sICAM-1, sVCAM-1, and E-selectin values obtained in subjects with low and high HDL-c, either among the patients or the healthy controls. In conclusion, low HDL-c levels are not associated with CAM overexpression in normolipidemic CAD patients and healthy subjects.

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Heart-type fatty acid-binding protein (h-FABP) is a novel diagnostic marker for myocardial infarction, but its prognostic value has not been established in patients with acute coronary syndrome (ACS). We sought to determine the value of qualitative analysis of h-FABP for predicting 30-day adverse events in patients with ACS. A retrospective observational study was conducted on patients at a community hospital, and 130 patients admitted through the emergency room (ER) for ACS were identified among 12,077 patients who presented to the ER between January and June 2003. Of these 130 patients, 90 (mean age, 66.8 years, 67 males) who had ACS were eligible for this study. Qualitative tests for serum h-FABP and troponin T (cTnT) were performed on presentation. Follow-up information on adverse events within 30 days after admission, defined as cardiac death or recurrent ACS, was obtained from the medical records. The qualitative tests for h-FABP and troponin T were positive in 62.2% and 36.7%, respectively. The cumulative adverse event rate at 30 days was 14.8% in the h-FABP-positive group and 3.2% in the negative group. The adjusted relative risk of a positive h-FABP test for adverse events was 44.98 (95% CI: 1.48 to 1364.88). A positive h-FABP test was an independent predictor of adverse events within 30 days in these patients.

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The objective of the present study was to compare left ventricular (LV) function and clinical outcomes in diabetics versus nondiabetics with acute myocardial infarction (AMI) treated by primary coronary angioplasty.
A total of 327 consecutive AMI subjects were reperfused by primary coronary angioplasty within 12 hours from onset. Diabetes mellitus (DM) was present in 104 of the 327 patients. LV function was serially determined by left ventriculograms taken in the acute and chronic phases (6 months after onset). (I) The early ST-segment resolution rate was lower in DM patients compared with non-DM patients (59% versus 83%, P < 0.0001). (II) During a 6-month follow-up, the percentages of target vessel revascularization (TVR), coronary aorta bypass grafting (CABG), and cardiac death were higher in the DM patients compared with the non-DM patients (TVR: 29% versus 19%; P < 0.05, CABG: 10% versus 5% ; P < 0.05, cardiac death: 12% versus 4%; P = 0.01). (III) The differences in left ventricular ejection fraction (LVEF) between two stages (delta-LVEF) were significantly lower in the DM patients than the non-DM patients (1 ± 9% versus 7 ± 10%, P < 0.0001). (IV) Multivariate analysis identified DM as an independent predictor of cardiac death (Odds ratio 5.5, 95% CI, 1.3-23.7, P < 0.05) and as a sole independent predictor of LVEF deterioration (Odds ratio 5.8, 95% CI, 2.8-11.8, P < 0.001).
In patients with AMI treated using primary coronary angioplasty, DM is closely related to left-ventricular systolic dysfunction and a poor patient outcome, including mortality.

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Hypercholesterolemia is a risk factor for development of coronary artery disease (CAD), however, several reports have suggested that low serum cholesterol is associated with a worse prognosis in patients with congestive heart failure (CHF). The objective of this study was to determine the prognostic value of cholesterol for CHF. The study subjects consisted of 133 consecutive patients hospitalized in our institution for progressive heart failure from April 2000 to March 2003. Thirty-two percent of the patients had CAD. After improvement of congestive heart failure and discharge from the hospital, lipid profiles, including serum total cholesterol (TC), triglycerides, and high and low density lipoprotein cholesterol (HDL, LDL, respectively), were obtained. During the follow-up period (2.3 ± 0.9 years), 21 patients died. There was a significant difference between survivors and nonsurvivors in HDL (53 ± 15, 43 ± 15 mg/dL, P = 0.01), but no differences were observed in other variables. In patients with CAD, survivors had significantly lower TC concentrations (179 ± 30 versus 246 ± 55 mg/dL, P = 0.004), although in patients without CAD, survivors had significantly higher TC concentrations (203 ± 37 versus 170 ± 40 mg/dL, P = 0.02). Multivariate analysis showed high TC predicted a worse outcome in patients with CAD (odds ratio (OR) = 1.052, 95% confidence interval (CI) 1.002-1.104, P = 0.04), but a better outcome in patients without CAD (OR = 0.972, 95% CI 0.948-0.997, P = 0.03), independent of age, gender, medication, and complications. Thus, low serum cholesterol is associated with an improved outcome in patients with CAD, while it predicts a worse outcome in patients without CAD.

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To determine whether the presence of anticardiolipin (aCL) antibodies in patients with acute coronary syndome is predictive of recurrent cardiac events in hospital stay and follow-up.
The study population consisted of 80 patients with acute coronary syndrome. IgM and IgG aCL levels were determined before hospital discharge. We divided the patients into those with an aCL IgG ≥ 40 IgG phospholipid units (group I, n = 30) and those with an aCL IgG < 40 IgG phospholipid units (group II, n = 50). All patients underwent coronary angiography. Follow-up coronary angiography was performed 12 months after percutaneous coronary intervention (PCI). Infectious and autoimmune diseases were exclusion criteria. Patients were observed to determine overall mortality, reinfarction, and restenosis.
There were no differences between the groups with respect to the prevalence of hypertension, diabetes mellitus, and cigarette smoking, sex, or ejection fraction. The prevalence of left ventricular thrombus was similar between the groups (group I: 16% versus group II: 16.7%, P > 0.05). Although the presence of left atrial thrombus was much more frequent in cardiolipin positive patients (13% versus 4%, respectively), the difference was not statistically significant (P = 0.19). Restenosis was observed in 40% of the cardiolipin positive patients and 14% of the cardiolipin negative patients (P < 0.01). There was no significant association between reinfarction and anticardiolipin positivity during follow-up (26% versus 10%, P > 0.05). In group I patients, in-hospital mortality was somewhat more frequent compared to group II patients (4% versus 10%), but the difference was not statistically significant (P = 0.27). One year mortality was similar between the groups.
These results suggest that 1) restenosis occurs more frequently in anticardiolipin positive patients and 2) no association is evident between positive aCL and mortality, rein-farction, and intracardiac thrombus.

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Diabetic retinopathy (DR) is an early and frequent marker of other vascular complications of diabetes and its relation with coronary ischemia is known. The aim of the present study was to evaluate the association between DR and indices of coronary artery disease (CAD) severity and extent determined by coronary angiography.
Sixty-nine diabetic patients undergoing coronary angiography for suspected CAD were evaluated. The severity and extent of CAD were scored from coronary angiograms by using 3 scores. Retinopathy was graded by fundus examination.
There were differences in the severity score, extent score, number of vessels with disease, duration of diabetes, diabetes therapy, history of previous myocardial infarction (MI), and serum creatinine level among patients with and without DR. CAD severity was associated with the presence of DR (r: 0.53, P < 0.001), grade of DR (r: 0.52, P < 0.001), duration of diabetes (r: 0.28, P: 0.019), history of previous MI (r: 0.36, P: 0.002); and serum creatinine level (r: 0.24, P: 0.049) where the presence of DR was the only independent factor related to the severity score in multivariate analysis (r: 0.48, P < 0.001). The parameters related to the extent score were the presence of DR (r: 0.50, P < 0.001); grade of DR (r: 0.48, P < 0.001); previous MI (r: 0.37, P: 0.002) and age of the patient (r: 0.26, P: 0.033). Factors independently related to the extent score in multivariate analysis were the presence of DR (r: 0.37, P: 0.001), previous MI (r: 0.30, P: 0.006), and age of the patient (r: 0.22, P: 0.003).
Among diabetics who are suspected of having CAD, those with retinopathy have more diffuse and severe coronary atherosclerosis, compared with diabetics without retinopathy. This cannot be explained by a longer duration or inferior control of the disease.

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Ventricular tachycardia (VT), which causes hemodynamic instability, and ventricular fibrillation (VF) sometimes occur in patients with severe underlying cardiovascular disease such as myocardial ischemia or infarction, and are associated with high mortality. This report presents the efficacy of nifekalant hydrochloride (nifekalant), a pure class III antiarrhythmic agent, in treating life-threatening ventricular arrhythmia in such patients.
From June 2000, when nifekalant became commercially available in Japan, to May 2003, 30 ischemic heart disease (IHD) patients with VT/VF resistant to direct-current (DC) countershock received nifekalant in our hospital. These 30 patients served as the nifekalant group in this study. As a control group, we also included 33 IHD patients with VT/VF that had been resistant to DC countershock upon or during hospitalization between January 1996 and May 2000 before nifekalant became commercially available.
No significant differences were observed in patient background factors and treatments between the two groups. The rates of death within 48 hours of occurrence of VT/VF were significantly lower in the nifekalant group (7%, 2/30) than in the control group (27%, 9/33; P < 0.03). The rates of cardiac death during hospitalization were also significantly lower in the nifekalant group (40%, 12/30) than in the control group (67%, 22/33; P < 0.03). The rates of survival until hospital discharge were significantly higher in the nifekalant group (57%, 17/30) than in the control group (30%, 10/33; P < 0.03). Multivariate analysis of all 63 patients revealed nifekalant administration was the factor that significantly improved the mortality (odds ratio for cardiac death, 0.26; 95% confidence interval (CI), 0.07 to 0.95; P = 0.041).
Nifekalant improves the prognosis for life-threatening ventricular arrhythmia in IHD patients.

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So-called unipolar ‘PQS pattern’ is widely accepted as a hallmark of successful catheter ablation of the left-sided atrioventricular accessory pathway. However, the unipolar nature of the electrogram and the site-dependent appearance of this characteristic pattern are poorly understood. Therefore, unipolar coronary sinus (CS) mapping was performed using a multipolar fine electrode in patients with Wolff-Parkinson-White (WPW) syndrome associated with an antegrade left-sided accessory pathway (case group) and those with a concealed left-sided accessory pathway or atrioventricular nodal reentrant tachycardia (control group) under sinus rhythm and fixed high right atrial, CS ostial, and distal pacing. In both groups, the unipolar CS atrial electrogram showed intrinsic negative deflection (initial positive followed by negative parts) with considerable variation depending on the recording site. This unipolar configuration of the atrial electrogram was not influenced by different activation sequences during pacing at various sites. The case group exhibited a unipolar ‘PQS pattern’ at successful ablation sites for the left lateral to anterolateral accessory pathway. However, this was not true for the left posteroseptal accessory pathway, possibly because the negative part of the atrial electrogram distorted the ‘PQS pattern’ as an intervening dip. In conclusion, the site-dependent variations of the unipolar CS atrial electrogram underlie the limited usefulness of the ‘PQS pattern’ in left posteroseptal accessory pathway localization.

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Atrial fibrillation (AF) is well known to be male-dominant. Female sex hormones may be involved, since very few premenopausal women experience AF. However, a possible gender difference in older subjects has not been fully elucidated yet.
We retrospectively reviewed the symptoms of 133 patients (111 males and 22 females) with paroxysmal AF (PAF) from the medical records at our hospital from 1995 to 2000, and classified the patients according to the time of the attacks as day type, night type, or unspecific type.
In females, the age at the first diagnosis of PAF was significantly higher (males: 57 ± 1 year old, females: 65 ± 2 years old; P = 0.006) and the proportion of cases younger than 61 years old was significantly smaller (63%, 32%; P = 0.007). As in previous reports, the female group had more cases with unspecific type (26.5%, 47.6%) or with long duration (> 24 hours) (16.9%, 37.5%). In contrast to these published results, fewer women (10.5%) had frequent attacks (more than twice a week) than men (39.8%). The incidence of regular alcohol consumption, one of the most important PAF triggers, was significantly higher in men than women (84.7%, 13.6%; P < 0.0001). Even when we focused on cases older than 60 years old, the female group still had more cases with unspecific type (53.3% versus 23.1%) or with long duration (27.3% versus 14.7%) than men, and fewer with frequent attacks (0% versus 51.7%) or regular alcohol consumption (6.7% versus 82.9%; P < 0.0001) than men.
The gender difference in symptoms related to PAF may depend not only on sex hormones, but also on intrinsic or social gender differences.

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Kawasaki disease (KD) has not been frequently reported from developing countries, especially from India. In this series from a tertiary level center in North India, we report on the clinical features and management of patients with KD seen between January 1994 to November 2004. KD was diagnosed on the basis of standard diagnostic criteria. Investigations included work-up for other causes of fever along with chest X-rays, electrocardiograms, and 2-D echocardiography. Thallium scintigraphy and coronary angiography were performed in 20 and 3 cases, respectively. Sixty-nine children (49 boys and 20 girls) fulfilled the diagnostic criteria. Mean age at diagnosis was 4.9 ± 3.0 years (range 0.3-14 years) and as many as 23 cases (33.3%) were above 5 years of age. Clustering was seen during the winter months. Extreme irritability, out of proportion to the degree of fever, was a characteristic feature. Redness of the lips and tongue was common but rash was seen only in 43 cases and lymphadenopathy in 47 cases. Thrombocytosis was present in 52.2% of the patients. Sixty-four patients received intravenous immunoglobulin. Cardiac abnormalities included extrasystoles in 1, coronary artery dilatation in 5, valvular regurgitation in 3, and perfusion defects on thallium scintigraphy in 4. There was no mortality. KD appears to occur at an older age in Indian children as compared to reports from Japan. Irritability is a characteristic clinical finding. Cardiac abnormalities are frequent during the acute stage but regress gradually. The disease needs to be considered in the differential diagnosis of all children with persistent unexplained fever.

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The significance of pulse pressure (PP) and mean blood pressure (MBP) for blood pressure (BP) control is unclear. The aim of this study was to examine the relationship between PP and MBP and BP control.
We obtained home BP measurements for 117 patients aged 40-75 years with either office systolic BP (SBP) ≥ 140 mmHg or office diastolic BP (DBP) ≥ 90 mmHg. Patients were treated with 1 to 2 antihypertensive drugs for 6 months to achieve home SBP < 135 mmHg and home DBP < 85 mmHg.
At follow-up, 72 patients were taking a single drug with good BP control, 23 were taking two drugs with good BP control, and 22 were taking two drugs without good BP control. Although office SBP and DBP at baseline were similar in the three groups, home SBP and DBP at baseline in the single drug group were lowest among the three groups (P < 0.01). Home MBP at baseline in the single drug group was lowest among the three groups (P < 0.01). Home PP at baseline was highest in the two-drug without good control group (P < 0.001). In multivariate logistic regression analysis, only home MBP at baseline was significantly correlated with a lack of BP control.
Home MBP rather than home PP is associated with achieving adequate BP control.

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The objective of the present study was to compare the effects of imidapril hydrochloride, an angiotensin converting enzyme inhibitor, and dilazep hydrochloride, an antiplatelet agent, on urinary protein excretion and renal function in patients with chronic glomerulonephritis.
Imidapril (2.5 or 5 mg/day) or dilazep (300 or 450 mg/day) was administered for 3 years. Blood pressure, proteinuria, and renal function were measured before and during the treatment. In the group administered imidapril (n = 11), urinary protein decreased by approximately 50% (2.16 ± 1.57 versus 0.90 ± 0.53 g/g Cr, P < 0.01) and blood pressure by 14/10 mmHg (139.6 ± 17.4/93.6 ± 8.7 mmHg versus 122.7 ± 10.5/81.8 ± 9.9 mmHg, P < 0.01) and both remained at low levels during the three years of treatment. No correlation was observed between the extent of blood pressure reduction and changes in urinary protein. Serum creatinine concentrations did not change significantly (1.3 ± 0.3 versus 1.3 ± 0.3 mg/dL, NS). In the dilazep group (n = 12), there were no significant changes in blood pressure, urinary protein, or serum creatinine.
These findings demonstrate that imidapril reduces proteinuria and contributes to preserve renal function, suggesting its usefulness in the treatment of patients with chronic glomerulonephritis.

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Thiol-modifying agents induce the release of nitric oxide (NO) from endothelial epithelium and the release of reactive oxygen free radicals in the vascular system. Moreover, thiol groups are essential for the functioning of the ATP dependent potassium channel (K-ATP). The effects of thiol-modifying agents and their molecular mechanisms on arrhythmia have not been widely studied. In this study, we investigated the effect of the hydrophilic SH-group-oxidizing substance thimerosal on the arrhythmia induced by reperfusion/ischemia after coronary artery ligation in rats. We studied the possible involvement of the K-ATP and NOS on the effect of thimerosal. Thimerosal pretreatment (3, 30 mg/kg dose iv. 10 minutes before coronary occlusion) significantly decreased the length of total arrhythmia, ventricular tachycardia, and the arrhythmia score. This effect of thimerosal was reversed by the K-ATP opener pinacidil but not by the K-ATP blocker glibenclamide. The inhibition of iNOS by L-NAME did not alter the antiarrhythmic effect of thimerosal. These data clearly suggest that the antiarrhythmic effect of thimerosal is dependent upon the blockage of K-ATP.

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This report describes a 77-year-old woman with a single coronary artery who suffered an acute anterior wall myocardial infarction. The single coronary artery arose from the right coronary artery through the transverse trunk, and there were no other cardiovascular anomalies. Coronary angiography did not reveal significant coronary artery stenosis in the left anterior descending artery. The patient was treated medically in the acute phase. She developed typical angina and evidence of myocardial ischemia, and underwent successful coronary artery bypass grafting in the chronic phase with anterior chest pain.

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This case report describes a 37-year-old man with manifest atriofascicular and fasciculoventricular connections who developed complete atrioventricular block. After resumption of 1:1 atrioventricular conduction, an electrophysiological study was conducted. During sinus rhythm, manifest ventricular preexcitation was observed and the AH and HV intervals were 80 msec and 50 msec, respectively. No change in AH interval during constant atrial pacing was observed by bolus injection of 20 mg of adenosine triphosphate. No changes in the morphology of the delta wave or HV interval were observed by changing the atrial pacing site. This patient developed HV block by atrial extrastimulus (S1S1: 600 msec, S1S2 ≤ 350 msec). Thus, the patient was diagnosed as having combined atriofascicular and fasciculoventricular connections.

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We describe a 66-year-old woman who had an alternating bundle branch block consisting of coexisting occurrence of right bundle branch block (RBBB) and left bundle branch block (LBBB) combined with Mobitz type II atrioventricular block (AVB). A prolonged PQ interval was associated with the RBBB pattern whereas it was not apparent in the LBBB pattern. Electrophysiologic study revealed that the LBBB pattern was combined with a double His bundle potential. On the other hand, the RBBB pattern was combined with a markedly prolonged HV interval with a low voltage monophasic His bundle potential, which we speculated was the former part of the split His bundle potential seen during the LBBB pattern. A combination of the longitudinal dissociation in the His bundle and the gap phenomenon at the intra-Hisian block portion may account for this observation.

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Arterial aneurysms represent a severe complication of Behcet's disease. A 42-year-old woman with Behcet's disease had a recurrence of an aneurysm after two surgical repair attempts using grafts. A covered stent-graft was implanted in her iliac external artery to occlude the neck of the aneurysm at the anastomosis of the bypass graft to her external iliac artery. The procedure reduced the size of the aneurysm by allowing the formation of a thrombus within its cavity. The implantation of an endovascular stent-graft may be a sound alternative to surgical repair for aneurysms associated with Behcet's disease.

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Cardiovascular beriberi is caused by thiamine deficiency and usually arises for one of two reasons: alcoholism or diet. Shoshin beriberi is a fulminant form of cardiac beriberi. We investigated the histopathological features of biopsied myocardial tissue samples from two patients with Shoshin beriberi (one patient with nonalcoholic beriberi and another patient with alcoholic beriberi). Interstitial fibrosis and a variation in size of the myocardial fibers were the main findings in the sample from these patients after thiamine treatment. These findings are persistent histopathological features in the myocardium of patients with Shoshin beriberi after thiamine treatment.

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