Recent epidemiological studies suggest that periodontitis is an important risk factor for coronary heart disease (CHD). The aim of this study was to evaluate the association between periodontitis and CHD, particularly acute coronary syndrome (ACS), focusing on microbiological and immunological features.
Twenty-eight CHD patients, 15 with ACS and 13 with chronic CHD, were included in this study. Coronary angiography, periodontal examination, and dental radiography were performed in all patients. Subgingival plaque, saliva, and blood samples were analyzed for the periodontopathogens Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythensis, Treponema denticola, and Prevotella intermedia using polymerase chain reaction.
Specific serum antibody titers to the 5 periodontal pathogens were determined by enzyme-linked immunosorbent assay. It was found that 33% of the ACS patients (5/15) harbored A. actinomycetemcomitans in oral samples, whereas no A. actinomycetemcomitans (0/13) was found in the chronic CHD patients (P < 0.05). Furthermore, ACS patients showed significantly higher serum IgG titers to A. actinomycetemcomitans (P < 0.05) compared with chronic CHD. More tooth loss and alveolar bone loss were noted in ACS patients than in chronic CHD patients, although the differences were not statistically significant.
Periodontal pathogens, particularly A. actinomycetemcomitans, may play a role in the development of ACS.

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Statins provide effective secondary prevention of cardiovascular events after acute coronary syndrome (ACS). Current guidelines recommend that statins be initiated in ACS patients before hospital discharge. In this retrospective study, we investigated the influence of early compared with late in-hospital initiation of statin therapy on the clinical outcomes of ACS patients.
Two hundred and ten ACS patients who had no history of statin treatment before hospitalization were enrolled. The patients were divided into early (statin treatment initiated ≤ 2 days after admission) and late (statin treatment initiated > 2 days after admission and before discharge) statin groups. We examined the association between early statin use and clinical outcomes in these patients using Cox proportional hazards models. Four months after discharge, event-free survival was 85% in the early statin group and 79% in the late statin group. In multivariate analyses, Killip IV classification and abnormal renal function were independent predictors of the composite endpoint of cardiovascular death, recurrent myocardial infarction, angina requiring rehospitalization, revascularization, and stroke. Early statin treatment had no significant influence (hazard ratio: 1.11; 95% confidence interval: 0.54 to 2.25; P = 0.78) on the composite endpoint 4 months after discharge. At 12 months after discharge, early statin treatment still had no significant influence on the composite endpoint (hazard ratio: 1.53; 95% confidence interval: 0.83 to 2.81; P = 0.17).
We concluded that ensuring all eligible ACS patients begin statin therapy during their hospital stay is more important than emphasizing immediate statin use after admission.

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Poor clinical outcomes for hemodialysis (HD) patients compared to non-HD patients after coronary intervention have been reported. Although coronary intervention using sirolimus-eluting stents (SESs) might be expected to reduce restenosis in HD patients, little is known about the efficacy of the SESs. The purpose of the present study was to compare the clinical and angiographic outcomes of HD patients with non-HD patients after SES implantation. The study population consisted of 170 consecutive patients (234 lesions) who had undergone successful coronary SES implantation. The patients were classified into 2 groups, an HD group (18 patients, 27 lesions) and a non-HD group (152 patients, 207 lesions). The incidence of any clinical event was significantly higher in the HD group than in the non-HD group (50.0% versus 12.5%, P < 0.0001). Target lesion revascularization was necessary in 6 patients (33.3%) in the HD group and in 7 patients (4.6%) in the non-HD group (P < 0.0001). The Cox proportional-hazards regression model on cardiac events identified HD patients (P = 0.0301, hazard ratio = 2.704) as an explanatory factor. Moreover, the Cox proportional-hazards regression model on target lesion revascularization identified HD (P = 0.0004, hazard ratio = 6.921) and in-stent re-stenosis lesion (P = 0.0293, hazard ratio = 3.323) as explanatory factors. The present study suggests that compared with non-HD patients, HD patients with coronary artery disease treated by SESs have a poorer clinical outcome.

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Noninvasive risk stratification is important for screening for lethal arrhythmia.
We developed a 187-channel signal-averaged vector-projected high-resolution electrocardiograph (187-ch SAVP-ECG) for detecting abnormalities in the spatial location of ventricular high-frequency late potentials (HFLPs) and ventricular repolarization.
The subjects consisted of 30 normal controls (CONTROL) and 13 patients with HFLPs (6 with myocardial infarction [MI], 6 with cardiomyopathy, and 1 with Brugada syndrome). The modified X, Y, Z-lead ECG and the synthesized signals from vector-projected 187-channel ECGs were amplified and passed through a digital filter. We calculated the integration of the HFLPs area between QRS_end and 30 ms before QRS_end. The integrated HFLPs map was superimposed on the corrected recovery time (RTc) and Tpeak-end dispersion maps composed by 187-ch SAVP-ECG. All patients received an examination by 64-channel magnetocardiography (64-ch MCG) on the same day.
The spatial distribution of HFLPs by the 187-ch SAVP-ECG map was in agreement with the location of increased RT dispersion in MI. The spatial distribution of HFLPs in DCM demonstrated a wide variety of patterns. Interestingly, the spatial distribution of HFLPs in cases with ARVC was located at around a right ventricular outflow region. The spatial distribution of HFLPs by 187-ch SAVP-ECG was in agreement with those determined by 64-ch MCG.
The 187-ch SAVP-ECG might be useful for evaluating the spatial distribution of nonuniform conduction and ventricular repolarization heterogeneity.

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A randomized and prospective study was designed to prove the efficacy of angiotensin II receptor blockers (ARB) in the amelioration of myocardial impairment in hypertrophic nonobstructive cardiomyopathy (HNCM).
Nineteen consecutive patients with HNCM were randomly assigned to two groups and then underwent cine magnetic resonance evaluation of left ventricular mass (LVM) twice just before and after one year of observation. In the ARB group, 50 mg of losartan potassium was administered once daily during the observation period. The ratio of LVM after the observation period over that before the period was blindly compared between the two groups to estimate morphologically the ameliorative effect of ARB.
In the ARB group, LVM was 203 ± 47 cm³ before the treatment period and 190 ± 55 cm³ after the period and the ratio of the final LVM over the initial LVM was 0.93 ± 0.10. In the non-ARB group the initial and final LVM values were 177 ± 48 cm³ and 179 ± 45 cm³, and the ratio of the final LVM over the initial LVM was 1.02 ± 0.07. The ratio of the final LVM over the initial LVM in the ARB group was significantly smaller (P = 0.03) than that in the non-ARB group.
The smaller ratio in the ARB group strongly indicates that ARB ameliorated the natural course of HNCM during the one year observation period. Thus, this is the first demonstration of the therapeutic efficacy of ARB in human HNCM.

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It has been reported that green tea consumption reduces the risk of coronary artery disease and cardiac events. Catechin is a major constituent of Japanese green tea and an antioxidant. Lipids and oxidization of low-density lipoprotein cholesterol (LDL-C) play important roles in atherosclerosis. Therefore, we evaluated the effect of catechin intake on the lipid profile and plasma oxidized LDL. The study population consisted of 40 healthy adult volunteers (10 men, 30 women). Catechin was extracted from green tea leaves. The subjects were randomly divided into two groups, a catechin group (n = 29) and a control group (n = 11). In the catechin group, catechin (500 mg: equivalent to 6 or 7 cups of green tea) was administered orally. Venous blood samples were obtained before eating a meal at the start and after 4 weeks without any lifestyle modification. Plasma oxidized LDL assay was performed with a sandwich-type enzyme immunoassay using anti-oxidized phosphatidylcholine monoclonal antibody. The baseline lipid profiles and tea consumptions were similar between the two groups. Plasma oxidized LDL was significantly decreased after catechin administration (from 9.56 ± 9.2 to 7.76 ± 7.7 U/mL, P = 0.005), while plasma LDL-C, triglyceride, and HDL-C concentrations did not change. Catechin decreased the plasma oxidized LDL concentration without significant change in plasma LDL concentration. The mechanism of the beneficial effects of green tea on coronary artery disease might result from a decrease in plasma oxidized LDL.

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The aim of this study was to evaluate the effect of obesity on renal functions and the possible relationship between TGF-β1 and obesity in hypertensive patients. Seventy newly diagnosed, hypertensive patients (male/female 36/34, aged 45.0 ± 8.0 years) and 30 (male/female 17/13, aged 41.8 ± 7.7 years) normotensive controls were included. Patients in both groups were analyzed for serum levels of glucose, creatinine, uric acid, lipids, and TGF-β1. A 24-hour urine sample was also obtained; creatinine clearance rate and urinary albumin excretion (UEA) were investigated. TGF-β1 levels were significantly higher (40.7 ± 13.6 versus 34.2 ± 12.1 pg/mL, P = 0.02), and creatinine clearance was significantly lower in patients compared with controls (98.9 ± 25.5 versus 124.5 ± 23.1 mL/min. per. 1.73 m², P = 0.001). Serum TGF-β1 levels (45.2 ± 14 versis 38.0 ± 12.8 pg/mL, P = 0.03), creatinine clearance rates (109.8 29.9 versus 93.0 ± 20.8 mL/min. per. 1.73 m², P = 0.001), and urinary albumin excretion (55.7 ± 62.0 versus 12.7 ± 12.6 mg/24 h, P = 0.002) were higher in obese hypertensive patients than in nonobese patients. In hypertensive patients, TGF-β1 levels correlated with body mass index (r = 0.296, P = 0.01) and creatinine clearance (r = 0.238, P = 0.04). The results suggest that increased body mass index is associated with increased creatinine clearance, urinary albumin excretion, and TGF-β1 levels in essential hypertension. In addition, TGF-β1 is positively correlated with body mass index and creatinine clearance in patients with essential hypertension.

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The objective of this study was to analyze the early predictive factors for successful weaning from a percutaneous cardiopulmonary support system (PCPS) in patients with low cardiac output syndrome after cardiovascular surgery.
A total of 938 patients underwent cardiovascular surgery with cardiopulmonary bypass (CPB) from January 1991 to September 2006 at Gunma University Hospital. Of these 938 patients, 13 (1.4%) required PCPS to maintain hemodynamics within 48 hours after surgery. The mean age of the 13 patients was 66 years (range, 45 to 86 years). Nine patients underwent open-heart surgery, 3 repair of a thoracic aortic aneurysm, and 1 a pericardiectomy. The patients were divided into 2 groups; group A (n = 4) who were removed from PCPS and group B (n = 9) who were not removed from PCPS. The conditions during the operation and after PCPS support were compared between the 2 groups.
The mean age was higher, and operation time, CPB time, and aortic cross-clamping time were significantly (P < 0.05) longer in patients with PCPS than in those without PCPS. The mean PCPS time in all 13 patients was 190 ± 122 hours. The mean age was higher, and CPB time and the aortic cross-clamping time were longer in group B than in group A (NS). The mean duration of PCPS support was significantly (P < 0.05) shorter in group A than in group B (117 ± 42 hours versus 235 ± 136 hours). PCPS flow in group A could be reduced from 48 hours after PCPS induction. However, PCPC flow in group B could not be reduced, and there were significant (P < 0.05) differences in PCPS flow at 72 and 96 hours after starting PCPS. Significant (P < 0.05) differences in the absolute values of the APACHE II score, serum lactate levels, administered epinephrine dose, and levels of total bilirubin (T-Bil), serum creatinine (sCr), and lactate dehydrogenase (LDH) were found between the 2 groups within 96 hours after PCPS induction. In addition, there were significant (P < 0.05) differences in the rate of change compared with the baseline control value obtained prior to PCPS use in PCPS flow, APACHE II score, and levels of T-Bil, sCr, and LDH within 96 hours after PCPS induction. Significant differences in the rate of change of sCr and LDH were found, especially from the early phase after PCPS use, compared with other parameters.
In the patients removed from PCPS, PCPS flow could be reduced within 48 hours after commencement of PCPS. Improvements in the APACHE II score and biochemical variables within 96 hours appear to be reliable prognostic factors for PCPS patients.

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The present study aimed to investigate the hypothesis that the function of the Na,Ca-exchanger (NCX) is of higher importance for contractility and Ca²⁺-homeostasis in left ventricle from terminally failing than from nonfailing human hearts.
The effect of decreasing extracellular [Na]_e (140 to 25 mmol/L) on force of contraction in isolated left ventricular papillary muscle strips was studied as a reflection of NCX function in multicellular preparations (terminally failing, DCM, dilated cardiomyopathy, NYHA IV, n = 13; nonfailing, NF, donor hearts, n = 10). Decreasing [Na]_e has previously been shown to increase contractility in vitro secondary to a decreased Ca²⁺-extrusion by the NCX. In addition, the NCX activity was measured as Na⁺-dependent ⁴⁵Ca²⁺-uptake into isolated myocardial vesicles as a function of time and Ca²⁺-concentration (DCM n = 8, NF n = 8). Decreasing [Na]_e enhanced the contractility of papillary muscle strips in both DCM and NF, but the contractility of DCM was increased at smaller reductions of [Na]_e than NF. The NCX activity in isolated myocardial vesicles was unchanged as a function of time (T_1/2: DCM 2.4 ± 0.3 s versus NF 2.5 ± 0.3 s) and as a function of Ca²⁺ (DCM 0.99 ± 0.08 versus NF 0.96 ± 0.07 nmol/mg protein × 3 s, K_1/2: DCM 39.2 μM versus NF 38.3 μM).
These results demonstrate a higher sensitivity of the failing human myocardium towards Na,Ca-exchanger mediated positive inotropic effects, suggesting a higher significance of the Na,Ca-exchanger for the extrusion of Ca²⁺-ions in intact failing versus nonfailing human myocardium. Since the activity and the Ca ²⁺-affinity of the Na,Ca-exchanger in isolated vesicles was unchanged, we propose that alterations in Ca²⁺-and Na⁺-homeostasis (due to impaired function of the sarcoplasmic reticulum and the Na⁺, K⁺-ATPase) or the prolonged action potential are the reason for this observation.

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We report a case of late multiple stent fractures following the deployment of sirolimus-eluting stents (SESs) for diffuse right coronary artery (RCA) stenosis. A 44-year-old male with hyperlipidemia was referred to our hospital for acute myocardial infarction (AMI). Percutaneous coronary intervention (PCI) was performed for total occlusion of the proximal segment of the RCA, and 5 SESs were consecutively implanted for long, diffuse stenotic lesions. A follow-up coronary angiography (CAG) performed 8 months later revealed strut fractures in the middle of all the stents, except the most proximal one. Multislice computed tomography confirmed the locations of the fractured struts inside of the stents.

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We present a 60-year-old woman with chest pain preceded by emotional stress. Trans-thoracic echocardiography demonstrated localized left ventricular hypokinesis around the apical area. Multi-detector row computed tomography (MDCT) revealed no significant stenosis in the coronary arteries, which comfirmed Takotsubo-like cardiomyopathy. We show here the usefulness of MDCT for the noninvasive differentiation of Takotsubo cardiomyopathy from acute coronary syndrome.

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