Heart failure: mechanisms for progression 781 of circulating proBNP1-108 with our immunodepletion process, we are now able to assess the remaining "true" BNP and NT-proBNP molecules and evaluate their clinical relevance.

Purpose: Although indoxyl sulfate (IS), one of a uremic toxin, is suggested be a novel prognostic marker in patients with chronic kidney disease, its clinical characteristics has remained uncertain in patients with heart failure (HF) and preserved renal function (RF). We aimed to determine the clinical characteristics of IS in patients with HF. Methods: We studied 726 participants without overt HF and renal disease from a community-living, and prospectively enrolled 154 consecutive hospitalized acute and chronic heart failure (CHF) patients with preserved RF (eGFR >40 ml/min/1.73 m2) (24 acute HF patients and 130 CHF patients, respectively). We also performed right heart catheterization (RHC) in CHF patients (n = 105). Results: The plasma IS (PIS) levels in patients with CHF were significantly higher than that of healthy population matched with gender and eGFR of HF patients (0.79 [25th to 75th IQR: 0.45-1.19] μg/ml vs. 0.07 [0.04-0.11] μg/ml, respectively, p<0.001) (Figure A.), PIS levels were significantly correlated with right atrial pressure (r = 0.19, p = 0.028) and cardiac output (r = -0.30, p<0.001) in RHC study. Echocardiography revealed that LV mass index in High IS group (≥0.79 μg/ml) was significantly higher than that of Low IS group (<0.79 μg/ml) (Figure B.) in CHF patients. Interestingly, of 24 acute HF patients, PIS levels at discharge were significantly elevated compared with the baseline, as preliminary data (0.67 [0.36-0.90] μg/ml to 0.94 [0.76-1.68] μg/ml, p = 0.005) (Figure C). Figure 1 Figure 1 Conclusions: The plasma IS levels were suggested to be related to renal perfusion pressure with the prevalence of cardiac hypertrophy. From the change of IS levels during HF hospitalization, IS might be a novel marker to predict remote renal and cardiac status in patients with heart failure.

BACKGROUND:The efficacy of drug-eluting stents after rotational atherectomy (ROTA) has not been clarified.METHODS AND RESULTS:The 704 consecutive patients who underwent percutaneous coronary intervention (PCI) with a sirolimus-eluting stent (SES) (79 with and 625 without ROTA) were enrolled. The 2-year clinical outcome of these patients was compared with that of a group of 1,123 consecutive patients treated with bare-metal stents (BMS) (144 with and 979 without ROTA). At 2 years after index PCI, the use of SES after ROTA was associated with a lower crude incidence of major adverse cardiac events (MACE) than were BMS after ROTA (30.1% vs 43.1%, P=0.024). The difference was mainly derived from the reduction in target lesion revascularization (TLR) (25.0% vs 39.1%, P=0.022). After adjusting for confounders, ROTA-SES was associated with a reduction in MACE and TLR, with a similar hazard ratio to the non-ROTA group only with SES implantation. In a subgroup of dialysis patients, the incidence of TLR after ROTA with SES and BMS was similarly high.CONCLUSIONS:The use of SES after ROTA is an appropriate method for selected hard lesions, but has a limited effect in dialysis patients, even after lesion preparation with ROTA.

Background The efficacy of sirolimus-eluting stents (SESs) has not been established in dialysis patients.Methods and Results This study was a non-randomized observational single-center registry in a community hospital: data for 80 consecutive dialysis patients who underwent percutaneous coronary intervention (PCI) with SES were compared with those of a historical group of consecutive 124 dialysis patients treated with bare-metal stents (BMS). After 1 year, the cumulative incidence of major adverse cardiac events (MACE), comprising cardiac death, nonfatal myocardial infarction, stent thrombosis, or target lesion revascularization (TLR), was 25.2% in the SES group and 38.2% in the BMS group (p=0.048). In multivariate analysis, use of SES remained an independent predictor of MACE at I year after PCI (risk ratio 0.70, 95% confidence interval 0.52-0.93, p=0.015). Rates of TLR were 21.7% in the SES group and 30.9% in the BMS group and (p=0.15). Subgroup analysis showed that use of SES was effective in patients with small vessels, non-diabetic patients, and patients without highly calcified lesions.Conclusions In dialysis patients, the implantation of SES was moderately effective in reducing MACE at 1 year after PCI as compared with BMS. However, the TLR rate at 1 year was relatively higher than previously reported.

The role of plasma levels of oxidized low density lipoprotein (OxLDL) in the development of coronary heart disease (CHD) has not been fully elucidated. We examined the relationship among plasma levels of OxLDL, measured by an enzyme immunoassay using an antibody against OxLDL (FOH1a/DLH3) and apolipoprotein B, CHD, and modalities at the onset of acute coronary syndrome (ACS). A total of 115 individuals who underwent coronary angiography were studied. Of these, 21 patients complicated with extracoronary cardiovascular diseases were excluded. Consequently, 94 patients (63 men) (ACS: 23, stable angina pectoris (SAP): 46, and normal coronary artery (NCA):25) were eligible for inclusion in the study. Elevated plasma levels of OxLDL were associated with CHD, especially with ACS. In patients with NCA, hypertension was associated with plasma OxLDL. Plasma levels of OxLDL were significantly higher in patients with new-onset type ACS than in those with worsening type ACS (2.98 versus 1.53 mg/dL, P = 0.002). In conclusion, plasma levels of OxLDL are associated with CHD and significantly higher in patients with new-onset ACS. The findings of the present study suggest that plasma OxLDL can be a marker of the development of CHD and modalities of ACS.

A 74-year-old man who had been in good general state of health presented with coma. His pulse was 82 beats per minute and his blood pressure was 120/76 mm Hg. No heart murmurs or crackles were audible. Neurologic examination revealed no abnormalities except for consciousness. The electrocardiogram revealed ST segment elevation in leads V2 to V3 with ST depression in leads II, III, aVF and terminal T inversion in leads V2 to V5. We performed an urgent coronary arteriography and left ventriculography. We found no signs of the coronary arteries fixed stenoses despite persistent ST segment abnormalities. The left ventriculogram showed apical ballooning akinesis and basal hyperkinesis with an ejection fraction of 45%, as depicted (Fig. 1A and B). Creatine kinase concentrations rose over the next 24 h, peaking at 470 IU/l (normal, 53–288 IU/l). Serum electrolyte levels were as follows: sodium 113 mEq/l, potassium 4.8 mEq/l, and chloride 80 mEq/l. The results of endocrinological studies immediately after the sideration are shown in Table 1. Serum free triiodothyronine and free thyroxine were suppressed while thyrotropin (TSH) levels were within the normal range. Urine 17-hydroxycorticosteroid and 17-ketosteroid levels were suppressed, although basal levels of serum cortisol and plasma adrenocorticotropic hormone (ACTH) and urinary cortisol levels were within the lower limits of the normal range. The

Heme oxygenase-1 (HO-1) is a stress-inducible isoform of HO with potential cytoprotective effects. Monocyte activation/migration mediated by monocyte chemoattractant protein-1 (MCP-1) is one of the earliest and important events in the pathogenesis of atherosclerosis. We examined the effect of HO-1 on the production of lysophosphatidylcholine (Lyso-PC)-induced MCP-1 in the human promonocytic cell line U937. Increased HO-1 induction by hemin resulted in a significant decrease in the Lyso-PC-mediated induction of MCP-1 mRNA expression. SnPP (IX), the specific inhibitor of HO-1 enzymatic activity, prevented the hemin-mediated attenuation of MCP-1 mRNA expression. These results suggest that HO-1 may work as an anti-atherogenic agent through the attenuation of MCP-1 production.

BACKGROUND:Arterial stiffness measurements, generally from pulse wave velocity (PWV), are widely used with little knowledge of their relationship to long-term cardiovascular mortality in general populations.METHODS AND RESULTS:We studied a cohort of 492 Japanese-Americans living in Hawaii (mean age: 63.7 +/-8.8 years) to assess the relationship between PWV and cardiovascular disease mortality and all-cause mortality. During the 10-year follow-up, 43 patients died (14 from cardiovascular events). The cohort was divided into 2 groups by the cut-off value of PWV (9.9 m/s) represented in the receiver operating characteristic curve. The risk ratio for PWV values >9.9 m/s to all-cause mortality was 1.28 [95% confidence interval (CI): 1.14-1.42], and adjusted for other risk factors this ratio was 1.42 (95% CI: 0.96-2.11). The corresponding risk ratios for cardiovascular mortality was 4.46 (95% CI: 1.61-12.32) and 4.24 (95% CI: 1.39-12.96), respectively.CONCLUSIONS:The present study demonstrated that an increased PWV value is associated with future cardiovascular disease death in Japanese-Americans living in Hawaii.