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F-18 fluorodeoxyglucose ( 18F-FDG) positron emission tomography (PET) is a useful tool for the detection of local inflamed atherosclerotic lesions. This study used hybrid PET/computed tomography (CT) to examine the effects of 2 doses of atorvastatin on 18F-FDG uptake in atherosclerotic plaques in Japanese adults with stable angina pectoris who were scheduled to undergo percutaneous coronary intervention (PCI). This was a prospective, randomized, investigator-blinded, open-label study in patients with dyslipidemia (total cholesterol ≥220 mg/dL and/or LDL-C ≥140 mg/dL) who were scheduled to undergo PCI for stable angina pectoris and had not received any lipid-lowering drugs within 1 year before enrollment. Patients were randomly allocated to receive atorvastatin 5 or 20 mg/d for 6 months. At baseline (the day after PCI), 18F-FDG uptake in the ascending aorta and femoral artery was determined using PET/CT imaging, and the mean target-to-background ratio (TBR) was calculated in individual plaques. The same regions were assessed by PET/CT after 6 months of treatment. Changes from baseline to follow-up in the lipid profile, serum malondialdehyde-modified LDL-C (MDA–LDL-C), and serum high-sensitivity C-reactive protein (hs-CRP) were also examined. Drug adherence, adverse events, and changes in medications were monitored at monthly outpatient visits. Of 32 patients initially screened, 2 were excluded due to newly diagnosed cancer; thus, 30 patients were randomly assigned to treatment, 15 in each group. Patients were predominantly male (18 [60%]), with a mean (SD) age of 54 (11) years, mean body weight of 65 (12) kg, and mean total cholesterol, HDL-C, and triglyceride concentrations of 240 (29), 48 (14), and 180 (102) mg/dL, respectively. After 6 months, the 20-mg group had significant reductions from baseline in mean (SD) TBR in the ascending aorta (from 1.15 [0.14] to 1.05 [0.12]; percent change, −7.9% [9.4%]; P = 0.007) and the femoral artery (from 1.12 [0.11] to 1.02 [0.11]; percent change, −9.9% [13.8%]; P = 0.012). The corresponding changes from baseline were not statistically significant in the 5-mg group. The differences in percent change in TBR in the 2 locations were not significant between groups. When data from the 2 groups were combined, the overall reduction in TBR from baseline to 6 months was significant in both the ascending aorta ( P = 0.003) and the femoral artery ( P = 0.021). The decreases in TBR in both arteries were significantly correlated with reductions in LDL-C (ascending aorta: r 2 = 0.230 [ P = 0.012]; femoral artery: r 2 = 0.338 [ P = 0.003]), MDA–LDL-C (ascending aorta: r 2 = 0.183 [ P = 0.028]; femoral artery: r 2 = 0.247 [ P = 0.010]), and hs-CRP (ascending aorta: r 2 = 0.132 [ P = 0.048]; femoral artery: r 2 = 0.271 [ P = 0.007]). One patient in the 5-mg group and 2 patients in the 20-mg group had ∼2-fold increases in serum aminotransferases on a single occasion; however, no specific musculoskeletal or hepatic adverse events were observed, and aminotransferase values decreased to within normal ranges without changes in the atorvastatin dose. Six months of treatment with atorvastatin 20 mg, but not 5 mg, was associated with a significant reduction in TBR in the ascending aorta and femoral artery in these Japanese adults with dyslipidemia undergoing PCI for stable angina pectoris. University Hospital Medical Information Network Clinical Trials Registry identifier: C000000371.

Background: Depression increases the risk of mortality in hemodialysis patients. Alexithymia, a disorder of affect regulation, has also been reported to be associated with mortality risk in the general population. We conducted a prospective study to estimate the independent impact of depression and alexithymia on long-term mortality. Methods: A total of 230 hemodialysis outpatients, with a mean age of 56.3 ± 9.6 years, completed a batch of self-report measures including the Beck Depression Inventory-II (BDI-II), the 20-item Toronto Alexithymia Scale (TAS-20) and the 36-item Short Form Health Survey (SF-36). Survival status was confirmed every 6 months for up to 5 years. The presence of depression and alexithymia was defined by a BDI-II score of ≧14 and a TAS-20 score of ≧61, respectively. Results: During the follow-up period, 27 deaths were confirmed. Both depression and alexithymia were associated with an increased risk for all-cause mortality; the age- and sex-adjusted hazard ratio for depression was 2.36 (95% CI: 1.08–5.15; p = 0.03) and that for alexithymia was 4.29 (95% CI: 1.95–9.42; p < 0.001). Depression lost its statistical significance after controlling for alexithymia, whereas alexithymia remained significant even after adjusting for the baseline depression, health status (the summary scores of the SF-36), marital status and clinical covariates (multivariate adjusted hazard ratio = 3.62; 95% CI: 1.32–9.93; p = 0.01). Conclusions: Alexithymia is a strong independent risk factor for all-cause mortality in hemodialysis patients.

Background: Percutaneous transluminal angioplasty (PTA) for femoropopliteal lesions in peripheral artery disease has been performed in patients undergoing hemodialysis as well as in the general population. Cilostazol, a selective inhibitor of phosphodiesterase 3, has been reported to reduce target lesion revascularization after PTA for femoropopliteal lesions in the general population. Objective: This study investigated the effects of cilostazol use on long-term patency after PTA in patients with femoropopliteal disease undergoing hemodialysis. Methods: In this retrospective study, data from patients undergoing hemodialysis who underwent successful PTA for femoropopliteal disease, defined as a final luminal diameter stenosis <30% without angiographically visual arterial dissection and no in-hospital complications, were included. One study group received long-term treatment with oral cilostazol 100 mg BID after PTA; the control group did not. The duration of follow-up was ≤6 years. The primary outcome of interest was cumulative patency, as measured by the event-free rate 6 years after PTA, with event defined as restenosis of >50% of the vessel diameter in femoropopliteal lesions. Data on baseline characteristics, patency, and covariates (diabetes, hypertension, hyperlipidemia, smoking, coronary artery disease, critical limb ischemia, TransAtlantic Inter-Society Consensus classification, and stenting) were obtained from electronic medical records and telephone interviews with patients. To minimize the effects of selection bias for cilostazol administration, a propensity-matched analysis using Cox univariate and multivariate models including the previously mentioned covariates was conducted. The propensity scores of the 2 groups were matched 1:1 (AUC = 0.69 [receiving operating characteristics analysis]). Data were obtained from electronic medical records and telephone interviews with patients by trained personnel who were blinded to treatment assignment. Results: A total of 358 consecutive lesions of 174 patients undergoing hemodialysis were included (103 men, 71 women; mean [SD] age, 66 [11] years; cilostazol group, 61 patients, 121 lesions; control group, 113 patients, 237 lesions). The mean duration of follow-up was 37 (27) months. The 6-year event-free rate of restenosis of >50% of the vessel diameter was significantly higher in the cilostazol group than in the control group (72/121 [59.5%] vs 120/237 [50.6%]; P = 0.005 [logrank test]; hazard ratio [HR] = 0.63; 95% CI, 0.45-0.88; P = 0.008 [Cox univariate analysis]). Also, event-free rates of target lesion revascularization and limb amputation were significantly higher in the cilostazol group than in the control group (40/61 [65.6%] vs 57/113 [50.4%]; P = 0.013 [log-rank test] and 54/61 [88.5%] vs 90/113 [79.6%]; P = 0.047 [logrank test], respectively). On propensity score matching (105 lesions), the baseline characteristics were comparable between the 2 groups. The 6-year eventfree rate of restenosis was significantly higher in the cilostazol group than in the control group (66/105 [62.9%] vs 52/105 [49.5%]; HR = 0.58; 95% CI, 0.38-0.88; P = 0.012 [Cox univariate analysis]). On propensity-matched (Cox multivariate) analysis, cilostazol (HR = 0.51; 95% CI, 0.27-0.84; P = 0.008), age (HR = 1.01; 95% CI, 1.01–1.04; P = 0.031), and critical limb ischemia (HR = 2.21; 95% CI, 1.39-3.53; P = 0.001) were independent predictors of restenosis. None of the patients in the cilostazol group discontinued cilostazol treatment during the follow-up period. Four patients (6.6%) experienced mild headache. Conclusion: This study found that in these patients with femoropopliteal lesions in peripheral artery disease who were undergoing hemodialysis, those treated with cilostazol 100 mg BID after PTA had a higher mean rate of cumulative patency after PTA than those in the control group.

The renin-angiotensin-aldosterone system has an important role in the progression of both diabetic and nondiabetic nephropathy. Angiotensin-converting enzyme inhibitors and angiotensin-II receptor blocker can effectively retard or halt this progression. However, their renoprotective effect is not enough, because approximately 20% of patients have a progressive course to endstage renal disease. There is now clear evidence that combination therapy of two agents is more antiproteinuric and, likely renoprotective, than each agent alone. However, several critical issues should be addressed before recommending it as standard treatment in chronic renal disease.

Patients receiving hemodialysis for end-stage renal disease (ESRD) are at high risk for death from ischemic heart disease (IHD). Nicorandil, a hybrid compound of adenosine triphosphate-sensitive potassium channel opener and nitric oxide donor, has been reported to improve the clinical prognosis of patients with IHD. This study sought to investigate the efficacy of oral nicorandil in reducing the risks for cardiovascular events (CVEs) and CVE-related death in patients receiving hemodialysis for ESRD after undergoing percutaneous coronary intervention (PCI) for angina pectoris. For this retrospective chart review, we used data from telephone interviews and medical charts from 3 hospitals in Japan. Data from patients aged <80 years who were receiving hemodialysis for ESRD and who had undergone successful PCI for angina between January 1999 and December 2004 were included in the analysis. Patients were stratified based on status of nicorandil treatment before PCI, as follows: patients receiving nicorandil 5 mg PO TID (the recommended dosage in Japan) for >1 month before PCI (nicorandil group) or those who did not receive nicorandil (control group). We investigated 6-year follow-up data on the primary end point, defined as CVEs (ie, unplanned hospital admission for worsening anginal status, or CVE-related death). The secondary end point was CVE-related death. After the data were initially analyzed, we performed a propensity-matched analysis to minimize selection bias. Data from 356 patients were included in the study (235 men, 121 women; mean [SD] age, 69 [9] years; mean [SD] weight, 52.3 [9.1] kg; nicorandil group, 198 patients; control group, 158 patients). According to the estimated propensity scores, 107 patients from each group were matched. There were no differences between the 2 groups in the baseline characteristics. On propensity-matched patient analysis, the estimated rates of patients who were CVE-free at 6 years were 33.5% in the nicorandil group and 21.8% in the control group on Kaplan-Meier analysis (hazard ratio [HR] = 0.53; 95% CI, 0.36–0.78; P < 0.002), and the rates of 6-year survival (ie, patients who did not experience CVE-related death) were 92.7% in the nicorandil group and 85.8% in the control group (HR = 0.27; 95% CI, 0.07–0.89; P = 0.047). Cox multivariate analysis found that nico-randil treatment status was an independent predictor of CVEs (HR = 0.40; 95% CI, 0.18-0.91; P = 0.028) and CVE-related death (HR = 0.38; 95% CI, 0.14–0.78; P = 0.030). Results obtained in this retrospective study suggest the potential efficacy of nicorandil treatment in improving clinical outcomes in patients with IHD receiving hemodialysis following PCI.

Circulating CD34-positive (CD34+) cells, a population that includes endothelial progenitor cells, are believed to contribute to vascular homeostasis. Here we determine the prognostic value of CD34+ cell measurements in 216 chronic hemodialysis patients. A total of 43 cardiovascular events and 13 deaths occurred over an average 23 months follow-up in this cohort. A cutoff number for circulating CD34+ cells was determined by receiver operating characteristic curve analysis to maximize the power of the CD34+ cell count in predicting future cardiovascular events. Based on this, 93 patients were categorized as having low and 123 patients as having high numbers of CD34+ cells, determined by flow cytometry at the time of enrollment. Both cumulative cardiovascular event-free survival and all-cause survival were significantly less in the group of patients with low numbers of CD34+ cells. By multivariate analyses, a low level of circulating CD34+ cells was an independent and significant predictor for both cardiovascular events and all-cause mortality. Our study shows that a reduced number of circulating CD34+ cells is significantly associated with vascular risks and all-cause mortality in patients on chronic hemodialysis. These cells may be a useful biomarker.

Background/Aims: Adiponectin is an adipocyte-derived protein with antiatherogenic properties. Chronic kidney disease (CKD) is one of the risk factors for cardiovascular disease. We investigated the potential association between adiponectin and carotid arteriosclerosis in patients with predialysis CKD. Methods: We enrolled 95 CKD patients without dialysis and 81 non-CKD patients. Intima-media thickness (IMT) and plaque score (PS) in the common carotid artery were measured using an ultrasound system. Carotid arteriosclerosis was defined as IMT >1.2 mm and/or PS >5.0 mm. Results: The prevalence of CKD was independently associated with carotid arteriosclerosis after adjustment for other risk factors. Higher adiponectin levels were observed in CKD patients compared with non-CKD patients. Adiponectin levels were not independently correlated with the presence of carotid arteriosclerosis in all subjects. To evaluate the association between adiponectin and carotid arteriosclerosis among a CKD population, we divided the CKD patients into 2 groups according to a cutoff level of adiponectin determined by ROC analysis. The prevalence of carotid arteriosclerosis was significantly higher in the low-adiponectin group than in the high-adiponectin group among CKD patients. After adjusting for other risk factors, low levels of adiponectin were independently correlated with carotid arteriosclerosis in CKD patients. Conclusion: Our data document that adiponectin is associated with increased risk of carotid atherosclerosis in a predialysis CKD population.

F-18 fluorodeoxyglucose (18 F-FDG) positron emission tomography (PET) is a useful tool for the detection of local inflamed atherosclerotic lesions. This study used hybrid PET/computed tomography (CT) to examine the effects of 2 doses of atorvastatin on 18 F-FDG uptake in atherosclerotic plaques in Japanese adults with stable angina pectoris who were scheduled to undergo percutaneous coronary intervention (PCI). This was a prospective, randomized, investigator-blinded, open-label study in patients with dyslipidemia (total cholesterol ≥220 mg/dL and/or LDL-C ≥140 mg/dL) who were scheduled to undergo PCI for stable angina pectoris and had not received any lipid-lowering drugs within 1 year before enrollment. Patients were randomly allocated to receive atorvastatin 5 or 20 mg/d for 6 months. At baseline (the day after PCI), 18 F-FDG uptake in the ascending aorta and femoral artery was determined using PET/CT imaging, and the mean target-to-background ratio (TBR) was calculated in individual plaques. The same regions were assessed by PET/CT after 6 months of treatment. Changes from baseline to follow-up in the lipid profile, serum malondialdehyde-modified LDL-C (MDA-LDL-C), and serum high-sensitivity C-reactive protein (hs-CRP) were also examined. Drug adherence, adverse events, and changes in medications were monitored at monthly outpatient visits. Of 32 patients initially screened, 2 were excluded due to newly diagnosed cancer; thus, 30 patients were randomly assigned to treatment, 15 in each group. Patients were predominantly male (18 [60%]), with a mean (SD) age of 54 (11) years, mean body weight of 65 (12) kg, and mean total cholesterol, HDL-C, and triglyceride concentrations of 240 (29), 48 (14), and 180 (102) mg/dL, respectively. After 6 months, the 20-mg group had significant reductions from baseline in mean (SD) TBR in the ascending aorta (from 1.15 [0.14] to 1.05 [0.12]; percent change, -7.9% [9.4%]; P = 0.007) and the femoral artery (from 1.12 [0.11] to 1.02 [0.11]; percent change, -9.9% [13.8%]; P = 0.012). The corresponding changes from baseline were not statistically significant in the 5-mg group. The differences in percent change in TBR in the 2 locations were not significant between groups. When data from the 2 groups were combined, the overall reduction in TBR from baseline to 6 months was significant in both the ascending aorta (P = 0.003) and the femoral artery (P = 0.021). The decreases in TBR in both arteries were significantly correlated with reductions in LDL-C (ascending aorta: r2 = 0.230 [P = 0.012]; femoral artery: r2 = 0.338 [P = 0.003]), MDA-LDL-C (ascending aorta: r2 = 0.183 [P = 0.028]; femoral artery: r2 = 0.247 [P = 0.010]), and hs-CRP (ascending aorta: r2 = 0.132 [P = 0.048]; femoral artery: r2 = 0.271 [P = 0.007]). One patient in the 5-mg group and 2 patients in the 20-mg group had ∼2-fold increases in serum aminotransferases on a single occasion; however, no specific musculoskeletal or hepatic adverse events were observed, and aminotransferase values decreased to within normal ranges without changes in the atorvastatin dose. Six months of treatment with atorvastatin 20 mg, but not 5 mg, was associated with a significant reduction in TBR in the ascending aorta and femoral artery in these Japanese adults with dyslipidemia undergoing PCI for stable angina pectoris. University Hospital Medical Information Network Clinical Trials Registry identifier: C000000371.

In the COOPERATE trial, the combination treatment of the angiotensin-II receptor blocker losartan and the angiotensin-converting-enzyme inhibitor trandolapril significantly retarded progression of non-diabetic kidney disease compared with each monotherapy. The benefit could be greatly attributable to the potent reduction of proteinuria, because the three treatment groups showed the same reductions of office blood pressure (OBP). Ambulatory blood pressure (ABP) is reported to be better than OBP in predicting progression of kidney disease. Ninety-two patients enrolled in the COOPERATE trial underwent 24-hour ABP monitoring at randomization and at month 6, year 1, year 2 and year 3 on randomized treatment. Both OBP and ABP were similarly reduced among the three groups at all measurement points (p = NS) and throughout the whole study period (p = NS). No significant correlation between the change in 24-hour ABP and the change in proteinuria was seen (p = NS). A Cox-multivariable analysis showed that covariates affecting the renal outcomes (a doubling serum-Cr level and/or end-stage renal failure) were the change in proteinuria (hazard ratio 0.49, 95% CI 0.34-0.78, p = 0.01) and treatments (0.58, 0.45-0.99, 0.03), but not 24-hour ABP (0.98, 0.89-2.01, 0.17). The better renoprotective effect of the combination treatment is attributed to BP-independent mechanisms by more complete renin-angiotensin system blockade.

Prognostic value of nonlinear heart rate dynamics in hemodialysis patients with coronary artery disease. Although altered nonlinear heart rate dynamics predicts death in patients with coronary artery disease (CAD), its prognostic value in chronic hemodialysis patients with CAD is unknown. We analyzed 24-hour electrocardiogram for nonlinear heart rate dynamics and heart rate variability in a retrospective cohort of 81 chronic hemodialysis patients with CAD. During a follow-up period of 31 ± 20months, 19 cardiac and 8 noncardiac deaths were observed. Cox hazards model, including diabetes, left ventricular ejection fraction, and the number of diseased coronary arteries, revealed that abnormal α2 (defined as both increase and decrease in α2 because of its J curve relationship with cardiac mortality), decreased approximate entropy and decreased heart rate variability (triangular index and ultra-low frequency power) were significant and independent predictors of cardiac death. No significant and independent predictive power for noncardiac death was observed in either the heart rate dynamics or the heart rate variability measures. The predictive power of α2 and approximate entropy was independent of that of triangular index and ultra-low frequency power. Combinations of two categories of measures improved the predictive accuracy; overall accuracy of approximate entropy + ultra-low frequency power for cardiac death was 87%. Altered nonlinear heart rate dynamics are independent predictors of cardiac death in chronic hemodialysis patients with CAD and their combinations with decreased heart rate variability provide clinically useful markers for risk stratification.