NDT Advance Access originally published online on January 23, 2006
Nephrology Dialysis Transplantation 2006 21(6):1640-1647; doi:10.1093/ndt/gfk088
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Original Articles: Dialysis and Transplantation
Association of the circulating adiponectin concentration with coronary in-stent restenosis in haemodialysis patients
1 Cardiovascular Division, 2 Division of Urology and 3 Division of Surgery, Toujinkai Hospital, Kyoto, 4 Department of Interventional Cardiology, Kyoto Second Red Cross Hospital, Kyoto and 5 Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University, Moriguchi, Japan
Correspondence and offprint requests to: Masato Nishimura, MD, Cardiovascular Division, Toujinkai Hospital, 83-1, Iga, Momoyama-cho, Fushimi-ku, Kyoto 612-8026, Japan. Email: mnishimura{at}tea.ocn.ne.jp
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Abstract |
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Background. Success of coronary stenting is limited by in-stent restenosis. We aimed to determine whether circulating levels of the cytokines, which have anti-inflammatory properties such as adiponectin or interleukin-10, could be associated with the occurrence of coronary in-stent restenosis in patients with end-stage renal disease (ESRD).
Methods. We enrolled 71 consecutive ESRD patients undergoing haemodialysis (mean age: 64.9±8.9 years; 19 women, 52 men; mean haemodialysis duration: 78.2±87.5 months), who received stenting for a single coronary lesion. Plasma concentrations of adiponectin and IL-10 were measured within one week before coronary stenting.
Results. Of the 71 patients who had received stenting, in-stent restenosis occurred in 37 patients (52.1%) within 6 months after stenting. In univariate logistic analysis, the homeostasis model assessment index of insulin resistance, blood haemoglobin, serum concentrations of high density lipoprotein–cholesterol or triglycerides and plasma concentrations of insulin or adiponectin were significantly associated with coronary in-stent restenosis. In a multiple logistic regression analysis among these variables, however, only the plasma adiponectin concentration was associated with the coronary in-stent restenosis: the odds ratio of the increase in 1 µg/ml of plasma adiponectin concentration for having restenosis was 0.651 (P = 0.001, 95% confidence interval: 0.506–0.839). Patients with restenosis had lower plasma adiponectin concentrations than those without [6.2±2.2 µg/ml (2.1–10.4 µg/ml; n = 37) vs 27.2±10.8 µg/ml (17.9–79.8 µg/ml; n = 34); P = 0.0001].
Conclusions. Circulating adiponectin concentrations may be associated with the occurrence of coronary in-stent restenosis in ESRD patients undergoing maintenance haemodialysis.
Keywords: adiponectin; coronary artery disease; haemodialysis; restenosis; stenting
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Introduction |
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Patients with end-stage renal disease (ESRD) have a 20–40-fold higher cardiovascular mortality than people without renal disease. Percutaneous coronary revascularization procedures have been underutilized in the ESRD population, because the use of balloon coronary angioplasty in this group is associated with a high incidence of repeat revascularization for restenosis [1]. However, the widespread use of coronary stents has improved the outcome of percutaneous coronary angioplasty in ESRD patients [2] as well as in non-ESRD patients. Long-term success of coronary stenting is limited by in-stent restenosis, which usually occurs within the first 6 months after stent implantation. In-stent restenosis is caused by exaggerated neointimal formation, a specific inflammatory/proliferative response of the vascular wall to the trauma induced by angioplasty and stent implantation. Many clinical, angiographic and procedural variables have been studied to determine the causes or predictors of restenosis [3], but no definite factors that play a role in in-stent restenosis have ever been established in ESRD patients.
Circulating concentrations of C-reactive protein (CRP), which reflect the baseline level of systemic inflammation, predict the long-term risk of cardiovascular diseases. In contrast, interleukin-10 (IL-10) and adiponectin seem to be cytokines that inhibit the inflammatory response. IL-10 downregulates inflammatory activation of monocytes and macrophages by transcriptional and post-transcriptional inhibition of a wide range of pro-inflammatory cytokines [4]. Adiponectin is a recently discovered adipocytokine [5], also referred to as gelatin-binding protein-28. This cytokine is a 244 amino acid protein, the product of the apM1 gene, which is specifically and highly expressed in human adipose cells. Adiponectin is likely to play a protective role in experimental models of vascular injury, probably by suppressing the adhesion of monocytes to endothelial cells [6] and may act as a protective factor for the cardiovascular system in ESRD patients [7]. Furthermore, circulating adiponectin concentration reportedly correlates with humoral markers of coagulation or fibrinolysis such as plasminogen activator inhibitor, thrombin-activatable fibrinolysis inhibitor, or tissue factor pathway inhibitor in ESRD patients [8]. In the present study, we wanted to determine whether circulating levels of adiponectin or IL-10 were associated with the occurrence of coronary in-stent restenosis in ESRD patients undergoing maintenance haemodialysis.
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Patients
We enrolled 71 consecutive ESRD patients undergoing maintenance haemodialysis (mean age: 64.9±8.9 years; 19 women, 52 men; mean haemodialysis duration: 78.2±87.5 months), who underwent ad hoc stenting for a single coronary lesion on the same day as their diagnostic coronary angiography at the Kyoto Second Red Cross Hospital. Of the 71 haemodialysis patients, 39 patients had diabetes mellitus (DM). Type II DM had been treated before initiation of haemodialysis in all diabetic patients, but they had received neither insulin nor oral antidiabetic drugs for at least 6 months preceding the start of this study; of 39 diabetic patients, 29 patients had stopped insulin therapy, and 10 patients had stopped medication of antidiabetic drugs after initiation of haemodialysis. Their mean serum haemoglobin A1c value at this study was 5.9±0.8%. Four patients had a past history of cerebrovascular accidents (two patients each in the restenosis and non-restenosis groups). Patients having old myocardial infarction were excluded from this study. No patients suffered acute myocardial infarction or acute cerebrovascular accidents during this study. Mean systolic and diastolic blood pressures before dialysis were 145.5±13.7 mmHg (n = 71) and 73.5±11.2 mmHg (n = 71), and mean systolic and diastolic blood pressures after dialysis were 137.0±16.6 mmHg (n = 71) and 66.3±7.4 mmHg (n = 71), respectively. Lesions in the coronary arteries that received stent implantation were located in the right coronary artery (n = 21), the left anterior descending artery (n = 34) and the left circumflex artery (n = 16), respectively. Coronary lesions were type A for six patients, type B1 for 29 patients, type B2 for 24 patients and type C for 12 patients. According to the American College of Cardiology/American Heart Association classification [9], type A lesions are discrete (<10 mm length) and concentric, and have a high success rate of >85% in percutaneous coronary intervention; type B lesions are tubular (10–20 mm length) and eccentric, and have a moderate success rate of 60–85% in percutaneous coronary intervention (type B1 contains one of the type B criteria and type B2 contains more than one B criterion); and type C lesions are diffuse (>20 mm length) and extremely angulated, and have a low success rate of <60% in percutaneous coronary intervention: type B2 and type C lesions are thought to be complex ones according to these guidelines; 50.7% in the present study. Follow-up coronary angiography was performed approximately 6 months after stent implantation as described below. The Ethics Committee for Human Research of Toujinkai Hospital approved this study, and all patients provided informed consent for participation.
Haemodialysis
Haemodialysis was performed three times weekly using a dialysate containing Na+ (140 mEq/l), K+ (2.0 mEq/l), Cl– (110 mEq/l), Ca2+ (3.0 mEq/l), Mg2+ (1.0 mEq/l), HCO3– (30 mEq/l) and CH3COO– (10–15 mEq/l). Membranes used in the dialyser were cellulose triacetate (FB-190F, NIPRO, Tokyo, Japan), surface modified regenerated cellulose (AMBC-20X, Asahi Medical, Tokyo, Japan), polymethyl methacrylate (FB-2.1F, TORAY Medical, Tokyo, Japan) or polysulfone (PS-1.9UW, Kawasumi Laboratory, Tokyo, Japan). The dialysis filter surface area was 1.8–2.1 m2. Blood pressure was measured hourly during dialysis using a mercury sphygmomanometer. Blood pressure was determined at the last mid-week haemodialysis session before the coronary angiography and stenting.
Stent implantation and clinical and angiographic follow-up
Patients with coronary artery disease who underwent the procedures were treated with IV heparin and combined antiplatelet therapy (200 mg/day of ticlopidine hydrochloride and 200 mg/day of aspirin). Customized bare-metal stents mounted on expandable balloons were implanted. Drug-eluting stents were not used in this study. A minimal balloon inflation pressure was 12 atm, and the mean balloon inflation pressure was 18.6±3.2 atm. Rotational atherectomy with the Rotablator system (Boston Scientific, Natick, MA) was performed in 41 patients having coronary calcification prior to stenting. In 30 patients, only balloon coronary angioplasty was performed prior to stenting. Procedures of stenting had been performed with success in all 71 patients. Follow-up coronary angiography was performed within 6 months after coronary stenting. Quantitative coronary angiographic analysis was performed using a validated automated edge-detection programme (CCIP-310/W, CATHEX, Tokyo, Japan) by experienced interventional cardiologists. Reference diameter, minimal luminal diameter (MLD) and percent diameter stenosis before intervention, after intervention and at follow-up were measured from diastolic frames in single-matched views showing the smallest luminal diameter. Lesion length was measured on the baseline angiogram as the distance from the proximal to distal shoulder of the lesion in the least foreshortened projection. In addition, the following parameters were assessed: acute gain (MLD (after the procedure) – MLD (before the procedure)); late loss (MLD (after the procedure) – MLD (at follow-up)); net gain (difference between acute gain and late loss); and restenosis (presence of >50% diameter stenosis at follow-up). The parameters before and after stent implantation and at 6-month angiographic follow-up are summarized in Table 1.
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Biochemical and haematologic determinations
Blood samples (5 ml) for the measurement of plasma concentrations of adiponectin and IL-10 were obtained at the initiation of a mid-week haemodialysis within one week before coronary angiography and coronary stenting, after the patient had been in the supine position for at least 10 min. The plasma IL-10 concentration was measured using a high-sensitive enzyme-linked immunosorbent assay (ELISA) method (Human IL-10 EIA kit, Immunotech International, Marseille Cedex, France). The intra- and inter-assay coefficient of variation for this test ranged from 3.3 to 4.0% and from 5.6 to 8.6%, respectively. The plasma adiponectin concentration was determined by an ELISA method (Human Adiponectin/Acrp30 Immunoassay, Quantikine, R&D systems, Minneapolis, MN). The intra- and inter-assay coefficient of variation for this test ranged from 2.5 to 4.7% and from 5.8 to 6.9%, respectively. In addition to before coronary stenting, plasma adiponectin concentrations were again measured at the initiation of a mid-week haemodialysis session 1–2 years after coronary stenting in all the patients. Further, we measured plasma adiponectin concentrations in 20 Japanese healthy individuals (mean age: 33±7 years; 10 women, 10 men) to assess the validation of the ELISA method used in this study; the mean plasma adiponectin concentration was 6.4±2.1 µg/ml (3.1–11.7 µg/ml) in these healthy individuals. Blood samples for the measurement of blood haemoglobin and serum concentrations of calcium, inorganic phosphorus, total protein, albumin, total cholesterol, high-density lipoprotein (HDL)–cholesterol, triglycerides, CRP and intact parathyroid hormone were obtained at the initiation of the mid-week haemodialysis session within one week before coronary angiography and stenting. The serum CRP concentration was measured using a high sensitive assay kit (N-Assay LA CRP-S, D-type, Nittobo, Tokyo, Japan); the intra- and inter-assay coefficient of variation for this assay ranged from 0.6 to 1.6% and from 0.7 to 2.1%, respectively. Serum intact parathyroid hormone was measured using a chemiluminescent assay (Chemiluminescence Intact PTH 100T kit, Nichols Institute Diagnostics, San Juan Capistrano, CA).
Assessment of insulin sensitivity
We used the fasting glucose and insulin values to calculate the homeostasis model assessment index of insulin resistance (HOMA-IR) according to the following formula: HOMA-IR = [baseline glucose concentration (mmol/l) x baseline insulin concentration (µU/ml)/22.5)]. Blood was collected on a midweek non-dialysis day within 2 weeks before coronary stenting, for the measurement of HOMA-IR.
Statistical analysis
Values are expressed as mean±SD. The statistical analysis software system (SPSS for Windows, version 9.0J & 11.0J, SPSS Inc., Chicago, IL) was used for statistical analyses. Differences in continuous variables between groups were evaluated by Wilcoxon rank-sum test, and differences in categorical data between groups were evaluated by 
2 test. Difference in mean plasma adiponectin concentrations between before stenting and within 1–2 years after stenting was evaluated by paired Student's t-analysis. The associations of coronary in-stent restenosis with continuous or categorical variables were firstly analysed by using the univariate logistic regression model and the continuous or categorical variables that were related or tended to be related to the occurrence/absence of in-stent restenosis were further analysed by using multiple logistic regression models. As a measure of the relative risk for the occurrence of in-stent restenosis, the odds ratio and 95% CIs were calculated in order to summarize the effects of each covariate. All statistical tests were two-sided with a value for P<0.05 considered significant.
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Coronary in-stent restenosis
Follow-up coronary angiography revealed that in-stent restenosis occurred in 37 patients (52.1%) of 71 haemodialysis patients who had received coronary stenting. No patients had died between coronary stenting and follow-up angiography. In four of the 37 patients (10.8%), in-stent restenosis was diagnosed by coronary angiography before 6 months after stenting because of symptoms such as chest pain or discomfort. However, no angina symptoms were recognized in the other 33 patients with in-stent restenosis (89.2%) until the follow-up angiography 6 months after stenting. The angiographic and clinical characteristics in the non-restenosis (n = 34) and restenosis (n = 37) groups are summarized in Tables 1 and 2, respectively. Of the 71 patients who had undergone coronary stenting, 41 patients had received the rotational atherectomy at stenting because of severe plaque calcification. In-stent restenosis was found in 25 of all 41 patients (61%) in the rotational atherectomy group: 12 of 18 in diabetic patients (67%) and 13 of 23 in non-diabetic patients (57%). In the balloon angioplasty and stenting group, in-stent restenosis was found in 12 of all 30 patients (40%); nine of 21 in diabetic patients (43%) and three of nine in non-diabetic patients (33%).
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Differences in clinical factors between patients with or without restenosis
Patients with restenosis had higher HOMA-IR [Figure 1B; 4.86±1.81 mM·µU/ml (n = 37) vs 3.35±1.49 mM µU/ml (n = 34); P = 0.0003], diastolic blood pressure before dialysis, blood haemoglobin, serum triglyceride concentration and plasma fasting immunoreactive insulin concentration (Table 2). Serum HDL–cholesterol concentration was lower in patients with restenosis than in patients without restenosis. The mean serum CRP concentration before stenting did not differ between patients with or without in-stent restenosis. The incidences of use of the drugs that may affect the cardiovascular system did not differ between patients with or without in-stent restenosis. The mean plasma adiponectin concentration before stenting was 16.2±13.0 µg/ml in all of the haemodialysis subjects, and patients with restenosis had a lower mean plasma adiponectin concentration than those without [Figure 1A; 6.2±2.2 µg/ml (2.1–10.4 µg/ml; n = 37) vs 27.2±10.8 µg/ml (17.9–79.8 µg/ml; n = 34); P = 0.0001]; plasma adiponectin concentrations in patients without restenosis were higher than the mean value in all haemodialysis patients. The overlap of the distribution of adiponectin concentrations was not found between the patients with or without restenosis. The plasma adiponectin concentration did not differ between female and male patients [16.74±17.78 µg/ml (n = 19) vs 16.02±10.97 µg/ml (n = 52)], and was lower in patients with restenosis than in those without in both female and male haemodialysis patients [female: 6.37±2.69 µg/ml (n = 11) vs 31.01±20.03 µg/ml (n = 8), P = 0.0008; male: 6.09±2.04 µg/ml (n = 26) vs 25.96±6.00 µg/ml (n = 26), P = 0.0001]. The mean plasma adiponectin concentrations did not differ between before coronary stenting and 1–2 years after stenting in patients with in-stent restenosis (6.2±2.2 µg/ml vs 6.4±2.4 µg/ml, n = 37) and in patients without restenosis (27.2±10.8 µg/ml vs 25.6±8.4 µg/ml, n = 34). On the other hand, the plasma IL-10 concentration before stenting did not differ between patients with or without restenosis [27.1±7.1 pg/ml [n = 37] vs 24.3±6.5 pg/ml [n = 34]). There were no significant differences in gender, age, haemodialysis duration and coronary risk factors including systolic hypertension, smoking, obesity, DM, or serum concentrations of calcium, inorganic phosphorus, total protein, albumin and total cholesterol between patients with or without restenosis (Table 2).
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Logistic analysis of coronary in-stent restenosis
In univariate logistic analysis, HOMA-IR, blood haemoglobin, serum concentrations of HDL–cholesterol or triglycerides, plasma fasting immunoreactive insulin concentration and plasma adiponectin concentration were significantly associated with the occurrence of coronary in-stent restenosis, and diastolic blood pressure before dialysis and rotational atherectomy prior to stenting tended to be associated with in-stent restenosis (Table 3). Classic coronary risk factors such as systolic hypertension, smoking, total cholesterol, DM or obesity were not related to in-stent restenosis. In addition, coronary angiographic parameters determined by quantitative analysis were not related to the occurrence of in-stent restenosis. On the other hand, in multiple logistic regression analysis among the variables that were related or tended to be related with the occurrence/absence of in-stent restenosis, only the plasma adiponectin concentration measured before stenting was associated with the occurrence of coronary in-stent restenosis (Table 4). The odds ratio of increase in 1 µg/ml of plasma adiponectin concentration for having restenosis was 0.651 (P = 0.001, 95%(CI): 0.506–0.839). In the coronary angiographic analysis, the plasma adiponectin concentration correlated positively with net gain (r = 0.691, P = 0.0001, n = 71), and inversely with late loss (r = –0.650, P = 0.0001, n = 71) and diameter stenosis at follow-up (r = –0.686, P = 0.0001, n = 71).
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Discussion |
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In-stent restenosis due to intimal hyperplasia occurs after percutaneous coronary intervention with stent implantation in 10–40% of cases at 6 months, depending on various clinical, angiographic and procedural features. Mechanisms involved in the pathogenesis of in-stent restenosis include platelets and inflammatory cell activation due to procedural vascular injury with subsequent local release of cytokines and growth factors, leukocyte adherence, smooth muscle cell proliferation and extracellular matrix synthesis [10]. Both retrospective and prospective studies have shown that impaired brachial artery flow-mediated dilation is independently associated with the occurrence of restenosis in patients undergoing percutaneous coronary intervention using bare-metal stents [11,12]. Since brachial artery flow-mediated dilation depends largely on nitric oxide synthesis and local release of other endothelium-derived factors such as prostacyclin or bradykinin, endothelial dysfunction is thought to be deeply involved in the genesis of in-stent restenosis. Local production by dysfunctional endothelium of pro-inflammatory cytokines, growth factors, tumour necrosis factor (TNF), adhesion molecules and chaemotactic factors seems to play a role in in-stent restenosis via activation of local inflammatory pathways, enhanced migration of smooth muscle cells and intimal hyperplasia.
Although a physiological role of adiponectin has not been fully established, previous experimental data indicate that adiponectin has anti-atherogenic and anti-inflammatory properties. In cultured human smooth muscle cells, adiponectin attenuates DNA synthesis induced by growth factors such as platelet-derived growth factor, heparin-binding epidermal growth factor and basic fibroblast growth factor [13]. Adiponectin also inhibits the expression of intracellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin in endothelial cells in vitro, and prevents the adhesion of monocytes to TNF-
stimulated human aortic endothelial cells [6,14]. Adiponectin reportedly has an inhibitory effect on the proliferation of myelomonocytic progenitors, as well as on phagocytic activity and TNF- production by macrophages [15]. Adiponectin-deficient mice have severe neointimal thickening, and deficiency of plasma adiponectin is associated with excess neointimal formation in injured arteries using a spring wire [16,17]. Therefore, circulating adiponcetin is expected to play a role in prevention to coronary in-stent restenosis by inhibiting the pathologic responses induced by dysfunctional endothelium to the inflammatory stimuli such as coronary stenting.
Zoccali et al. [7] reported that circulating adiponectin concentrations are 2.5 times higher among dialysis patients than among healthy individuals. Changes in clearance rates or other unknown factors are thought to account for the elevated circulating concentrations in ESRD patients, although renal metabolism of adiponectin has not been determined. In their study, the mean plasma adiponectin concentration was 15.0±7.7 µg/ml in haemodialysis patients and 6.3±2.0 µg/ml in healthy subjects. In the study of Chudek et al. [18], the mean plasma adiponectin concentrations were 20.8±8.3 µg/ml in maintenance haemodialysis patients and 8.7±4.8 µg/ml in healthy subjects. Further, Guebre-Egziabher et al. [19] reported that the mean adiponectin concentrations were 9.8±2.9 µg/ml in male patients and 16.6±5.0 µg/ml in female patients, who had early stages of chronic kidney diseases. On the other hand, ESRD patients undergoing continuous ambulatory peritoneal dialysis reportedly had higher mean plasma adiponectin concentrations in Malyszko et al.'s [8] study (36.1±23.2 µg/ml). Since the mean plasma adiponectin concentration in healthy individuals measured in our ELISA method (6.4±2.1 µg/ml, n = 20) was almost the same as those measured by Zoccali et al. [7] or Chudek et al. [18], plasma adiponectin concentrations determined in this study seem to be as reliable as those in their studies. The mean adiponectin concentration in all of the ESRD patients in the present study was 16.2±13.0 µg/ml, which was similar to that reported by Zoccali et al. However, in our present study, plasma adiponectin concentrations were lower in patients with in-stent restenosis (6.6±3.4 µg/ml), whereas plasma adiponectin concentrations were much higher in patients without in-stent restenosis (27.3±10.9 µg/ml). On the other hand, Shimada et al. [20] reported that circulating concentrations of adiponectin were not related to the occurrence of in-stent restenosis after percutaneous coronary intervention in non-ESRD patients. The plasma adiponectin concentrations in their study were 5.9±3.6 µg/ml for the non-restenosis group and 5.7±2.8 µg/ml for the restenosis group, both of which were similar to the values in ESRD patients having in-stent restenosis in the present study. No overlap of the distribution of plasma adiponectin concentrations was found between the restenosis (2.1–10.4 µg/ml) and non-restenosis (17.9–79.8 µg/ml) groups in the present study. These findings indicate that circulating adiponectin concentrations higher than the mean value among dialysis patients may be necessary for inhibiting the neointimal formation after coronary stenting in maintenance haemodialysis patients.
Our study has several potential limitations. Firstly, plasma adiponectin concentrations had been measured before stenting, but not checked between coronary stenting and follow-up angiography. Therefore, we cannot deny the possibility that plasma adiponectin concentrations may have changed after coronary stenting. However, plasma adiponectin concentrations are expected not to have significantly altered even after coronary stenting, because the mean plasma adiponectin concentrations did not differ between before stenting and 1–2 years after stenting in patients with in-stent restenosis as well as those without restenosis. Secondly, the incidence of coronary in-stent restenosis was higher in the present study than in the previous studies of ESRD patients; 19–21% in Hase et al.'s study [21] and 31% in Le Feuvre et al.'s study [2]. Although we cannot clearly explain the higher incidence of coronary in-stent restenosis of the present study, clinical characteristics in the study participants such as high mean age (64.9±8.9 years), relatively high prevalence of DM (54.9%; 39/71), or very low use of statins may have been involved in the higher restenosis rate in our study. The relatively high incidence of complex coronary lesions such as type B2 or C (49.3%; 35/71) was also likely to be related with the higher restenosis rate in our study. Thirdly, this study was performed with traditional bare-metal stents; therefore, our present data cannot be directly extrapolated to patients receiving drug-eluting stents. Fourthly, since the number of patients was small, the quality of data does not allow us to draw conclusions with the same confidence like a large-scale trial.
In conclusion, the circulating adiponectin concentration before coronary stenting is expected to be associated with in-stent restenosis after percutaneous coronary intervention in ESRD patients undergoing maintenance haemodialysis. The lower circulating adiponectin concentrations which are the same levels as non-ESRD subjects are likely to indicate the possible occurrence of coronary in-stent restenosis in haemodialysis patients, although we do not have direct evidence to prove it. On the other hand, the circulating adiponectin concentrations higher than the mean value in dialysis patients may play a protective role for the occurrence of in-stent restenosis possibly by inhibiting the intimal hyperplasia after coronary stenting. Possible early identification of patients with lower or higher risk of restenosis after coronary in-stent restenosis by plasma adiponectin concentrations would affect the timing of follow-up coronary angiography and contribute to protection of haemodialysis patients from secondary cardiac events caused by restenosis such as acute myocardial ischaemia or congestive heart failure. ESRD patients are thought to have potential endothelial dysfunction; therefore, the role of circulating adiponectin in inhibiting the pathologic responses induced by dysfunctional endothelium may be greater in dialysis patients than non-ESRD patients. Results obtained from the present study indicate that more attention should be paid to the relationship between plasma adiponectin concentrations and coronary in-stent restenosis in ESRD patients undergoing maintenance haemodialysis.
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Acknowledgments |
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The authors deeply appreciate the staff of the Department of Interventional Cardiology at the Kyoto Second Red Cross Hospital for coronary angiography and percutaneous coronary intervention. The authors also thank Mr Masao Shimotsuma and Mr Masaji Ushiyama in the Laboratory Department of the Kyoto Prefectural University of Medicine regarding the technical assistance for measuring plasma adiponectin and interleukin-10 concentrations.
Conflict of interest statement. We declare that we have no conflict of interest on this study.
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[Abstract/Free Full Text]
Accepted in revised form: 3. 1.06
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