Prevalence and prognostic implication of restenosis or dilatation at the aortic coarctation repair site assessed by cardiovascular MRI in adult patients late after coarctation repair.

BACKGROUND: Cardiovascular magnetic resonance (CMR) is ideal for assessing patients with repaired aortic coarctation (CoA). Little is known on the relation between long-term complications of CoA repair as assessed by CMR and clinical outcome. We examined the prevalence of restenosis and dilatation at the repair site and the long-term outcome in patients with repaired CoA. METHODS AND RESULTS: CMR imaging and clinical data for adult CoA patients (247 patients aged 33.0 ± 12.8 years, 60% male), were analyzed. The diameter of the aorta at the repair site was measured on CMR and its ratio to the aortic diameter at the diaphragm (repair site-diaphragm ratio, RDR) was calculated. Restenosis (RDR≤70%) was present in 31% of patients (and significant in 9% [RDR<50%]), and dilatation (RDR>150%) in 13.0%. A discrete aneurysm at the repair site was observed in 9%. Restenosis was more likely after resection and end-end anastomosis, whereas dilatation after patch repair. Systemic hypertension was present in 69% of patients. Of the hypertensive patients, blood pressure (133 ± 20/73 ± 10 mm Hg) was well controlled in 93% with antihypertensive therapy. Mortality rate over a median length of 5.9 years was low (0.69% per year, 95% CI: 0.33-1.26), but significantly higher than age-matched healthy controls (standardised mortality ratio 2.86, CI 1.43-5.72, p<0.001). CONCLUSION: Restenosis or dilatation at the CoA repair site as assessed by CMR is not uncommon. Medium term survival remains good, however, albeit lower than in the general population. Life-long follow-up and optimal blood pressure control are likely to secure a good longer term outlook in these patients.

Lower epicardial adipose tissue adiponectin in patients with metabolic syndrome.

BACKGROUND: Adiponectin is an anti-atherogenic insulin-sensitizer hormone whose plasma concentration is lower in patients with metabolic syndrome (MS). Visceral adiposity, including epicardial adipose tissue (EAT), is closely related to the development of MS and coronary artery disease (CAD). We sought to study whether EAT and subcutaneous adipose tissue (SAT) adiponectin mRNA levels are similar in patients with and without MS. METHODS: EAT, SAT and blood samples were collected from patients undergoing elective cardiac surgery, for revascularization (n=19) or other procedures (n=27). Plasma adiponectin was measured using ELISA. mRNA was purified and adiponectin mRNA quantified by real time RT-PCR. RESULTS: Mean (SD) age was 71.6 (9.6) years. Patients who met Adult Treatment Panel III MS criteria (n=29) presented lower plasma adiponectin concentrations (11.2 (7.4) vs. 19.6 (8.4) mg/l, P=0.004), lower EAT adiponectin mRNA (12.7 (3.0) vs. 15.1 (3.7) a.u., P=0.029) and similar SAT adiponectin mRNA levels (13.7 (4.2) vs. 15.6 (5.7) a.u., P=0.25) than those without MS. After adjusting for age, sex, CAD and heart failure, the association with MS remained statistically significant for plasma adiponectin (OR 0.862 (0.762-0.974)), was of borderline significance for EAT adiponectin mRNA (OR 0.796 (0.630-1.005)) and not significant for SAT adiponectin mRNA (OR 0.958 (0.818-1.122)). Patients in the lower quartiles of EAT adiponectin mRNA and plasma adiponectin presented a higher mean of components of the MS. CONCLUSIONS: Subjects with MS present lower EAT adiponectin mRNA levels than those without MS, whereas SAT adiponectin mRNA levels do not seem to differ between both groups. EAT might be the link between MS and its atherothrombotic cardiac complications.

Receptor for advanced glycation end-products expression in subcutaneous adipose tissue is related to coronary artery disease.

OBJECTIVE: Obesity, a risk factor for coronary artery disease (CAD), is associated with inflammation and reactive oxygen species (ROS) production, while advanced glycation end-products, through their receptor (AGER or RAGE), play an important role on these processes. The aim of this study was to analyze the expression levels of RAGE, NADPH oxidase subunits, and catalase in adipose tissue in relation with CAD. DESIGN AND METHODS: Patients undergoing heart surgery were included in two groups: with and without CAD. Epicardial adipose tissue (EAT) and subcutaneous adipose tissue (SAT) biopsies were analyzed for gene expression by RT-quantitative PCR, immunohistochemistry, or western blot. RESULTS: RAGE mRNA and protein expression in SAT from patients with CAD was lower than in patients without CAD. However, there was no change in EAT from patients with or without CAD. P22-PHOX and RAGE gene expression were higher in EAT than in SAT, whereas catalase mRNA levels were lower. NADPH oxidase subunits and catalase mRNA expression were not influenced by CAD. Whereas NADPH oxidase-dependent oxidative response of SAT and EAT to lipid circulating levels could be different; glycemic levels were not related with the analyzed genes expression. CONCLUSIONS: This study demonstrates that RAGE expression in SAT, but not in EAT, is down-regulated in patients with CAD with respect to those without CAD. Although changes were not observed for NADPH oxidase subunits or catalase expression between CAD and non-CAD patients, a possible relationship between ROS production and RAGE expression in adipose tissues cannot be ruled out.

Diabetic and nondiabetic patients express similar adipose tissue adiponectin and leptin levels.

OBJECTIVE: Epicardial adipose tissue (EAT) is an interesting visceral fat pad with a particular location. EAT and subcutaneous adipose tissue (SAT) produce a wide range of adipokines. Some of them, including adiponectin and leptin, can influence the risk of development of diabetes and other associated metabolic and cardiovascular conditions. We sought to assess whether EAT and SAT adiponectin and leptin expression levels are different in diabetic patients with respect to nondiabetic subjects. SUBJECTS AND METHODS: We collected samples of EAT from 120 patients and samples of SAT from 88 of the same group of patients undergoing elective cardiac surgery for coronary artery bypass grafting (n=69) or other procedures (n=51). After RNA isolation, adiponectin and leptin expression levels were analyzed by real-time reverse transcriptase PCR. Plasma levels were determined in small subsamples of subjects. Baseline clinical and treatment data were obtained from medical records. RESULTS: A total of 45 diabetic and 75 nondiabetic subjects were included in the study. Mean (s.d.) age was 70.1 (7.8) years and there were 32% women. EAT and SAT adiponectin and leptin mRNA expression levels were similar in the diabetic and the nondiabetic groups (EAT adiponectin 14.4 (4.3) vs 14.6 (3.4) arbitrary units (a.u.), P=0.79; SAT adiponectin 15.6 (4.7) vs 15.1 (3.9), P=0.54; EAT leptin 9.3 (interquartile range 2.5) vs 9.5 (1.9) a.u., P=0.72; SAT leptin 9.9 (3.6) vs 10.0 (2.5) a.u., P=0.96). These findings persisted after stratification for sex and coronary artery disease. Logistic regression models including possible confounders and a combination of diabetes and impaired fasting glucose as a dependent variable led to similar results. Plasma adiponectin levels were lower in diabetic patients, whereas leptin levels showed a nonsignificant trend. CONCLUSION: Diabetic and nondiabetic subjects express similar EAT and SAT adiponectin and leptin levels. Counter-regulatory mechanisms of adiponectin and leptin expression in patients with established diabetes might partly account for these findings.

Epicardial adipose tissue expression of adiponectin is lower in patients with hypertension.

Low plasma adiponectin levels are related to a higher risk of development of metabolic and cardiovascular disorders, including hypertension (HT). To date, there have been no studies supporting the relationship between epicardial adipose tissue (EAT) expression of adiponectin and HT. We collected samples of EAT from 116 patients undergoing elective cardiac surgery, mostly for coronary artery bypass grafting (n = 54), valve surgery (n = 49) or both (n = 12). Samples of subcutaneous adipose tissue (SAT) were harvested from 85 patients. After RNA isolation, the expression of adiponectin was analysed by real-time retrotranscriptase (RT)-PCR. Baseline clinical data were obtained from medical records. The diagnosis of HT was established mostly by the patients' general physicians following current guidelines. We included 84 hypertensive and 32 non-hypertensive patients. Mean (+/-s.d.) age was 70.3+/-7.9 years. EAT expression levels of adiponectin were lower in hypertensives (14.0+/-3.6 vs 15.3+/-3.6 arbitrary units (a.u.), P = 0.06). This difference was statistically significant (odds ratio (OR) 0.828 per a.u., P = 0.020) after adjustment for age, gender, body mass index, diabetes mellitus, heart failure, coronary artery disease (CAD), total cholesterol and triglyceride levels. However, SAT adiponectin mRNA levels were similar in hypertensive and non-hypertensive patients (15.3+/-4.2 vs 15.3+/-5.0 a.u., P > 0.99). Adjustment for potential confounding factors hardly altered this result. Our findings indicate that EAT expression of adiponectin may be associated with HT status independently of CAD or other comorbidities, whereas SAT expression does not. These results support the hypothesis that EAT is actively implicated in global cardiovascular risk, describing its association with HT.