Differences in the inflammatory response between patients with and those without diabetes mellitus after coronary stenting.
ABSTRACT Patients with diabetes mellitus who undergo coronary stenting are at increased risk of restenosis. It is known that inflammation plays a crucial role in restenosis.
We assessed the inflammatory response to elective coronary stent implantation (CSI) in stable diabetic and nondiabetic patients.
C-reactive protein (CRP), soluble (s) P-selectin, and soluble intercellular adhesion molecule (sICAM)-1 plasma levels were determined in diabetic (n = 51) and nondiabetic (n = 56) patients before and 48 hours and 4 weeks after bare metal stenting (BMS).
Diabetic patients presented significantly higher inflammatory marker levels before and after CSI. Nonetheless, diabetic and nondiabetic patients had postintervention peak of markers attained within 48 hours. At baseline, diabetic and nondiabetic patients presented CRP levels of 5.0 +/- 20.1 (P < or = 0.04) and 3.8 +/- 9.4 microg/ml and, at 48 hours postintervention, 22.0 +/- 20.2 (P = 0.001; P = 0.002) and 12.6 +/- 11.3 (P < or = 0.0001) microg/ml. Regarding sP-selectin, diabetic and nondiabetic patients obtained levels of, at baseline, 182 +/- 118 (P < or = 0.04) and 105 +/- 48 ng/ml and, at 48 hours, 455 +/- 290 (P = 0.001; P < or = 0.01) and 215 +/- 120 (P < or = 0.04) ng/ml. For diabetic and nondiabetic patients, sICAM-1 levels were, at baseline, 248 +/- 98 (P < or = 0.04) and 199 +/- 94 ng/ml and, at 48 hours, 601 +/- 201 (P = 0.001; P < or = 0.01) and 283 +/- 220 (P = 0.001) ng/ml. At 4 weeks, for all patients, markers returned to preprocedural levels: versus before PCI: *P = 0.001, (section sign)P < or = 0.0001; versus nondiabetic patients: (#)P < or = 0.04, (paragraph sign)P = 0.002, (Upsilon)P < or = 0.01.
Diabetic and nondiabetic patients exhibited a temporal inflammatory response after an elective BMS. However, diabetic patients present higher preprocedural levels of CRP, sP-selectin, and sICAM-1 and reveal a further exacerbated inflammatory response after intervention. The differences in inflammatory response may have implications in restenosis within these two sets of patients.
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ABSTRACT: BACKGROUND: HIGH SENSITIVITY C-REACTIVE PROTEIN (HSCRP) HAS BEEN IDENTIFIED AS A PREDICTOR OF ADVERSE CARDIOVASCULAR OUTCOMES. WHETHER HSCRP IS A USEFUL BIOMARKER FOR RISK STRATIFICATION IN CONTEMPORARY PERCUTANEOUS CORONARY INTERVENTION REMAINS UNKNOWN.METHODS AND RESULTS: WE CONDUCTED A PROSPECTIVE STUDY AMONG 513 PATIENTS UNDERGOING NON-EMERGENCY PERCUTANEOUS CORONARY INTERVENTION AND EXAMINED THE RELATIONSHIP BETWEEN PRE- AND POSTPROCEDURAL HSCRP LEVELS AND OUTCOMES. THE PATIENTS WERE DIVIDED ACCORDING TO THE MEDIAN PREPROCEDURAL HSCRP LEVEL (0.3 MG/DL). PATIENTS WITH HIGH HSCRP HAD SIGNIFICANTLY MORE ADVERSE CLINICAL CHARACTERISTICS. PREPROCEDURAL HSCRP LEVEL WAS AN INDEPENDENT PREDICTOR OF PERIPROCEDURAL MYOCARDIAL INFARCTION (ODDS RATIO PER DOUBLING OF HSCRP 1.15 [95% CONFIDENCE INTERVAL, 1.011.31]; P=0.038). UNADJUSTED MORTALITY (29.7% VERSUS 9.9%; P0.001) AND THE COMBINED END POINT OF DEATH OR MYOCARDIAL INFARCTION (36.5% VERSUS 16.0%, P0.001) DURING A FOLLOW-UP OF 5 YEARS WERE MARKEDLY GREATER IN PATIENTS WITH HIGH PREPROCEDURAL HSCRP. SIMILAR RELATIONSHIPS EXISTED FOR POSTPROCEDURAL HSCRP. HOWEVER, AFTER MULTIVARIABLE ADJUSTMENT, NEITHER PREPROCEDURAL HSCRP LEVELS (HAZARD RATIO PER DOUBLING 0.96 [0.92, 1.00]; P=0.066) NOR POSTPROCEDURAL HSCRP LEVELS (HAZARD RATIO 0.98 [0.94, 1.02]; P=0.27) WERE SIGNIFICANTLY ASSOCIATED WITH MORTALITY.CONCLUSIONS: High hsCRP is associated with a greater independent risk of periprocedural myocardial infarction, as defined by the universal definition, but is not an independent determinant of mortality after percutaneous coronary intervention. Our findings suggest that routine measurement of hsCRP in patients undergoing percutaneous coronary intervention in contemporary practice is unlikely to be beneficial.Circulation Cardiovascular Interventions 12/2012; 5(6). DOI:10.1161/CIRCINTERVENTIONS.112.972182 · 6.98 Impact Factor
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ABSTRACT: Endothelial colony-forming cells (ECFCs) isolated from peripheral blood are a highly promising cell source for a wide range of applications, including tissue engineering, in vivo vasculogenesis and anti-cancer therapeutics. Because of the potential for clinical translation, it is increasingly important to isolate and study ECFCs from patient cohorts that may benefit from such technologies. The primary objective of this investigation was to determine whether ECFCs could be obtained from patients with chronic kidney disease and diabetes (CKD-DM), using techniques that can be readily applied in the clinical setting. We also investigated the impact of autologous vs commercially available (i.e. allogeneic) human serum on ECFCs isolation. Surprisingly, the efficacy of ECFCs isolation from the CKD-DM group was comparable to a healthy control group when autologous serum was used. In contrast, substitution of allogeneic serum reduced ECFCs isolation in CKD-DM and control groups. In characterization studies, ECFCs were positive for several endothelial cell markers. ECFCs from the CKD-DM group were sensitive to inflammatory activation but their cellular proliferation was compromised. The concentrations of IL-4 and IL-8 were significantly increased in allogeneic serum, which induced a pro-inflammatory environment, including the release of IL-4, IL-6, IL-8 and MCP-1 into the conditioned media of cell cultures. Taken together, these data support further investigation into the use of autologous serum and cells for ECFC-based therapeutics and underscore the importance of the cytokine content in serum used for ECFCs isolation. Copyright © 2012 John Wiley & Sons, Ltd.Journal of Tissue Engineering and Regenerative Medicine 09/2014; 8(9). DOI:10.1002/term.1580 · 4.43 Impact Factor
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ABSTRACT: It is widely accepted that diabetes mellitus (DM) impairs endothelial nitric oxide synthase activity as well as enhances the production of reactive oxygen species, thus resulting in diminished nitric oxide bioavailability and the consequent pro-atherogenetic alterations. Important biomarkers of the vasculature are related to endothelial dysfunction, to inflammatory and coagulation processes, and to oxidative stress in DM. Several therapeutic strategies might exert favorable effects on the vasculature of diabetic patients, such as insulin analogues, antihypertensive agents, statins, and hypoglycemic agents, whereas in spite of the prominent role of oxidative stress in diabetes, antioxidant therapy remains controversial. The use of specific biomarkers related to vascular function could be a useful therapeutic approach in such patients.Journal of the American College of Cardiology 08/2013; 62(8):667-76. DOI:10.1016/j.jacc.2013.03.089 · 15.34 Impact Factor