- Email: [email protected]
133: Predictive value of coronary artery stenoses and C-reactive protein levels in patients with stable coronary artery disease
Journal of Clinical Lipidology, Vol 2, No 5S, October 2008
patients with angina and negative cTnT. Further investigation is required in order to evaluate whether IMA provides information about the risk of an oncoming acute ischemic event. Funding: none
132 INTERACTIONS OF GENETIC MARKERS OF INFLAMMATION AND MULTIPLE RISK FACTORS IN CAD (CORONARY ARTERY DISEASE) C. Boiocchi1, C. Falcone2, S. Bozzini1, A. Pirotta1, M. Cuccia1. 1Department of Genetic and Microbiology, University of Pavia, Pavia, Italy, 2 CIRMC University of Pavia, Pavia, Italy
133 PREDICTIVE VALUE OF CORONARY ARTERY STENOSES AND C-REACTIVE PROTEIN LEVELS IN PATIENTS WITH STABLE CORONARY ARTERY DISEASE P. Avanzas1, R. Arroyo-Espliguero2, J. Quiles3, J.C. Kaski4. 1Hospital Universitario Central de Asturias, Department of Cardiology, Oviedo, Spain, 2Hospital de Guadalajara, Department of Cardiology, Guadalajara, Spain, 3Hospital de San Juan, Department of Cardiology, Alicante, Spain, 4 St. George´s Hospital, University of London, London, United Kingdom
Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous elements in the large arteries; it constitute the single most important contributor to the growing burden of cardiovascular disease. Starting from these considerations, that highlight the strong inflammatory component involved in formation and progression of the atherosclerotic plaque, it was investigated the possible involvement of polymorphisms of molecules known for playing a crucial role in the inflammatory process, in order to identify the interaction of specific genes and factors involved in the early predisposition, in the amplification and in chronicity of the phenomena behind the inflammatory process: RAGE -374 T/A; -429 T/C; +82 G/S; TNF: -308 G/A; TNF -857 G/A and its two receptors: TNFR1 MspA1 I; TNFR2 NlaIII; TLR4 Asp299Gly and for complement receptors: CR1 Pro1827Arg; CR2 Glu1003Ala). In this study a case-control investigation was performed on 800 patients and 240 healthy controls matched for age, sex and ethnicity,genotype and allele frequencies obtained were compared with healthy controls. Data were then analyzed according to the various risk factors for atherosclerosis: age of onset of clinical symptoms, body mass index, hypertension, diabetes, hypercholesterolemia, family history of CAD, gender and smoking habits. Multivariated analysis of these risk factors and related polymorphisms will be presented.
Objective: We sought to assess the prognostic value of non obstructive coronary stenoses and Creactive protein (CRP) levels in patients with chronic stable angina (CSA). Methods: We studied 790 consecutive CSA patients who underwent coronary arteriography. High sensitivity CRP was measured and coronary angiograms were scored according to Sullivan et al: vessel score (number of coronary arteries showing at least 50% reduction in lumen diameter) and extension score (proportion of the coronary artery tree showing angiographically detectable atheroma). Patients were followed up for one year. Results: 368 patients (46.6%) underwent revascularization. 71 patients (9%) had at least one of the events comprised in the combined study endpoint (unstable angina, myocardial infarction and cardiac death). Patients who suffered events had a significantly higher vessel score (n) (2.0[2.0-3.0] vs. 2.0[1.0-2.0], P<0.001), extension score (%) (23.5 [17-34.5] vs. 16.0 [6.0-27.0], P<0.001) and CRP levels (mg/L) (3.0[1.8-7.2] vs. 2.3 [1.1-4.7], P=0.001) compared to patients without events. Multivariate analysis showed extension score (OR 5.3 [2.8 to 10.3] CI 95%; P<0.001), revascularization (OR 0.26 [0.14 to 0.48] CI 95%; P<0.001) and CRP levels (OR 1.9 [1.1 to 3.2] CI 95%; P=0.03), but not vessel score (p=0.1), to be independent predictors of the combined end-point. Conclusions: In patients with CSA, independently of revascularization, extension score and CRP levels predict cardiac adverse events, regardless of the presence or absence of flow limiting coronary lesions.
Funding: none
Funding: none
S61
patients with angina and negative cTnT. Further investigation is required in order to evaluate whether IMA provides information about the risk of an oncoming acute ischemic event. Funding: none
132 INTERACTIONS OF GENETIC MARKERS OF INFLAMMATION AND MULTIPLE RISK FACTORS IN CAD (CORONARY ARTERY DISEASE) C. Boiocchi1, C. Falcone2, S. Bozzini1, A. Pirotta1, M. Cuccia1. 1Department of Genetic and Microbiology, University of Pavia, Pavia, Italy, 2 CIRMC University of Pavia, Pavia, Italy
133 PREDICTIVE VALUE OF CORONARY ARTERY STENOSES AND C-REACTIVE PROTEIN LEVELS IN PATIENTS WITH STABLE CORONARY ARTERY DISEASE P. Avanzas1, R. Arroyo-Espliguero2, J. Quiles3, J.C. Kaski4. 1Hospital Universitario Central de Asturias, Department of Cardiology, Oviedo, Spain, 2Hospital de Guadalajara, Department of Cardiology, Guadalajara, Spain, 3Hospital de San Juan, Department of Cardiology, Alicante, Spain, 4 St. George´s Hospital, University of London, London, United Kingdom
Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous elements in the large arteries; it constitute the single most important contributor to the growing burden of cardiovascular disease. Starting from these considerations, that highlight the strong inflammatory component involved in formation and progression of the atherosclerotic plaque, it was investigated the possible involvement of polymorphisms of molecules known for playing a crucial role in the inflammatory process, in order to identify the interaction of specific genes and factors involved in the early predisposition, in the amplification and in chronicity of the phenomena behind the inflammatory process: RAGE -374 T/A; -429 T/C; +82 G/S; TNF: -308 G/A; TNF -857 G/A and its two receptors: TNFR1 MspA1 I; TNFR2 NlaIII; TLR4 Asp299Gly and for complement receptors: CR1 Pro1827Arg; CR2 Glu1003Ala). In this study a case-control investigation was performed on 800 patients and 240 healthy controls matched for age, sex and ethnicity,genotype and allele frequencies obtained were compared with healthy controls. Data were then analyzed according to the various risk factors for atherosclerosis: age of onset of clinical symptoms, body mass index, hypertension, diabetes, hypercholesterolemia, family history of CAD, gender and smoking habits. Multivariated analysis of these risk factors and related polymorphisms will be presented.
Objective: We sought to assess the prognostic value of non obstructive coronary stenoses and Creactive protein (CRP) levels in patients with chronic stable angina (CSA). Methods: We studied 790 consecutive CSA patients who underwent coronary arteriography. High sensitivity CRP was measured and coronary angiograms were scored according to Sullivan et al: vessel score (number of coronary arteries showing at least 50% reduction in lumen diameter) and extension score (proportion of the coronary artery tree showing angiographically detectable atheroma). Patients were followed up for one year. Results: 368 patients (46.6%) underwent revascularization. 71 patients (9%) had at least one of the events comprised in the combined study endpoint (unstable angina, myocardial infarction and cardiac death). Patients who suffered events had a significantly higher vessel score (n) (2.0[2.0-3.0] vs. 2.0[1.0-2.0], P<0.001), extension score (%) (23.5 [17-34.5] vs. 16.0 [6.0-27.0], P<0.001) and CRP levels (mg/L) (3.0[1.8-7.2] vs. 2.3 [1.1-4.7], P=0.001) compared to patients without events. Multivariate analysis showed extension score (OR 5.3 [2.8 to 10.3] CI 95%; P<0.001), revascularization (OR 0.26 [0.14 to 0.48] CI 95%; P<0.001) and CRP levels (OR 1.9 [1.1 to 3.2] CI 95%; P=0.03), but not vessel score (p=0.1), to be independent predictors of the combined end-point. Conclusions: In patients with CSA, independently of revascularization, extension score and CRP levels predict cardiac adverse events, regardless of the presence or absence of flow limiting coronary lesions.
Funding: none
Funding: none
S61