44 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 RISK FACTORS AND DIABETES EUROPEAN CARDIOVASCULAR DISEASE STATISTICS: THE EUROPEAN HEART HEALTH II (EUROHEART II) PROJECT N. Townsend 1 , M. Nichols 2 , P. Scarborough 1 , M. Rayner 1 1 Public Health, University of Oxford, Oxford, United Kingdom 2 Faculty of Health, Deakin University, Geelong, Australia Background: European Cardiovascular Disease Statistics 2012, part of the EuroHeart II project, is the most recent update in a series of comprehensive Europe-wide reports on the mortality, morbidity, treatment, risk factors and costs of cardiovascular disease (CVD) in Europe. Methods: The report draws on international data sources that provide comparable data across the greatest number of European countries. The 53 member states of the WHO European region were included in the definition of Europe. In addition, a new cost of disease study was carried out to estimate the total costs (direct and indirect) of CVD in the EU. Results: Every year, CVD causes over 4 million deaths in Europe (47% of all deaths), and 1.9 million in the EU (40%). There are important inequalities between countries in mortality, morbidity, and in many risk factors that indicate the possible extent of the future burden. CVD is estimated to cost the EU almost EUR196 billion per year, of which 54% is due to direct costs to the health care system. Comparable data on incidence and prevalence of CVD are very limited, as are high quality data on important contributing risk factors, particularly diet and obesity. Conclusions: CVD remains the leading cause of death in Europe, and places a considerable burden on the health systems and economies of Europe. Further, the report highlights that there remain substantial gaps in the quality of data available to monitor and evaluate efforts to reduce CVD and CHD in Europe. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 45 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 RISK FACTORS AND DIABETES EFFECT OF FACTOR XIII POLYMORPHISMS ON THE RISK OF MYOCARDIAL INFARCTION Z. Bereczky 1 , Z.A. Mezei 1 , L. Balogh 2 , E. Katona 1 , E. Balogh 2 , I. Czuriga 2 , I. Édes 2 , L. Muszbek 3 1 Clinical Research Center, University of Debrecen Medical and Health Science Center, Debrecen, Hungary 2 Institute of Cardiology, University of Debrecen Medical and Health Science Center, Debrecen, Hungary 3 Clinical Research Center and Vascular Biology Thrombosis and Haemostasis Re- search Group of the Hungarian Academy of Sciences, University of Debrecen Medical and Health Science Center, Debrecen, Hungary Elevated factor XIII (FXIII) levels were demonstrated to be associated with increased risk of myocardial infarction (MI) in females, but not in males. Moreover, in our population FXIII-A Val34Leu polymorphism was protective against MI in patients with elevated fibrinogen levels. The role of FXIII-B subunit His95Arg and IntronK (nt29756C>G) polymorphisms in cardiovascular diseases has not been investigated, yet. In this study the above-mentioned polymorphisms were determined in 882 consecutive patients admitted for coronary angiography and in 1000 individuals representing the general Hungarian population. The rare allele frequencies of the His95Arg and IntronK (nt29756C>G) polymorphisms in the population were 0.08 and 0.15, respectively, which are similar to the results for Caucasians available in the HapMap database. The allele frequencies in the clinical controls (without MI and no significant coronary stenosis, n=276) did not differ significantly from the respective values in the general population. Individuals carrying the rare allele of FXIII-B IntronK polymorphism had significantly (p<0.0001) lower FXIII activity (94±21% vs. 103±21%) and FXIIIA 2 B 2 antigen (20.7±4.7 mg/L vs. 23.1±5.0 mg/L) levels compared to individuals homozygous for the frequent allele. FXIII-B IntronK polymorphism decreased the risk of MI by 60% in patients with elevated fibrinogen level (OR:0.37, 95% CI:0.17-0. 84, p=0.017). Moreover, an interactive effect was demonstrated between FXIII-B IntronK and FXIII-A Val34Leu polymorphisms; OR for MI in the case of double carriers with elevated fibrinogen was 0.031 (95% CI:0.01-0.21, p<0.0001). Our results confirm that the well-known effect of high fibrinogen level as a risk factor of MI is considerably modified by FXIII polymorphisms. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 46 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION Mitochondrial dynamics and mitophagy in the diabetic endothelium J.A. Vita 1 1 Medicine/Cardiology, Boston University, Boston, USA There is growing recognition that the vascular endothelium plays a central role in the regulation of vascular homeostasis. Abnormalities of endothelium-dependent vasodilatio n are detectable at all stages of atherosclerosis. In addition to loss of the bioactivity of endothelium-derived nitric oxide, these conditions are also associated with abnormalities of many other aspects of "endothelial function" including control of thrombosis, inflammation, and intimal growth. Patients with type 2 diabetes mellitus, obesity, and the metabolic syndrome, have increased risk for cardiovascular disease, and such patients also display endothelial dysfunction. Recent studies suggest links between m itochondria dysfunction and endothelial dysfunction in patients with type 2 diabetes mellitus. In par ticular, endothelial cells show evidence of increased mitochondrial fission and impaired autophagy compared to cells from age-matched healthy control subjects. Interventions that reduce excess fission under diabetic conditions tend to restore endothelial function, while inhibiting autophagy in healthy ce lls has a detrimental effect. Overall, these studies suggest that altered mitochondrial dynamics and loss of mitochondrial quality control contribute to endothelial dysfunction in patients with diabetes mellitus. The se findings may suggest new approaches for patient management. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 47 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION EFFECT OF DPP4-INHIBITOR ON VASCULAR FUNCTION IN PATIENTS WITH ISCHEMIC HEART DISEASE H. Adachi 1 , H. Kan 1 , J. Tomono 1 1 Dep. of Cardiology, Gunma Prefectural Cardiovascular Center, Maebashi Gunma, Japan Background and Purpose : It is well documented that vascular function is attenuated in patients with diabetes mellitus, and vascular dysfunction is the first step of coronary arteriosclerosis. Therefore, treatment for diabetes mellitus is important to prevent heart disease, however, it is not well studied what kind of pharmaceutical agent is optimal. Recently, DPP4 inhibitor can be used and many favorable effects on glycemic control are reported. Hereby, we planned to investigate the effect of DPP4 inhibitor on vascular function in ischemic heart disease (IHD) patients with diabetes mellitus. Method : Twenty-two IHD patients with mild diabetes mellitus were prescribed DPP4 inhibitor and assigned to Group D, and seventeen control patients without DPP4 inhibitor were to Group C. Flow mediated dilatation(FMD) and cardio-ankle vascular index(CAVI) were measured before administration and 6 months later. Results : HbA1c improved from 6.7±0.5% to 6.1±0.5 (p<0.01) in Group D, 6.3±0.6 to 6.5±0.5 (n.s.) in Group C. FMD and CAVI improved in Group D from 3.8±1.5 to 4.4±1,7(P<0.05), 9.3±0.9 to 8.9±0.8(P<0.05), respectively, while they failed to improve in Group C (3.9±2.3 to 4.2±2.1, 9.2±0.9 to 9.3 ±1.1, respectively). Even if we compared Group D with patients who showed improvement of glycemic control in Group C, neither FMD nor CAVI had shown any improvement. Conclusion : DPP4 inhibitor was revealed to improve vascular function regardless of glycemic control. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 48 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION VALUE AND LIMITATIONS OF HAGEN-POISEUILLE'S LAW IN THE ESTIMATION OF CORONARY WALL SHEAR STRESS. E. Wellnhofer 1 , J. Osman 2 , R. Mevert 2 , U. Kertzscher 2 , K. Affeld 2 , L. Goubergrits 2 1 Internal Medicine/Cardiology, German Heart Center Berlin, Berlin, Germany 2 Biofluidmechanics laboratory, Charité Universitätsmedizin Berlin, Berlin, Germany Background: Hagen-Poiseuille's law (HP) is widely used to estimate wall shear stress (WSS, WSS_HP) in medicine. Only flow rate and local vessel diameter are needed as input data. This advantage is achieved at the cost of accuracy due to simplified assumptions concerning vessel shape. Calculation of WSS by numerical integration of the Navier-Stokes differential equations for incompressible fluids (CFD, WSS_CFD) in three-dimensional finite element vessel reconstructions is more accurate, but also more demanding and time-consuming. Methods: Vascular trees from 17 right (RCA) and 15 left (LCA) coronary arteries stratified with respect to luminal remodeling (controls (C), aneurysmatic (AnCAD) and non-aneurysmatic coronary artery disease (CAD)) were reconstructed from biplane angiograms. Patient specific flow simulations were performed by CFD. Results for WSS_ CFD and WSS_HP were compared. Results: Mean WSS_CFD was 2.6±2.6 Pa and WSS_HP was 2.4±2.6 Pa. The mean difference was 0.23 (-0.09-0.58) was not significant and correlation was 0.942. There were major differences in distribution particularly in the low WSS range (minimum (min) WSS (r=0.494), percent area <0.4 Pa (A_.4) (r=0.811)), however. Min WSS is over-estimated (p=0.01) and A_0.4 WSS is under-estimated (p=0.01) significantly by HP. The estimation of maximum (max) WSS can be improved (r=0.933; r=0.816 with max WSS_HP) by estimation from mean WSS_HP using a factor of 2 in RCA and 3 in LCA due to a strong trend of max WSS_ CFD with mean WSS_CFD (different slopes in RCA/LCA). Conclusion: Estimation of WSS by Hagen Poiseuille's law performs well for mean and maximum values, but is a poor estimate in low WSS areas. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 49 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION ADIPONECTIN AND CARDIOVASCULAR RISK PREDICTION: STRATIFICATION OF CHEST PAIN PATIENTS BY A CLUSTER ANALYSIS C. Caselli 1 , M. Coceani 1 , T. Prescimone 1 , M. Cabiati 1 , A. Mazzarisi 1 , M. Schlueter 1 , S. Del Ry 1 , F. Cocci 1 , D. Giannessi 1 , P. Marraccini 1 1 CNR, Institute of Clinical Physiology Pisa, Pisa, Italy The new European guidelines on cardiovascular disease (CVD) prevention report the need to a better identification of population at high risk of CVD, the major ca use of premature death in Europe. With an unbiased statistical approach, we sought to identify clusters of patients with chest pain in order to better stratify their CVD risk. We prospectively included 202 consecutive patients with chest pain (63% males, age 62±12 yr) undergone to CT coronary angiography (CTCA). Patients were classified using K-means cluster analysis of clinical, imaging and bio-humoral data, selected for their relevance to CVD. The relevance of this classification was validated using presence of atherosclerosis (ATS) and significant stenosis (>50%) as assessed by CTCA. The most relevant patient classification resulted in three phenotypes distinguished according to Framingham Risk Score (FRS) and high molecular weigth (HMW) adiponectin plasma levels: Phenotype 1 (n=39) included subjects at very high CVD risk (FRS 34.6±9.7%) and ver y low HMW adiponectin (1.6±1.3 mg/mL); Phenotype 2 (n=124) subjects with lower FRS (11.8±5.4%) and hig her HMW (1.9±1.1); Phenotype 3 (n=16) the less severe patients (FRS 8.1±4.5%) with high levels of HMW (7.8±2.8). Presence and severity of ATS (existence of significant stenosis and number of diseased vessels) were significantly identified trough these phenotypes (Figure). By K-means cluster analysis, we identified three different CVD phenotypes allowing to stratify chest pain patients. Subjects within these phenotypes may required different diagnostic and therapeutic approach to improve their outcome.
ADIPONECTIN AND CARDIOVASCULAR RISK PREDICTION: STRATIFICATION OF CHEST PAIN PATIENTS BY A CLUSTER ANALYSIS
Caselli C;Prescimone T;Cabiati M;Mazzarisi A;Del Ry S;Giannessi D;Marraccini P
2013
Abstract
44 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 RISK FACTORS AND DIABETES EUROPEAN CARDIOVASCULAR DISEASE STATISTICS: THE EUROPEAN HEART HEALTH II (EUROHEART II) PROJECT N. Townsend 1 , M. Nichols 2 , P. Scarborough 1 , M. Rayner 1 1 Public Health, University of Oxford, Oxford, United Kingdom 2 Faculty of Health, Deakin University, Geelong, Australia Background: European Cardiovascular Disease Statistics 2012, part of the EuroHeart II project, is the most recent update in a series of comprehensive Europe-wide reports on the mortality, morbidity, treatment, risk factors and costs of cardiovascular disease (CVD) in Europe. Methods: The report draws on international data sources that provide comparable data across the greatest number of European countries. The 53 member states of the WHO European region were included in the definition of Europe. In addition, a new cost of disease study was carried out to estimate the total costs (direct and indirect) of CVD in the EU. Results: Every year, CVD causes over 4 million deaths in Europe (47% of all deaths), and 1.9 million in the EU (40%). There are important inequalities between countries in mortality, morbidity, and in many risk factors that indicate the possible extent of the future burden. CVD is estimated to cost the EU almost EUR196 billion per year, of which 54% is due to direct costs to the health care system. Comparable data on incidence and prevalence of CVD are very limited, as are high quality data on important contributing risk factors, particularly diet and obesity. Conclusions: CVD remains the leading cause of death in Europe, and places a considerable burden on the health systems and economies of Europe. Further, the report highlights that there remain substantial gaps in the quality of data available to monitor and evaluate efforts to reduce CVD and CHD in Europe. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 45 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 RISK FACTORS AND DIABETES EFFECT OF FACTOR XIII POLYMORPHISMS ON THE RISK OF MYOCARDIAL INFARCTION Z. Bereczky 1 , Z.A. Mezei 1 , L. Balogh 2 , E. Katona 1 , E. Balogh 2 , I. Czuriga 2 , I. Édes 2 , L. Muszbek 3 1 Clinical Research Center, University of Debrecen Medical and Health Science Center, Debrecen, Hungary 2 Institute of Cardiology, University of Debrecen Medical and Health Science Center, Debrecen, Hungary 3 Clinical Research Center and Vascular Biology Thrombosis and Haemostasis Re- search Group of the Hungarian Academy of Sciences, University of Debrecen Medical and Health Science Center, Debrecen, Hungary Elevated factor XIII (FXIII) levels were demonstrated to be associated with increased risk of myocardial infarction (MI) in females, but not in males. Moreover, in our population FXIII-A Val34Leu polymorphism was protective against MI in patients with elevated fibrinogen levels. The role of FXIII-B subunit His95Arg and IntronK (nt29756C>G) polymorphisms in cardiovascular diseases has not been investigated, yet. In this study the above-mentioned polymorphisms were determined in 882 consecutive patients admitted for coronary angiography and in 1000 individuals representing the general Hungarian population. The rare allele frequencies of the His95Arg and IntronK (nt29756C>G) polymorphisms in the population were 0.08 and 0.15, respectively, which are similar to the results for Caucasians available in the HapMap database. The allele frequencies in the clinical controls (without MI and no significant coronary stenosis, n=276) did not differ significantly from the respective values in the general population. Individuals carrying the rare allele of FXIII-B IntronK polymorphism had significantly (p<0.0001) lower FXIII activity (94±21% vs. 103±21%) and FXIIIA 2 B 2 antigen (20.7±4.7 mg/L vs. 23.1±5.0 mg/L) levels compared to individuals homozygous for the frequent allele. FXIII-B IntronK polymorphism decreased the risk of MI by 60% in patients with elevated fibrinogen level (OR:0.37, 95% CI:0.17-0. 84, p=0.017). Moreover, an interactive effect was demonstrated between FXIII-B IntronK and FXIII-A Val34Leu polymorphisms; OR for MI in the case of double carriers with elevated fibrinogen was 0.031 (95% CI:0.01-0.21, p<0.0001). Our results confirm that the well-known effect of high fibrinogen level as a risk factor of MI is considerably modified by FXIII polymorphisms. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 46 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION Mitochondrial dynamics and mitophagy in the diabetic endothelium J.A. Vita 1 1 Medicine/Cardiology, Boston University, Boston, USA There is growing recognition that the vascular endothelium plays a central role in the regulation of vascular homeostasis. Abnormalities of endothelium-dependent vasodilatio n are detectable at all stages of atherosclerosis. In addition to loss of the bioactivity of endothelium-derived nitric oxide, these conditions are also associated with abnormalities of many other aspects of "endothelial function" including control of thrombosis, inflammation, and intimal growth. Patients with type 2 diabetes mellitus, obesity, and the metabolic syndrome, have increased risk for cardiovascular disease, and such patients also display endothelial dysfunction. Recent studies suggest links between m itochondria dysfunction and endothelial dysfunction in patients with type 2 diabetes mellitus. In par ticular, endothelial cells show evidence of increased mitochondrial fission and impaired autophagy compared to cells from age-matched healthy control subjects. Interventions that reduce excess fission under diabetic conditions tend to restore endothelial function, while inhibiting autophagy in healthy ce lls has a detrimental effect. Overall, these studies suggest that altered mitochondrial dynamics and loss of mitochondrial quality control contribute to endothelial dysfunction in patients with diabetes mellitus. The se findings may suggest new approaches for patient management. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 47 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION EFFECT OF DPP4-INHIBITOR ON VASCULAR FUNCTION IN PATIENTS WITH ISCHEMIC HEART DISEASE H. Adachi 1 , H. Kan 1 , J. Tomono 1 1 Dep. of Cardiology, Gunma Prefectural Cardiovascular Center, Maebashi Gunma, Japan Background and Purpose : It is well documented that vascular function is attenuated in patients with diabetes mellitus, and vascular dysfunction is the first step of coronary arteriosclerosis. Therefore, treatment for diabetes mellitus is important to prevent heart disease, however, it is not well studied what kind of pharmaceutical agent is optimal. Recently, DPP4 inhibitor can be used and many favorable effects on glycemic control are reported. Hereby, we planned to investigate the effect of DPP4 inhibitor on vascular function in ischemic heart disease (IHD) patients with diabetes mellitus. Method : Twenty-two IHD patients with mild diabetes mellitus were prescribed DPP4 inhibitor and assigned to Group D, and seventeen control patients without DPP4 inhibitor were to Group C. Flow mediated dilatation(FMD) and cardio-ankle vascular index(CAVI) were measured before administration and 6 months later. Results : HbA1c improved from 6.7±0.5% to 6.1±0.5 (p<0.01) in Group D, 6.3±0.6 to 6.5±0.5 (n.s.) in Group C. FMD and CAVI improved in Group D from 3.8±1.5 to 4.4±1,7(P<0.05), 9.3±0.9 to 8.9±0.8(P<0.05), respectively, while they failed to improve in Group C (3.9±2.3 to 4.2±2.1, 9.2±0.9 to 9.3 ±1.1, respectively). Even if we compared Group D with patients who showed improvement of glycemic control in Group C, neither FMD nor CAVI had shown any improvement. Conclusion : DPP4 inhibitor was revealed to improve vascular function regardless of glycemic control. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 48 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION VALUE AND LIMITATIONS OF HAGEN-POISEUILLE'S LAW IN THE ESTIMATION OF CORONARY WALL SHEAR STRESS. E. Wellnhofer 1 , J. Osman 2 , R. Mevert 2 , U. Kertzscher 2 , K. Affeld 2 , L. Goubergrits 2 1 Internal Medicine/Cardiology, German Heart Center Berlin, Berlin, Germany 2 Biofluidmechanics laboratory, Charité Universitätsmedizin Berlin, Berlin, Germany Background: Hagen-Poiseuille's law (HP) is widely used to estimate wall shear stress (WSS, WSS_HP) in medicine. Only flow rate and local vessel diameter are needed as input data. This advantage is achieved at the cost of accuracy due to simplified assumptions concerning vessel shape. Calculation of WSS by numerical integration of the Navier-Stokes differential equations for incompressible fluids (CFD, WSS_CFD) in three-dimensional finite element vessel reconstructions is more accurate, but also more demanding and time-consuming. Methods: Vascular trees from 17 right (RCA) and 15 left (LCA) coronary arteries stratified with respect to luminal remodeling (controls (C), aneurysmatic (AnCAD) and non-aneurysmatic coronary artery disease (CAD)) were reconstructed from biplane angiograms. Patient specific flow simulations were performed by CFD. Results for WSS_ CFD and WSS_HP were compared. Results: Mean WSS_CFD was 2.6±2.6 Pa and WSS_HP was 2.4±2.6 Pa. The mean difference was 0.23 (-0.09-0.58) was not significant and correlation was 0.942. There were major differences in distribution particularly in the low WSS range (minimum (min) WSS (r=0.494), percent area <0.4 Pa (A_.4) (r=0.811)), however. Min WSS is over-estimated (p=0.01) and A_0.4 WSS is under-estimated (p=0.01) significantly by HP. The estimation of maximum (max) WSS can be improved (r=0.933; r=0.816 with max WSS_HP) by estimation from mean WSS_HP using a factor of 2 in RCA and 3 in LCA due to a strong trend of max WSS_ CFD with mean WSS_CFD (different slopes in RCA/LCA). Conclusion: Estimation of WSS by Hagen Poiseuille's law performs well for mean and maximum values, but is a poor estimate in low WSS areas. No conflict of interest Downloaded by: 146.48.70.161 - 2/27/2015 3:17:22 PM 49 ABSTRACTS PRESENTED AT THE 10 TH INTERNATIONAL CONGRESS ON CORONARY ARTERY DISEASE, OCTOBER 13-16, 2013 VASCULAR BIOLOGY AND ENDOTHELIAL FUNCTION ADIPONECTIN AND CARDIOVASCULAR RISK PREDICTION: STRATIFICATION OF CHEST PAIN PATIENTS BY A CLUSTER ANALYSIS C. Caselli 1 , M. Coceani 1 , T. Prescimone 1 , M. Cabiati 1 , A. Mazzarisi 1 , M. Schlueter 1 , S. Del Ry 1 , F. Cocci 1 , D. Giannessi 1 , P. Marraccini 1 1 CNR, Institute of Clinical Physiology Pisa, Pisa, Italy The new European guidelines on cardiovascular disease (CVD) prevention report the need to a better identification of population at high risk of CVD, the major ca use of premature death in Europe. With an unbiased statistical approach, we sought to identify clusters of patients with chest pain in order to better stratify their CVD risk. We prospectively included 202 consecutive patients with chest pain (63% males, age 62±12 yr) undergone to CT coronary angiography (CTCA). Patients were classified using K-means cluster analysis of clinical, imaging and bio-humoral data, selected for their relevance to CVD. The relevance of this classification was validated using presence of atherosclerosis (ATS) and significant stenosis (>50%) as assessed by CTCA. The most relevant patient classification resulted in three phenotypes distinguished according to Framingham Risk Score (FRS) and high molecular weigth (HMW) adiponectin plasma levels: Phenotype 1 (n=39) included subjects at very high CVD risk (FRS 34.6±9.7%) and ver y low HMW adiponectin (1.6±1.3 mg/mL); Phenotype 2 (n=124) subjects with lower FRS (11.8±5.4%) and hig her HMW (1.9±1.1); Phenotype 3 (n=16) the less severe patients (FRS 8.1±4.5%) with high levels of HMW (7.8±2.8). Presence and severity of ATS (existence of significant stenosis and number of diseased vessels) were significantly identified trough these phenotypes (Figure). By K-means cluster analysis, we identified three different CVD phenotypes allowing to stratify chest pain patients. Subjects within these phenotypes may required different diagnostic and therapeutic approach to improve their outcome.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
