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Association between inflammation and low HDL cholesterol levels. Results from the InChianti study
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XVIII S.I.S.A. National Congress
ASSOCIATION BETWEEN INFLAMMATION AND LOW HDL CHOLESTEROL LEVELS. RESULTS FROM THE InCHIANTI STUDY
C REACTIVE PROTEIN AND ENDOTHELIAL DYSFUNCTION IN NEVER TREATED HYPERTENSIVE PATIENTS
G. Zuliani, S. Volpato, A. BI6. S. Bandinelli*, A.R. Atti, A.M. Corsi*, L. Ferrucci*§, R. Fellin
A Sciacqua, G lemma, F. Borrello, E Ruberto, M Perticone, S Cassano, G Colangelo, A Pujia, G Sesti, F. Perticone
Department of Clinical and Experimental Medicine, Section of Internal Medicine, Gerontology & Geriatrics, University di Ferrara, Italy.
Cardiovascular Disease Unit, University Magna Graecia of Catanzaro,
Low HDL-C levels are a risk factor for CHD. A growing level of attention has been devoted to the relationship between inflammation and plasma lipoproteins. We investigated the association between some markers of flogosis and low HDL-C in the InChianti Study, a large sample of community dwelling Italian subjects, including 1270 older subjects. Low HDL-C was defined <10th gender specific percentile (36 mg/dL M, 41 mg/dL F). Acute phase marker considered were: IL-6, IL-10, IL-18, IL1beta, TNFalpha, and CRP. At linear multivariate analysis only IL-6, IL-18 e CRP were inversely correlated with HDL-C (adjusted R2:0.12). Stepwise multivariate logistic regression analysis showed that IL-6 levels (111vs I tertile, OR: 2,57; 95%Chl.26-5.22), TG (111vs I tertile O.R.: 28.64; 6.82120.23), and fasting insulin (111 vs I tertile O.R.:2.47; 1.20-5.08) were associated with low HDL-C levels independently from age, smoking, daily alcohol intake, BMI, waist circumference, hypertension, diabetes, fasting blood glucose, uric acid, insulin therapy, oral hypoglicemic drugs, last-year physical activity, CRP, IL-18, IL-10, IL-lbeta, and TNF alpha levels. We conclude that: I) some markers of inflammation a r e associated with HDLC levels in older individuals; 2) although both low HDL-C and IL-6 levels were associated with the main traits of the metabolic syndrome their association was independent.
VASCULAR STIFFNESS AND INTIMAL MEDIA THICKNESS IN HYPERTENSIVE NEVER-TREATED PATIENTS M. Vatrano, R Maio, F Borrello, A Scozzafava, M Perticone, A Castagna, E Santillo, A Pujia, G Sesti, F. Perticone Cardiovascular Disease Unit, University Magna Greecia of Catanzaro Atherosclerosis is an inflammatory, chronic disease that is characterized by functional and structural alterations that reduce the elasticity of the arterial wall. The not-invasive evaluation of these alterations is a preclinic indicator of atherosclerotic disease, allowing a better therapeutic approach. Vascular echography is an useful and easy instrument to do it. Recently, some studies have demonstrated an important association between the vascular alterations, evaluated by echography, and the arterial stiffness in diabetic patients. The aim of this study was to evaluate, in uncomplicated hypertensive patients, the correlation between intimal media thickness (IMT) and arterial stiffness evaluated by sfigmocardiography. Twenty-four patients (17M/7F; age 52+10 yrs) have been enrolled. The evaluation of arterial stiffness has been performed by measuring the Augmentation Index (AIx) and the Pulse Wave Velocity (PWV) in carotid and femoral artery by tonometric method (SphygmoCor). IMT determination was echographically evaluated at the level of the Common Carotid (CC) Artery. Data analysis has demonstrated a significant correlation (P<0,0001) between carotid IMT and AIx (r=0,752) and PWV (r=0,807, P<0,000); these results have been confirmed by multivariate analysis, in fact PWV was the most important determinant of IMT, justifying the 65,2% of the variation, and AIx added another 11,1% (P<0,000). In conclusion, our data demonstrate, in hypertensive uncomplicated patients, the utility of sfigmocardiografy to study the vascular damage.
Atherosclerosis is an inflammatory, chronic disease. Initially it begins with endothelial dysfunction and, then, it makes progress until the plaque formation and clinic manifestations. It's known the association between some inflammatory markers, as C reactive protein (CRP), and acute vasular complications during the conclamate coronary artery disease (CAD). Recently, our group has demonstrated the independent prognostic value of reduced endothelium-dependent vasodilation in hypertensive patients. Thus, the aim of this study was to evaluate, in a group of hypertensive never treated patients, the possible association between CRP levels and the endothelium-dependent vasodilation. Seventy-two patients (46M/26F; age 45+8 yrs) have been enrolled, all were affected by essential uncomplicated hypertension. The CRP levels were evaluated by nephelometric method. Endothelium-dependent and -independent vasodilation were assessed by strain-gauge plethysmography, during a dose-response curve to intrabrachial-arterial infusion of acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. Data analysis has demonstrated an inverse correlation (r=-0.457; P<0.001) between CRP levels and endothelium-dependent vasodilation; this result has been confirmed by multivariate analysis. In fact CRP levels were the most important determinant of the forearm blood flow increment, justifying the 20.9% of the variation. In conclusion, our data demonstrate, in a group of uncomplicated hypertensive patients, that an inflammatory marker as CRP, is associated with endothelial dysfunction, an early atherosclerotic marker.
EFFECTS OF THROMBOXANE SYNDROMES
ROFECOXIB ON A S P I R I N - I N S E N S I T I V E BIOSYNTHESIS IN ACUTE CORONARY
Francesco Cipollone,* Giovanni Ciabattoni,* Annalisa lezzi,* Maria Fazia,* Elena Toniato,* Stefano Martinotti,* Barbara Pini,* Chiara Cuccurullo,* Cesare di Iorio,# Massimo Pasquale,# Valeria Venti,* Franco Cuccurullo,* Andrea Mezzetti,* Carlo Patrono.* "G.d'Annunzio" University Foundation, Chieti (*); "SS. Annunziata" Hospital, ChieU (#). Aspirin fails to suppress enhanced thromboxane (TX) biosynthesis in a subset of episodes of platelet activation in patients with acute coronary syndromes (ACS). In this study we examined whether platelet or monocyte cyclooxygenase (COX)-2 may contribute to aspirin-insensitive TXA2 synthesis and be inhibited by short-term treatment with rofecoxib, a COX-2 inhibitor. Twenty-four aspirin-treated patients with ACS were randomized to a 3-day course of rofecoxib (25 mg/die) or placebo. Peripheral blood samples were collected 3 times daily, while 4- to 6-hour urine samples during the whole study pedod. Platelet arid monocyte COX2 level was measured by FACS, immunocytochemistry, Western blot; 11dehydro-TXB2 (11-dH-TXB2), urinary metabolite of TXA2, was measured by validated RIA, COX-2 expression was detected both in platelets (7+2%) as in monocytes (10+2%). Whereas baseline 11-dH-TXB2 did not differ between the rofecoxib and the control groups (305+116 vs 294±100 pg/mg creatinin, P=NS), rofecoxib reduced 11-dH-TXB2 levels by -70% in the last sample (99±54 pg/mg creatinine, n=24; P>0.0001). Placebo had no significant effect (274±85 pg/mg creatinine, n=24; P=NS). This study shows that aspirin-insensitive TXA2 synthesis in ACS may reflect platelet and monocyte COX-2 expression, possibly in response to a local inflammatory milieu. Coxibs could be an ideal tool to test the clinical relevance of the COX-2 pathway in this setting.
XVIII S.I.S.A. National Congress
ASSOCIATION BETWEEN INFLAMMATION AND LOW HDL CHOLESTEROL LEVELS. RESULTS FROM THE InCHIANTI STUDY
C REACTIVE PROTEIN AND ENDOTHELIAL DYSFUNCTION IN NEVER TREATED HYPERTENSIVE PATIENTS
G. Zuliani, S. Volpato, A. BI6. S. Bandinelli*, A.R. Atti, A.M. Corsi*, L. Ferrucci*§, R. Fellin
A Sciacqua, G lemma, F. Borrello, E Ruberto, M Perticone, S Cassano, G Colangelo, A Pujia, G Sesti, F. Perticone
Department of Clinical and Experimental Medicine, Section of Internal Medicine, Gerontology & Geriatrics, University di Ferrara, Italy.
Cardiovascular Disease Unit, University Magna Graecia of Catanzaro,
Low HDL-C levels are a risk factor for CHD. A growing level of attention has been devoted to the relationship between inflammation and plasma lipoproteins. We investigated the association between some markers of flogosis and low HDL-C in the InChianti Study, a large sample of community dwelling Italian subjects, including 1270 older subjects. Low HDL-C was defined <10th gender specific percentile (36 mg/dL M, 41 mg/dL F). Acute phase marker considered were: IL-6, IL-10, IL-18, IL1beta, TNFalpha, and CRP. At linear multivariate analysis only IL-6, IL-18 e CRP were inversely correlated with HDL-C (adjusted R2:0.12). Stepwise multivariate logistic regression analysis showed that IL-6 levels (111vs I tertile, OR: 2,57; 95%Chl.26-5.22), TG (111vs I tertile O.R.: 28.64; 6.82120.23), and fasting insulin (111 vs I tertile O.R.:2.47; 1.20-5.08) were associated with low HDL-C levels independently from age, smoking, daily alcohol intake, BMI, waist circumference, hypertension, diabetes, fasting blood glucose, uric acid, insulin therapy, oral hypoglicemic drugs, last-year physical activity, CRP, IL-18, IL-10, IL-lbeta, and TNF alpha levels. We conclude that: I) some markers of inflammation a r e associated with HDLC levels in older individuals; 2) although both low HDL-C and IL-6 levels were associated with the main traits of the metabolic syndrome their association was independent.
VASCULAR STIFFNESS AND INTIMAL MEDIA THICKNESS IN HYPERTENSIVE NEVER-TREATED PATIENTS M. Vatrano, R Maio, F Borrello, A Scozzafava, M Perticone, A Castagna, E Santillo, A Pujia, G Sesti, F. Perticone Cardiovascular Disease Unit, University Magna Greecia of Catanzaro Atherosclerosis is an inflammatory, chronic disease that is characterized by functional and structural alterations that reduce the elasticity of the arterial wall. The not-invasive evaluation of these alterations is a preclinic indicator of atherosclerotic disease, allowing a better therapeutic approach. Vascular echography is an useful and easy instrument to do it. Recently, some studies have demonstrated an important association between the vascular alterations, evaluated by echography, and the arterial stiffness in diabetic patients. The aim of this study was to evaluate, in uncomplicated hypertensive patients, the correlation between intimal media thickness (IMT) and arterial stiffness evaluated by sfigmocardiography. Twenty-four patients (17M/7F; age 52+10 yrs) have been enrolled. The evaluation of arterial stiffness has been performed by measuring the Augmentation Index (AIx) and the Pulse Wave Velocity (PWV) in carotid and femoral artery by tonometric method (SphygmoCor). IMT determination was echographically evaluated at the level of the Common Carotid (CC) Artery. Data analysis has demonstrated a significant correlation (P<0,0001) between carotid IMT and AIx (r=0,752) and PWV (r=0,807, P<0,000); these results have been confirmed by multivariate analysis, in fact PWV was the most important determinant of IMT, justifying the 65,2% of the variation, and AIx added another 11,1% (P<0,000). In conclusion, our data demonstrate, in hypertensive uncomplicated patients, the utility of sfigmocardiografy to study the vascular damage.
Atherosclerosis is an inflammatory, chronic disease. Initially it begins with endothelial dysfunction and, then, it makes progress until the plaque formation and clinic manifestations. It's known the association between some inflammatory markers, as C reactive protein (CRP), and acute vasular complications during the conclamate coronary artery disease (CAD). Recently, our group has demonstrated the independent prognostic value of reduced endothelium-dependent vasodilation in hypertensive patients. Thus, the aim of this study was to evaluate, in a group of hypertensive never treated patients, the possible association between CRP levels and the endothelium-dependent vasodilation. Seventy-two patients (46M/26F; age 45+8 yrs) have been enrolled, all were affected by essential uncomplicated hypertension. The CRP levels were evaluated by nephelometric method. Endothelium-dependent and -independent vasodilation were assessed by strain-gauge plethysmography, during a dose-response curve to intrabrachial-arterial infusion of acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. Data analysis has demonstrated an inverse correlation (r=-0.457; P<0.001) between CRP levels and endothelium-dependent vasodilation; this result has been confirmed by multivariate analysis. In fact CRP levels were the most important determinant of the forearm blood flow increment, justifying the 20.9% of the variation. In conclusion, our data demonstrate, in a group of uncomplicated hypertensive patients, that an inflammatory marker as CRP, is associated with endothelial dysfunction, an early atherosclerotic marker.
EFFECTS OF THROMBOXANE SYNDROMES
ROFECOXIB ON A S P I R I N - I N S E N S I T I V E BIOSYNTHESIS IN ACUTE CORONARY
Francesco Cipollone,* Giovanni Ciabattoni,* Annalisa lezzi,* Maria Fazia,* Elena Toniato,* Stefano Martinotti,* Barbara Pini,* Chiara Cuccurullo,* Cesare di Iorio,# Massimo Pasquale,# Valeria Venti,* Franco Cuccurullo,* Andrea Mezzetti,* Carlo Patrono.* "G.d'Annunzio" University Foundation, Chieti (*); "SS. Annunziata" Hospital, ChieU (#). Aspirin fails to suppress enhanced thromboxane (TX) biosynthesis in a subset of episodes of platelet activation in patients with acute coronary syndromes (ACS). In this study we examined whether platelet or monocyte cyclooxygenase (COX)-2 may contribute to aspirin-insensitive TXA2 synthesis and be inhibited by short-term treatment with rofecoxib, a COX-2 inhibitor. Twenty-four aspirin-treated patients with ACS were randomized to a 3-day course of rofecoxib (25 mg/die) or placebo. Peripheral blood samples were collected 3 times daily, while 4- to 6-hour urine samples during the whole study pedod. Platelet arid monocyte COX2 level was measured by FACS, immunocytochemistry, Western blot; 11dehydro-TXB2 (11-dH-TXB2), urinary metabolite of TXA2, was measured by validated RIA, COX-2 expression was detected both in platelets (7+2%) as in monocytes (10+2%). Whereas baseline 11-dH-TXB2 did not differ between the rofecoxib and the control groups (305+116 vs 294±100 pg/mg creatinin, P=NS), rofecoxib reduced 11-dH-TXB2 levels by -70% in the last sample (99±54 pg/mg creatinine, n=24; P>0.0001). Placebo had no significant effect (274±85 pg/mg creatinine, n=24; P=NS). This study shows that aspirin-insensitive TXA2 synthesis in ACS may reflect platelet and monocyte COX-2 expression, possibly in response to a local inflammatory milieu. Coxibs could be an ideal tool to test the clinical relevance of the COX-2 pathway in this setting.