- Email: [email protected]
103 Efficacy of meloxicam oral suspension in controlling pain and inflammation following castration in horses
e228
Abstracts / Atherosclerosis 241 (2015) e149ee229
Methods and materials: 120 patients with confirmed ischemicCHF were examined. 50%had permanent AF and 50%had sinus rhythm. To estimate arterial wall status volume sphygmography was done with VaSera VS1000 device (Fucuda, Japan). To evaluate collagen matrix condition of arterial wall plasma level of TIMP-I had been used. Results: PWV both in ankle-brachial segment and in muscle type vessels in patients with AF did not differ significantly from patients with sinus rhythm.PWV in carotid-femoral segment was reliably lower in patients with AF(10,26[6,45;14,22]m/sec vs 8,76[4,21;10,43]m/sec, (p<0,001)).Also, there was significant distinction in CAVI1 between the groups: in AF patient it was8,11±0,65, and9,49±1,53 in sinus rhythm patients,(p<0,001).Groups differed significantly in PWV in aorta: 6,87 [3,18;8,54]m/sec vs 8,90[6,21;10,86]m/sec,(p<0,001).Augmentation indices were differ significantly between the groups: R-AI 1,68±0,03 vs 1,98±0,76(p¼0,049), C-AI 1,16±0,23vs1,76±0,35(p<0,001). Correlation analysis showed direct reliable interconnection of severe dependency between PWVcf, PWVao(r¼0,51;?¼0,032;r¼0,65;?¼0,005); CAVI1 and augmentation indices(r¼0,50;?¼0,045;r¼0,53;?¼0,018;r¼0,61;?<0,001) and presence of permanent AF. In both groups shift to rise collagen conformation was indicated according to TIMP-1, but without significant difference between the groups994,73[510,10;1244,23]ng/dL; vs932,70ng/dL [569,35;1365,98] (?¼0,464).Correlation analysis showed direct interconnections in patients with permanent AF between TIMP-1 and: PWVcf (r¼0,58; ?¼0,002); PVWao(r¼0,67; ?¼0,003); CAVI-1 (r¼0,57; ?¼0,018); augmentation indices (r¼0,63; ?¼0,011; r¼0,62; ? <0,001). Conclusion: in patients with permanent AF and ischemic CHF structural and functional remodeling of arterial wall appears as increase of genuine stiffness, decrease of elasticity and distensibility and elevation of collagen conformation in intercellular matrix of smooth muscle layer of arteries.
EAS-0709. DYNAMICS OF STRUCTURE AND FUNCTION OF ARTERIAL WALL IN PATIENTS WITH PERMANENT ATRIAL FIBRILLATION AFTER TREATMENT WITH OMEGA-3 UNSATURATED FATTY ACIDS N. Koziolova, E. Polyanskaya, Y. Shilova, J. Nikonova. Propaedeutics of Internal Diseases #2, Perm State Medical Academy, Perm, Russia Aim: Dynamics of structural and functional parameters of arterial wall in patients with permanent atrial fibrillation (AF) and ischemic CHF after complex treatment with u3-unsaturated fatty acids (u3-UFA). Methods and materials: 60 patients with permanent AF and ischemic CHF were examined. To estimate arterial wall status volume sphygmography was done with VaSera VS-1000 device (Fucuda, Japan). To evaluate collagen matrix condition of arterial wall plasma level of TIMP-I had been used. All the patients were randomized into 2 groups: the 1st received standardized u3-UFA for 6 months additionally to basic treatment, and the 2nd one get just basic therapy of ischemicCHF. Results: In patients who were treated with u3-UFA there was reliably more evident decrease in PVWab(0,7±0,2%and 1,4±0,1% vs14,8±2,4% and17,9±7,7%(?<0,001)).After 6-months therapy including u3-UFA patients had significant CAVI1 decrease in compare with group without u3UFA in treatment: -14,4±5,9%vs -4,2±1,3%,(?<0,001).Positive dynamics was estimated in B-PWV and it was more evident in the 1st group: -12,3±10,3 %vs -5,3±3,5%(?<0,001).Also, PVWcf decreased reliably -29,4±8,2%vs -15,4±4,2%,(?<0,005) during treatment with u3-UFA .Carotid and aorta PVW decreased more after treatment with u3UFA(22,7±9,2% and20,1±9,5% vs10,3±5,5 and6,3±0,6% respectively(? <0,001).Indices of augmentation decreased significantly after using of u3UFA and more than in another group(R-AI 0,9±0,3% vs 0,3±0,1%; C-AI 0,5±0,2%vs -0,1±0,01%(p<0,001)).Positive dynamics in common marker of arterial wall fibrosis was indicated after treatment with u3-UFA (TIMP1decreased significantly:?17,6+4,8%). Conclusion: Including of u3-UFA in complex therapy of patients with permanent AF and ischemic CHF provides protective effects on arterial wall. It seems that one of mechanisms is suppression of collagen conformation in intercellular matrix of arteries.
EAS-0568. ATHEROSCLEROSIS AND MITOCHODRIAL GENOME
AGEING:
COMMON
MUTATIONS
OF
M.A. Sazonova a, V.V. Sinyov b, A.I. Ryzhkova c, V.A. Barinova b, A.V. Zhelankin b, K.Y. Mitrofanov a, A.Y. Postnov b, I.A. Sobenin b, A.N. Orekhov a. a Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia; b Laboratory of Medical Genetics, Cardiology Research Complex MH RF, Moscow, Russia; c Biological Faculty, K.I.Skryabin Moscow State Academy of Veterinary Medicine and Biotechnology, Moscow, Russia Aim: In the preliminary study it was detected that mitochondrial genome mutations m.C3256T, m.652delG, m.T3336C, m.C5178A, m.G12315A, m.G14459A and m.G15059A are atherogenic and mutations m.A1555G, m.652insG, m.G13513A and m.G14846A are antiatherogenic. The aim of the present study was the analysis of the association of heteroplasmy level in these mitochondrial mutations with ageing. Methods: The participants of the study were 700 women and men from Moscow region. High-resolution B-mode ultrasonography of carotids was used to estimate the extent of carotid atherosclerosis by measuring of the carotid intima-media thickness and the size of atherosclerotic plaques. DNA samples were obtained from whole venous blood. After the extraction of total DNA, the samples were amplified and pyrosequenced. An estimation of heteroplasmy level percent was carried out by an original method developed by M. A. Sazonova et al., based on pyrosequencing technology. Results: A significantly positive correlation was found between the age of the study participants and the heteroplasmy level of mitochondrial genome mutations G12315A, G14459A and G15059A (p0,05). A negative correlation with the age was highly significant for mutations A1555G and G14846A (p0,05), for 652insG and G13513A the level of significance was p0,1. Conclusion: The obtained results suggest that mitochondrial genome mutations, associated with atherosclerosis, correlate with the age of participants of the study. Atherogenic mutations correlate with the age positively and antiatherogenic have a negative correlation with it. These facts prompt suggestions that the processes of atherogenesis and ageing have a common origin. This study was supported by Russian Scientific Foundation, grant #14-1500112.
EAS-0587. ASSOCIATION OF MITOCHONDRIAL MUTATION LIPOFIBROUS PLAQUES IN HUMAN AORTIC INTIMA
T3336C
WITH
V.A. Barinova a, M.A. Sazonova b, V.V. Sinyov a, A.I. Ryzhkova c, A.V. Zhelankin a, K.Y. Mitrofanov b, A.Y. Postnov a, A.N. Orekhov b, I.A. Sobenin a. a Laboratory of Medical Genetics, Cardiology Research Complex MH RF, Moscow, Russia; b Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia; c Biological Faculty, K.I.Skryabin Moscow State Academy of Veterinary Medicine and Biotechnology, Moscow, Russia Aim: A detection of mitochondrial mutations associated with atherosclerosis can be an important addition to the existing systems of cardiovascular risk assessment. The aim of this study was an analysis of an association of the heteroplasmy level in mitochondrial genome mutation T3336C, localized in a gene of the first subunit of NADH dehydrogenase, with atherosclerotic lesions in aortas. Methods: The materials for the study were tissue samples from normal aortic intima and lipofibrous plaques of 7 individuals. DNA was obtained from tissue samples by a method of phenol-chloroform extraction. A pyrosequencing of PCR-fragments was carried out by an automatic pyrosequenator PSQTMHS96MA. To estimate the heteroplasmy percent in mutations according to the data of pyrogram there was used a method of quantitative assessment of a mutant allele in mitochondrial genome,
Abstracts / Atherosclerosis 241 (2015) e149ee229
developed by Sazonova M.A. et al. (2009) on the basis of pyrosequencing technology. Results: The obtained results showed that the heteroplasmy level in mutation T3336C for 29% of aortas is higher in lipofibrous plaques compared to normal intima. Conclusions: Atherogenicity of silencing mutation T3336C, which doesn’t lead to amino acid substitution in the protein chain of enzyme
e229
of NADH dehydrogenase, can be explained by an association of this mutation with haplotype correlating with atherosclerosis. Therefore, a somatic mutation in mitochondrial gene of the first subunit of NADH dehydrogenase can be involved in mechanisms of development of atherosclerosis. The study was supported by Russian Science Foundation, grant #14-1401038.
Abstracts / Atherosclerosis 241 (2015) e149ee229
Methods and materials: 120 patients with confirmed ischemicCHF were examined. 50%had permanent AF and 50%had sinus rhythm. To estimate arterial wall status volume sphygmography was done with VaSera VS1000 device (Fucuda, Japan). To evaluate collagen matrix condition of arterial wall plasma level of TIMP-I had been used. Results: PWV both in ankle-brachial segment and in muscle type vessels in patients with AF did not differ significantly from patients with sinus rhythm.PWV in carotid-femoral segment was reliably lower in patients with AF(10,26[6,45;14,22]m/sec vs 8,76[4,21;10,43]m/sec, (p<0,001)).Also, there was significant distinction in CAVI1 between the groups: in AF patient it was8,11±0,65, and9,49±1,53 in sinus rhythm patients,(p<0,001).Groups differed significantly in PWV in aorta: 6,87 [3,18;8,54]m/sec vs 8,90[6,21;10,86]m/sec,(p<0,001).Augmentation indices were differ significantly between the groups: R-AI 1,68±0,03 vs 1,98±0,76(p¼0,049), C-AI 1,16±0,23vs1,76±0,35(p<0,001). Correlation analysis showed direct reliable interconnection of severe dependency between PWVcf, PWVao(r¼0,51;?¼0,032;r¼0,65;?¼0,005); CAVI1 and augmentation indices(r¼0,50;?¼0,045;r¼0,53;?¼0,018;r¼0,61;?<0,001) and presence of permanent AF. In both groups shift to rise collagen conformation was indicated according to TIMP-1, but without significant difference between the groups994,73[510,10;1244,23]ng/dL; vs932,70ng/dL [569,35;1365,98] (?¼0,464).Correlation analysis showed direct interconnections in patients with permanent AF between TIMP-1 and: PWVcf (r¼0,58; ?¼0,002); PVWao(r¼0,67; ?¼0,003); CAVI-1 (r¼0,57; ?¼0,018); augmentation indices (r¼0,63; ?¼0,011; r¼0,62; ? <0,001). Conclusion: in patients with permanent AF and ischemic CHF structural and functional remodeling of arterial wall appears as increase of genuine stiffness, decrease of elasticity and distensibility and elevation of collagen conformation in intercellular matrix of smooth muscle layer of arteries.
EAS-0709. DYNAMICS OF STRUCTURE AND FUNCTION OF ARTERIAL WALL IN PATIENTS WITH PERMANENT ATRIAL FIBRILLATION AFTER TREATMENT WITH OMEGA-3 UNSATURATED FATTY ACIDS N. Koziolova, E. Polyanskaya, Y. Shilova, J. Nikonova. Propaedeutics of Internal Diseases #2, Perm State Medical Academy, Perm, Russia Aim: Dynamics of structural and functional parameters of arterial wall in patients with permanent atrial fibrillation (AF) and ischemic CHF after complex treatment with u3-unsaturated fatty acids (u3-UFA). Methods and materials: 60 patients with permanent AF and ischemic CHF were examined. To estimate arterial wall status volume sphygmography was done with VaSera VS-1000 device (Fucuda, Japan). To evaluate collagen matrix condition of arterial wall plasma level of TIMP-I had been used. All the patients were randomized into 2 groups: the 1st received standardized u3-UFA for 6 months additionally to basic treatment, and the 2nd one get just basic therapy of ischemicCHF. Results: In patients who were treated with u3-UFA there was reliably more evident decrease in PVWab(0,7±0,2%and 1,4±0,1% vs14,8±2,4% and17,9±7,7%(?<0,001)).After 6-months therapy including u3-UFA patients had significant CAVI1 decrease in compare with group without u3UFA in treatment: -14,4±5,9%vs -4,2±1,3%,(?<0,001).Positive dynamics was estimated in B-PWV and it was more evident in the 1st group: -12,3±10,3 %vs -5,3±3,5%(?<0,001).Also, PVWcf decreased reliably -29,4±8,2%vs -15,4±4,2%,(?<0,005) during treatment with u3-UFA .Carotid and aorta PVW decreased more after treatment with u3UFA(22,7±9,2% and20,1±9,5% vs10,3±5,5 and6,3±0,6% respectively(? <0,001).Indices of augmentation decreased significantly after using of u3UFA and more than in another group(R-AI 0,9±0,3% vs 0,3±0,1%; C-AI 0,5±0,2%vs -0,1±0,01%(p<0,001)).Positive dynamics in common marker of arterial wall fibrosis was indicated after treatment with u3-UFA (TIMP1decreased significantly:?17,6+4,8%). Conclusion: Including of u3-UFA in complex therapy of patients with permanent AF and ischemic CHF provides protective effects on arterial wall. It seems that one of mechanisms is suppression of collagen conformation in intercellular matrix of arteries.
EAS-0568. ATHEROSCLEROSIS AND MITOCHODRIAL GENOME
AGEING:
COMMON
MUTATIONS
OF
M.A. Sazonova a, V.V. Sinyov b, A.I. Ryzhkova c, V.A. Barinova b, A.V. Zhelankin b, K.Y. Mitrofanov a, A.Y. Postnov b, I.A. Sobenin b, A.N. Orekhov a. a Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia; b Laboratory of Medical Genetics, Cardiology Research Complex MH RF, Moscow, Russia; c Biological Faculty, K.I.Skryabin Moscow State Academy of Veterinary Medicine and Biotechnology, Moscow, Russia Aim: In the preliminary study it was detected that mitochondrial genome mutations m.C3256T, m.652delG, m.T3336C, m.C5178A, m.G12315A, m.G14459A and m.G15059A are atherogenic and mutations m.A1555G, m.652insG, m.G13513A and m.G14846A are antiatherogenic. The aim of the present study was the analysis of the association of heteroplasmy level in these mitochondrial mutations with ageing. Methods: The participants of the study were 700 women and men from Moscow region. High-resolution B-mode ultrasonography of carotids was used to estimate the extent of carotid atherosclerosis by measuring of the carotid intima-media thickness and the size of atherosclerotic plaques. DNA samples were obtained from whole venous blood. After the extraction of total DNA, the samples were amplified and pyrosequenced. An estimation of heteroplasmy level percent was carried out by an original method developed by M. A. Sazonova et al., based on pyrosequencing technology. Results: A significantly positive correlation was found between the age of the study participants and the heteroplasmy level of mitochondrial genome mutations G12315A, G14459A and G15059A (p0,05). A negative correlation with the age was highly significant for mutations A1555G and G14846A (p0,05), for 652insG and G13513A the level of significance was p0,1. Conclusion: The obtained results suggest that mitochondrial genome mutations, associated with atherosclerosis, correlate with the age of participants of the study. Atherogenic mutations correlate with the age positively and antiatherogenic have a negative correlation with it. These facts prompt suggestions that the processes of atherogenesis and ageing have a common origin. This study was supported by Russian Scientific Foundation, grant #14-1500112.
EAS-0587. ASSOCIATION OF MITOCHONDRIAL MUTATION LIPOFIBROUS PLAQUES IN HUMAN AORTIC INTIMA
T3336C
WITH
V.A. Barinova a, M.A. Sazonova b, V.V. Sinyov a, A.I. Ryzhkova c, A.V. Zhelankin a, K.Y. Mitrofanov b, A.Y. Postnov a, A.N. Orekhov b, I.A. Sobenin a. a Laboratory of Medical Genetics, Cardiology Research Complex MH RF, Moscow, Russia; b Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia; c Biological Faculty, K.I.Skryabin Moscow State Academy of Veterinary Medicine and Biotechnology, Moscow, Russia Aim: A detection of mitochondrial mutations associated with atherosclerosis can be an important addition to the existing systems of cardiovascular risk assessment. The aim of this study was an analysis of an association of the heteroplasmy level in mitochondrial genome mutation T3336C, localized in a gene of the first subunit of NADH dehydrogenase, with atherosclerotic lesions in aortas. Methods: The materials for the study were tissue samples from normal aortic intima and lipofibrous plaques of 7 individuals. DNA was obtained from tissue samples by a method of phenol-chloroform extraction. A pyrosequencing of PCR-fragments was carried out by an automatic pyrosequenator PSQTMHS96MA. To estimate the heteroplasmy percent in mutations according to the data of pyrogram there was used a method of quantitative assessment of a mutant allele in mitochondrial genome,
Abstracts / Atherosclerosis 241 (2015) e149ee229
developed by Sazonova M.A. et al. (2009) on the basis of pyrosequencing technology. Results: The obtained results showed that the heteroplasmy level in mutation T3336C for 29% of aortas is higher in lipofibrous plaques compared to normal intima. Conclusions: Atherogenicity of silencing mutation T3336C, which doesn’t lead to amino acid substitution in the protein chain of enzyme
e229
of NADH dehydrogenase, can be explained by an association of this mutation with haplotype correlating with atherosclerosis. Therefore, a somatic mutation in mitochondrial gene of the first subunit of NADH dehydrogenase can be involved in mechanisms of development of atherosclerosis. The study was supported by Russian Science Foundation, grant #14-1401038.