Increased ROS production and DNA damage in monocytes are biomarkers of aging and atherosclerosis.

BACKGROUND: New evidence demonstrates that aging and dyslipidemia are closely associated with oxidative stress, DNA damage and apoptosis in some cells and extravascular tissues. However, in monocytes, which are naturally involved in progression and/or resolution of plaque in atherosclerosis, this concurrence has not yet been fully investigated. In this study, we evaluated the influence of aging and hypercholesterolemia on serum pro-inflammatory cytokines, oxidative stress, DNA damage and apoptosis in monocytes from apolipoprotein E-deficient (apoE-/-) mice compared with age-matched wild-type C57BL/6 (WT) mice. Experiments were performed in young (2-months) and in old (18-months) male wild-type (WT) and apoE-/- mice. RESULTS: Besides the expected differences in serum lipid profile and plaque formation, we observed that atherosclerotic mice exhibited a significant increase in monocytosis and in serum levels of pro-inflammatory cytokines compared to WT mice. Moreover, it was observed that the overproduction of ROS, led to an increased DNA fragmentation and, consequently, apoptosis in monocytes from normocholesterolemic old mice, which was aggravated in age-matched atherosclerotic mice. CONCLUSIONS: In this study, we demonstrate that a pro-inflammatory systemic status is associated with an impairment of functionality of monocytes during aging and that these parameters are fundamental extra-arterial contributors to the aggravation of atherosclerosis. The present data open new avenues for the development of future strategies with the purpose of treating atherosclerosis.

Increased ROS production and DNA damage in monocytes are biomarkers of aging and atherosclerosis

BACKGROUND: New evidence demonstrates that aging and dyslipidemia are closely associated with oxidative stress, DNA damage and apoptosis in some cells and extravascular tissues. However, in monocytes, which are naturally involved in progression and/or resolution of plaque in atherosclerosis, this concurrence has not yet been fully investigated. In this study, we evaluated the influence of aging and hypercholesterolemia on serum pro-inflammatory cytokines, oxidative stress, DNA damage and apoptosis in monocytes from apolipoprotein E-deficient (apoE-/-) mice compared with age-matched wild-type C57BL/6 (WT) mice. Experiments were performed in young (2-months) and in old (18-months) male wild-type (WT) and apoE-/- mice. RESULTS: Besides the expected differences in serum lipid profile and plaque formation, we observed that atherosclerotic mice exhibited a significant increase in monocytosis and in serum levels of pro-inflammatory cytokines compared to WT mice. Moreover, it was observed that the overproduction of ROS, led to an increased DNA fragmentation and, consequently, apoptosis in monocytes from normocholesterolemic old mice, which was aggravated in age-matched atherosclerotic mice. CONCLUSIONS: In this study, we demonstrate that a pro-inflammatory systemic status is associated with an impairment of functionality of monocytes during aging and that these parameters are fundamental extra-arterial contributors to the aggravation of atherosclerosis. The present data open new avenues for the development of future strategies with the purpose of treating atherosclerosis.

Estimation of cardiovascular risk and detection of subclinical carotid atheromatosis in patients with diabetes without a history of cardiovascular disease

ABSTRACT Objectives Cardiovascular risk estimated by several scores in patients with diabetes mellitus without a cardiovascular disease history and the association with carotid atherosclerotic plaque (CAP) were the aims of this study. Materials and methods Cardiovascular risk was calculate using United Kingdom Prospective Diabetes Study (UKPDS) risk engine, Framingham risk score for cardiovascular (FSCV) and coronary disease (FSCD), and the new score (NS) proposed by the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol. Ultrasound was used to assess CAP occurrence. A receiver operating characteristic (ROC) analysis was performed. Results One hundred seventy patients (mean age 61.4 ± 11 years, 58.8% men) were included. Average FSCV, FSCD and NS values were 33.6% ± 21%, 20.6% ± 12% and 24.8% ± 18%, respectively. According to the UKPDS score, average risk of coronary disease and stroke were 22.1% ± 16% and 14.3% ± 19% respectively. Comparing the risks estimated by the different scores a significant correlation was found. The prevalence of CAP was 51%, in patients with the higher scores this prevalence was increased. ROC analysis showed a good discrimination power between subjects with or without CAP. Conclusion The cardiovascular risk estimated was high but heterogenic. The prevalence of CAP increased according to the strata of risk. Understanding the relationship between CAP and scores could improve the risk estimation in subjects with diabetes.

Estimation of cardiovascular risk and detection of subclinical carotid atheromatosis in patients with diabetes without a history of cardiovascular disease.

OBJECTIVES: Cardiovascular risk estimated by several scores in patients with diabetes mellitus without a cardiovascular disease history and the association with carotid atherosclerotic plaque (CAP) were the aims of this study. MATERIALS AND METHODS: Cardiovascular risk was calculate using United Kingdom Prospective Diabetes Study (UKPDS) risk engine, Framingham risk score for cardiovascular (FSCV) and coronary disease (FSCD), and the new score (NS) proposed by the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol. Ultrasound was used to assess CAP occurrence. A receiver operating characteristic (ROC) analysis was performed. RESULTS: One hundred seventy patients (mean age 61.4 ± 11 years, 58.8% men) were included. Average FSCV, FSCD and NS values were 33.6% ± 21%, 20.6% ± 12% and 24.8% ± 18%, respectively. According to the UKPDS score, average risk of coronary disease and stroke were 22.1% ± 16% and 14.3% ± 19% respectively. Comparing the risks estimated by the different scores a significant correlation was found. The prevalence of CAP was 51%, in patients with the higher scores this prevalence was increased. ROC analysis showed a good discrimination power between subjects with or without CAP. CONCLUSION: The cardiovascular risk estimated was high but heterogenic. The prevalence of CAP increased according to the strata of risk. Understanding the relationship between CAP and scores could improve the risk estimation in subjects with diabetes.

Preventive and therapeutic moderate aerobic exercise programs convert atherosclerotic plaques into a more stable phenotype.

UNLABELLED: The mechanisms by which exercise affects atherosclerotic plaque stability remain incompletely understood. We evaluated the effects of two training protocols on both atherosclerotic plaque structure and the signaling pathways involved in plaque rupture. METHODS: Male low-density lipoprotein (LDL) receptor knockout mice were fed a high-fat, high-cholesterol diet (HFD). One group was subjected to moderate exercise using a treadmill for 14weeks (preventive protocol). The other group started an exercise regimen after 16weeks of the HFD (therapeutic group). Atherosclerotic plaques within the aorta were evaluated for lipid and collagen contents, as well as for inflammatory markers. Plasma cholesterol and cytokine levels were also determined. RESULTS: The mice receiving a HFD developed hypercholesterolemia and atherosclerotic plaques within the aorta. The aortas from the animals in the preventive protocol exhibited smaller lipid cores and higher collagen content. These animals also exhibited lower CD40 expression within the plaques. The aortas of the mice in the therapeutic group exhibited higher collagen content, but no differences in either lipid core size or plaque size were noted. No differences in blood pressure, plasma cholesterol, cytokine levels, plaque size or metalloproteinase 9 expression were observed in the trained animals compared with the sedentary animals. CONCLUSION: Moderate aerobic exercise modified atherosclerotic plaque characteristics and converted the plaques into a more stable phenotype, increasing the collagen content in response to both exercise programs. Furthermore, moderate aerobic exercise reduced the animals' fat content and decreased the activity of the CD40-CD40L signaling pathway in the preventive group.

Pontes de miocárdio em corações de suínos (SUS domesticus) e suas possíveis influências sobre lesões ateroscleróticas em artérias coronárias / Myocardial bridge of pigs (Sus domesticus) hearts associated with lesions of coronary arteries

Seek, therefore, to analyze in adults and young pigs, under light microscopy, the morphological characteristics of the coronary arterial branches under of the myocardial bridges, as well as the prepontine and postpontine segments, attempting to establish morphofunctional correlations between these. Was used for the study 40 pig hearts, all mongrel females, being 20 young and 20 adults, all with myocardial bridges, of which were removed prepontine, pontine and postpontine segments of the coronary arteries, together with the surrounding tissue. The segments were submitted with usual techniques of the light microscopy and stained with hematoxylin and eosin. Changes were observed in tunica intima, such as thickening, cells with clear cytoplasm, disruption and duplication of the limiting internal elastic lamina. The statistical test was significant for the position in adult pigs, confirming that there is a highter frequency of lesions in prepontine segment of the tunica intima of the coronary arteries when compared with the pontine and postpontine segments. The statistical test confirmed variation in the lesions frequency between sample studied, being highter in young animals when compared with adult animals. For the young animals, the test was not significant for the variable positions between of the segments compared with each other. There is statistically a highter occurrence of atherosclerotic lesions which precedes the myocardial bridge in relation to the others segments studied.

Buscou-se analisar em suínos jovens e adultos, sob microscopia de luz, as características morfológicas dos ramos arteriais coronarianos sob as pontes de miocárdio, bem como dos segmentos pré-pontino e pós-pontino, na tentativa de estabelecer correlações morfofuncionais entre eles. Foram utilizados 40 corações de suínos para a pesquisa, todos fêmeas sem raça definida, sendo 20 jovens e 20 adultos, todos portadores de pontes de miocárdio, dos quais foram retirados fragmentos pré-pontino, pontino e pós-pontino de ramos da artéria coronária direita e esquerda, junto com o tecido circunjacente. Os segmentos foram submetidos às técnicas habituais da microscopia de luz e corados pela hematoxilina-eosina. Observou-se alterações da íntima, tais como espessamentos, células com citoplasma claro, ruptura e/ou duplicação da lâmina limitante elástica interna. O teste estatístico se mostrou significativo para posição em suínos adultos, confirmando que existe uma maior frequência de lesões no segmento pré-pontino da túnica íntima das artérias coronárias quando comparado com o segmento pontino e com o pós-pontino. O mesmo teste confirmou uma variação na frequência de lesões entre as amostras estudadas, sendo maior em animais jovens quando defrontado com animais adultos. Paraos animais jovens, o teste não se apresentou significativo para a variável posição entre nenhum dos segmentos comparados entre si. Concluiu-se, estatisticamente, uma maior ocorrência de lesões ateroscleróticas nos segmentos arteriais que antecedem a ponte de miocárdio em relação aos demais segmentos estudados.

Pontes de miocárdio em corações de suínos (SUS domesticus) e suas possíveis influências sobre lesões ateroscleróticas em artérias coronárias / Myocardial bridge of pigs (Sus domesticus) hearts associated with lesions of coronary arteries

Seek, therefore, to analyze in adults and young pigs, under light microscopy, the morphological characteristics of the coronary arterial branches under of the myocardial bridges, as well as the prepontine and postpontine segments, attempting to establish morphofunctional correlations between these. Was used for the study 40 pig hearts, all mongrel females, being 20 young and 20 adults, all with myocardial bridges, of which were removed prepontine, pontine and postpontine segments of the coronary arteries, together with the surrounding tissue. The segments were submitted with usual techniques of the light microscopy and stained with hematoxylin and eosin. Changes were observed in tunica intima, such as thickening, cells with clear cytoplasm, disruption and duplication of the limiting internal elastic lamina. The statistical test was significant for the position in adult pigs, confirming that there is a highter frequency of lesions in prepontine segment of the tunica intima of the coronary arteries when compared with the pontine and postpontine segments. The statistical test confirmed variation in the lesions frequency between sample studied, being highter in young animals when compared with adult animals. For the young animals, the test was not significant for the variable positions between of the segments compared with each other. There is statistically a highter occurrence of atherosclerotic lesions which precedes the myocardial bridge in relation to the others segments studied. (AU)

Buscou-se analisar em suínos jovens e adultos, sob microscopia de luz, as características morfológicas dos ramos arteriais coronarianos sob as pontes de miocárdio, bem como dos segmentos pré-pontino e pós-pontino, na tentativa de estabelecer correlações morfofuncionais entre eles. Foram utilizados 40 corações de suínos para a pesquisa, todos fêmeas sem raça definida, sendo 20 jovens e 20 adultos, todos portadores de pontes de miocárdio, dos quais foram retirados fragmentos pré-pontino, pontino e pós-pontino de ramos da artéria coronária direita e esquerda, junto com o tecido circunjacente. Os segmentos foram submetidos às técnicas habituais da microscopia de luz e corados pela hematoxilina-eosina. Observou-se alterações da íntima, tais como espessamentos, células com citoplasma claro, ruptura e/ou duplicação da lâmina limitante elástica interna. O teste estatístico se mostrou significativo para posição em suínos adultos, confirmando que existe uma maior frequência de lesões no segmento pré-pontino da túnica íntima das artérias coronárias quando comparado com o segmento pontino e com o pós-pontino. O mesmo teste confirmou uma variação na frequência de lesões entre as amostras estudadas, sendo maior em animais jovens quando defrontado com animais adultos. Paraos animais jovens, o teste não se apresentou significativo para a variável posição entre nenhum dos segmentos comparados entre si. Concluiu-se, estatisticamente, uma maior ocorrência de lesões ateroscleróticas nos segmentos arteriais que antecedem a ponte de miocárdio em relação aos demais segmentos estudados.(AU)

Vascular calcification in atherosclerosis: potential roles of macrophages and non-coding micro-RNAs / Calcificación vascular en aterosclerosis: posibles funciones de macrófagos y micro-ARNs no codificantes

Coronary heart disease, a leading cause of death in western societies, is caused by the presence of atherosclerotic plaques in the coronary arteries. Calcification is a frequent complication of atherosclerotic plaques, and often a contributing factor to their instability and rupture. Endothelial cells, smooth muscle cells and plaque macrophages, all contribute to the calcification process, which is reminiscent of that underlying bone formation. In particular, the role of macrophages in calcification has long been recognized, but whether or not distinct macrophage subsets ­v.g., M1 or inflammatory, and M2 or antinflammatory have specific functions in osteogenic signaling within the context of plaque calcification remains poorly understood. Over the past few years, accumulated evidence has revealed novel roles of non-coding micro-RNAs (miRs) in atherorelevant functions of macrophages and in mechanisms linked to macrophage divergence into different subtypes. In this article we discuss some salient findings on potential roles of miRs in vascular calcification, with focus on those miRs that have also been associated to macrophage differentiation, and speculate on their potential relation to M1 and M2 macrophages in the context of calcification of atherosclerotic plaques. (AU)

La enfermedad cardíaca coronaria, principal causa de muerte en occidente, es causada por la presencia de placas ateroscleróticas en las arterias coronarias. La presencia de depósitos de calcificación es una complicación frecuente de la placa, y puede contribuir a la inestabilidad y ruptura de la misma. El proceso de calcificación de la placa es similar al que ocurre en hueso, y contribuyen al mismo, mecanismos dependientes de células endoteliales, células musculares lisas y macrófagos, células que están presentes en todas las etapas de desarrollo de la placa aterosclerótica. El rol de los macrófagos en la calcificación de la placa se conoce desde hace tiempo, pero la contribución de los distintos tipos de macrófagos ­por ejemplo, M1 o tipo inflamatorio, y M2 o tipo antiinflamatorio a mecanismos de señalización osteogénica en dicho contexto aún no se conoce. Recientemente varios trabajos experimentales han revelado la existencia de nuevos roles de micro-ARNs no codificantes (miRs) en varias funciones de los macrófagos que son de relevancia en el proceso aterogénico, como así también en mecanismos relacionados a la diferenciación de macrófagos en subtipos específicos. En este artículo discutimos algunos de los hallazgos más importantes sobre posibles nuevos roles de miRs en calcificación vascular, poniendo énfasis en aquellos miRs que han sido también asociados a la diferenciación de macrófagos, y especulamos acerca de su posible relación con macrófagos M1 y M2 en el contexto de la calcificación de la placa aterosclerótica. (AU)

A Novel Algorithm to Quantify Coronary Remodeling Using Inferred Normal Dimensions.

BACKGROUND: Vascular remodeling, the dynamic dimensional change in face of stress, can assume different directions as well as magnitudes in atherosclerotic disease. Classical measurements rely on reference to segments at a distance, risking inappropriate comparison between dislike vessel portions. OBJECTIVE: to explore a new method for quantifying vessel remodeling, based on the comparison between a given target segment and its inferred normal dimensions. METHODS: Geometric parameters and plaque composition were determined in 67 patients using three-vessel intravascular ultrasound with virtual histology (IVUS-VH). Coronary vessel remodeling at cross-section (n = 27.639) and lesion (n = 618) levels was assessed using classical metrics and a novel analytic algorithm based on the fractional vessel remodeling index (FVRI), which quantifies the total change in arterial wall dimensions related to the estimated normal dimension of the vessel. A prediction model was built to estimate the normal dimension of the vessel for calculation of FVRI. RESULTS: According to the new algorithm, "Ectatic" remodeling pattern was least common, "Complete compensatory" remodeling was present in approximately half of the instances, and "Negative" and "Incomplete compensatory" remodeling types were detected in the remaining. Compared to a traditional diagnostic scheme, FVRI-based classification seemed to better discriminate plaque composition by IVUS-VH. CONCLUSION: Quantitative assessment of coronary remodeling using target segment dimensions offers a promising approach to evaluate the vessel response to plaque growth/regression.

A Novel Algorithm to Quantify Coronary Remodeling Using Inferred Normal Dimensions / Novo Algoritmo para Quantificar o Remodelamento Coronário Utilizando Dimensões Normais Preditas

Background:Vascular remodeling, the dynamic dimensional change in face of stress, can assume different directions as well as magnitudes in atherosclerotic disease. Classical measurements rely on reference to segments at a distance, risking inappropriate comparison between dislike vessel portions.Objective:to explore a new method for quantifying vessel remodeling, based on the comparison between a given target segment and its inferred normal dimensions.Methods:Geometric parameters and plaque composition were determined in 67 patients using three-vessel intravascular ultrasound with virtual histology (IVUS-VH). Coronary vessel remodeling at cross-section (n = 27.639) and lesion (n = 618) levels was assessed using classical metrics and a novel analytic algorithm based on the fractional vessel remodeling index (FVRI), which quantifies the total change in arterial wall dimensions related to the estimated normal dimension of the vessel. A prediction model was built to estimate the normal dimension of the vessel for calculation of FVRI.Results:According to the new algorithm, “Ectatic” remodeling pattern was least common, “Complete compensatory” remodeling was present in approximately half of the instances, and “Negative” and “Incomplete compensatory” remodeling types were detected in the remaining. Compared to a traditional diagnostic scheme, FVRI-based classification seemed to better discriminate plaque composition by IVUS-VH.Conclusion:Quantitative assessment of coronary remodeling using target segment dimensions offers a promising approach to evaluate the vessel response to plaque growth/regression.

Fundamento:O remodelamento vascular, alteração dimensional dinâmica frente ao estresse, pode assumir diferentes direções e magnitudes na doença aterosclerótica. As medidas clássicas baseiam-se em referências a distância do segmento-alvo, com risco de comparação inadequada pela seleção de porções vasculares indesejáveis.Objetivo:Explorar um novo método para quantificar remodelamento vascular, baseado na comparação entre um determinado segmento-alvo e suas dimensões normais inferidas.Métodos:Parâmetros geométricos e a composição da placa foram determinados em 67 pacientes usando-se ultrassom intravascular de três vasos com histologia virtual (IVUS-VH). Avaliou-se o remodelamento coronário ao nível da seção transversal (n = 27.639) e da lesão (n = 618) usando-se métrica clássica e um novo algoritmo analítico baseado no índice de remodelamento vascular fracionado (FVRI) que quantifica a alteração total nas dimensões da parede arterial em relação a dimensão normal estimada do vaso. Construiu-se um modelo preditivo para estimar a dimensão normal do vaso para calcular o FVRI.Resultados:De acordo com o novo algoritmo, o padrão de remodelamento “ectásico” foi o menos comum, o remodelamento “completo compensatório” foi observado em metade dos casos, e os tipos “negativo” e “incompleto compensatório” foram detectados nos restantes. Comparada ao esquema tradicional diagnóstico, a classificação baseada no FVRI pareceu melhor discriminar a composição da placa através de IVUS-VH.Conclusão:A análise quantitativa do remodelamento coronário utilizando dimensões do segmento-alvo oferece uma abordagem promissora para avaliar a resposta vascular ao crescimento e à regressão da placa.

Role of chemokines in promoting instability of coronary atherosclerotic plaques and the underlying molecular mechanism

Our aim was to investigate the role of chemokines in promoting instability of coronary atherosclerotic plaques and the underlying molecular mechanism. Coronary angiography and intravascular ultrasound (IVUS) were performed in 60 stable angina pectoris (SAP) patients and 60 unstable angina pectoris (UAP) patients. The chemotactic activity of monocytes in the 2 groups of patients was examined in Transwell chambers. High-sensitivity C-reactive protein (hs-CRP), monocyte chemoattractant protein-1 (MCP-1), regulated on activation in normal T-cell expressed and secreted (RANTES), and fractalkine in serum were examined with ELISA kits, and expression of MCP-1, RANTES, and fractalkine mRNA was examined with real-time PCR. In the SAP group, 92 plaques were detected with IVUS. In the UAP group, 96 plaques were detected with IVUS. The plaques in the UAP group were mainly lipid 51.04% (49/96) and the plaques in the SAP group were mainly fibrous 52.17% (48/92). Compared with the SAP group, the plaque burden and vascular remodeling index in the UAP group were significantly greater than in the SAP group (P<0.01). Chemotactic activity and the number of mobile monocytes in the UAP group were significantly greater than in the SAP group (P<0.01). Concentrations of hs-CRP, MCP-1, RANTES, and fractalkine in the serum of the UAP group were significantly higher than in the serum of the SAP group (P<0.05 or P<0.01), and expression of MCP-1, RANTES, and fractalkine mRNA was significantly higher than in the SAP group (P<0.05). MCP-1, RANTES, and fractalkine probably promote instability of coronary atherosclerotic plaque.

Role of chemokines in promoting instability of coronary atherosclerotic plaques and the underlying molecular mechanism.

Our aim was to investigate the role of chemokines in promoting instability of coronary atherosclerotic plaques and the underlying molecular mechanism. Coronary angiography and intravascular ultrasound (IVUS) were performed in 60 stable angina pectoris (SAP) patients and 60 unstable angina pectoris (UAP) patients. The chemotactic activity of monocytes in the 2 groups of patients was examined in Transwell chambers. High-sensitivity C-reactive protein (hs-CRP), monocyte chemoattractant protein-1 (MCP-1), regulated on activation in normal T-cell expressed and secreted (RANTES), and fractalkine in serum were examined with ELISA kits, and expression of MCP-1, RANTES, and fractalkine mRNA was examined with real-time PCR. In the SAP group, 92 plaques were detected with IVUS. In the UAP group, 96 plaques were detected with IVUS. The plaques in the UAP group were mainly lipid 51.04% (49/96) and the plaques in the SAP group were mainly fibrous 52.17% (48/92). Compared with the SAP group, the plaque burden and vascular remodeling index in the UAP group were significantly greater than in the SAP group (P<0.01). Chemotactic activity and the number of mobile monocytes in the UAP group were significantly greater than in the SAP group (P<0.01). Concentrations of hs-CRP, MCP-1, RANTES, and fractalkine in the serum of the UAP group were significantly higher than in the serum of the SAP group (P<0.05 or P<0.01), and expression of MCP-1, RANTES, and fractalkine mRNA was significantly higher than in the SAP group (P<0.05). MCP-1, RANTES, and fractalkine probably promote instability of coronary atherosclerotic plaque.

Coronary plaque rupture in patients with myocardial infarction after noncardiac surgery: frequent and dangerous.

PURPOSE: The pathophysiology of acute coronary syndromes (ACS) after noncardiac surgery is not established yet. Thrombosis over a vulnerable plaque or decreased oxygen supply secondary to anemia or hypotension may be involved. The purpose of this study was to investigate the pathophysiology of ACS complicating noncardiac surgery. METHODS: Clinical and angiographic data were prospectively recorded into a database for 120 consecutive patients that had an ACS after noncardiac surgery (PACS), for 120 patients with spontaneous ACS (SACS), and 240 patients with stable coronary artery disease (CAD). Coronary lesions with obstructions greater than 50% were classified based on two criteria: Ambrose's classification and complex morphology. The presence of Ambrose's type II or complex lesions were compared between the three groups. RESULTS: We analyzed 1470 lesions in 480 patients. In PACS group, 45% of patients had Ambrose's type II lesions vs. 56.7% in SACS group and 16.4% in stable CAD group (P<0.001). Both PACS and SACS patients had more complex lesions than patients in stable CAD group (56.7% vs. 79.2% vs. 31.8%, respectively; P<0.001). Overall, the independent predictors of plaque rupture were being in the group PACS (P<0.001, OR 2.86; CI, 1.82-4.52 for complex lesions and P<0.001, OR 3.43; CI, 2.1-5.6 for Ambrose's type II lesions) or SACS (P<0.001, OR 8.71; CI, 5.15-14.73 for complex lesions and P<0.001, OR 5.99; CI, 3.66-9.81 for Ambrose's type II lesions). CONCLUSIONS: Nearly 50% of patients with perioperative ACS have evidence of coronary plaque rupture, characterizing a type 1 myocardial infarction.

Effects of linseed consumption for a short period of time on lipid profile and atherosclerotic lesions in rabbits fed a hypercholesterolaemic diet.

Linseed contains biologically active substances, such as lignans, fibres and linoleic acid, which are believed to provide cardioprotective effects. The objective of the present study was to assess the potential hypolipaemic, anti-atherogenic and anti-inflammatory effects of linseed consumption using an experimental animal model, with rabbits fed a hypercholesterolaemic diet (1 % cholesterol extracted from lyophilised egg). A total of twenty white male rabbits were selected and divided into two groups: group I (GI), control group, ten rabbits; group II (GII), ten rabbits. The animals were fed a hypercholesterolaemic diet for 56 d. For the GII diet, ground linseed was added from day 29 through to day 56. Animals underwent aortic arch and descending aorta dissection on day 56 for histological, morphometric and immunohistochemical analysis. At the end of the experiment, GII animals presented with lower levels of total cholesterol (TC, 10 068·3 v. 16 767·0 mg/l; P < 0·05) and lower levels of LDL-cholesterol (LDL-C; 10 743·2 v. 15 961·2 mg/l; P < 0·05) when compared with the GI control group. There was no significant difference in serum HDL-cholesterol and TAG between the two groups. Almost all animals exhibited type III atherosclerotic lesions in the descending aorta. There was no statistically significant difference between the intima area and the intima:media layer area ratio in both groups. There was no difference between the positive areas for vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 molecules between the groups. Linseed consumption showed hypolipaemic action by reducing LDL-C and TC levels; however, this cholesterol-lowering effect did not reduce the atherosclerotic lesions induced by a hypercholesterolaemic diet (1 % cholesterol) for a short period of time.