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Cholesterol crystal embolism is the effect of the destabilization of an atherosclerotic plaque after a triggering event, producing the migration of cholesterol crystals to peripheral arterioles, triggering an endothelial inflammatory process; the clinical spectrum varies from being asymptomatic to having multiple organ involvement; diagnostic suspicion is mainly clinical and the skin biopsy will confirm the diagnosis due to its easy accessibility. The treatment is still controversial and there is no consensus on the therapeutic measures to apply. Below is the case of a 72-year-old male patient with atheroembolism due to cholesterol crystals in the lower limbs, secondary to endovascular manipulation by prior angioplasty. [ABSTRACT FROM AUTHOR]

Copyright of Revista Argentina de Cardiología is the property of Sociedad Argentina de Cardiologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Latinoamericana de Hipertension is the property of Revista Latinoamericana de Hipertension and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Despite advancements in multi-modal imaging techniques, a substantial portion of ischemic stroke patients today remain without a diagnosed etiology after conventional workup. Based on existing diagnostic criteria, these ischemic stroke patients are subcategorized into having cryptogenic stroke (CS) or embolic stroke of undetermined source (ESUS). There is growing evidence that in these patients, non-cardiogenic embolic sources, in particular non-stenosing atherosclerotic plaque, may have significant contributory roles in their ischemic strokes. Recent advancements in vessel wall MRI (VW-MRI) have enabled imaging of vessel walls beyond the degree of luminal stenosis, and allows further characterization of atherosclerotic plaque components. Using this imaging technique, we are able to identify potential imaging biomarkers of vulnerable atherosclerotic plaques such as intraplaque hemorrhage, lipid rich necrotic core, and thin or ruptured fibrous caps. This review focuses on the existing evidence on the advantages of utilizing VW-MRI in ischemic stroke patients to identify culprit plaques in key anatomical areas, namely the cervical carotid arteries, intracranial arteries, and the aortic arch. For each anatomical area, the literature on potential imaging biomarkers of vulnerable plaques on VW-MRI as well as the VW-MRI literature in ESUS and CS patients are reviewed. Future directions on further elucidating ESUS and CS by the use of VW-MRI as well as exciting emerging techniques are reviewed. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular diseases are the principal cause of morbidity and mortality worldwide. Obesity, sarcopenia, insufficient physical activity, and sedentary behaviors synergistically impact cardiovascular risk. Objective: Evaluate cardiovascular risk in relation to physical activity, sedentary behaviors, and body composition. Materials and Methods: Cross-sectional observational study in 95 total males and females. Cardiovascular risk was determined using the Framingham score, which corrects for total area of atherosclerotic plaque. Risk was also determined using body composition, anthropometry, bioimpedance and dynamometry as indirect indicators, physical activity, sedentary behaviors, and a validated questionnaire. Descriptive, correlation and association analyses were conducted with 95% confidence. Results: 95% of women and 98% of men presented with an elevated cardiovascular risk; 51.5% with obesity, 95.5% central obesity, and 47.3% with diminished muscular strength. Significant positive associations were observed between cardiovascular risk and waist circumference (rho=0.26; p=0.024). There was no significant association between muscle strength and cardiovascular risk (rho=-0.21, p=0.065). Sedentary behavior increased cardiovascular risk (OR=3.9; p=0.033). Conclusions: Central obesity and staying more than six hours per day in a sitting position are factors associated with cardiovascular risk. [ABSTRACT FROM AUTHOR]

Copyright of Revista Latinoamericana de Hipertension is the property of Revista Latinoamericana de Hipertension and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Latinoamericana de Hipertension is the property of Revista Latinoamericana de Hipertension and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Argentina de Cardiología is the property of Sociedad Argentina de Cardiologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Coronary atherosclerotic disease is a major cause of death in Cuba and elsewhere. The volume of epicardial fat is considered a new cardiovascular risk factor because of its association with coronary atherogenesis. Objective: To determine, by multislice computed tomography, the association between epicardial fat volume and the presence of coronary atherosclerotic plaques. Method: A descriptive study was conducted with a universe of 130 patients with chest pain suggestive of ischemic heart disease, of which 117 were selected by opinion sampling. These patients underwent a calcium score study, a coronary angiography and a measurement of the epicardial fat volume. Results: Male patients predominated (54.7%) and those aged 60-69 years (32.5%). A high volume of epicardial fat was found in 51.3% of patients, affecting 52.8% of women; 78.9% of patients with a calcium score between 100 and 399 UH had a high volume of epicardial fat, just as 71.2% of those with plaques and 100% of those with 4 or 5 plaques; 41% of patients had various types of plaque, which were mainly located in the anterior descending artery (88.1%). Conclusions: The measurement of the volume of epicardial fat is a useful tool to estimate the presence of coronary disease. When it was high, it was associated with older age, female gender and the presence of a higher calcium score, more plaques, more injuries and a greater involvement of the anterior descending artery. [ABSTRACT FROM AUTHOR]

The asymmetric dimethylarginine (ADMA) is an inhibitor of nitric oxide synthase (NOS) and a mediator of endothelial dysfunction and cardiovascular diasease. The objective of the present study was to determine serum concentration ADMA and its relationship with aortic lesions development in rabbits. Thirty male New Zealand rabbits, divided into two similar groups were used in this study: Group 1: fed with a commercial rabbit food (Conejarina) and vegetables, Group 2: fed with eggs and Conejarina. The experiment lasted 12 weeks and the lipid profile was assayed by enzymatic methods, ADMA was assayed by ELISA at weeks 0, 6 and 12. A histological study of rabbits aorta was done. Results revealed that in group 2, ADMA showed increased levels at week 6 and 12 of the study (p <0.05). Regarding atheroma development, group 2 presented arterial lesions. In conclusion, ADMA can be considered as a marker of atherosclerosis according to our experimental results. [ABSTRACT FROM AUTHOR]

Evolution of atheroma usually take many years and this process is stimulated by a high dietary intake of cholesterol and both, saturated and trans fatty acids, added to accelerating factors such as tobacco, stress, diabetes, arterial hypertension, sedentary life style and obesity. Histopathology of the plaque reveals recruitment of Th 1 helper lymphocytes which destabilizes the atheroma, making it vulnerable to occlusion because of erosions and fissures; then adhering platelets and blood cells to its surface ensuing a myocardial infarction. On the contrary, plaque stabilization avoids its rupture, a result that can be achieved through reduction of the inflammatory activity in the plaque with medications that reduce its lipid content or by impairing macrophage activity inside the plaque. The former objectives can be obtained by 1) stoping LDL-c deposit 2) increasing reverse cholesterol transport with HDL-c 3) promoting foam cells death or macrophage migration or 4) remotion of the necrotic core of the atheroma. Studies of pharmacological regression of the atheromatous plaque in humans started several years ago with niacin; then with simvastatin (a HMG CoA reductase inhibitor) combined to niacin that increased by 26% HDL-c and reduced 42% LDL-c, a finding associated to 0,4% reduction of angiographically demonstrated coronary stenosis and surprisingly to 87% lowering of acute coronary risk events. On the other hand, recombinant apoA-I Milano, intravenously injected, also induce 4,2% regression of the atheroma volume in comparison to 0,14% decreased volume reduction with placebo. It is worth to consider renin-angiotensin-aldosterone system actively participate in atheroma development because olmesartan, an angiotensin II antagonist molecule (ARA II), reduce in 5,4% coronary atheroma volume, compared to 0,6% reduction obtained with a control treatment; this change was associated to a longer survival of patients without major cardiovascular events in comparison to the control group. This result points to an important cardiovascular protecting effect of ARA II agents. [ABSTRACT FROM AUTHOR]

Objetive: identify the extent or presence of periodontal disease presenting patients hospitalized with diagnosis established by TAC of ischemic stroke within the first seven days of evolution. Introduction: ischemic attack or cerebral ischemia is damage to the brain due to reduced blood supply, oxygen and nutrients when vessels responsible for this task are clogged. In this case the nerve cells in the affected area may die within minutes. This damage can cause impairments in body functions such as speech, memory and /or movement depending on the brain area affected. When this obstruction is greater than 24 hours is established ischemic cerebrovascular event, but when this is shorter than the time range is called a transient ischemic attack. The pathogenesis of periodontal disease is complex because it is a combination of the initiation and maintenance of chronic inflammation by diverse flora and microbio I products plaque. Subsequent host response to this infection is mediated by a pattern of tissue destruction. Periodontitis is associated with elevated markers of inflammation that are considered themselves as risk for ischemic stroke, and there is evidence that these bacteria are found in carotid plaques, although their role in atherogenesis is not welld defined. Materials and methods: we included patients hospitalized for four health institutions with confirmed diagnosis of ischemic stroke associated with periodontal disease, previous valuation Critical Medicine and then are evaluated periodontally. PS.NI were evaluated, was included in laboratory studies BH, QS and examinations of the CT cabinet. Results: the results show that patients with a diagnosis of ischemic stroke periodontal disease had moderate to severe against hospital controls and population groups, this allows the two entities associated pathologies in order to make prevention and treatment of various patient groups. Conclusions: in this study it was determined that 1 00% of patients with periodontal indices showed ACI characteristic moderate and advanced chronic EP, as well as the need for specialized dental care for patients in hospitals of intensive, where inability exists that patients have good control of oral hygiene. [ABSTRACT FROM AUTHOR]

Background. Cardiovascular diseases are the leading cause of death in the world. In developed countries there are technological advances that help detect diseases using ultrasound studies designed by research groups at different French and British universities. Regrettably, government hospitals in Mexico do not have access to them on account of their high cost. Purpose. Offer the medical community a software tool that provides automated diagnoses to identify and quantify cardiovascular risk and lesions. Method. Computerized methods were implemented with the intention of obtaining results, quickly and accurately, in calculating cardiovascular risk and detecting atherosclerosis, atheromatous plaques, and endothelial dysfunction, all by means of digital image processing algorithms based on rules of prediction that use statistical definitions for pattern generation and acquisition systems, thereby complementing detection methods using arterial images and pattern extraction to determine diameters and thicknesses of vascular layers, which indicate the presence and severity of vascular disorders, with the precision needed to favor clinical monitoring of patients. Conclusions. The software system developed for this project is capable of diagnosing atherosclerosis, endothelial dysfunction, and atheromatous plaques, providing accurate measurements on areas which comprise only the zones of analysis without phase shift or omission. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVD) are the leading cause of death in the world. Among them the ischemic type are of great importance, where the development of atherosclerotic plaques is the central pathophysiological process. The study of atherosclerosis is critical to understand how this disease process begins and factors influencing its development. Various laboratory methods, including immunohistochemistry, allow the recognition of ceils and molecules involved in the atheromatous process that are interacting according to the progression of the lesion. A marker of endothelial dysfunction is the increased expression of intercellular adhesion molecule ICAM- 1. In this paper, an immunohistochemistry method was standardized for the adhesion molecule ICAM- 1, and its expression was studied in healthy human arteries with atheromatous plaque. In samples of human arteries with atherosclerotic disease, the expression of ICAM- 1 was observed to be increased, but was hardly recognizable. This mainly because the tissue used as a control for standardization was a tonsil with an inflammatory process and hyperplasia, which significantly increases the expression of ICAM-1. The implementation of the immunohistochemistry method for ICAM- 1 in human arteries will reveal endothelial dysfunction states that will enable a future design and implementation of methods of diag- nosis in atherosclerotic processes in the early stages. [ABSTRACT FROM AUTHOR]

Phytosterols and phytostanols, are molecules that have identical structure, except that the latter are saturated (no double bonds in their structure base). In nature are found in all plant foods, especially vegetable oils and stanols are not abundant, but can also be obtained chemically by hydrogenation of sterols. Molecules are structurally similar to cholesterol and have been shown that their intake has a number of beneficial effects on our body. The most obvious is the inhibition of cholesterol absorption (lowers total cholesterol and LDL cholesterol). Risk factor for the formation and progression of atherosclerotic plaque recommended daily intake of 2 g. They have, other properties: immunomodulatory, anti-inflammatory, antitumor, antibacterial and antifungal. (Rev Horiz Med 2011;11(2):93) [ABSTRACT FROM AUTHOR]

Whereas hormonal therapy (HT) may increase the risk of coronary heart disease (CHD) and stroke in menopausal women, epidemiological studies (protection in premenopausal women) suggest and experimental studies (prevention of fatty streak development in animals) demonstrate a major atheroprotective action of estradiol (E2). The understanding of the deleterious and beneficial effects of estrogens is thus required at both a cellular and molecular level. Both the endothelium and the immuno-inflammatory system play a key role in the development of fatty streak deposit as well as in the rupture of the atherosclerotic plaque. Whereas E2 favors an anti-inflammatory effect in vitro (cultured cells), it rather elicits a pro-inflammatory response in vivo at the level of several subpopulations of the immuno-inflammatory system, which could contribute to plaque destabilization. E2 promotes beneficial actions on the endothelium such as nitric oxide and prostacyclin production. E2 actions are essentially mediated by two molecular targets: estrogen receptor α (ER-α) and β (ER-β, but the former appears to mediate most of the actions of E2 on the endothelium and on the immune system. ER-α modulates target gene transcription through two activation functions (AF), AF-I and AF-2, even though signalling via ER-α located at the plasma membrane (responsible for membrane-initiated steroid signalling [MISS]/ [extra-genomic]) can also lead to an indirect effect on gene transcription. Recently, we demonstrated that ER-α AF-I is not required for the vasculoprotective actions of E2, whereas it is necessary for the effects of E2 on its reproductive targets. These results suggest that selective estrogen receptor modulators stimulating ER-α with minimal activation of ER-α AF-I could retain beneficial vascular actions, while minimizing the sexual effects. [ABSTRACT FROM AUTHOR]

The aortic aneurysm is part of the acute aortic syndromes (AAS). Aortic aneurysms have a weakened tunica media. Acute aneurysm expansion may herald rupture with high morbility and mortality. Five percent of AAS are diagnosed as pentetrating atherosclerotic ulcer which is an ulceration of an atherosclerotic lesion of the aorta that penetrates the internal elastic lamina and allows hematoma formation within the tunica media of the aortic wall. Endovascular treatment is an alternative to surgery and has provided an adequate rate of successful repair. There is another type of treatment which combines surgery and endovascular repair (the hybrid open-endovascular repair) which provides adequate results. The afford mention case is about a patient with a penetrating atherosclerotic ulcer. The hematoma that results from this ulcer extends and self-contains the aneurysm, with a high risk of rupture. We will also describe the aneurysm treatment options. [ABSTRACT FROM AUTHOR]

Introduction: We studied plasmatic TNF-α, nitric oxide (NO) and citrulline behaviors and probable morphological mitochondrial alterations in aortic smooth muscle cells, in rats with atherogenesis induced by hyperfibrinogenemia in: A) control, B) multiple injured for 30 days and C) multiple injured for 60 days. Material and methods: Hyperfibrinogenemia induction: adrenaline injection (0,1mg/rat/day). TNF-α (pg/dL) was determined by Elisa and NO (μM) and citrulline (mM) by spectrophotometry. Morphological mitochondrial alterations were studied by electronic microscopy. Variables were analized: ANOVA, r coefficient and X² test. Results: We observed a significant increment of TNF-α in multiple injured for 30 days (B) (50.05±2.29) as well as in multiple injured for 60 days (C) (74.99±2.82) related to control (A) (33.01±1.49) (p<0.001 in both groups). Citrulline presented a significant increased in (B) (5.56±0.20) and (C) (6.84±0.13) when compared to (A) (4.41±0.23) (p<0.001 in both situations). Mean while NO biodisponibility diminished significantly in (B) (8.97±0.70) and in (C) (5.32±0.68) when compared to (A) (21.65±1.74) (p<0.001 in both situations). Conclusions: Hyperfibrinogenemia could modify the NO physiopathological pathway and produced morphological mitochondrial alterations in aortic smooth muscle cells, probably producing ischemic lesions in the vascular wall and altering the vasodilatation response. [ABSTRACT FROM AUTHOR]

Inflammation plays an important role in the development of atherosclerotic lesions, affecting several stages of the atheroma's development going from the initial leukocyte recruitment to the eventual rupture of the unstable atherosclerotic plaque. The inflammatory reactions within coronary atheroscterotic plaques influence the clinical outcome of acute coronary syndromes and coronary artery disease. Recent studies suggest that inflammation markers may reflect different aspects of the atherothrombotic process in relation to the stages of acute coronary syndrome. These markers play an important rote in the risk of developing coronary artery disease, and may correlate with its severity. Some cytokines, acute phase proteins, acute phase reactants proteins, and adhesion molecules released from the inflammatory cells may reflect the inflammatory process in atherosclerotic plaques. However, it remains to be determined whether these pro- and anti-inflammation markers may confer risk or protection for cardiovascular disease, or simply reflect the underlying disease process. The analysis of the markers may be useful for the development of new strategies for coronary disease prevention and treatment. Therefore, we need a well-designed evaluation of these markers before their use in the clinical practice. [ABSTRACT FROM AUTHOR]

Antioxidants have been used to slow down or inhibit atherosclerosis. The objective of the present study was to compare the effect of pinus maritime, and of vitamins C and E, separately and combined, on serum concentration of oxLDL, E-selectin, IL-6, CRP and on the formation of aortic lesions in rabbits. 84 rabbits were studied: Group 1: commercial rabbit food (CRF) and vegetables. Group 2: Egg and (CRF). Group 3: Egg, (CRF) and Pinus maritime. Group 4: Egg, (CRF) and vitamin C. Group 5: Egg, (CRF) and vitamin E. Group 6: Egg, (CRF), Pinus maritime and vitamin C. Group 7: Egg, (CRF), Pinus maritime and vitamin E. The experiment lasted 12 weeks. Lipid profile, oxLDL, E-selectin, IL-6, vitamin E, vitamin C, PCR and histological study of rabbits' aorta were performed. Antioxidant supplement decreased oxLDL, E-selectine, IL-6 (p<0,05) and inhibited aortic lesions. In conclusion, antioxidants were effective in slowing down inflammation and oxidation markers, and the formation and progression of atheroma. [ABSTRACT FROM AUTHOR]

An ideal experimental model of cerebral aneurysm is of great importance for studying the pathogenesis of this lesion and also for testing new techniques for diagnosis and treatment. Objective: we evaluated the feasibility and usefulness of an experimental model of sidewall sacular aneurysm made of a vein graft from the inferior cava vein anastomosed in situ to the infrarenal abdominal aorta of a Wistar rat. Methods: an experimental model of aneurysm was developed, using 36 rats operated with microsurgery technique; we anastomose a segment of the inferior cava vein to the infrarenal abdominal aorta of a Wistar rat. After a follow-up of 2 months, the rats were sacrifice for histological analysis. Results: thirty rats complete the follow up, with a good tolerance to the occlusion of the inferior cava vein; there were no cases of spontaneous occlusion of the aneurysms. Seventy percent of the aneurysm increase their initial diameter, we confirm the presence of intra-aneurysmal thrombi specially on those aneurysms that grew, some develop two or more lobulations on the aneurysm sac, and atheromatous plaque on the aneurysmatic wall. Conclusions: this model of sidewall aneurysms has a low incidence of spontaneous trombosis, the microsurgery technique is easy, reproducible and we do not need to take out an additional venous graft. Most of these aneurysms increase their initial length and have resamblance with the hystologic features of the human giant aneurysms. [ABSTRACT FROM AUTHOR]

Objectives: To demonstrate that inflammatory atheromatose carotid plaques can be visualized with positron emission tomography with 18F-fluorodeoxyglucose (18FDG PET) in symptomatic patients, in order to correlate them with systemic inflammatory markers, such as CRP. Method: Fifteen patients with cerebral ischemia due to atherosclerotic carotid disease were studied. 18FDG uptake with PET was considered and blood samples were taken for determining high sensibility C reactive protein (HsCRP). Results: The mean age of the patients was 66 years; 11 of them were males (73%) and 4 were females (27%). 18FDG PET was positive in 12 patients (80%), while 100% of the studied population had low risk HsCRP with normal white cell count. Conclusions: 18FDG PET proves active inflammation in carotid atheromatose plaques. There was no significant correlation between the presence of ahteromatose carotid plaques, HsCRP serum levels, and 18FDG PET study. [ABSTRACT FROM AUTHOR]

Antecedents. At the present time in diverse studies as North American Symptomatic Carotid Endarterectomy Trial and Europe Carotid Surgery Trial, surgery in patients with equal or greater 50% stenosis in the carotid bifurcation result in a statistically significant diminution in the average of apoplexies compared with groups with medical treatment. Objective. To describe Service of Angiología and Vascular Surgery of the Hospital Central Militar experience in atherosclerotic disease of the carotid surgical treatment. Method. Descriptive retrospective-prospective study of patients subjected to surgical treatment of atherosclerotic disease of the carotid from January 2004 to April 2006. A descriptive statistical analysis was applied. Results. A total of 72 endarterectomies was made, in 61 patients. The greater mortality average and neurological deficit was of 2%, NASCET, ACAS and ESCT studies, report a mortality index from 2.8 to 3.5%, with complications of the wound (infection and hematomas) index below the reported in these publications. Conclusion. Secondary mortality and morbidity to the surgical treatment of the atherosclerotic disease of the carotid are similar to reported in the international studies. [ABSTRACT FROM AUTHOR]