Arteriosclerose, aterosclerose, arteriolosclerose e esclerose calcificante da média de Monckeberg: qual a diferença? / Arteriosclerosis, atherosclerosis, arteriolosclerosis, and Monckeberg medial calcific sclerosis: what is the difference?

Resumo A principal causa de óbito na contemporaneidade são as doenças cardiovasculares. Arteriosclerose, aterosclerose, arteriolosclerose e arteriosclerose de Monckeberg são termos frequentemente utilizados como sinônimos, mas traduzem alterações distintas. O objetivo desta revisão foi discutir os conceitos de arteriosclerose, aterosclerose, arteriolosclerose e esclerose calcificante da média de Monckeberg. O termo arteriosclerose é considerado mais genérico, significando o enrijecimento e a consequente perda de elasticidade da parede arterial, abarcando os demais tipos. A aterosclerose é uma doença inflamatória secundária a lesões na camada íntima, que tem como principal complicação obstrução crônica e aguda do lúmen arterial. A arteriolosclerose se refere ao espessamento das arteríolas, particularmente relacionada à hipertensão arterial sistêmica. Já a esclerose calcificante da média de Monckeberg designa a calcificação, não obstrutiva, da lâmina elástica interna ou da túnica média de artérias musculares. As calcificações vasculares, que incluem lesões ateroscleróticas e a esclerose calcificante da média de Monckeberg, vêm sendo estudadas como um fator de risco para a morbimortalidade cardiovascular.

Abstract Cardiovascular diseases are the main cause of death in contemporary times. Arteriosclerosis, atherosclerosis, arteriolosclerosis, and Monckeberg's arteriosclerosis are terms that are often used interchangeably, but they refer to different vascular pathologies. The objective of this study is to review the concepts of atherosclerosis, atherosclerosis, arteriosclerosis and Monckeberg medial calcific sclerosis (MMCS). The term arteriosclerosis is more generic, meaning the stiffening and consequent loss of elasticity of the arterial wall, and encompasses the other terms. Atherosclerosis is an inflammatory disease secondary to lesions in the intimal layer and whose main complication is acute and chronic obstruction of the arterial lumen. Arteriolosclerosis refers to thickening of arterioles, particularly in association with systemic arterial hypertension. MMCS refers to non-obstructive calcification in the internal elastic lamina or the tunica media of muscular arteries. Vascular calcifications, which include atherosclerotic lesions and MMCS, have been studied as a risk factor for cardiovascular morbidity and mortality.

Intra- and extracranial atherosclerotic disease: casting a new light on emerging trends.

Intra- and extracranial atherosclerotic stenosis has been shown to be associated with an increased risk of secondary stroke mortality. Advances in invasive and non-invasive imaging modalities have improved analysis of hemodynamic changes and allowed better delineation of the integrity of intracranial collateralization and plague morphology in patients with artery stenosis. This review focuses on new imaging modalities and clinical applications of currently available techniques, and provides significant insight into future directions in comprehensive analysis of intra- and extracranial atherosclerotic stenosis.

Arteriosclerosis: facts and fancy.

Arterial vascular diseases comprise the leading cause of death in the industrialized world. Every physician learns about the pathology of these diseases in medical school. All pathologists evaluate arterial disease in surgical pathology and/or autopsy specimens. All clinicians encounter patients with clinical manifestations of these diseases. With such a common and clinically-important group of entities one would think there would be a general understanding of the "known" information that exists. That is, physicians and scientists should be able to separate what is fact and what is fancy. This review article is intended to generate thought in this regard.

Age-related changes in hypothalamic-pituitary-adrenal axis activity in patients with manifest arterial disease.

Reports on age-related changes of hypothalamic-pituitary-adrenal (HPA) axis activity are equivocal. In addition, subtle changes in HPA axis activity are associated with cardiovascular risk factors. This study evaluates the effect of age in a large sample of patients with arterial disease on several parts of the circadian rhythm of the HPA axis. Within the Second Manifestations of Arterial Disease-Magnetic Resonance (SMART-MR) study, a prospective cohort study among patients with manifest arterial disease, cross-sectional analyses were performed in 419 patients (age 63 ± 9 years). Circadian cortisol rhythm was assessed with six saliva samples, collected at awakening and 30, 45, and 60 min thereafter and at 10 and 11 pm. Furthermore, a low dose of dexamethasone (0.5 mg) was administered at 11 pm, and saliva was sampled the next morning to test the cortisol suppression. Linear regression analyses adjusted for sex, awakening time, workday, smoking, blood pressure, BMI, diabetes mellitus, and dyslipidemia showed that older age was associated with a blunted cortisol awakening response. Per year increase, the rise (ß = -0.15 nmol/l; 95%CI -0.25 to -0.05) and diurnal pattern (ß = -0.14 nmol/l; 95%CI -0.25 to -0.02) decreased. Furthermore, older age was associated with higher evening levels (ß log transformed = 0.01; 95%CI 0.01-0.02) and higher mean cortisol after dexamethasone (ß log transformed = 0.01; 95%CI 0.002-0.02). In patients with arterial disease, HPA axis activity showed reduced variability with older age, independent of cardiovascular risk factors.

Importancia del estudio del perfil lipídico en niños obesos / Importance of studying the lipid profile in obese children

La arterioesclerosis, es un proceso complejo y multifactorial que se inicia con la identificación de la estría lipídica a los 3 años de edad, lesión que progresa a placa fibrosa y lesión complicada en los años posteriores. La obesidad, es definida como una deposición excesiva de grasa en el cuerpo, que está asociado con consecuencias adversas para parámetros metabólicos, también consecuencias a corto y largo plazo y usualmente también con problemas psicosociales significativos y el desarrollo de enfermedades crónicas. Las dislipemias son uno conjunto de entidades que afectan al metabolismo lipídico y cuyos efectos nocivos son determinantes en el desarrollo del proceso de arteriosclerosis.

Atherosclerosis is a multifactorial complex process that begins with the identification of lipid streak at 3 years of age, injury progressing to fibrous plaque and complicated lesión in subsequent years. Obesity is defined as an excessive deposition of fat in the body, wich is associated with adverse metabolic parameters, also the short-and long-term and usually also with significant psychosocial problems and chronic disease development. The dyslipidemias are one set of entities that affect lipid metabolism and the harmful effects are crucial in the development of aterosclerosis process.

Accelerated arteriosclerosis: a form of transplant arteriopathy.

PURPOSE OF REVIEW: Terminology for posttransplant renal arterial lesions is confusing, with multiple terms being applied, the more common among them being the comprehensive terms, transplant arteriosclerosis and transplant atherosclerosis; endarteritis, for intimal lesions with an inflammatory component; and finally for advanced lesions with or without intimal inflammation, transplant arteriopathy. However, these latter lesions may present the appearance of banal arteriosclerosis, albeit more advanced expected on the basis of donor age. This review explores the distinctions to be drawn among these various descriptive terms. RECENT FINDINGS: Cell-mediated arterial lesions due to T-cell cell-endothelial interactions and antibody-mediated lesions, due to antiendothelial cell antibodies, show many common features: myofibroblasts, some of recipient origin, laying down extracellular matrix. However, they differ in that cell-mediated intimal lesions initially have a prominent leukocytic component, usually absent in antibody-mediated lesions. The antibodies most frequently implicated are antihuman leukocyte antigen class I and class 2 antibodies. With the exception of a sometimes more cellular intima and initial absence of dense collagen and elastic fibers, these latter lesions resemble those of arteriosclerosis of aging. SUMMARY: Many instances of lesions designated as transplant arteriopathy are morphologically similar or identical to typical renal arteriosclerosis and could equally be regarded as accelerated arteriosclerosis.

Arteriosclerosis: rethinking the current classification.

CONTEXT: Arteriosclerosis is the vascular disease that is the leading cause of mortality in industrialized countries. Currently, there are 3 lesions within the broader category of arteriosclerosis: atherosclerosis, Mönckeberg medial calcific sclerosis, and arteriolosclerosis. OBJECTIVE: In this review, we discuss the history of the terminology and current classification of arteriosclerosis and problems with the current classification. We also discuss recently described new arterial lesions that are not in the current classification. DATA SOURCES: In spite of the prevalence and importance of arteriosclerotic vascular disease, and the widespread use of the current terminology, there are major problems with the current classification: (1) the current classification has an inconsistent naming convention, (2) the classification fails to use terms that accurately describe the lesions, and (3) important arterial lesions are absent from the classification. In addition, although the terms arteriosclerosis and atherosclerosis describe different lesions, these terms are often used interchangeably. CONCLUSION: Consideration should be given for a new more inclusive and accurate classification of "arteriosclerotic" lesions that more accurately reflects the pathology of these important vascular lesions.

Primary sclerosing cholangitis--the arteriosclerosis of the bile duct?

Primary sclerosing cholangitis (PSC) is a chronic inflammatory disease of unknown aetiology affecting the large bile ducts and characterized by periductal fibrosis and stricture formation, which ultimately result in biliary cirrhosis and liver failure. Arteriosclerosis involves the accumulation of altered lipids and lipoproteins in large arteries; this drives inflammation and fibrosis and ultimately leads to narrowing of the arteries and hypoperfusion of dependent organs and tissues. Knowledge of the causative factors is crucial to the understanding of disease mechanisms and the development of specific treatment. Based on pathogenetic similarities between PSC and arteriosclerosis, we hypothesize that PSC represents "arteriosclerosis of the bile duct" initiated by toxic biliary lipids. This hypothesis is based on common molecular, cellular, and morphological features providing the conceptual framework for a deeper understanding of their pathogenesis. This hypothesis should stimulate translational research to facilitate the search for novel treatment strategies for both diseases.

Expression of alpha2-macroglobulin, neutrophil elastase, and interleukin-1alpha differs in early-stage and late-stage atherosclerotic lesions in the arteries of the circle of Willis.

Different types of atherosclerotic (AS) lesions can be distinguished histologically and represent different stages of AS plaque development. Late-stage lesions more frequently develop complications such as plaque rupture and thrombosis with vessel occlusion than early AS lesions. To clarify whether protective, destructive, and inflammatory proteins are differentially expressed in early-stage and late-stage AS plaques we examined the proteinase inhibitor alpha(2)-macroglobulin (A2M), the neutrophil elastase (NE)-an enzyme degrading elastin and collagen fibers-and the proinflammatory protein interleukin-1alpha (IL-1alpha) in all types of AS plaques in the arteries of the circle of Willis from 78 human autopsy cases of both genders (61-91 years of age). Paraffin sections of AS plaques were immunostained with antibodies directed against A2M, NE and IL-1alpha. In initial AS lesions A2M was found, whereas NE and IL-1alpha were absent. NE and IL-1alpha became detectable as soon as a significant number of macrophages occurred within AS lesions. With increasing histopathological type of AS lesions, a marked increase of the area of the plaque exhibiting NE and IL-1alpha was observed. The area which exhibits A2M in AS plaques, on the other hand, did not vary significantly between the different stages. Thus, our results indicate a disproportionately high increase of the destructive enzyme NE and the proinflammatory protein IL-1alpha in relation to A2M with the progression of the grade of AS lesions pointing to the transgression of the protective capacity of A2M by NE and IL-1alpha in late-stage plaques. Therefore, our findings support the hypothesis that NE-induced tissue damage in late-stage AS plaques contributes to the development of plaque rupture and subsequent thrombosis.

[Vulnerable plaque and internal atherosclerosis plaque angiogenesis].

The instability of atherosclerotic plaque would lead to the rupture of plaque, even acute coronary syndrome (ACS). To prevent the internal atherosclerosis plaque angiogenesis may play a very important role in stabilizing the vulnerable plaque. Traditional Chinese drugs show potential advantages in stabilizing AS plaque by its characteristics of multi-way, multi-link and multi-target all-sided treatment.

Endovascular therapies for noncoronary atherosclerosis in the elderly: supra-aortic vessels and thoracoabdominal aorta lesions.

Due to the aging of the population and the fact that people are living longer, there are increasing numbers of older patients with noncoronary atherosclerosis. Carotid and subclavian arteries are often the first involved vessels in atherosclerosis, and thoracoabdominal aortic involvement is becoming even more frequent. New techniques, such as intra-arterial thrombolysis, protection and thrombo-aspiration devices, and new stent graft designs are becoming available for percutaneous treatment of atherosclerosis in such vessels. In this review, the authors offer geriatric cardiologists an overview and an update of the most recent advances in techniques and results in the field of interventional treatments of atherosclerosis of supra-aortic vessels and thoracoabdominal aorta in the elderly.

Atherosclerosis is associated with delirium after coronary artery bypass graft surgery.

OBJECTIVES: To investigate whether atherosclerosis of the ascending aorta, internal carotid arteries, and coronary arteries is predictive of postoperative delirium in subjects undergoing coronary artery bypass graft (CABG) surgery. DESIGN: Prospective cohort study. SETTING: Boston Veterans Affairs Healthcare System. PARTICIPANTS: Thirty-six male veterans undergoing primary CABG surgery. MEASUREMENTS: Subjects underwent Duplex ultrasound to assess stenosis in the internal carotid arteries. Information on the ascending aortic plaque, as assessed by transesophageal echocardiogram, and the number of coronary vessels bypassed was collected. To create an atherosclerosis score, the number of atherosclerotic areas was added. A validated delirium battery was administered to the subjects preoperatively and on postoperative Days 2 and 5. RESULTS: Fifteen subjects (41.7%) developed delirium postoperatively. In bivariate analysis, carotid stenosis of 50% or more (relative risk (RR)=3.5, 95% confidence interval (CI)=1.5-8.1) and moderate-severe ascending aortic plaque (RR=2.9, 95% CI=1.0-8.5) were significantly associated with the development of delirium. There was a trend toward a significant association for three or more vessels bypassed (RR=9.6, 95% CI=0.6-145.3). After controlling for age, baseline cognition, and medical comorbidity, the atherosclerosis score was significantly associated with postoperative delirium (adjusted RR=2.7, 95% CI=1.1-6.8). CONCLUSION: In this preliminary report, atherosclerosis in the carotid arteries, aorta, and coronary circulation is associated with the development of delirium after CABG surgery. Further investigation into atherosclerosis as a risk factor for delirium is warranted.

Circulating adhesion molecules in apoE-deficient mouse strains with different atherosclerosis susceptibility.

Recruitment of inflammatory cells in the arterial wall by vascular adhesion molecules plays a key role in development of atherosclerosis. Apolipoprotein E-deficient (apoE(-/-)) mice have spontaneous hyperlipidemia and develop all phases of atherosclerotic lesions. We sought to examine plasma levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) and sP-selectin in two apoE(-/-) strains C57BL/6 (B6) and BALB/c with early or advanced lesions. Mice were fed chow or a Western diet containing 42% fat, 0.15% cholesterol, and 19.5% casein. On either diet, BALB/c.apoE(-/-) mice developed much smaller atherosclerotic lesions and displayed significantly lower levels of sVCAM-1 and sP-selectin than B6.apoE(-/-) mice. The Western diet significantly elevated sVCAM-1 levels in both strains and sP-selectin levels in B6.apoE(-/-) mice. BALB/c.apoE(-/-) mice exhibited 2-fold higher HDL cholesterol levels on the chow diet and 15-fold higher HDL levels on the Western diet than B6.apoE(-/-) mice, although the two strains had comparable levels of total cholesterol and triglyceride. Thus, increased atherosclerosis is accompanied by increases in circulating VCAM-1 and P-selectin levels in the two apoE(-/-) mouse strains, and the high HDL level may protect against atherosclerosis by inhibiting the expression of adhesion molecules in BALB/c.apoE(-/-) mice.

Predictive factors of in-stent restenosis in renal artery stenting: a retrospective analysis.

PURPOSE: To retrospectively evaluate the role of clinical and procedural factors in predicting in-stent restenosis in patients with renovascular disease treated by renal artery stenting. METHODS: From 1995 to 2002, 147 patients underwent renal artery stenting for the treatment of significant ostial atherosclerotic stenosis. Patients underwent strict clinical and color-coded duplex ultrasound follow-up. Ninety-nine patients (111 stents), with over 6 months of continuous follow-up (mean 22+/-12 months, range 6-60 months), were selected and classified according to the presence (group A, 30 patients, 32 lesions) or absence (group B, 69 patients, 79 lesions) of significant in-stent restenosis. A statistical analysis was performed to identify possible preprocedural and procedural predictors of restenosis considering the following data: sex, age, smoking habit, diabetes mellitus, hypertension, serum creatinine, cholesterol and triglyceride levels, renal artery stenosis grade, and stent type, length and diameter. RESULTS: Comparing group A and B patients (chi(2) test), a statistically significant relation was demonstrated between stent diameter and length and restenosis: the risk of in-stent restenosis decreased when the stent was >/=6 mm in diameter and between 15 and 20 mm in length. This finding was confirmed by multiple logistic regression analysis. Stent diameter and length were proved to be significantly related to in-stent restenosis also when evaluating only patients treated by Palmaz stent (71 stents). CONCLUSION: Although it is based on a retrospective analysis, the present study confirms the importance of correct stent selection in increasing long-term patency, using stents of at least 6 mm in diameter and with a length of approximately 15-20 mm.

Role of thrombogenic factors in the development of atherosclerosis.

Hemostatic factors play a crucial role in generating thrombotic plugs at sites of vascular damage (atherothrombosis). However, whether hemostatic factors contribute directly or indirectly to the pathogenesis of atherosclerosis remains uncertain. Autopsy studies have revealed that intimal thickening represents the first stage of atherosclerosis and that lipid-rich plaque arises from such lesions. Several factors contribute to the start of intimal thickening. Platelets release several growth factors and bioactive agents that play a central role in development of not only thrombus but also of intimal thickening. We have been investigating which coagulation factors simultaneously, or subsequently with platelet aggregation, participate in thrombus formation. Tissue factor (TF) is an essential initiator of blood coagulation that is expressed in various stages of atherosclerotic lesions in humans and other animals. Factors including thrombin and fibrin, which are downstream of the coagulation cascade activated by TF, also contribute to atherosclerosis. TF is involved in cell migration, embryogenesis and angiogenesis. Thus TF, in addition to factors downstream of the coagulation cascade and the protease-activated receptor 2 activation system, would be a multifactorial regulator of atherogenesis.

Atheroscleritis is a more rational term for the pathological entity currently known as atherosclerosis.

The term "atheroma", a Latin word was first used in 1755 by Albrecht von Halles to designate the plaque deposited on the innermost layer of systemic artery walls. In 1940, however, Félix Marchand suggested the word "atherosclerosis" should be better instead of "atheroma", which is derived from two Greek roots: athéré means gruel or porridge and sclerosis signifies hardening. It is obviously an improvement over the older designation arteriosclerosis. Atherosclerosis is still used up to data because it describes the two components of plaque: the lipid-filled core of atheroma encased in a shell of sclerosis or fibrosis, which presents the feature of atherosclerotic structure. Although atherosclerosis has been considered to be multi-factorial disease in which genetic, environmental, metabolic factors have been implicated, the gaps remain in our knowledge of the etiopathogenesis of atherosclerosis. More recently, there is mounting evidence that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis. The data from animals as well as humans indicated that an inflammatory process was involved in all stages of atherosclerosis appeared in different clinical settings, including atheromatous development, plaque rupture, restenotic process. The anti-inflammatory approach has been showed as one of the most promising strategies for atherosclerosis, such as statin intervention. Based on evidence and in light of the new understanding that inflammation is an intrinsic part of the process, we would like to propose a further change of nomenclature, call the disease atheroscleritis.

Degree of atherosclerosis predicts short-term commitment for smoking cessation therapy.

BACKGROUND: Only little is known about factors that influence the smokers' propensity to start smoking cessation therapy and stay within such programs. METHODS: One hundred fifteen subjects that were current smokers and presented at the angiologic outpatient unit were enrolled in a prospective cohort study. All patients were invited to take part in a smoking cessation program. Patients' history, noninvasive vascular, cardiac, and pulmonary parameters, state of atherosclerotic disease (SMART-score), smoking history, and Fagerström index were obtained and the carbon monoxide breathing test was performed. RESULTS: Lower age and heavy smoking were associated with less propensity to start smoking cessation therapy. The degree of atherosclerosis significantly predicted short-term commitment to smoking cessation therapy (relative risk for discontinuation: 0.82; 95% CI: 0.70-0.96). Single factors predictive for staying within the therapy were peripheral arterial occlusive disease and hyperlipidemia, while neither prior myocardial infarction nor pulmonary function was associated with compliance. Fifty-four percent of patients that completed 3 months of therapy quit smoking. CONCLUSIONS: Counseling in smokers with preexistent or newly diagnosed atherosclerotic diseases or risk factors should include their specific vascular condition and information on positive consequences on the progress of these conditions. Counseling for initiation of smoking cessation therapy should apply different strategies as used in the maintenance phase of therapy.