الفهرس 
Metabolic SyndromeOnly 14 pages are availabe for public view
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Abstract
M
etS is a constellation of vascular risk factors that increase the risk of subsequent cardiovascular and cerebrovascular occlusive events. Multiple attempts have been made to define the diagnostic criteria for MetS. The most recent definition is the consensus definition in 2009; MetS is diagnosed when 3 or more out of 5 vascular risk factors exist (increased fasting blood glucose, increased systolic and/or diastolic bl. P., increased TGs., reduced HDL and abdominal obesity); all with specific cut off values except abdominal obesity which has ethnic specific values. Variable studies have investigated the effect of MetS on large vessel atherosclerosis as well as small vessel disease (SBI and WMLs.) aiming to determine the possible risk of future TIA or stroke in neurologically asymptomatic MetS patients.
It’s become clear now that inflammation represents a core component in the process of atherogenesis Attention has been drawn to the importance of blood markers for atherosclerosis, atherosclerotic plaque instability and endothelial dysfunction.
A number of blood markers indicate the presence of the atherosclerotic process and represent risk for the development of Cerebro-vascular (CV) events. Further, they may be used for identifying subjects predisposed to plaque disruption and vascular obstruction. Elevated levels of several inflammatory mediators among apparently healthy men and women have proven to have predictive value for future vascular events, particularly cytokines such as IL-6 and tumor necrosis factor alpha (TNF-a), cell adhesion molecules like ICAM-1, P-selectin, E-selectin, and acute-phase reactants such as high sensitive C-reactive protein (hsCRP), fibrinogen, and serum amyloid A.
Inflammation has a fundamental role in the development and progression of the atherosclerotic plaques. Stable plaques are characterized by a chronic inflammatory infiltrate, while vulnerable and ruptured plaques are characterized by an active inflammation and “plaque activity” processes involved in the thinning of the fibrous cap. High plaque neovascularization is confirmed to be an important predictor of unstable lesions in symptomatic and asymptomatic plaques, through different mechanisms that may be connected with plaque inflammation. It is believed that the absence of pericytes in new vessels causes “leak” of potentially noxious and inflammatory plasma components into the extracellular matrix of the media/intima, increasing the plaque volume, gradually reducing vessel wall oxygen diffusion, enhancing further angiogenesis. In the final phase, the plaque is enveloped in adventitial vasa vasorum and a rich network of small caliber microvessels, a hallmark of symptomatic atherosclerosis
The term “silent” may not be entirely appropriate since these lesions could be often associated with unnoticed or subtle symptoms in patients that never asked for an evaluation, making impossible a diagnosis of stroke.
The clinical event of stroke is not always a good guide to the existence of cerebral infarction. Advanced neuroimaging detected that up to one third of patients with TIA and no physical examination changes have infarcts on scans. These patients are at even higher risk for subsequent stroke as are other patients with SBI. In consequence, SBI is recognized as part of a spectrum of cerebrovascular disease, which also includes TIA to stroke.
SBI are commonly diagnosed by MRI in both first ever ischemic stroke and healthy elderly patients. It is also common in patients with hypertension and coronary artery disease, and in those undergoing haemodialysis. In different series, the reported frequency of MRI defined SBI ranges from 5-50%.
Several studies were launched to detect the prognosis of SBI and demonstrated that SBI carries the risk of several subsequent neurological diseases such as new SBI, stroke, dementia and depression.
To clarify whether the clustering of vascular risk factors that form the MetS constitute a significant difference in the risk of cerebral large and small vessel atherosclerotic disease and to determine the proportion and pattern of extracranial cerebrovascular atherosclerosis as well as SBI in Egyptian MetS patients.
A cross sectional observational study was conducted on 30 subjects, aged 40-60 years old, completely asymptomatic neurologically, recruited from internal medicine & diabetes mellitus outpatient clinics of Nasser Institute for Research and Treatment hospital. Subjects were divided into group 1 (20 subjects with MetS) and group 2 (10 controls with only 1 or 2 vascular risk factors). All subjects underwent complete neurological examination, assessment of previously mentioned vascular risk factors, a complete extracranial neurovascular U/S survey and brain MRI. Variables investigated were isolated elevation of CCA mean IMT, extracranial atherosclerotic plaques, SBI and WMLs.
MetS had a significant effect on the presence of extracranial atherosclerotic plaques, but not on isolated IMT elevation. There was also no significant effect regarding the number or laterality of plaques found. Lastly, MetS had a highly significant effect on the presence of SBI and WMLs. Multivariate analysis of different vascular risk factors amongst MetS subjects showed that none of the risk factors to be an independent predictor of atherosclerotic plaques or MRI pathological findings.
The presence of MetS carries a heavier atherosclerotic burden on extracranial large arteries, at least partially, and on cerebral parenchymal small vessels than does the presence of only 1 or 2 random vascular risk factors.