کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9959715 | 1577534 | 2005 | 18 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Atherothrombosis and High-Risk Plaque
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کلمات کلیدی
MMPNCPTCFAOPNIELHDLTLRACSAHAthin-cap fibroatheroma - fibroatheroma نازک کاپhigh-density lipoprotein - HDL یا لیپوپروتئین با دانسیته بالا یا چگالی بالاapo - آپوapolipoprotein - آپولیپوپروتئینOsteopontin - استئوپنتینAmerican Heart Association - انجمن قلب آمریکاToll-like receptor - تیالآرCAM - ساخت به کمک کامپیوترAcute coronary syndrome - سندرم کرونری حادTissue factor - عامل بافتinternal elastic lamina - لمینا کشویی داخلیLow-density lipoprotein - لیپوپروتئین کم چگالی یا الدیال LDL - لیپوپروتئین کم چگالی(کلسترول بد)matrix metalloproteinase - ماتریکس متالوپروتئینازC-reactive protein - پروتئین واکنشی سیCRP - پروتئین واکنشی سی یا سی. آر. پی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Atherothrombosis and High-Risk Plaque Atherothrombosis and High-Risk Plaque](/preview/png/9959715.png)
چکیده انگلیسی
Atherothrombosis is a complex disease in which cholesterol deposition, inflammation, and thrombus formation play a major role. Rupture of high-risk, vulnerable plaques is responsible for coronary thrombosis, the main cause of unstable angina, acute myocardial infarction, and sudden cardiac death. In addition to rupture, plaque erosion may also lead to occlusive thrombosis and acute coronary events. Atherothrombosis can be evaluated according to histologic criteria, most commonly categorized by the American Heart Association (AHA) classification. However, this classification does not include the thin cap fibroatheroma, the most common form of high-risk, vulnerable plaque. Furthermore, the AHA classification does not include plaque erosion. As a result, new classifications have emerged and are reviewed in this article. The disease is asymptomatic during a long period and dramatically changes its course when complicated by thrombosis. This is summarized in five phases, from early lesions to plaque rupture, followed by plaque healing and fibrocalcification. For the early phases, the role of endothelial dysfunction, cholesterol transport, high-density lipoprotein, and proteoglycans are discussed. Furthermore, the innate and adaptive immune response to autoantigens, the Toll-like receptors, and the mechanisms of calcification are carefully analyzed. For the advanced phases, the role of eccentric remodeling, vasa vasorum neovascularization, and mechanisms of plaque rupture are systematically evaluated. In the final thrombosis section, focal and circulating tissue factor associated with apoptotic macrophages and circulatory monocytes is examined, closing the link between inflammation, plaque rupture, and blood thrombogenicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the American College of Cardiology - Volume 46, Issue 6, 20 September 2005, Pages 937-954
Journal: Journal of the American College of Cardiology - Volume 46, Issue 6, 20 September 2005, Pages 937-954
نویسندگان
Valentin (FACC), Pedro R. (FACC), Zahi A. (FACC), Roberto (FACC), Juan J. (FACC),