الفهرس 
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Abstract
Over the last decade, cardiovascular disease (CVD) has become the single largest cause of death worldwide. Like many high-income countries during the last century, low- and middle-income countries are seeing an alarming increase in the rates of CVD, and this change is accelerating (Gaziano and Gaziano, 2012).
Stable ischemic heart disease (IHD) is most commonly caused by obstruction of the coronary arteries by atheromatous plaque. After the plaque burden exceeds the capacity of the artery to remodel outward, encroachment on the arterial lumen begins, eventually; the stenoses may progress to a degree that impedes blood flow through the artery (Libby, 2012).
In the acute coronary syndromes, the culprit lesion is often a plaque complicated by thrombosis extending into the lumen. Such plaques are termed “thrombosed plaques” (Schaar et al 2004).
The primary clinical and preventive goal is to identify patients who are vulnerable to acute coronary thrombosis. Such patients are likely to have a high atherosclerotic burden, high-risk/vulnerable plaques, and/or thrombogenic blood (Schaar et al, 2004).
from the view of vulnerable plaque detection, morphological studies should provide valuable insight regarding which criteria are important for localizing high-risk lesions using imaging modalities and assessing the potential risk for rupture (Finn et al, 2010).
A noninvasive technology gaining clinical acceptance is computed tomography (CT) angiography. It is used primarily for the detection of calcium; however, recently it has been shown that it may be useful in detecting the plaques that may be responsible for ACS (Finn et al, 2010).
There also has been intense interest in the evaluation of coronary CT angiography as a tool for risk stratification and for monitoring risk factor management. The rationale behind these efforts is our growing understanding of the relationship between plaque composition and the different clinical manifestations of CAD (Bastarrika et al, 2009).
Beyond detection of coronary stenosis or coronary artery calcification, non-calcified plaque detection is an appealing but still un-validated approach to the risk assessment (Taylor, 2012).
Attenuation-based atherosclerotic plaque characterization at coronary CT angiography has been shown to correlate reasonably well with histologic findings (Becker et al, 2003).
The basic plaque features proposed to be associated with greater risk for plaque rupture or acute coronary syndromes include low-attenuation plaque (plaque <30 HU), outward arterial remodeling (artery diameter ratio of the involved segment to a proximal reference of 1.1 or greater), and a spotty pattern (<3 mm in size) of calcification (Motoyama et al, 2007).
Newly developed software algorithms that can volumetrically quantify calcified and non-calcified atherosclerotic plaque components may additionally permit use of multidetector CT in risk stratification and monitoring therapies designed to manage and reduce risk of major adverse cardiac events (Naghavi et al, 2003)
More recently, automated segmentation tools for plaque quantification have been introduced by all manufacturers, with a reported improved inter-observer variability between 12%–17% (Sun et al, 2008).
Our study – using semi-automated plaque quantification tool after scanning by a 64-row MDCT – aimed to demonstrate the differences in plaque compositions among patients presented with acute coronary syndrome to those presented with stable angina, based on tissue characterization based on their Hounsfield unit (HU).
Our study showed excellent visualization of the proximal and middle vascular segments of the coronary arteries; moreover, using the Sureplaque ® tool, the plaques were easily identified and volumetrically quantified along the examined vascular segments.
In our experience the plaques examined in both patients with ACS (culprit lesions), and those presented with stable angina showed higher degrees of vascular stenosis, larger lipid cores with statistically significant differences. Also the culprit plaques showed a rather spotty pattern of calcifications and relatively lower calcification percentages from the total plaque volumes.
However, the percentages of soft tissue/fibrous tissue components were not significantly difference between patients with ACS and SA.