• Alia Zubair
  • Azhar Mubarik
  • Shahid Jamal
  • Salma Naz


Background: Recent clinical and histopathologic data suggests that inflammation plays a key role incoronary artery plaque instability and subsequent occlusive thrombosis. The intima has received muchattention as a site of inflammation, while the adventitia has remained relatively unexplored. The aim ofthe present study was to investigate the frequency of inflammatory activity in the cap and shoulderregion of unruptured, atherosclerotic lesions in coronary arteries and to correlate these findings withdistribution of inflammatory cells in adventitia. Methods: The study was carried out in HistopathologyDepartment, Army Medical College, Rawalpindi and National University of Sciences & Technology(NUST), from August 2008 to July 2009. Sixty-seven autopsy cases performed at Military HospitalRawalpindi, Pakistan were selected. The cases were divided into study group and control group. Casegroup (n=35) included those where cause of death was ischemic heart disease. Those coronary arterieswere taken as control (n=32) where atherosclerotic changes were found by chance (death withouthistory of ischemic heart disease). Plaques in each group were assessed by light microscopy and byimmunohistochemistry. Results: The ages of the deceased ranged from 38 to 49 years. Within studygroup, adventitial lymphocytes exhibited strong correlation with erosion, thrombus formation in culpritplaque (p=0.001). No correlation was found between adventitial T-lymphocytes and erosion of plaque(p=0.700) in control group. In 72% of culprit plaques moderate staining for T-lymphocytes wasobserved in adventitia as well as intima. In control group, most of the cases contained scattered cells.Few cases of stable plaques revealed lymphocytes as clusters, both in adventitia and in intima.Conclusion: Adventitial inflammation may play a pivotal role for atherosclerotic lesion histology andatheroma instability. With the help of these autopsy findings, we hope to be able to reduce the incidenceof culprit plaques related to inflammatory reaction in patients of ischemic heart disease.Keywords: Atherosclerosis, Culprit plaque, Adventitial inflammation, T-lymphocytes


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