A MORPHOLOGICAL STUDY OF CELIAC, SUPERIOR MESENTERIC AND INFERIOR MESENTERIC ARTERIES IN ATHEROSCLEROSIS

Authors

  • Amjad Naeem
  • Nadia Nasim
  • Umaira Ihsan
  • Atika Masood

Abstract

Background: Depolymerisation of acid-mucopolysaccharides results in the loss of metachormasia of
the ground substance followed by visible fibre crumbling, complete dissolution and replacement by
lipid droplets and cholesterol. The objective of this study was to assess the distribution of different
atherosclerotic lesions in celiac, superior mesenteric and inferior mesenteric arteries relation to age and
sex. Methods: A prospective descriptive observation study was conducted at Mortuary of King Edward
Medical University Lahore, and Department of Pathology Allama Iqbal Medical College Lahore. A
total of 30 human autopsies were carried out. Celiac, Superior mesenteric and inferior mesenteric
arteries were taken out and opened length-wise. One to four areas of tissue were taken from each artery
for histological examination. Slides were prepared from each paraffin block. Sections were stained with
haematoxylin and eosin. Special stains were performed on sections to display each component of
atherosclerosis. Results: The fibrolipid plaques were seen in 6 cases. The complicated lesions were
present in 5 cases. Of these, 4 showed ulceration and 1 showed thrombus formation. The calcified
lesions were observed in 5 cases. The morphological changes in media and elastica were present in 4
cases. In superior mesenteric artery fatty streaks were present in 8 cases. The fibrolipid plaques were
confirmed in 5 cases. Three cases showed ulceration, 1 case showed intimal vascularisation,
haemorrhage, and thrombus formation. The calcified lesions were present in 2 cases. The
morphological changes in media and elastica were seen in 4 cases in anterior mesenteric artery. Fatty
streaks were present in 8 cases. The fibrolipid plaques were grossly observed in 6 cases. The
complicated lesions were present in 4 cases; of these, 3 cases showed ulceration, and 1 showed intimal
vascularisation and haemorrhage along with thrombus formation. The calcified lesions were present in
3 cases. The morphological changes in media and elastica were present in 4 cases. Conclusion: This
data indicates the incidence of ischemic changes in abdominal viscera due to atherosclerotic narrowing.
Keywords: Celiac, Superior, Inferior, mesenteric, atherosclerosis, arteries

References

Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ.

Weight in infancy and death from ischaemic heart disease.

Lancet 1989;2:577-80.

Oliveria SA, Ellison RC, Moore LL, Gillman MW, Garrahie

EJ, Singer MR. Parent-child relationships in nutrient intake: the

Framingham children's Study. Am J Clin Nutr 1992;56:593-8.

Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis

GJ. Compensatory enlargement of human atherosclerotic

coronary arteries. N Engl J Med 1987;316:1371-5.

Kronmal RA, Mc Clelland RL, Detrano R, Shea S, Lima

JA, Cushman M, et al. Risk factors for the progression of

coronary artery calcification in asymptomatic subjects: results

from the Multi-Ethnic Study of Atherosclerosis (MESA).

Circulation 2007;115:2722-30.

Chironi G, Simon A, Denarie N, Védie B, Séné V, Mégnien JL,

et al. Determinants of progression of coronary artery calcification

in asymptomatic men at high cardiovascular risk. Angiology

;53:677-83.

Margolis KL, Dunn K, Simpson LM, Ford CE, Williamson JD,

Gordon DJ, et al. Coronary heart disease in moderately

hypercholesterolemic, hypertensive blackand non- black patients

randomized to pravastatin versus usual care: theantihypertensive

and lipid lowering to prevent heart attack trial (ALLHAT-LLT).

Am Heart J 2009;158:948-55.

Ross. R. Atherosclerosis: the role of endothelial injury, smooth

muscle proliferation and platelet factors. Triangle 1976;15:45-51.

Dalferes ER Jr, Radhakrishnamurthy B, Ruiz HA, Berenson GS.

Composition of proteoglycans from human atherosclerotic

lesions. Exp Mol Pathol 1987;47:363-76.

Gordon RC, Julie HC. Recent advance in Molecular Pathology:

Smooth muscle phenotypic changes in arterial wall homeostasis:

Implications for the pathogensis of Atherosclerosis. Exp Mol

Pathol 1985;42:139-62.

Rahilly-Tierney CR, Lawler EV, Scranton RE, Gaziano JM.

Lawler, Cardiovascular benefit of magnitude of Low-Density

Lipoprotein Cholesterol Reduction A Comparison of subgroups

by Age. Circulation 2009;120:1491-7.

James, EC, Mashtaq, AK, Gregory C, Henderson G, Kruth HS.

Cytometric study of Cholesteryl ester containing foam cells. II,

analysis of aorta from cholesterol fed swine. Experimental and

Molecular Pathology 1987;46:52-63.

Smith, EB, Staples EM, Dietz HS, Smith RH. Role of

endothelium in Sequestraton of lipoprotein and fibrinogen in

aortic lesions, thrombi and Graft Pseudo-intimsas. Lancet

;2(8147):812-6.

Hoff HF, Heideman CL, Gaubatz JW, Scott DW, Titus JL, Gotto

AM Jr. Correlation of Apolipoprotein B retention with the

structure of atherosclerotic plaques from human aorta: Lab Invest

:38:560-7.

Lewis, JG, Richard G. Taylor BS, St Clair RW, Cornhill JF.

Endotheilal surface characteristics in Pigeon coronary artery

atherosclerosis. Lab Invest 1982; 46(2):123-38.

Elesber AA, Redfield MM, Rihal CS, Prasad A, Lavi S, Lennon

R. Coronary endothelial dysfunction hyperlipidemia are

independently associated with diastolic dysfunction in humans,

Am Heart J 2007;153:1081ˆ’7.

Kanazawa T, Izawa M, Kaneko H, Onodera K, Metoki H, Oike

Y, et al. Comparison among Lipid constituents in Native LDL,

ultra water soluble LDL, and Vessel wall and their significance in

atherosclerosis. Experimental and Molecular Pathology

;47:166ˆ’74.

Rivera JJ, Nasir K, Katz R, Takasu J, Allison M, Wong ND, et

al. Relationship of Thoracic Aortic Calcium to Coronary

Calcium and its Progression (from the Multi-Ethnic Study of

Atherosclerosis [MESA]). Am J Cardiol 2009;103:1562-7.

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Published

2012-06-01

How to Cite

1.
Naeem A, Nasim N, Ihsan U, Masood A. A MORPHOLOGICAL STUDY OF CELIAC, SUPERIOR MESENTERIC AND INFERIOR MESENTERIC ARTERIES IN ATHEROSCLEROSIS. J Ayub Med Coll Abbottabad [Internet]. 2012 Jun. 1 [cited 2025 Jul. 1];24(2):18-21. Available from: https://jamc.ayubmed.edu.pk/index.php/jamc/article/view/2181

Issue

Vol. 24 No. 2 (2012): JOURNAL OF AYUB MEDICAL COLLEGE, ABBOTTABAD

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ORIGINAL ARTICLE

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