You could be reading the full-text of this article now if you...

If you have access to this article through your institution,
you can view this article in

Correlations Between CCN1 Immunoexpression and Myocardial Histologic Lesions in Sudden Cardiac Death

Papetta, Angela MD, PhD; Gakiopoulou, Hariklia MD; Agapitos, Emmanouil MD; Patsouris, Efstratios S. MD; Lazaris, Andreas C. MD

American Journal of Forensic Medicine & Pathology:
doi: 10.1097/PAF.0b013e31828d69b5
Original Articles
Abstract

Abstract: CCN1 (CYR61) is a member of the CCN family of secreted matricellular proteins; it can regulate the expression of genes involved in angiogenesis and matrix remodeling. The latter mechanisms seem to be of vital importance in the pathophysiology of sudden cardiac death. We performed an immunohistochemical analysis on 62 cardiac tissue specimens derived from individuals of young and middle age who had died of sudden cardiac death. CCN1 immunopositivity was detected in 80.6% of all specimens. Semiquantitative statistical analysis of the staining results revealed that CCN1 immunoreactivity was significantly associated with ischemic morphology and hypertrophy of myocardial fibers, interstitial edema, and atheromatosis of coronary arteries in more than 10% of the myocardial fibers. Taking the previously mentioned correlations into account, ischemia seems to induce myocardial expression of CCN1; therefore, CCN1 immunostaining could be evaluated as a complementary tool in the assessment of ischemic areas when no tissue evidence of necrosis is available.

Author Information

From the First Department of Pathology, Medical School, The Athens National and Kapodistrian University, Athens, Greece.

Manuscript received November 29, 2011; accepted June 6, 2012.

The authors report no conflicts of interest.

Reprints: Angela Papetta, MD, PhD, First Department of Pathology, Medical School, The Athens National and Kapodistrian University, 75 Mikras Asias St, Goudi, GR-115 27, Athens, Greece. E-mail: angel.doc@hotmail.com.

© 2013 by Lippincott Williams & Wilkins.