The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Abnormalities of cardiocytes in regions bordering fibrous scars of dogs with heart failure.
V G Sharov; H N Sabbah; A S Ali; H Shimoyama; M Lesch; S Goldstein (Profiled Author: Hani N Sabbah)
Department of Medicine, Henry Ford Heart and Vascular Institute, Detroit, MI 48202, USA.
International journal of cardiology 1997;60(3):273-9.
Progressive deterioration of left ventricular function is a characteristic feature of the heart failure state and is often speculated to result from ongoing loss of viable myocytes. We previously showed that in dogs with chronic heart failure, cardiocyte death through apoptosis occurs in the border region of fibrous scars (old infarcts). In the present study we examined the structural integrity of cardiocytes in regions bordering fibrous scars using transmission electron microscopy. Morphometric studies were performed using left ventricular tissue obtained from ten dogs with chronic heart failure produced by intracoronary microembolizations. Mitochondrial number increased significantly with proximity to the scar, while mitochondrial size decreased leading to a gradual decrease in mitochondrial volume fraction. Severe injury to mitochondria was present in only 5% of organelles in myocytes far from the scar but increased markedly to 28-41% in myocytes adjacent to or incorporated within the scar. Similarly, severe myofibrillar abnormalities were present in only 3% of myocytes that were far from the scar but increased significantly to 12-73% in myocytes adjacent to or incorporated within the scar. These results indicate that in dogs with chronic heart failure, constituent myocytes of left ventricular regions bordering fibrous scars manifest heterogeneity in the extent of degeneration. The extent of degeneration is greatest in myocytes closest to the scar and least in myocytes far from the scar. We postulate that this wavefront of myocyte degeneration is a dynamic process that may lead to progressive expansion of the scar through loss of viable myocytes and ultimately may contribute, in part, to the progressive left ventricular dysfunction that characterizes the heart failure state.
1 Originating Grant
Sabbah, Hani N
1 April 1994 - 31 December 2003
NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Total Funding: $ 2,329,997
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
1 February 1995 - 31 January 2004
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 2,130,658
STEIN, PAUL D
Total Funding: $ 1,041,629
SLOANE, BONNIE F
1 June 2010 - 31 March 2013
FOGARTY INTERNATIONAL CENTER
Total Funding: $ 179,490
H N Sabbah; P D Stein; T Kono; M Gheorghiade; T B Levine; S Jafri; E T Hawkins; S GoldsteinThe American journal of physiology 1991;260(4 Pt 2):H1379-84.
Hani N Sabbah; Victor G Sharov; Ramesh C Gupta; Sudhish Mishra; Sharad Rastogi; Albertas I Undrovinas; Pervaiz A Chaudhry; Anastassia Todor; Takayuki Mishima; Elaine J Tanhehco; et al.Circulation research 2003;93(11):1095-101.
Victor G Sharov; Anastassia V Todor; Makoto Imai; Hani N SabbahHeart failure reviews 2005;10(4):305-10.
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