This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maron, B. J. Articles by Roberts, W. C. Search for Related Content PubMed PubMed Citation Articles by Maron, B. J. Articles by Roberts, W. C.

American Journal of Pathology, Vol 79, 387-434, Copyright © 1975 by American Society for Investigative Pathology

REGULAR ARTICLES

Ultrastructural features of degenerated cardiac muscle cells in patients with cardiac hypertrophy

BJ Maron, VJ Ferrans and WC Roberts

Degenerated cardiac muscle cells were present in hypertrophied ventricular muscle obtained at operation from 12 (38%) of 32 patients with asymmetric septal hypertrophy (hypertrophic cardiomyopathy) or aortic valvular disease. Degenerated cells demonstrated a wide variety of ultrastructural alterations. Mildly altered cells were normal-sized or hypertrophied and showed focal changes, including preferential loss of thick (myosin) filaments, streaming and clumping of Z band material, and proliferation of the tubules of sarcoplasmic reticulum. Moderately and severely degenerated cells were normal-sized or atrophic and showed additional changes, including extensive myofibrillar lysis and loss of T tubules. The appearance of the most severely degenerated cells usually reflected the cytoplasmic organelle (sarcoplasmic reticulum, glycogen, or mitochondria) which underwent proliferation and filled the myofibril-free areas of these cells. Moderately and severely degenerated cells were present in areas of fibrosis, had thickened basement membranes, and had lost their intercellular connections. These observations suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic ventricular hypertrophy.

This article has been cited by other articles:

				K.-i. Okada, T. Minamino, Y. Tsukamoto, Y. Liao, O. Tsukamoto, S. Takashima, A. Hirata, M. Fujita, Y. Nagamachi, T. Nakatani, et al. Prolonged Endoplasmic Reticulum Stress in Hypertrophic and Failing Heart After Aortic Constriction: Possible Contribution of Endoplasmic Reticulum Stress to Cardiac Myocyte Apoptosis Circulation, August 10, 2004; 110(6): 705 - 712. [Abstract] [Full Text] [PDF]

				J. Marin-Garcia, M. J Goldenthal, and G. W Moe Mitochondrial pathology in cardiac failure Cardiovasc Res, January 1, 2001; 49(1): 17 - 26. [Full Text] [PDF]

				G. Pons-Llado, M. Ballester, X. Borras, F. Carreras, I. Carrio, J. Lopez-Contreras, A. Roca-Cusachs, J. Marrugat, and J. Narula Myocardial cell damage in human hypertension J. Am. Coll. Cardiol., December 1, 2000; 36(7): 2198 - 2203. [Abstract] [Full Text] [PDF]

				M. Kanoh, G. Takemura, J. Misao, Y. Hayakawa, T. Aoyama, K. Nishigaki, T. Noda, T. Fujiwara, K. Fukuda, S. Minatoguchi, et al. Significance of Myocytes With Positive DNA In Situ Nick End-Labeling (TUNEL) in Hearts With Dilated Cardiomyopathy : Not Apoptosis but DNA Repair Circulation, June 1, 1999; 99(21): 2757 - 2764. [Abstract] [Full Text] [PDF]

				G Takemura, Y Takatsu, and H Fujiwara Luminal narrowing of coronary capillaries in human hypertrophic hearts: an ultrastructural morphometrical study using endomyocardial biopsy specimens Heart, January 1, 1998; 79(1): 78 - 85. [Abstract] [Full Text] [PDF]

				A. M. Gerdes, T. Onodera, X. Wang, and S. A. McCune Myocyte Remodeling During the Progression to Failure in Rats With Hypertension Hypertension, October 1, 1996; 28(4): 609 - 614. [Abstract] [Full Text]