Structural remodeling of cardiac myocytes in patients with ischemic cardiomyopathy
- PMID: 1638711
- DOI: 10.1161/01.cir.86.2.426
Structural remodeling of cardiac myocytes in patients with ischemic cardiomyopathy
Abstract
Background: Chronic ischemic heart disease may lead to ventricular dilation and congestive heart failure (ischemic cardiomyopathy [ICM]). The changes in cardiac myocyte shape associated with this dilation, however, are not known.
Methods and results: Left ventricular myocyte dimensions were assessed in cells isolated from explanted human hearts obtained from patients with ICM (n = 6) who were undergoing heart transplantation. Cells were also examined from three nonfailing donor hearts with normal coronary arteries (NCA). Compared with cells from patients with NCA, myocyte length was 40% longer in hearts from patients with ICM (197 +/- 8 versus 141 +/- 9 microns, p less than 0.01), cell width was not significantly different, and cell length/width ratio was 49% greater (11.2 +/- 0.9 versus 7.5 +/- 0.6, p less than 0.01). Sarcomere length was the same in myocytes from both groups. The extent of myocyte lengthening is comparable to the increase in end-diastolic diameter commonly reported in patients with ICM.
Conclusions: These data suggest that increased myocyte length (an intracellular event), instead of myocyte slippage (an extracellular event), is largely responsible for the chamber dilation in ICM. Furthermore, maladaptive remodeling of myocyte shape (e.g., increased myocyte length/width ratio) may contribute to the elevated wall stress (e.g., increased chamber radius/wall thickness) in ICM.
Similar articles
-
The cellular basis of dilated cardiomyopathy in humans.J Mol Cell Cardiol. 1995 Jan;27(1):291-305. doi: 10.1016/s0022-2828(08)80028-4. J Mol Cell Cardiol. 1995. PMID: 7760353
-
Structural basis of end-stage failure in ischemic cardiomyopathy in humans.Circulation. 1994 Jan;89(1):151-63. doi: 10.1161/01.cir.89.1.151. Circulation. 1994. PMID: 8281642
-
The cellular basis of pacing-induced dilated cardiomyopathy. Myocyte cell loss and myocyte cellular reactive hypertrophy.Circulation. 1995 Oct 15;92(8):2306-17. doi: 10.1161/01.cir.92.8.2306. Circulation. 1995. PMID: 7554216
-
Structural remodeling and mechanical dysfunction of cardiac myocytes in heart failure.J Mol Cell Cardiol. 1995 Mar;27(3):849-56. doi: 10.1016/0022-2828(95)90000-4. J Mol Cell Cardiol. 1995. PMID: 7602601 Review.
-
Changing the remodeling process in heart failure: basic mechanisms and laboratory results.Curr Opin Cardiol. 1998 May;13(3):156-61. Curr Opin Cardiol. 1998. PMID: 9649937 Review.
Cited by
-
A human ventricular myocyte model with a refined representation of excitation-contraction coupling.Biophys J. 2015 Jul 21;109(2):415-27. doi: 10.1016/j.bpj.2015.06.017. Biophys J. 2015. PMID: 26200878 Free PMC article.
-
Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart.Cell Res. 2017 Oct;27(10):1195-1215. doi: 10.1038/cr.2017.87. Epub 2017 Aug 8. Cell Res. 2017. PMID: 28785017 Free PMC article.
-
Multiphysics and multiscale modelling, data-model fusion and integration of organ physiology in the clinic: ventricular cardiac mechanics.Interface Focus. 2016 Apr 6;6(2):20150083. doi: 10.1098/rsfs.2015.0083. Interface Focus. 2016. PMID: 27051509 Free PMC article. Review.
-
MicroRNA-34a Plays a Key Role in Cardiac Repair and Regeneration Following Myocardial Infarction.Circ Res. 2015 Aug 14;117(5):450-9. doi: 10.1161/CIRCRESAHA.117.305962. Epub 2015 Jun 16. Circ Res. 2015. PMID: 26082557 Free PMC article.
-
Dystrophin and the cardiomyocyte membrane cytoskeleton in the healthy and failing heart.Heart Fail Rev. 2000 Oct;5(3):221-38. doi: 10.1023/A:1009805419285. Heart Fail Rev. 2000. PMID: 16228906
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
