Abstract
The aim of the study was to detect changes in left ventricular cardiomyocyte size and shape in response to chronic ischemia and loss of cardiac tissue (myocardial infarction) during the course of ischemic heart disease (IHD). Left ventricular cardiomyocyte dimensions (diameter and length) were estimated histomorphometrically, and their cross-sectional area and volume were assessed in 85 males who died suddenly out of hospital (within 6 hours of the onset of the terminal event) due to the acute first (preinfarction IHD group, n=53, aged 48.6+/-2.9 years) or repeated (postinfarction IHD group, n=32, aged 51.7+/-2.9 years) IHD attack, and had no other causes for the increased heart load. Twenty-nine males of similar age (mean age, 46.0+/-3.1 years) who succumbed to external causes served as controls. We have found cardiomyocyte hypertrophy in the preinfarction IHD group already. The cardiomyocyte volume was increased by 32.0% in comparison with the same index in the control group, and cross-sectional area and length--by 17.2 and 12.5%, respectively. In postinfarction IHD group, all studied cardiomyocyte parameters did not differ significantly from the analogous indices in the preinfarction IHD group (P>0.05). Cardiomyocyte hypertrophy was related to the increase in left ventricular cardiomyocyte parameters. Left ventricular cardiomyocyte hypertrophy occurs before the first myocardial infarction. In postinfarction myocardium, cardiomyocyte dimensions do not differ significantly at least prior to the appearance of congestive heart failure syndrome.
Highlights
The essential function of the heart – to generate force to pump blood – depends upon the coordinated contraction of cardiomyocytes
We have found cardiomyocyte hypertrophy in the preinfarction ischemic heart disease (IHD) group already
The cardiomyocyte volume was increased by 32.0% in comparison with the same index in the control group, and cross-sectional area and length – by 17.2 and 12.5%, respectively
Summary
The essential function of the heart – to generate force to pump blood – depends upon the coordinated contraction of cardiomyocytes. The unit of contraction represents sarcomeres, longitudinally arranged within all muscle cells. This protein complex is organized into thick (myosin) and thin (actin, troponin, and tropomyosin) filaments, which in the presence of calcium and ATP, slide past each other and generate the force of contraction. Structural and functional integrity between neighboring cardiomyocytes is supported by complex protein structures, called desmosomes. These complexes may transmit force between cells and participate in transduction of signals. They are important for the propagation of electric potential and ensure synchronized contraction of cardiomyocytes [1]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
