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Morphometric and immunohistochemical study of left ventricular cardiomyocytes’ morphology during remodelling in progressing ischemic heart failure (HF)
Date Issued | Volume | Issue | Start Page | End Page |
---|---|---|---|---|
2023-09-02 | 483 | S1 | 173 | 173 |
E-PS-03 | E-Posters Cardiovascular Pathology. E-PS-03-007.
Background & objectives: Ischemic injury initiates cardiomyocytes’ compensatory remodelling causing cellular resilience and hemodynamic function changes towards HF. Cardiomyocyte geometry and nonsarcomeric flament desmin expression analysis in diferent ischemic HF stages (adult heart model) is attempt to identify morphologic criteria monitoring HF progress. Methods: Cardiomyocyte’s length-diameter ratio and immunohistochemical reaction against desmin in left cardiac ventriclular segments were analysed in test groups (deceased or after heart transplantation due to ischemic injury): 1st – A, 2nd – B, 3rd – C/D stages of HF by ACC/AHA; control group – samples of patients with no cardiovascular disorders. Statistical analysis – ANOVA with post-hoc LSD tests (p<0.05). Results: Mean value of cardiomyocyte length-diameter ratio was smaller in 1st group compared to control (5.137 (0.374) vs. 5.392 (0.354), p=0.015). It increased in 3rd group compared to 1st and 2nd groups (5.582 (0.448) vs. 5.137 (0.374) and 5.3 (0.245), p<0.05). Cardiomyocytes of 1st group had more intensive immunohistochemical reaction against desmin compared to control group (p<0.001), also more intensive in 3rd compared to 2nd group (p<0.001), and control group (p<0.001), whereas intensity was similar in 1st and 2nd groups (p=0.159). Positive weak correlation between changes in cardiomyocyte geometry and expression of desmin was detected (r=0.2453, p=0.012). Conclusion: Morphofunctional changes of cardiomyocyte geometry and desmin expression during remodelling in response to ischemic injury are detected before HF, and progress in symptomatic HF, presenting morphometric and immunohistochemical diagnostic criteria to monitor myocardial disease progress at its earliest structural manifestation.