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In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Anatomy and quantification of myocardial cell death
1Department of Pathological Anatomy, University of Milan Medical School, Sacco Hospital, Italy.
Abstract:
Irreversible damage of the myocardial cells may show different morphologic aspects in relation to the type of dysfunction of their contraction-relaxation cycle. Attenuation of the muscle fibers with elongation of the sarcomeres and nuclei are the earliest modifications (systolic paradoxical bulging and stretching by the intraventricular pressure) when the myocells stop their function in irreversible relaxation. This 'atonic' death is pathognomonic of myocardial infarction (infarct or coagulation necrosis) and the lesion evolves with typical structural changes. An opposite and entirely different morphologic pattern is seen in the 'tetanic' death in which the myocardial cells arrest in irreversible contraction (coagulative myocytolysis or contraction band necrosis). Segmental (paradiscal bands) or pancellular hypercontraction with extreme shortening of the sarcomeres and subsequent myofibrillar rhexis alternated with irregular cross band formations (holocytic bands) are characteristic of this necrosis seen in numerous human and experimental conditions and specific of catecholamine toxicity. The third type of damage is observed in low output syndromes in which increasing edematous vacuolization and disappearance of the myofibrils (colliquative myocytolysis) are the main structural alterations. They are suggestive of progressive functional reduction leading to dilatative insufficiency ('failing' death). These clear-cut morphofunctional patterns indicate distinctive biochemical impairments and pathogenesis. In particular their frequent presence in and possible association with the different aspects of the ischemic heart disease presuppose other non-ischemic mechanisms responsible for complications and death in this modern epidemic.
Insights
Myocardial cell death presents distinct morphologic patterns based on contraction-relaxation cycle dysfunction. Understanding these patterns, like
Area of Science:
- Cardiovascular Pathology
- Cellular Biology
- Pathogenesis of Heart Disease
Background:
- Myocardial cell death exhibits diverse morphological features linked to contraction-relaxation cycle abnormalities.
- Three primary patterns of myocardial cell death are identified: 'atonic' (relaxation failure), 'tetanic' (contraction failure), and 'colliquative' (edematous vacuolization).
- These distinct patterns are associated with specific biochemical impairments and pathogenic mechanisms.
Purpose of the Study:
- To elucidate the distinct morphofunctional patterns of myocardial cell death.
- To correlate these patterns with specific functional dysfunctions and underlying pathogenetic mechanisms.
- To investigate the implications of these patterns in ischemic heart disease and non-ischemic complications.
Main Methods:
- Morphological analysis of myocardial cells under various conditions of dysfunction.
- Correlation of observed structural changes with functional states (relaxation, contraction, low output).
- Pathogenetic and biochemical investigation of identified cell death patterns.
Main Results:
- 'Atonic' death (myocardial infarction) shows attenuated fibers and elongated sarcomeres due to irreversible relaxation.
- 'Tetanic' death (catecholamine toxicity) exhibits hypercontraction, sarcomere shortening, and myofibrillar rhexis (contraction band necrosis).
- 'Colliquative' myocytolysis (low output syndromes) is characterized by edematous vacuolization and myofibril loss, indicating dilatative insufficiency.
Conclusions:
- Distinct morphofunctional patterns of myocardial cell death ('atonic', 'tetanic', 'colliquative') reflect specific functional impairments and biochemical alterations.
- These patterns provide insights into the pathogenesis of various cardiac conditions, including myocardial infarction, catecholamine toxicity, and heart failure.
- The presence of these patterns, particularly in ischemic heart disease, suggests the involvement of non-ischemic mechanisms in cardiac complications and mortality.
