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The pathogenesis of cardiac infarction. A few comments on some unanswered questions
Insights
Coronary insufficiency, a 50-year-old concept, involves elective myocardial necrosis due to inadequate coronary perfusion. This process is influenced by coronary artery narrowing, cardiac muscle mass, and heart effort during critical damage periods.
Area of Science:
- Cardiology
- Pathology
- Cellular Biology
Background:
- Coronary heart disease has been studied for over 200 years, with the concept of coronary insufficiency emerging 50 years ago.
- The pathological anatomy of coronary insufficiency is complex and variable.
- Coronary insufficiency is a superimposed concept, with cardiac infarcts and inner myocardial layer damage as subordinate conditions.
Purpose of the Study:
- To elucidate the underlying mechanisms of coronary insufficiency and its morphological consequences.
- To analyze the factors contributing to myocardial necrosis in the context of coronary perfusion.
- To clarify the relationship between coronary artery anatomy, cardiac workload, and myocardial damage.
Main Methods:
- Analysis of pathological anatomy and morphological consequences of coronary insufficiency.
- Investigation of the role of coronary perfusion and "vis a tergo" in myocardial damage.
- Examination of cellular mechanisms, including ion behavior and energy metabolism, in cardiac muscle fibers.
Main Results:
- Coronary insufficiency is characterized by elective parenchyma necrosis, resulting from inadequate coronary perfusion pressure ("vis a tergo").
- Three key factors contribute to coronary insufficiency: critical coronary artery narrowing, cardiac muscle mass, and cardiac effort.
- Disturbances in cellular respiration and calcium ion influx lead to energy depletion and necrosis of cardiac muscle fibers.
Conclusions:
- Cardiac infarcts are a "dyscirculatory" phenomenon, dependent on coronary circulation, with specific sites of predilection.
- Myocardial necrosis can occur through various pathways, distinct from those leading to cardiac infarcts.
- Understanding the interplay of anatomical, functional, and cellular factors is crucial for analyzing individual cases of coronary insufficiency.
Abstract:
1. Questions concerning coronary heart disease have been raised for more than 200 years, but the concept of coronary insufficiency is only 50 years old. 2. The pathological anatomy of coronary insufficiency is variable, unexpectedly rich and stratified, and full of pecularities. 3. "Coronary insufficiency" is the superimposed concept; "cardiac infarcts" and "inner myocardial layer damage" are subordinate. 4. The logical connection linking all the morphological consequences of so-called coronary insufficiency is the elective necrosis of the parenchyma. The anatomically demonstrable equivalents of coronary insufficiency are, from the point of view of coronary perfusion, the result of an inadequate "vis a tergo". 5. This principle is enshrined in a complex of conditions which has to be disentangled if an individual case is to be analysed. The complex comprises three sets of factors: (a) the critical narrowing of the lumen of the coronary arteries and all their branches leading to a given territory; (b) the weight of the functioning mass of the cardiac muscle; (c) cardiac effort required of the heart during the critical period of damage. 6. The presence of anastomoses between the coronary arteries is no proof of their functional efficiency or readiness in an emergency. The conditions which determine their responsiveness, particularly as far as time is concerned, are at the moment still not adequately known. 7. The behaviour of ions at the membranes of living cells, particularly of muscle fibres, is a fundamental phenomenon, fascinating in its primitive aspects. A disturbance of cellular respiration, produced in the cardiac muscle "regularly" by the "inadequate vis a tergo" of coronary perfusion, leads to an exhaustion of energy stores, and to an increased influx of calcium ions. This activates the ATP-ase of the myofibrils, and thereby reduces the level of adenin nucleotides. This loss of energy-rich substances not only militates against the function of the muscle fibres, it also initiates their necrosis. 8. The cardiac infarct is a phenomenon of a disturbed circulation-- a "dyscirculatory" change. It is found in certain sites of predilection, whose choice becomes intelligible only through an understanding of the developmental history of the coronary arteries. The cardiac infarct is "coronary-dependent"! There are, however, also other forms of, and possibilities leading to, the development of myocardial necrosis. The nosology of the cardiac infarct clearly distinguishes the latter from these other forms. In damage of the inner layers of the myocardium infarcts do not develop by the confluence of necroses of individual fibres or of groups of fibres. Infarcts are not a phenomenon of addition, they do not have the "character of a mosaic". 9. As in other tissues, in the human myocardium also there are lysosomes. They are found in hypertrophied muscle fibres. Topical relations to zones of necrosis have not been found. 10...