| Abstract |
Diseases of the arteries are responsible for morbidity and mortality more than any other human disease. The anomalies and pathologies of arteries cause clinical disease in two basic mechanisms, narrowing or complete obstruction of the lumen or the presence of acute phenomenon (eg, thrombosis, embolism). Theories about the inaugural events of atherogenesis started out early, but today dominates the theory of the inflammatory response to endothelial damage due to synergistic hemodynamic disorders, adverse effects of hypercholesterolemia and contribution of infectious agents. The most studied situation which contributes greatly both to the genesis and the evolution of the atherosclerotic lesion is hypercholesterolemia, which through production of free radicals, causes endothelial damage, dysfunction, and the creation of increased levels of oxidized subendothelial LDL.
Exploring the epidemiological characteristics, regarding the symptoms and therefore sudden death, these are observed at much younger ages, which often involve the 3 rd decade of life, while in the genesis and progression are involved both familial and environmental factors. Each plaque has a starting point of genesis, where the vascular environment and the above factors regulate its further development. As the earlier phase is defined the fatty streak, while the lumen of the vessel may be blocked gradually or after an acute episode. In any case, the lethal mechanism is the release of ventricular arrhythmias or fibrillation, after coronary spasm. The concept of vulnerable plaque has been introduced in recent years, explaining how plaques causing mild stenosis in the angiographic findings, give birth to acute coronary events and are prone to thrombosis, which is usually come after a rupture or erosion of plaque.
180 patients died of sudden coronary death constituted the study material as well as 40 witnesses, with extracardiac cause of death. The average stenosis was calculated digitally at 86.1%, while the microscopic examination showed 87.3%. Specifically, they found 101 cases out of 180 total observations in which the digitally measured stenosis was less than originally estimated, and 21 cases in which the final measured lumen was narrowed by less than 75%. The difference in measurements is attributed to the wrong microscopic estimation in the first place, the error which is included in the measurement after processing tissues with formalin and parafin, not taking into account the shape of the plaque and the extent of the damage in the coronary arterial tree, regardless of the degree of stenosis caused by them.
The main conclusion resulting from the second part of the study is that the plaque does not grow by getting through specific and predetermined stages, increasing proportionally the composition of its various components, but reasonably present differences between them and each one follows a different pattern , while the opposite results would indicate a linear and smooth volume change of the plaque with the ingredients.
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