Leukotriene production by human vascular tissues: possible link between the nature of the atherosclerotic lesions and their clinical activity

Abstract

The idea that angiographic assessment of coronary atherosclerosis is a poor predictor of the occurrence of clinical complications is being appreciated more and more. Over a certain age, atherosclerotic lesions in the coronary arteries become common in humans [1]. Clinical manifestations of coronary artery disease are, on the contrary, relatively uncommon phenomena, sometimes occurring erratically and unpredictably in the patient’s life. This is especially true of the most catastrophic clinical complications of coronary artery disease, namely unstable angina, myocardial infarction, and sudden cardiac death. On the other hand, a long established and more understandable relationship exists between the angiographic degree of coronary artery lesions and chronic stable angina. Here, the progressive reduction of coronary reserve as a function of the degree of lumen obstruction can easily explain the occurrence of myocardial ischemia in conditions of an increased myocardial oxygen demand. However, stable angina is rarely an unmanageable situation, and we are mostly faced with the problem of unstable events only loosely correlated with quantitative assessment of lumen reductions. Given the strong evidence still relating the proven mechanisms of “coronary instability” — thrombosis and alterations in the vasomotor tone — to atherosclerotic plaques in the coronary arteries [2–6], one is left with the recognition of the limitations of quantitative assessment of lumen reduction as given by angiography, and with the need to explore qualitative features of the atherosclerotic plaque in search for hints that predict the “activation” of the disease.