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Atherosclerosis was found in humans who lived thousands years ago. Paleopathologist Marc Armand Ruffer (1859-1917) identified atherosclerotic plaques in the aorta as well as in several large arteries of numerous Egyptian mummies, noting that atherosclerosis was a widespread disease in antiquity. Russian researchers tried to induce experimental atherosclerosis in an animal model, feeding laboratory animals with pure cholesterol. They demonstrated that cholesterol alone caused atherosclerotic lesions in the artery wall. Many studies have shown that blood cholesterol levels are largely determined by the amount of fat in the diet. The Study of the Seven Countries was the first epidemiological evidence that linked the increase in cholesterol to cardiovascular events. In the genetic approach, one of the first indications that coronary artery disease was related to cholesterol came from anecdotal case reports of children with xanthomas (large deposits of lipids just under the skin or attached to tendon sheaths, on the back of the hands or ankles), who had sudden death or myocardial infarction before the age of 10 years. The first cases of homozygous familial hypercholesterolemia were described. The 2019 European Guideline, for example, considers for high-risk patients, a target LDL-c < 70 mg/dl and a reduction > 50% compared to baseline; for very high risk, a target LDL-c < 55 mg/dl and a reduction > 50% compared to baseline; and for patients with acute coronary syndrome, within a two-year period, a target LDL< 40 mg/dl. In order to achieve these more aggressive goals, the combination of drugs is necessary, especially in patients with eligibility criteria for the new lipid-lowering drugs, based on molecular biology techniques, in addition to an adequate clinical judgment. |
