Abstract

This is not a play on words, but a key to solving a problem that has been deadlocked. The science of atherosclerosis is still based on the experiments of N. N. Anichkov. It always prioritizes lipid infiltration of vessel's walls. In fact, the lipid infiltration of the vessel's walls is not related to the origin of lipids in atheromas. Their origin is always associated with fatty degeneration of myofibroblasts in places of sclerosis (fibrous plaques), but not with hematogenous infiltration. The key to solving this problem lies in a disclosure of the genesis of sclerotic changes in intima. On the one hand it concerns a primary age sclerosis (compensatory) as well as secondary sclerosis (inflammatory, etc). On the other hand it is important to establish causes of degradation (fatty degeneration) and death of myofibroblasts (the so-called Langgans'cells) in places of sclerosis (fibrous plaques), followed by atheroma formation. We have first showed in vivo (at the cellular level) that a death of myofibroblasts in plaques with following release of lipids occurs due to the fact that these myofibroblasts reach the Heiflik's limit much faster than myofibroblasts on healthy vessels. These occurs due to shortening of telomeres in myofibroblasts that intensively multiply in places of reparative sclerosis. The authors propose replacing the term “atherosclerosis” with “scleroatherosis”, which more accurately reflects the essence of the disease and the sequence of events in its pathogenesis. Considering "scleroarethosis" as a nosological form, two periods of development of the process should be emphasized: the first – sclerotic period (compensatory) and the second – atheromatous (period of decompensation). The second period is accompanied by all manifestations and complications known for scleroatherosis that can't be eliminated. It is no need to spend billions on senseless "purifying” blood vessels and "lowering" cholesterol in blood plasma. It is more important to focus on a healthy lifestyle and, above all, to fight with arterial hypertension as with a main factor of blood vessels' deterioration.

Highlights

  • Это не «игра слов», а ключ к решению проблемы, которое в настоящее время зашло в тупик.

  • Основным постулатом в патогенезе атеросклероза в настоящее время является утверждение о ведущей роли проникновения липидов (холестерола) из плазмы крови в стенку сосуда.

  • В них, как компенсаторную реакцию, для сохранения постоянства ёмкости сосудистого русла, наблюдают разрастание и утолщение интимы с формированием в ней так называемого эластически-гиперпластического слоя из миофибробластов, мигрирующих в интиму из средней оболочки сосуда

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Summary

Introduction

Это не «игра слов», а ключ к решению проблемы, которое в настоящее время зашло в тупик. Основным постулатом в патогенезе атеросклероза в настоящее время является утверждение о ведущей роли проникновения липидов (холестерола) из плазмы крови в стенку сосуда. В них, как компенсаторную реакцию, для сохранения постоянства ёмкости сосудистого русла, наблюдают разрастание и утолщение интимы с формированием в ней так называемого эластически-гиперпластического слоя из миофибробластов, мигрирующих в интиму из средней оболочки сосуда

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