A third-year student sees an aorta with yellow spots in the dissecting room. A fifth-year student sees the same person no longer as a specimen but as a patient with retrosternal pain. A first-year resident reads a lipid profile and has to say whether it changes management. The course is built so that these three views converge in a single chain: morphological stage → clinical syndrome of a specific vascular territory → work-up plan → the number in the lipid profile that actually moves the decision.
Atherosclerosis is a chronic progressive disease of elastic and muscular-elastic arteries, based on the accumulation in the intima of atherogenic lipoproteins containing apolipoprotein B, followed by inflammation, plaque formation and its complications. The ESC/EAS 2025 Focused Update states it directly: atherosclerosis is caused by the progressive deposition of low-density lipoprotein cholesterol (LDL-C) and other ApoB-containing lipoproteins in the arterial wall; LDL-C is not only a risk factor for atherosclerotic cardiovascular disease (ASCVD) but, like other ApoB lipoproteins, a direct cause of ASCVD.
The course is intended for 3rd–5th-year students of the general medicine faculty and first-year residents. The learning outcome of the four modules is this: link the morphological stage to the clinical picture; build a work-up plan when atherosclerotic disease is suspected; read a lipid profile and explain what in it changes management; name the complications of each location.
How the programme is organised. Module 1 covers aetiology and risk factors, including the SCORE2/SCORE2-OP scales and familial dyslipidaemias. Module 2 covers the pathogenesis and morphology of the stages: fatty spots and streaks → fibrous plaques → complicated lesions (atheromatosis, ulceration, thrombus) → atherocalcinosis; separately, saccular abdominal aortic aneurysm with rupture, atherosclerotic nephrosclerosis, and diffuse small-focal (atherosclerotic) cardiosclerosis. Module 3 covers the clinical picture by vascular territory. Module 4 covers diagnosis, treatment and prevention. After each module there is a checkpoint of eight questions, passing score 70%. The final exam has 25 questions, passing score 75%, two attempts. At least one third of the questions are analyses of a teaching case construct: generalised, without real names or dates.
The clinical basis of the course is named by the current editions of the documents, not by outdated tables recalled "from memory".
- The full 2019 ESC/EAS Guidelines for the management of dyslipidaemias (European Heart Journal 2020;41:111–188, doi:10.1093/eurheartj/ehz455). This is where the LDL-C target levels by risk category are set.
- The 2025 Focused Update of these guidelines (doi:10.1093/eurheartj/ehaf190). This is not a new full edition: the document changes only those provisions for which, after 2019, sufficient data emerged for new or modified class I/IIa or III recommendations. The LDL-C target levels are unchanged. Risk assessment has changed: SCORE2 and SCORE2-OP replace SCORE.
- The 2024 ESC Guidelines for the management of chronic coronary syndromes (doi:10.1093/eurheartj/ehae177).
- Clinical protocol of the Ministry of Health of the Republic of Kazakhstan «Атерогенные нарушения липидного обмена (дислипидемии)» [Atherogenic lipid metabolism disorders (dyslipidaemias)], Joint Commission on the Quality of Medical Services (JCQMS) [рус.: ОККМУ], protocol No. 196 of 07 December 2023.
What the course does not cover — and this is a boundary, not a minor caveat.
The course does not replace a full course in cardiology, neurology, angiology and pathological anatomy. It does not teach how to perform coronary intervention, does not cover thrombolysis protocols in stroke, and does not cover vasculitides, syphilitic mesaortitis (inflammation of the tunica media of the aorta in syphilis — a non-atherosclerotic cause of aneurysm), Erdheim cystic medial necrosis (cystic degeneration of the aortic media, also a non-atherosclerotic aortopathy) or connective tissue dysplasias as causes of aneurysms. It is not a guide to acute coronary syndrome: ACS appears here only as an outcome of a complicated plaque and as the moment when the 2025 Focused Update requires intensification of lipid-lowering therapy. It does not teach interpreting coronary calcium as screening of the whole population: ESC/EAS 2025 states directly that coronary imaging and the calcium score are not indicated as a broad screening test for risk assessment. It does not prescribe dietary supplements: the 2025 focused update gives a class III, level B recommendation — nutraceuticals and vitamins without documented safety and significant LDL-C lowering are not recommended to reduce ASCVD risk.
One more boundary concerning sources. A separate current full text of a Ministry of Health of the Republic of Kazakhstan clinical protocol on stable ischaemic heart disease, 2020–2025 edition, was not found in open access. Therefore the clinical picture and treatment of chronic coronary syndromes rely on ESC 2024, and the Kazakhstani standard for dyslipidaemias and codes I20–I25 relies on protocol No. 196/2023. If a different local document is in force in a particular organisation in practice, it must be opened separately: this course does not substitute for it.
The course never retells an observational association as an effect. INTERHEART is a case-control study in 52 countries: it shows what proportion of first myocardial infarctions is associated with nine factors, but by itself does not prove that eliminating each factor reduces risk in the same proportion. Risk reduction with LDL-C lowering is proven by randomised trials and the CTT meta-analysis. These are different levels of claim, and the lessons do not mix them.
After this lesson the theory begins. Not before.