The fourth teaching stage is atherocalcinosis: the deposition of calcium salts in plaques. In the Stary scheme, calcified lesions were designated type Vb (later in common usage type VII), and purely fibrous lesions with minimal lipid type Vc (type VIII). Calcium makes the plaque rigid, the artery a pipe, and the pulse wave fast. This is the stage of "old" atherosclerosis of the aorta: white stony plaques, the aorta does not collapse, it crunches on cutting.
Calcification is not a synonym for safety and not a synonym for catastrophe. ESC/EAS 2025 gives an important caveat: statins can reduce the lipid core and at the same time increase calcification — this is a sign of stabilisation, so a rise in CAC on a statin cannot be read as "the treatment is not working". On the other hand, a high CAC in a person without clinical ASCVD is associated with an event risk comparable to secondary prevention at markedly high values (the document gives the reference point CAC ≥300 as an example of "unequivocally documented ASCVD on imaging"). The association is observational; the 2025 focused update directly considers an RCT that would randomise management by CAC and prove a reduction in events to be absent.
Three organ outcomes that the curriculum requires you to be able to name as morphological diagnoses.
Atherosclerotic saccular aneurysm of the abdominal aorta with rupture. Plaques and destruction of the media weaken the wall, more often below the renal arteries. A saccular (or fusiform) dilatation forms. The thrombotic masses of the aneurysm contain layers of fibrin; the wall shows atheromatosis and calcification. Rupture — into the retroperitoneal tissue or into the abdominal cavity — causes massive blood loss. The clinical threshold for elective treatment of a fusiform degenerative aneurysm is set not by morphology but by ESVS 2024: elective repair is not recommended in men with a diameter <55 mm and in women <50 mm; elective repair should be considered at ≥55 mm in men and ≥50 mm in women (the recommendations were downgraded to IIa C because of a lack of high-level evidence). The threshold is preferably measured by ultrasound; CTA is for planning when the ultrasound threshold has already been reached. A saccular aneurysm is singled out in the same document as a separate morphology with a different risk — an exact numerical threshold "for all saccular aneurysms" as a single number is not set out separately in the ESVS 2024 text open to the lesson; the teaching morphological diagnosis "saccular aneurysm with rupture" describes a complication that has occurred, not a screening threshold.
Atherosclerotic nephrosclerosis. Stenosing atherosclerosis of the renal arteries and arterioles leads to ischaemic shrinkage of the kidneys: the surface is finely granular, the cortex is thinned, the glomeruli are hyalinised, the stroma is sclerosed, the arterioles show hyalinosis. The clinical counterpart is renovascular hypertension and a decline in eGFR. The course does not substitute for a nephrology protocol for renal artery revascularisation: the outcomes of renal artery stenting in large RCTs (ASTRAL, CORAL) are not discussed here as management. The morphological diagnosis must be recognised on a specimen.
Diffuse small-focal (atherosclerotic) cardiosclerosis. Multiple small scars in the myocardium after repeated foci of ischaemic necrosis on a background of stenosing atherosclerosis of the coronary arteries, without a large transmural scar. Macroscopy: the heart is firm, the chambers may be dilated, on section there are small greyish foci. This is the morphological substrate of chronic ischaemic heart disease, arrhythmias and ischaemic cardiomyopathy. It must not be confused with a large-focal post-infarction scar (the outcome of a Q-wave infarction) or with diffuse myocarditis.
The boundary of the module. A morphological stage on the aorta is not assigned "from the clinical picture", and the clinical picture is not assigned "from the stage at another person's autopsy". The link the course requires you to be able to draw: spots — silent exposure; fibrous plaque — chronic ischaemia of the territory; complicated plaque — acute thrombosis/embolism; calcification — rigidity and a marker of disease burden; aneurysm, nephrosclerosis, cardiosclerosis — the organ end-points of the same disease in different territories.