Typical Sites of Stenosis and Occlusion
The atherosclerotic process affects the vascular bed unevenly. The formation of pathological stenoses and occlusions is most characteristic of the following arteries of the brain and neck circulatory system:
- Aortic arch (arcus aortae) and brachiocephalic trunk (truncus brachiocephalicus).
- Subclavian artery (a. subclavia).
- Carotid system: common carotid artery (a. carotis communis), as well as its main branches — internal (a. carotis interna) and external (a. carotis externa) carotid arteries.
- Vertebrobasilar system: vertebral artery (a. vertebralis) and basilar artery (a. basilaris).
- Intracranial cerebral arteries: anterior (a. cerebri anterior), middle (a. cerebri media), and posterior (a. cerebri posterior) cerebral arteries.
- Connecting branches of the Circle of Willis: anterior communicating (a. communicans anterior) and posterior communicating (a. communicans posterior) arteries.
Anatomy and Pathology of the Carotid Arteries
Normally, the common carotid artery (a. carotis communis) ascends toward the head and at the bifurcation (division) forms two major pathways: the internal carotid artery (ICA) and the external carotid artery (ECA).
Pathological narrowing of the vessel lumen occurs due to the formation of an atherosclerotic plaque. The typical localization of this process is precisely the bifurcation area of the common carotid artery extending into the proximal segment (origin) of the internal carotid artery. This creates ideal conditions for subsequent thrombosis and embolism.
Mechanism of Artery-to-Artery Embolism
Artery-to-artery embolism is the pathological process of embolus migration with the bloodstream from a proximal arterial segment to a distal one. In practice, this most often means the transfer of substrate from large major neck vessels to intracranial cerebral arteries (e.g., from the ICA to the retinal artery or branches of the middle cerebral artery).
The pathogenesis of artery-to-artery embolism involves a strict sequence of stages:
- Presence of an unstable atherosclerotic plaque in the lumen of the internal carotid artery.
- Formation of fresh thrombotic masses on the ulcerated surface of the plaque.
- Detachment of a thrombus fragment (or particles of the degenerating atherosclerotic plaque itself).
- Migration of the detached fragment (embolus) along the bloodstream upward through the ICA into the cerebral vessels, which logically leads to their acute occlusion.
Cardiogenic Embolism of Cerebral Arteries
Cardiogenic embolism is based on the formation of embolic fragments on heart valve leaflets or the formation of an intracardiac thrombus with their subsequent release into the cerebral arteries.
Two groups of risk factors contributing to this process are distinguished.
Proven Cardiogenic Risk Factors:
- Atrial fibrillation.
- Presence of a prosthetic heart valve.
- Rheumatic heart valve disease.
- Recent myocardial infarction (within the past 1 month).
- Presence of an intracardiac thrombus.
- Intracardiac mass (e.g., myxoma).
Possible Cardiogenic Risk Factors:
- Sick sinus syndrome (SSS).
- Patent foramen ovale.
- Atherosclerotic plaque in the thoracic aorta.
- Prior myocardial infarction within 2–6 months.
- Presence of a hypokinetic or akinetic left ventricular segment.
- Mitral or aortic valve calcification.
Briefly: answers to topical questions
What are the pathogenetic subtypes of ischemic stroke according to TOAST criteria?
According to the TOAST system, ischemic strokes are differentiated into four etiological subtypes.
- Large artery atherosclerosis — large vessel thromboembolic.
- Cardioembolic — cardioembolic.
- Small vessel occlusion — small vessel disease (small vessel).
- Other determined etiology — 'other' aetiologies.
Precise subtype distribution is sometimes difficult, and the cause of stroke frequently remains undetermined.
Which specific arteries form the Circle of Willis?
The Circle of Willis is formed by the following major arteries at the base of the brain:
- Basilar artery (a. basilaris) — formed by the union of the vertebral arteries.
- Internal carotid artery (a. carotis interna) — forms the carotid circulation.
- Anterior cerebral artery (a. cerebri anterior) — participates in the blood supply to the cerebral hemispheres.
- Anterior communicating artery (a. communicans anterior) — an element of the arterial circle.
- Posterior communicating artery (a. communicans posterior) — a crucial anastomosis between the carotid and vertebrobasilar systems.
- Posterior cerebral artery (a. cerebri posterior) — participates in the blood supply to the cerebral hemispheres.
To memorize the main sources of cardiogenic embolism, use the mnemonic "RHYTHM-VALVE-THROMBUS": RHYTHM disorders (atrial fibrillation), VALVE pathology (prosthetic, rheumatic), and THROMBUS sources (recent infarction up to 1 month, intracardiac thrombi, or myxomas).
Class and exam questions
What is the difference between artery-to-artery embolism and cardiogenic embolism?
In cardiogenic embolism, the source (a thrombus or a valve fragment) forms in the heart chambers. In artery-to-artery embolism, a thrombus forms in the proximal section of a large artery (e.g., on a plaque in the carotid artery) and migrates into smaller distal cerebral vessels.
Where do atherosclerotic plaques most commonly form in the carotid arteries?
The most typical localization is the region of the common carotid artery bifurcation (a. carotis communis) extending to the proximal segment (origin) of the internal carotid artery (a. carotis interna).
What cardiac pathology most frequently leads to cardiogenic embolism?
The vast majority of cardiogenic embolism cases are due to the presence of non-rheumatic atrial fibrillation in the patient.
What else to study on this topic
- Clinical presentation of lacunar stroke and its differentiation from embolic disorders.
- Symptoms of middle cerebral artery occlusion (a. cerebri media).
- Features of blood circulation in the vertebrobasilar territory in atherosclerosis.
- Pathogenesis of unstable atherosclerotic plaque formation.
- The role of patent foramen ovale in the development of paradoxical embolism.
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