How is vascular erosion classified in older adults with a history of hypertension, diabetes, or atherosclerosis?

Classification of Vascular Erosion

Vascular erosion is not formally classified by a standardized grading system in current guidelines; instead, it is characterized by its anatomical location, underlying pathology (arteriolosclerosis vs. cerebral amyloid angiopathy for cerebral vessels, or atherosclerotic plaque characteristics for coronary/peripheral vessels), and clinical presentation.

Anatomical Classification by Vascular Territory

Vascular erosion is best understood by the specific arterial bed affected:

Cerebrovascular Erosion

• Deep territory erosion occurs in penetrating arterioles of the basal ganglia, thalamus, brainstem, and deep cerebellar nuclei, typically associated with arteriolosclerosis (lipohyalinosis) 1
• Lobar territory erosion affects arterioles in the leptomeninges, cerebral cortex, and cerebellar hemispheres, primarily linked to cerebral amyloid angiopathy (CAA) 1
• Risk factors include hypertension, diabetes, and age for arteriolosclerosis; age and apolipoprotein E ε2/ε4 alleles for CAA 1

Aortic Erosion (Vertebral Body Erosion)

• Chronic contained rupture with vertebral body erosion (VBE) results from pulsatile trauma of thoracoabdominal aortic aneurysms causing progressive bone destruction 1
• Occurs predominantly in thoracolumbar spine (26/80 cases) with average aneurysm diameter of 7.056 ± 3.39 cm 1
• Associated with arterial hypertension (100% of cases), osteoporosis, and advanced age (average 65 years) 1
• Distinguished from infectious erosion by smooth, well-defined lytic margins versus irregular margins in spondylodiscitis 1

Coronary and Peripheral Arterial Erosion

• Plaque erosion accounts for approximately one-third of acute coronary syndromes and up to two-thirds of non-STEMI cases 2
• Characterized by intact fibrous cap with endothelial denudation, abundant extracellular matrix, few inflammatory cells, and neutrophil extracellular traps (NETs) 2, 3
• Occurs predominantly on stenotic plaques (median 31% diameter stenosis) in regions of elevated wall shear stress 4

Pathophysiological Classification

By Underlying Small Vessel Disease (Cerebrovascular)

• Arteriolosclerosis-related erosion: Concentric hyalinized vascular wall thickening in deep brain territories, driven by hypertension and diabetes 1
• CAA-related erosion: β-amyloid peptide deposition in cortical vessel walls, age-dependent with genetic predisposition 1

By Hemodynamic Mechanism (Coronary/Peripheral)

• High-flow erosion: Occurs in 15/17 cases at sites of elevated time-averaged wall shear stress, maximum wall shear stress, and wall shear stress gradient 4
• Oscillatory-flow erosion: Rare variant (2/17 cases) occurring in regions of elevated oscillatory shear stress without flow elevation 4

By Thrombotic Potential

• Erosion with thrombosis: Endothelial desquamation exposing thrombogenic subendothelial matrix, triggering platelet adhesion and NET formation 3
• Erosion without thrombosis: Subclinical endothelial dysfunction without acute thrombotic complications 2

Clinical Classification by Presentation

Symptomatic vs. Asymptomatic

• Symptomatic erosion presents with acute coronary syndromes, stroke/TIA, or critical limb ischemia depending on vascular bed 1
• Asymptomatic erosion detected incidentally on imaging or at autopsy 1

By Severity of Ischemia (Peripheral Arterial Disease)

• Intermittent claudication: Exertional leg symptoms with reproducible walking distance 1
• Critical limb ischemia: Chronic ischemic rest pain, ulcers, or gangrene threatening limb viability 1
• Acute limb ischemia: Sudden decrease in perfusion with the "5 Ps" (pain, pulselessness, pallor, paresthesias, paralysis) 1, 5

Risk Stratification in High-Risk Populations

Diabetic Patients

• 2-4 fold increased risk of peripheral arterial disease with more distal vessel involvement and medial arterial calcification 1, 6
• Combination of microvascular and macrovascular disease accelerates erosion pathophysiology 6
• Neuropathy may mask ischemic symptoms, allowing progression to tissue loss 1, 6

Hypertensive Patients

• Arterial hypertension present in 100% of aortic erosion cases with vertebral body involvement 1
• Elevated systolic blood pressure strongly associated with upper extremity artery disease (highest odds ratio among modifiable risk factors) 1

Atherosclerotic Disease Patients

• Multi-site atherosclerosis confers worse prognosis than single-location disease 1
• Smoking carries highest odds ratio (2.6) for upper extremity arterial disease among all risk factors 1

Critical Diagnostic Pitfalls

Never assume normal perfusion based on palpable pulses alone in diabetic patients—up to 50% of diabetic foot ulcer patients have peripheral arterial disease despite adequate examination findings 6. An ankle-brachial index (ABI) <0.90 has 75% sensitivity and 86% specificity for PAD diagnosis and should be measured in all patients over 70 years, age 50-69 with smoking or diabetes, or any age with diabetes plus one atherosclerosis risk factor 1, 6, 7.

Delayed recognition of "masked LEAD" (lower extremity arterial disease) in patients with comorbidities limiting walking capacity (heart failure, neuropathy) can allow severe PAD to progress without claudication symptoms 6, 7. ABI <0.5, ankle pressure <50 mmHg, or toe pressure <30 mmHg requires urgent vascular surgery referral to prevent catastrophic gangrene and amputation 6, 5.