# Stroke in a 32-year-old male with hypertension, hyperlipoproteinemia(a), and no large vessel disease: a case report

## TL;DR

A 32-year-old man with high Lp(a) levels had a stroke without large vessel disease, suggesting Lp(a) may cause small vessel damage.

## Contribution

This case report suggests Lp(a) may induce microthrombosis in small vessels, a novel mechanism for stroke.

## Key findings

- Elevated Lp(a) levels were associated with subcortical and thalamic brain lesions in a young patient.
- Treatment with PCSK9 inhibitors and antiplatelet therapy led to full recovery.
- Lp(a) may contribute to stroke via procoagulant effects in small vessels.

## Abstract

Lipoprotein(a) [Lp(a)] is associated with cardiovascular events through three primary mechanisms: promoting atherosclerosis, thrombosis, and inflammation. While evidence of Lp(a)-induced thrombosis in large vessels is limited, its effects on small vessels have not been previously reported.

A 32-year-old male with hypertension presented with 2 weeks of right-sided numbness. Magnetic resonance imaging of the brain revealed multiple punctate lesions in the subcortex of both cerebral hemispheres, as well as a subacute ischaemic lesion in the thalamus. Notablely, no significant evidence of vascular sclerosis or stenosis was found. Blood tests indicated elevated Lp(a) levels. Following treatment with a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor and dual antiplatelet therapy, the patient made a full recovery.

Multiple punctate lesions in the subcortex of both brain hemispheres are common but highly non-specific. Further research is needed to determine whether these lesions represent a clinical manifestation of microthrombosis induced by elevated serum Lp(a) levels. The subacute ischaemic lesion in the thalamus suggests that the procoagulant effect of Lp(a) may contribute to cardiovascular diseases, including those affecting small vessels. However, the potential impact of hypertension-induced damage cannot be excluded.

This case highlights the need for thorough etiologic evaluation in young stroke patients with unclear risk factors. Markedly elevated Lp(a) may contribute to a prothrombotic state even without large-vessel disease. Incorporating Lp(a) measurement into diagnostic and therapeutic assessments could aid management, with PCSK9 inhibitors and dual antiplatelet therapy offering potential benefit.