Morphological stabilization and regression of carotid plaque following therapy with evolocumab in a high-risk patient
Tiziana Claudia Aranzulla1, Giuseppe Musumeci1
1Mauriziano Umberto I Hospital, Torino, Italy.
Insights
Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors, alongside statins, may promote atherosclerotic plaque regression and remodeling. This case study shows significant carotid plaque reduction and stabilization with PCSK9 inhibitor therapy.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Medical Imaging
Background:
- Atherosclerosis, a leading cause of cardiovascular and cerebrovascular disease, necessitates effective lipid-lowering therapies.
- Low-density lipoprotein cholesterol (LDL-C) reduction correlates with decreased atherosclerosis progression and adverse events.
- Managing complex atherosclerotic disease requires optimizing lipid targets and considering advanced therapies.
Abstract:
Lipid-lowering therapy is a mainstay for the management of coronary and carotid disease. Actually, progression of atherosclerosis and adverse events are reduced in proportion to the achieved levels of LDL cholesterol (LDL-C). A 67-year-old patient underwent two hospitalizations 6 months apart due to acute coronary syndromes. In the first, PCI with drug-eluting stents (DES) was performed to treat ulcerated stenoses in the left anterior descending artery. In the second, lipid-rich critical disease was found on the right coronary artery and treated with PCI + DES. Later, carotid duplex ultra-sonography (DU) was done due to some episodes of dizziness. It showed an 80% critical stenosis (peak systolic velocity, PSV 239 cm/s) of the left internal carotid artery (LICA) with high-risk features (hypoechogenic and irregular plaque with "fluffy" components). In consideration of the plaque morphology and the unmet LDL-C targets, evolocumab was added to the ongoing statin therapy. In the following months, we observed a parallel trend between carotid plaque regression and LDL-C lowering. Initial plaque remodeling was seen after 5 months: the atheroma appeared fibrotic, with no more fluffy components. At 10 months, in conjunction with the achievement of LDL-C goal (23 mg/dl), a fibrocalcific atheroma was observed; PSV, after an initial rise, fell to 229 cm/s. No further cardiovascular event occurred at 46 months. Last DUS showed a 60% fibrocalcific mid LICA stenosis with PSV of 180 cm/s. Our experience highlights the important role of proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors in promoting remodeling and hopefully regression of atherosclerotic plaques.
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