AHA Scientific Sessions 2026 Abstract · Nov 2, 2026
A Case with Serial Ultrasound Observation of Carotid Plaque Regression and Progression
By Katayama M, Naqvi TZ
Introduction: Carotid plaque detected by ultrasound is subclinical atherosclerosis and an early imaging sign of elevated atherosclerotic cardiovascular disease (ASCVD) risk. However, the therapeutic strategy aimed for plaque regression is not established, and treatment response is variable. Case: A 70-year-old female with multiple cardiovascular risks (hypertension, dyslipidemia, and a positive family history of premature coronary artery disease) has been diagnosed carotid artery stenosis. She had an initial carotid ultrasound scan 15 years ago at the age of 55, which identified a plaque (1.6 mm maximum plaque height at the right carotid bulb, Figure A). She started statin but discontinued due to myalgia. She was diagnosed with rheumatoid arthritis (RA) in her 40’s and has been controlled well with adalimumab. Serial ultrasound findings and lab data: When she returned to the second ultrasound examination (12 yrs later, at the age 67), the plaque height progressed to 3.8 mm (Figure B). She had gained weight, and her LDL was 194 mg/dL after she discontinued statin. Lipoprotein(a) was 53 mg/dL. She started statin and ezetimibe and followed life-style modification instructions. Her LDL level decreased to 65 mg/dL in three months. She was compliant with medications, and her follow-up ultrasound (a year later) showed a regression in plaque size (Figure C). At that point, the initiation of PCSK9 inhibitor was considered due to elevated Lp(a), but the patient was reluctant to start any additional medication. She could continue statin with ezetimibe for about another 6 months but discontinued when she had viral infection. After that, she was unable to comply with lipid medication due to multiple unfavorable symptoms. Her LDL level was 179 mg/dL. At the age of 70, she returned to the fourth carotid ultrasound, which revealed the plaque progressed to moderate stenosis of the right internal carotid artery (Figure D). Therapeutic interventions: The PCSK9 inhibitor was initiated following the imaging result. Surgical intervention was recommended by a neurosurgeon, but she preferred medical therapy. She continues evolocumab with ezetimibe with achieved targeted LDL (<70 mg/dL). Conclusion: We experienced a case whose carotid artery plaque once regressed but subsequently progressed to significant stenosis. Several factors could contribute to the progression of atherosclerosis in this case; statin intolerance, chronic inflammatory state (RA), and elevated Lp(a). Personalized and aggressive strategies are essential in high-risk patients.