AHA Scientific Sessions 2026 Abstract · Nov 2, 2026
Fixed by the Stent? Detecting Hidden Polyvascular Disease and Risk-Adapted Lipid Therapy After PCI
By Mahajan K, HIMRAL S, Sharma JB et al.
Background: A successful PCI relieves symptoms and is taken, by patients and clinicians alike, as having “fixed” the problem. But atherosclerosis is systemic: concurrent plaque in the carotid and femoral beds marks a polyvascular extreme-risk phenotype with far worse outcomes, for which guidelines mandate a stricter LDL-cholesterol (LDL-C) target (<40 mg/dL) than other ASCVD (<55 mg/dL). These beds are rarely imaged, so the phenotype is routinely missed. Research Question: After PCI, does the hidden burden of extracoronary atherosclerosis, and the higher risk it signals, translate into more intensive LDL-C lowering and attainment of the stricter targets these patients are owed? Methods: In a prospective post-PCI registry, consecutive patients seen ≥1 month after PCI (n=889) underwent bilateral carotid and common femoral ultrasound. Plaque was focal luminal encroachment or intima-media thickness ≥2.0 mm (stricter Mannheim adaptation). Patients were ordered by burden: CAD only; CAD + 1 extracoronary bed; or CAD + ≥2 beds (polyvascular extreme risk). Lipid metrics and combination lipid-lowering therapy (LLT) were compared across ordered groups by the Cochran-Armitage test for trend. Results: Of 889 patients, 361 (40.6%) had CAD only, 314 (35.3%) had CAD + 1 bed, and 214 (24.1%) had CAD + ≥2 beds; nearly 1 in 4 carried an unrecognized polyvascular extreme-risk phenotype identified only by imaging. Risk markers rose monotonically with burden (male sex 74.5→86.9%, p-trend<0.001; hypertension 50.1→60.7%, p=0.01; BMI>25 47.6→63.3%, p<0.001), confirming a higher-risk gradient. Treatment did not follow: mean LDL-C (50.1/51.1/52.8 mg/dL) showed no decline; attainment of <55 (69.5/63.4/64.4%) and <40 mg/dL (31.1/31.5/24.8%) did not rise; combination LLT declined with burden (70.9/64.9/63.5%; p-trend=0.05). The highest-risk group, who owed the <40 mg/dL target, met it least often (24.8%). Lp(a) >50 mg/dL was prevalent and flat (47.3/48.1/51.8%), an untreated driver atop undertreated LDL-C. Conclusions: Routine carotid and femoral ultrasound after PCI unmasks a large hidden subgroup with polyvascular extreme-risk anatomy whose risk profile is worse, yet whose LDL-C, target attainment, and combination LLT are no more intensive and, for combination therapy, paradoxically less. This treatment-risk discordance shows that post-PCI reassurance can mask rising residual risk. Embedding non-coronary vascular assessment into post-PCI care is a low-cost trigger to align treatment with risk in those who benefit most.