ESC Congress 2026 Abstract · Oct 26, 2026
Beyond the stent: routine vascular ultrasound after PCI reveals polyvascular extreme risk without intensified LDL-cholesterol lowering therapy
By Mahajan K, Sharma JB, Himral SK et al.
Background/Introduction: After percutaneous coronary intervention (PCI), clinicians and patients are often reassured that coronary risk has been “treated”, yet substantial residual atherosclerosis may persist in non-coronary vascular beds. Polyvascular disease defines an extreme-risk phenotype for which guidelines recommend more aggressive LDL-cholesterol (LDL-C) lowering (target <40 mg/dL) than for other patients with established atherosclerotic cardiovascular disease (target <55 mg/dL). Systematic non-coronary vascular assessment after PCI could therefore reclassify risk and highlight opportunities to intensify secondary prevention. Purpose: To quantify the prevalence of ultrasound-detected polyvascular atherosclerosis after PCI and to test whether greater extra-coronary plaque burden is linked to more intensive LDL-C lowering and attainment of risk-adapted LDL-C targets. Methods: We analysed a prospective registry of consecutive patients attending a post-PCI clinic ≥1 month after the index procedure (n=889). All underwent a routine ultrasound of the bilateral carotid and common femoral arteries. Atherosclerotic plaque was defined as a focal structure encroaching into the lumen or intima–media thickness ≥2.0 mm, using a stricter adaptation of Mannheim criteria. Patients were classified as CAD only (no extra-coronary plaque), CAD + 1 extra-coronary bed, or CAD + ≥2 beds (polyvascular extreme-risk). Baseline characteristics and lipid metrics (LDL-C, LDL-C <55 mg/dL, LDL-C <40 mg/dL, combination lipid-lowering therapy) were compared with one-way ANOVA and chi-square tests. Results: Of 889 patients, 361 (40.6%) had CAD only, 314 (35.3%) CAD + 1 extra-coronary bed, and 214 (24.1%) CAD + ≥2 beds, so nearly one in four had an otherwise unrecognised extreme-risk polyvascular phenotype detected only by routine vascular imaging. Age, male sex, and BMI >25 kg/m² increased with plaque burden (all p≤0.001), whereas diabetes and hypertension were similarly prevalent. LDL-C management was not risk-aligned: mean LDL-C was 50.1, 51.1, and 52.8 mg/dL in the CAD only, CAD + 1 bed, and CAD + ≥2 bed groups (p=0.35), with comparable proportions achieving LDL-C <55 mg/dL (69.5%, 63.4%, 64.4%; p=0.20) and <40 mg/dL (31.1%, 31.5%, 24.8%; p=0.19). Combination lipid-lowering therapy also did not increase with plaque burden (70.9%, 64.9%, 63.5%; p=0.12). Conclusion(s): Routine carotid and femoral ultrasound after PCI uncovers a substantial hidden subgroup with polyvascular extreme-risk anatomy, yet their LDL-C levels, LDL-C target attainment, and use of combination lipid-lowering therapy are indistinguishable from those with CAD only. This treatment–risk paradox underscores that reassurance after PCI can mask residual polyvascular risk; embedding systematic non-coronary vascular assessment into post-PCI pathways offers a practical means to refine risk stratification and trigger intensification of secondary prevention in patients who stand to benefit most.Table.Baseline characteristics