Does diabetes mellitus increase intimal hyperplasia and restenosis measured by IVUS after catheter-based coronary interventions compared to non-diabetics?
Serial IVUS analysis demonstrates that the increased risk of restenosis in diabetic patients after coronary interventions is primarily driven by exaggerated intimal hyperplasia.
BACKGROUND: The increased risk of restenosis after catheter-based coronary interventions in diabetic patients has not been determined. Intravascular ultrasound (IVUS) has shown that the decrease in arterial area is responsible for most of the late lumen loss in nonstented lesions and that intimal hyperplasia is responsible for all of the late lumen loss in stented lesions. METHODS AND RESULTS: Serial (postintervention and follow-up at 5.6 +/- 3.3 months) IVUS was used to study 251 native coronary lesions in 241 patients; 63 patients had treated diabetes mellitus (oral hypoglycemic drugs or insulin). Interventional procedures included percutaneous transluminal coronary angioplasty, directional or rotational atherectomy, excimer laser angioplasty, or Palmaz-Schatz stents. The external elastic membrane (EEM), stent, and lumen areas were measured. The plaque+media (P+M) area in nonstented lesions was calculated as EEM minus lumen area, and the intimal hyperplasia (IH) area in stented lesions was calculated as stent minus lumen area. The anatomic slice selected for serial analysis had an axial location within the target lesion at the smallest follow-up lumen area. Nonstented lesions in diabetics and nondiabetics had a similar decrease in EEM cross-sectional area (CSA; 1.9 +/- 2.8 versus 1.8 +/- 4.2 mm2; P = .6350). However, nonstented lesions in diabetics had a greater increase in P+M CSA (1.3 +/- 2.8 versus 0.6 +/- 2.5 mm2, P = .0720), and the increase in P+M CSA contributed a greater percentage to the decrease in lumen CSA. In stented lesions, the decrease in lumen CSA (5.2 +/- 2.5 versus 2.0 +/- 2.3 mm2) and the increase in IH CSA (5.0 +/- 2.8 versus 1.8 +/- 2.0 mm2) were greater in diabetics than nondiabetics (P = .0009 and P = .0007, respectively). These findings were even more striking in (nonstented and stented) restenotic lesions. CONCLUSIONS: Serial IVUS analysis showed that the main reason for increased restenosis in diabetes mellitus was exaggerated intimal hyperplasia in both stented and nonstented lesions.
Kornowski et al. (1997) studied this question.