Intravascular ultrasound studies have shown that restenosis in both stented and non-stented lesions is due to intimal hyperplasia (Kornowski etal., 1997; Levine etal., 1997; Van Belle etal., 1997), which is a smooth-muscle-cell proliferative response. In one series of 241 patients (n = 63 with diabetes) who had 251 native lesions stented, follow-up angiography with intravascular ultrasound demonstrated the late lumen loss was more pronounced in both stented and non-stented lesions of diabetic patients (Kornowski etal., 1997).
Results from registries and clinical trials indicate that diabetic patients have an increased risk of restenosis, repeat revascularisation and death after PCI (Rozenman etal., 2000; Van Belle etal., 2001). A useful retrospective study of clinical trial participants was performed at the Cardialysis Core Laboratory in Rotterdam (West etal., 2004). Restenosis occurred in 550 of 2672 (21%) non-diabetic and 130 of 418 (31%) diabetic patients (P < 0.001). Reduced body mass index (BMI), larger reference diameter before stenting and longer stented length of vessel were multivariate predictors of restenosis.
In the ARTS trial, the incidence of death/stroke/MI at 3 years was similar in stented patients who, according to the BMI, were normal (BMI 18.5-24.9 kg/m2), overweight (BMI 25-30 kg/m2) or obese (BMI > 30 kg/m2; n = 124) at 30%, 37% and 32%, respectively (Gruberg etal., 2005). The rates for these respective groups managed by surgical revascularisation were 24%, 16% and 11%. The rates of repeat revascularisation, although much higher in PCI-treated patients than CABG-treated patients, were unrelated to BMI. Thus, in this trial BMI was unrelated to outcome in both PCI- and CABG-treated patients.
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