The role of serial carotid intima-media thickness assessment as a surrogate marker of atherosclerosis control in patients with recent myocardial infarction.

Introduction: Despite percutaneous coronary intervention (PCI), patients after their first myocardial infarction (MI) are at high risk of ischemic event recurrence. Therefore, there is a need for objective markers of adequate atherosclerosis control, independent of prescribed pharmacotherapy and patients' compliance. Such a potential indicator of major adverse cerebral and coronary event (MACCE) risk might be change in carotid intima-media thickness (CIMT), which indicates atherosclerosis growth.

Aim: To evaluate the potential associations between CIMT changes and the incidence of MACCE and recurrent MI.

Material And Methods: The CIMT assessments at baseline and during 2 follow-up visits were performed in 215 patients admitted with MI, in whom PCI was performed for an index lesion, followed by best medical treatment. The incidences of MACCE (cardiovascular death, recurrent MI, ischemic stroke) and new onset angina were recorded prospectively.

Results: The MACCE were recorded in 65 (30.2%) patients and angina due to coronary lesion progression (CLP) in 27 (12.5%) patients. Although initial CIMT values were similar in patients who suffered MACCE vs. MACCE-free patients (1.43 ±0.40 vs. 1.45 ±0.44 mm; = 0.486), patients in whom MACCE occurred had greater annual CIMT growth as assessed at the first (0.024 ±0.12 vs. 0.009 ±0.16 mm/year; < 0.001) and subsequent follow-up visit (0.050 ±0.1 vs. 0.001 ±0.1 mm/year; < 0.001), in mean 36.5 ±29.3 and 53.3 ±37.1 months, respectively. An optimal cut-off value for annual CIMT change of > 0.003 mm/year (sensitivity: 84.5%, specificity: 49.3%) for MI plus CLP (AUC = 0.673) occurred an independent indicator of MACCE (HR = 3.00; 95% CI: 1.496-6.016), recurrent MI (HR = 4.59, 95% CI: 1.591-13.217), and MI plus CLP (HR = 3.50, 95% CI: 1.759-6.964).

Conclusions: Annual CIMT change might be a potentially valuable marker of atherosclerosis response to post-MI treatment.