Background—: Systemic levels of myeloperoxidase predict prognosis in patients with acute coronary syndromes and are considered a marker of plaque vulnerability. It is not known whether myeloperoxidase is associated with different coronary morphologies (ie, rupture or erosion of the culprit lesion) in patients with acute coronary syndrome. Methods and Results—: Twenty-five consecutive patients (aged 67±11 years; 15 men [60%]; 13 [52%] with non–ST-segment elevation acute coronary syndrome and 12 [48%] with acute ST-segment elevation myocardial infarction) were enrolled. Optical coherence tomography classified the culprit lesion as ruptured in 18 (72%) or eroded in 7 patients (28%) and detected intraluminal thrombus in 89% of ruptured plaques and 100% of eroded plaques. Baseline systemic levels of serum myeloperoxidase were significantly higher in patients with an eroded plaque than in those with a ruptured plaque (median, 2500 ng/mL; 25th to 75th percentile, 1415 to 2920 versus median, 707 ng/mL; 25th to 75th percentile, 312 to 943; P =0.001), whereas C-reactive protein levels did not differ significantly (median, 11.3 mg/L; 25th to 75th percentile, 1.3 to 28.5 versus median, 3.9 mg/L; 25th to 75th percentile, 1.3 to 17.8; P =0.76, respectively). In addition, the density of myeloperoxidase-positive cells within thrombi overlying plaques in postmortem coronary specimens retrieved from sudden coronary death victims was significantly higher in lesions with erosion (n=11) than ruptures (n=11) (median, 1584; 25th to 75th percentile, 1088 to 2135 cells/mm ² versus median, 579; 25th to 75th percentile, 442 to 760 cells/mm ² ; P =0.0012). Conclusions—: Systemic myeloperoxidase levels are significantly elevated in patients with acute coronary syndrome presenting with eroded culprit plaque compared with patients presenting with ruptured culprit plaque. Consistently, in postmortem coronary specimens, luminal thrombi superimposed on eroded plaques contain a higher density of myeloperoxidase-positive cells than thrombi superimposed on ruptured plaques. This study supports the concept that elevations in selective inflammatory biomarkers reflect specific acute complications of coronary atherosclerosis.

Incomplete endothelialization has been found to be associated with late stent thrombosis, a rare but devastating phenomenon, more frequent after drug-eluting stent implantation. Optical coherence tomography (OCT) has 10 times greater resolution than intravascular ultrasound and thus appears to be a valuable modality for the assessment of stent strut coverage. The LEADERS trial was a multi-centre, randomized comparison of a biolimus-eluting stent (BES) with biodegradable polymer with a sirolimus-eluting stent (SES) using a durable polymer. This study sought to evaluate tissue coverage and apposition of stents using OCT in a group of patients from the randomized LEADERS trial. Fifty-six consecutive patients underwent OCT during angiographic follow-up at 9 months. OCT images were acquired using a non-occlusive technique at a pullback speed of 3 mm/s. Data were analysed using a Bayesian hierarchical random-effects model, which accounted for the correlation of lesion characteristics within patients and implicitly assigned analytical weights to each lesion depending on the number of struts observed per lesion. Primary outcome was the difference in percentage of uncovered struts between BESs and SESs. Twenty patients were included in the analysis in the BES group (29 lesions with 4592 struts) and 26 patients in the SES group (35 lesions with 6476 struts). A total of 83 struts were uncovered in the BES group and 407 out of 6476 struts were uncovered in the SES group [weighted difference −1.4%, 95% confidence interval (CI) −3.7 to 0.0, P = 0.04]. Results were similar after adjustment for pre-procedure lesion length, reference vessel diameter, number of implanted study stents, and presence of stent overlap. There were three lesions in the BES group and 15 lesions in the SES group that had ≥5% of all struts uncovered (difference −33.1%, 95% CI −61.7 to −10.3, P < 0.01). Strut coverage at an average follow-up of 9 months appears to be more complete in patients allocated to BESs when compared with SESs. The impact of this difference on clinical outcome and, in particular, on the risk of late stent thrombosis is yet to be determined.