Key result
T2D in first ACS is linked to worse atherosclerosis and a ~57% higher absolute rate of well-developed collaterals.
Why the study?
The study aimed to compare coronary artery disease severity and plaque features by angiography and OCT between type II diabetic and non-diabetic patients presenting with a first ACS.
Does type II diabetes affect the severity and phenotype of coronary atherosclerosis at the time of a first acute coronary syndrome compared to non-diabetic patients?
Observational (n=239)
Does type II diabetes affect the severity and phenotype of coronary atherosclerosis at the time of a first acute coronary syndrome compared to non-diabetic patients?
Absolute Event Rate: 73% vs 16%
p-value: p=0.001
At the time of a first ACS, diabetic patients paradoxically exhibit more severe coronary atherosclerosis, better collateral development, and a predominantly calcific plaque phenotype compared to non-diabetics.
Diabetes was associated with more severe CAD at first ACS; leaves open whether this supports earlier screening in diabetics.
AIMS: We aimed to compare coronary artery disease (CAD) at the time of a first acute coronary syndrome (ACS) in type II diabetic and non-diabetic patients by coronary angiography and by optical coherence tomography (OCT). METHODS AND RESULTS: Two different patient populations with a first ACS were enrolled for the angiographic (167 patients) and the OCT (72 patients) substudy. Angiographic CAD severity was assessed by Bogaty, Gensini, and Sullivan scores, whereas collateral development towards the culprit vessel was assessed by the Rentrop score. Optical coherence tomography plaque features were evaluated at the site of the minimum lumen area (MLA) and of culprit segment. In the angiographic substudy, at multivariate analysis, diabetes was associated with both the stenosis score and the extent index (P = 0.001). Furthermore, well-developed collateral circulation (Rentrop 2-3) towards the culprit vessel was more frequent in diabetic than in non-diabetic patients (73% vs. 16%, P = 0.001). In the OCT substudy, at MLA site lipid quadrants were less and the lipid arc was smaller in diabetic than in non-diabetic patients (2.3 ± 1.3 vs. 3.0 ± 1.2; P = 0.03 and 198° ± 121° vs. 260° ± 118°; P = 0.03). Furthermore, the most calcified cross-section along the culprit segment had a greater number of calcified quadrants and a wider calcified arc in diabetic than in non-diabetic patients (1.7 ± 1.0 vs. 1.2 ± 0.9; P = 0.03 and 126° ± 95° vs. 81° ± 80°; P = 0.03). Superficial calcified nodules were more frequently found in diabetic than in non-diabetic patients (79 vs. 54%, P = 0.04). CONCLUSIONS: In spite of potent pro-inflammatory, pro-oxidant and pro-thrombotic stimuli operating in type II diabetes, diabetic patients exhibit substantially more severe coronary atherosclerosis than non-diabetic patients at the time of a first acute coronary event. Better collateral development towards the culprit vessel, a predominantly calcific plaque phenotype and, probably, yet unknown protective factors operating in diabetic patients may explain these intriguing paradoxical findings.
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Niccoli et al. (2012) conducted an observational in First acute coronary syndrome (ACS) (n=239). Type II Diabetes vs. Non-diabetic was evaluated on Well-developed collateral circulation (Rentrop 2-3) towards the culprit vessel (p=0.001). Type II diabetic patients presenting with a first ACS exhibited more severe coronary atherosclerosis and more frequent well-developed collateral circulation (73% vs. 16%, P=0.001) than non-diabetics.
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