AI Article Synopsis

  • Patients with diabetes experience higher rates of major adverse cardiac events (MACEs), possibly due to differences in coronary plaque characteristics related to their condition.
  • In a study involving 898 patients with acute myocardial infarction, researchers used advanced imaging techniques to assess plaque morphology and found that diabetes significantly increased the risk of MACEs, particularly related to heart attacks from both treated and untreated lesions.
  • Despite the increased risks, the prevalence of high-risk plaque characteristics in diabetic patients was similar to that of non-diabetic patients, suggesting other factors contribute to the higher event rates in diabetics.

Article Abstract

Background: Patients with diabetes have increased rates of major adverse cardiac events (MACEs). We hypothesized that this is explained by diabetes-associated differences in coronary plaque morphology and lipid content.

Methods: In PROSPECT II (Providing Regional Observations to Study Predictors of Events in the Coronary Tree), 898 patients with acute myocardial infarction with or without ST-segment elevation underwent 3-vessel quantitative coronary angiography and coregistered near-infrared spectroscopy and intravascular ultrasound imaging after successful percutaneous coronary intervention. Subsequent MACEs were adjudicated to either treated culprit lesions or untreated nonculprit lesions. This substudy stratified patients by diabetes status and assessed baseline culprit and nonculprit prevalence of high-risk plaque characteristics defined as maximum plaque burden ≥70% and maximum lipid core burden index ≥324.7. Separate covariate-adjusted multivariable models were performed to identify whether diabetes was associated with nonculprit lesion-related MACEs and high-risk plaque characteristics.

Results: Diabetes was present in 109 of 898 patients (12.1%). During a median 3.7-year follow-up, MACEs occurred more frequently in patients with versus without diabetes (20.1% versus 13.5% [odds ratio (OR), 1.94 (95% CI, 1.14-3.30)]), primarily attributable to increased risk of myocardial infarction related to culprit lesion restenosis (4.3% versus 1.1% [OR, 3.78 (95% CI, 1.12-12.77)]) and nonculprit lesion-related spontaneous myocardial infarction (9.3% versus 3.8% [OR, 2.74 (95% CI, 1.25-6.04)]). However, baseline prevalence of high-risk plaque characteristics was similar for patients with versus without diabetes concerning culprit (maximum plaque burden ≥70%: 90% versus 93%, =0.34; maximum lipid core burden index ≥324.7: 66% versus 70%, =0.49) and nonculprit lesions (maximum plaque burden ≥70%: 23% versus 22%, =0.37; maximum lipid core burden index ≥324.7: 26% versus 24%, =0.47). In multivariable models, diabetes was associated with MACEs in nonculprit lesions (adjusted OR, 2.47 [95% CI, 1.21-5.04]) but not with prevalence of high-risk plaque characteristics (adjusted OR, 1.21 [95% CI, 0.86-1.69]).

Conclusions: Among patients with recent myocardial infarction, both treated and untreated lesions contributed to the diabetes-associated ≈2-fold increased MACE rate during the 3.7-year follow-up. Diabetes-related plaque characteristics that might underlie this increased risk were not identified by multimodality imaging.

Registration: URL: https://www.

Clinicaltrials: gov; Unique identifier: NCT02171065.

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Source
http://dx.doi.org/10.1161/CIRCULATIONAHA.122.061983DOI Listing

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