Elevated risk from diabetes in acute MI, PCI cohort not due to plaque composition
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Key takeaways:
- In patients with acute heart attack who had PCI, those with diabetes had more CV events after the procedure than those without it.
- The difference was not due to plaque amount or characteristics.
PHILADELPHIA — In patients with acute MI who had successful PCI and underwent imaging to assess plaque composition, diabetes raised risk for poor outcomes but the difference was not related to plaque, according to a presentation.
Ori Ben-Yehuda, MD, professor of medicine and director of the Cardiovascular Outcomes Group at Sulpizio Cardiovascular Institute, University of California, San Diego, discussed the results of a substudy of the PROSPECT II trial at the Heart in Diabetes CME Conference during a session highlighting cardiometabolic papers published in Circulation in 2023.
The trial evaluated 898 patients from Denmark, Norway and Sweden (mean age, 63 years; 17% women) with acute STEMI or non-STEMI who had successful PCI and afterward underwent three-vessel quantitative coronary angiography and co-registered near-infrared spectroscopy and IVUS.
Risk after PCI by diabetes status
For the present substudy, the researchers stratified patients by diabetes status and by whether they had maximum plaque burden of 70% or more and whether they had maximum core lipid burden index of 324.7 or more (highest quartile). The primary outcome was major adverse CV events, defined as cardiac death, MI, unstable angina and progressive angina requiring revascularization or with rapid lesion progression, evaluated in both culprit and nonculprit lesions from the index procedure. The median follow-up was 3.7 years.
“The predictors of events in nonculprit lesions were the presence of thin-capped fibroatheroma, as well as the narrowness of the artery and plaque burden greater than 70%,” Ben-Yehuda said. “When you have all of these together, your risk is quite high. We can actually measure the presence of cholesterol in tissue and [using near-infrared spectroscopy and IVUS] create maps of the coronary arteries.”
The primary outcome occurred more often in patients with diabetes than those without diabetes (20.1% vs. 13.5%; OR = 1.94; 95% CI, 1.14-3.3), driven by MI due to culprit lesion restenosis (4.3% vs. 1.1%; OR = 3.78; 95% CI, 1.12-12.77) and spontaneous MI in nonculprit lesions (9.3% vs. 3.8%; OR = 2.74; 95% CI, 1.25-6.04), Ben-Yehuda said during the presentation, noting that event rates were even higher for patients with insulin-treated diabetes.
In addition, he said, patients with maximum plaque burden of 70% or more (OR for patient-level events = 3.09; 95% CI, 1.65-5.76; OR for lesion-level events = 11.37; 95% CI, 5.6-23.11) and those with maximum core lipid burden index of 324.7 or more (OR for patient-level events = 2.07; 95% CI, 1.18-3.69; OR for lesion-level events = 7.47; 95% CI, 3.94-14.2) were more likely to have MACE than patients under those thresholds.
Minimum lumen area of nonculprit lesions, where high risk was defined as up to 4 mm2, was most predictive of progressive angina, Ben-Yehuda said.
However, in patients with MACE due to culprit or nonculprit lesions, there was no difference by diabetes status in maximum plaque burden of 70% or more (culprit lesions: diabetes, 90%; no diabetes, 93%; P = .34; nonculprit lesions: diabetes, 23%; no diabetes, 22%; P = .37) or in maximum core lipid burden index of 324.7 or more (culprit lesions: diabetes, 66%; no diabetes, 70%; P = .49; nonculprit lesions: diabetes, 26%; no diabetes, 24%; P = .47), according to the researchers.
‘The findings surprised us’
“This is where the findings surprised us,” Ben-Yehuda said during the presentation. “We expected to have more plaques in the diabetics. This was seen in PROSPECT I and other studies. Our prediction was that their plaque characteristics are going to be more severe, and that would explain the higher event rate. There are several reasons why a diabetic would have more events: more plaque, different type of plaque — which could be either the characteristics we are looking for or things we are not measuring — or ... other factors that are beyond the presence of the plaque and its characteristics [but] affect plaque rupture. There were no differences in plaque characteristics [by diabetes status], perhaps because this was a well-treated diabetic population and therefore we’re not seeing what usually occurs in a diabetic, but I think that actually gives us an advantage here, because it shows us that after controlling for the amount of atherosclerosis, we still have double the event rate, highlighting that [patients with diabetes] are indeed at higher risk, but not simply by having more atherosclerotic plaque.”
In multivariable models, diabetes was associated with MACE in nonculprit lesions (adjusted OR = 2.47; 95% CI, 1.21-5.04) but it was not associated with prevalence of high-risk plaque characteristics (aOR = 1.21; 95% CI, 0.86-1.69), Ben-Yehuda and colleagues found.
“We could not identify any characteristic that was studied in this study, suggesting that [higher event rates in diabetes are due to] either other factors in the plaque that we’re not measuring such as inflammation or something that is extrinsic to the plaque, which gives us more things that we can find,” Ben-Yehuda said during the presentation. “That leaves important questions for further study.”
Reference:
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Ben-Yehuda O. Joint session with Circulation. Presented at: Heart in Diabetes CME Conference; June 7-9, 2024; Philadelphia.
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