Key result
In nondiabetic post-MI survivors, a postload glucose spike >2.4 mmol/L was associated with a higher risk of MACE compared to ≤2.4 mmol/L (HR 1.63; 95% CI 1.17-2.27; P=0.004 in the matched cohort).
Why the study?
The effect of postload glucose spikes on post-myocardial infarction prognosis in nondiabetic patients was unexplored.
Does a higher postload glucose spike predict major adverse cardiac events in nondiabetic post-MI survivors?
Cohort (n=847)
Does a higher postload glucose spike predict major adverse cardiac events in nondiabetic post-MI survivors?
Postload glucose spikes independently predict MACE and offer better prognostic value than 2-hour post-load plasma glucose in nondiabetic post-MI patients.
Answers are grounded in this paper and cite their sources.
May support postload glucose in post-MI risk models; hypothesis-generating and requires prospective validation before practice change.
Background The effect of postload glucose spikes (PGS), the difference between 2 hour post‐load plasma glucose (2hPLPG) and fasting plasma glucose (FPG), on post–myocardial infarction (post‐MI) prognosis in nondiabetic patients is unexplored. Methods This is a retrospective cohort analysis of 847 nondiabetic post‐MI survivors who underwent a predischarge oral glucose tolerance test (median PGS: 2.4 mmol/L). Patients were divided into the unmatched groups 1 and 2 (PGS ≤ and > 2.4 mmol/L) and the propensity score‐matched groups 1M and 2M (355 pairs assembled from the overall cohort), and these groups were compared. Major adverse cardiac events (MACE: death and nonfatal reinfarction) were recorded during follow‐up (median: 3.4 years). Event‐free survival was compared by the Kaplan‐Meier method. Multivariate Cox proportional hazards regression determined the predictors of MACE. C‐statistics (change in area under the curve, δAUC), continuous net reclassification improvement (NRI >0 ), and integrated discrimination improvement (IDI) were used to compare models. Results The number of MACE was higher in groups 2 (27.3% vs 14.2%, P < .001) and 2M (24.5% vs 15.5%, P < .001). Event‐free survival was worse in groups 2 (hazard ratio [HR] 2.01; 95% CI, 1.49‐2.71; P < .001) and 2M (HR 1.63; 95% CI, 1.17‐2.27; P = .004). PGS independently predicted MACE‐free survival in the whole (HR 1.16; 95% CI, 1.06‐1.26; P = .002) and matched cohort (HR 1.12; 95% CI, 1.02‐1.24; P = .021). PGS, but not FPG or 2hPPG, improved the predictive performance of the base model (δAUC 0.013, P = .046), with greater improvement seen when PGS was added and compared to 2hPPG (δAUC 0.005, P = .034; NRI >0 0.2107, P = .013; IDI 0.0042, P = .046). Conclusion PGS is a better predictor of post‐MI prognosis than 2hPPG in nondiabetic patients.
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Chattopadhyay et al. (2021) conducted a cohort in post-myocardial infarction in nondiabetic patients (n=847). Postload glucose spike > 2.4 mmol/L vs. Postload glucose spike ≤ 2.4 mmol/L was evaluated on Major adverse cardiac events (MACE: death and nonfatal reinfarction) (HR 1.63, 95% CI 1.17-2.27, p=0.004). In nondiabetic post-MI survivors, a postload glucose spike >2.4 mmol/L was associated with a higher risk of MACE compared to ≤2.4 mmol/L (HR 1.63; 95% CI 1.17-2.27; P=0.004 in the matched cohort).
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