In individuals with type 1 diabetes, a 1 standard deviation increase in apolipoprotein B-100 was associated with a 31% increased risk of non-ST-elevation myocardial infarction (HR 1.31).
Cohort (n=4,215)
Yes
Do lipid and apolipoprotein profiles differentially affect the risk of STEMI versus NSTEMI in individuals with type 1 diabetes?
Lipid and apolipoprotein profiles have differential associations with the risk of STEMI versus NSTEMI in patients with type 1 diabetes, suggesting distinct pathophysiological mechanisms.
Hazard Ratio: 1.31 (95% CI 1.15–1.5)
p-value: p=<0.001
Non-ST-elevation myocardial infarction (NSTEMI) has become the main myocardial infarction subtype in type 1 diabetes compared to ST-elevation myocardial infarction (STEMI), accounting for nearly 80% of myocardial infarction-related hospitalizations. Yet, prior studies in type 1 diabetes have assessed myocardial infarctions as a single entity, potentially overlooking clinically relevant heterogeneity between subtypes in risk assessment. We aimed to study the role of lipids, apolipoproteins, insulin resistance, and the metabolic syndrome in risk stratification of all myocardial infarctions, STEMI and NSTEMI in individuals with type 1 diabetes stratified by the presence of microvascular complications. The current study is an observational follow-up study of 4215 individuals from the Finnish Diabetic Nephropathy Study. We verified 449 first-ever myocardial infarctions from medical records and death certificates and further categorized them into either STEMI or NSTEMI. Multivariable Cox regression models were used to assess the effect of a comprehensive lipid and apolipoprotein panel and insulin resistance on the risk of all myocardial infarctions, STEMI, and NSTEMI. Risk estimates for all myocardial infarctions were additionally stratified based on the presence of microvascular complications. For STEMI, apolipoprotein A-I (ApoA-I) (hazard ratio per 1 standard deviation 0.77 95% confidence interval 0.60–0.99; P = 0.043), HDL2 cholesterol (HDL2-C) (0.72 0.55–0.95; P = 0.019), and HDL-C/total cholesterol ratio (0.76 0.59–0.98; P = 0.035) were associated with reduced risk, while no variables were associated with increased risk. Regarding NSTEMI, apolipoprotein B-100 (ApoB-100) (1.31 1.15–1.50; P < 0.001) and ApoB-100 to apolipoprotein A-I (ApoA-I) ratio (1.29 1.18–1.41; P < 0.001) showed the strongest association with an increased risk, while the HDL-C/total cholesterol ratio was associated with reduced risk (0.71 0.62–0.82; P < 0.001). In stratified analyses, associations between selected lipid and apolipoprotein variables and myocardial infarction risk appeared stronger among individuals without microvascular complications. Higher estimated glucose disposal rate, indicating lesser insulin resistance, was associated with reduced risk of both STEMI (0.82 0.73–0.92; P < 0.001) and NSTEMI (0.92 0.86–0.99; P = 0.024). We demonstrated that the risk profile between STEMI and NSTEMI differs regarding lipids and apolipoproteins, while insulin resistance was associated with increased risk of both MI subtypes.
Smidtslund et al. (Sat,) conducted a cohort in Type 1 diabetes (n=4,215). Apolipoprotein B-100 (per 1 SD increase) vs. Lower levels was evaluated on First-ever non-ST-elevation myocardial infarction (NSTEMI) (HR 1.31, 95% CI 1.15-1.50, p=<0.001). In individuals with type 1 diabetes, a 1 standard deviation increase in apolipoprotein B-100 was associated with a 31% increased risk of non-ST-elevation myocardial infarction (HR 1.31).