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Association of Abnormal Glucose Metabolism and Inflammation With Prognosis in Patients With Acute Coronary Syndrome
Chong Zhang1, Wenjin Peng2,3,4,5,6, Tianqi Wang2,3,4,5,6,7
1Neuroscience Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Insights
Acute coronary syndrome patients with abnormal glucose metabolism and high inflammation face increased major adverse cardiovascular events (MACE) risk. Early treatment can mitigate this risk.
Area of Science:
- Cardiology
- Metabolic Syndrome
- Inflammation Research
Background:
- The interplay between glucose metabolism markers (triglyceride-glucose index, stress hyperglycemia ratio) and inflammation in acute coronary syndrome (ACS) is not well understood.
- The long-term prognostic impact of these interactions in ACS patients requires further clinical investigation.
Purpose of the Study:
- To investigate the relationship between glucose metabolism markers and inflammatory markers in ACS patients.
- To identify distinct patient phenotypes based on these markers.
- To assess the association between these phenotypes and 1-year major adverse cardiovascular events (MACE) risk.
Main Methods:
- K-means clustering was applied to triglyceride-glucose (TyG) index, stress hyperglycemia ratio (SHR), and specific inflammatory markers (HMGB1, PDGF, PGN, LPA, citrullinated H3).
- A Cox proportional hazards model analyzed the link between identified cluster phenotypes and 1-year MACE risk in 363 ACS patients.
Main Results:
- A positive correlation was observed between SHR, TyG index, and inflammatory markers.
- Two distinct phenotypes emerged: normal glucose metabolism/low inflammation and abnormal glucose metabolism/high inflammation.
- The abnormal glucose metabolism/high inflammation phenotype significantly increased 1-year MACE risk (aHR: 3.84, 95% CI: 1.93-7.64).
- Early guideline-directed medical therapy reduced MACE risk in the high-risk group.
Conclusions:
- ACS patients exhibiting both abnormal glucose metabolism and heightened inflammation possess a substantially elevated risk of long-term MACE.
- Targeted interventions, including guideline-directed medical therapy, anti-inflammatory agents, and hypoglycemic drugs, show promise for improving outcomes in this high-risk cohort.
Background:
In acute coronary syndrome (ACS) patients, the relationship between abnormal glucose metabolism markers, such as the triglyceride-glucose (TyG) index and stress hyperglycemia ratio (SHR), and inflammatory markers remains unclear. Furthermore, their interaction and impact on long-term prognosis have yet to be investigated in clinical cohorts.
Methods:
In this study, K-means clustering was performed on the TyG index, SHR, and inflammatory markers, including high mobility group box-1 protein, platelet-derived growth factor, phenylacetylglutamine, lysophosphatidic acid, and citrullinated histone H3. A Cox proportional hazards model was used to assess the association between cluster phenotypes and 1-year major adverse cardiovascular events (MACE) risk in ACS patients.
Results:
Among 363 ACS patients, 62 developed MACE during the 1-year follow-up. SHR correlated positively with the TyG index and inflammatory markers. K-means clustering identified two phenotypes: normal glucose metabolism/low inflammation and abnormal glucose metabolism/high inflammation. Multivariable Cox analysis showed the latter was strongly linked to MACE (adjusted hazard ratio: 3.84, 95% confidence interval: 1.93-7.64), and early guideline-directed medical therapy reduced MACE risk in this high-risk group.
Conclusions:
ACS patients with abnormal glucose metabolism and high inflammation have a higher long-term MACE risk than those with normal glucose metabolism and low inflammation. Early guideline-directed medical therapy, alongside anti-inflammatory therapy and hypoglycemic agents, may improve long-term outcomes in this high-risk group.
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