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Non-diabetic hyperglycaemia correlates with angiographic coronary artery disease prevalence and severity
D M Konstantinou1, Y S Chatzizisis, G E Louridas
11st Cardiology Department, AHEPA University Hospital, Aristotle University Medical School, 1, St. Kyriakidi Street, 54636 Thessaloniki, Greece. dimikon@auth.gr
Insights
Higher blood sugar levels, including non-diabetic hyperglycaemia, are linked to increased coronary artery disease (CAD) prevalence and severity. Haemoglobin A1c (HbA1c) predicts CAD outcomes, even in non-diabetics.
Area of Science:
- Cardiology
- Endocrinology
- Metabolic Syndrome
Background:
- The association between glycaemia and coronary artery disease (CAD) risk is debated.
- Optimal glucose levels for cardiovascular health remain unclear.
Purpose of the Study:
- To evaluate the prevalence and severity of angiographic CAD in relation to hyperglycaemia categories.
- To assess the predictive value of haemoglobin A1c (HbA1c) for CAD outcomes.
Main Methods:
- Coronary angiography was performed on 273 patients with suspected ischaemic pain.
- Patients were classified into normal fasting glucose (NFG), impaired fasting glucose (IFG), and diabetes mellitus (DM) groups.
- CAD severity was quantified using Gensini's score, extent score, and an arbitrary index.
Main Results:
- CAD prevalence was 2.5 times higher in IFG and DM groups compared to NFG.
- Poorer glycaemic control predicted worse angiographic CAD severity.
- Elevated HbA1c levels were associated with higher CAD prevalence and severity, independent of diabetes status.
Conclusions:
- Non-diabetic hyperglycaemia, indicated by fasting glucose or HbA1c, correlates with adverse angiographic outcomes.
- HbA1c is a significant predictor of CAD prevalence, even after accounting for conventional risk factors.
Aim:
The role of glycaemia as a coronary artery disease (CAD) risk factor is controversial, and the optimal glucose level is still a matter of debate. For this reason, we assessed the prevalence and severity of angiographic CAD across hyperglycaemia categories and in relation to haemoglobin A(1c) (HbA(1c)) levels.
Methods:
We studied 273 consecutive patients without prior revascularization undergoing coronary angiography for suspected ischaemic pain. CAD severity was assessed using three angiographic scores: the Gensini's score; extent score; and arbitrary index. Patients were grouped, according to 2003 American Diabetes Association criteria, into those with normal fasting glucose (NFG), impaired fasting glucose (IFG) and diabetes mellitus (DM).
Results:
CAD prevalence was 2.5-fold higher in both the IFG and DM groups compared with the NFG group. Deterioration of glycaemic profile was a multivariate predictor of angiographic CAD severity (extent score: P=0.027; arbitrary index: P=0.007). HbA(1c) levels were significantly higher among CAD patients (P=0.016) and in those with two or more diseased vessels (P=0.023) compared with the non-CAD group. HbA(1c) levels remained predictive of CAD prevalence even after adjusting for conventional risk factors, including DM (adjusted OR: 1.853; 95% CI: 1.269-2.704).
Conclusion:
Non-diabetic hyperglycaemia, assessed either categorically by fasting glucose categories or continuously by HbA(1c) levels, correlates with the poorest angiographic outcomes.
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