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HbA1c Identifies Subjects With Prediabetes and Subclinical Left Ventricular Diastolic Dysfunction
Antonino Di Pino1, Sarah Mangiafico2, Francesca Urbano1
1Department of Clinical and Experimental Medicine, Garibaldi Hospital, University of Catania, 95122 Catania, Italy.
Insights
Prediabetes identified by HbA1c shows early heart changes. These cardiac alterations are linked to glycation and inflammation markers, even with normal glucose levels.
Area of Science:
- Cardiology
- Endocrinology
- Metabolic Diseases
Background:
- Prediabetes is linked to subclinical cardiac changes, potentially leading to heart failure.
- Early detection of cardiac alterations in prediabetes is crucial for cardiovascular disease prevention.
Purpose of the Study:
- To investigate diastolic function in prediabetes defined by HbA1c.
- To explore the association between cardiac changes, glycation (HbA1c, sRAGEs, esRAGE), and inflammation in prediabetes.
Main Methods:
- Cross-sectional study of 167 subjects with normal fasting glucose/normal glucose tolerance.
- Stratification into control (<5.7% HbA1c) and prediabetes (5.7%-6.4% HbA1c) groups.
- Evaluation of Doppler echocardiography, HbA1c, OGTT, sRAGEs, and esRAGE.
Main Results:
- HbA1c prediabetes group showed impaired diastolic function (lower E/A ratio) and increased left atrial volume and sphericity.
- HbA1c, sRAGEs, and esRAGE were identified as key determinants of these cardiac alterations.
- These cardiac changes were present despite normal fasting glucose and oral glucose tolerance test results.
Conclusions:
- Prediabetes, particularly when identified by HbA1c, is associated with subclinical cardiac alterations.
- Glycation markers (HbA1c, sRAGEs, esRAGE) play a significant role in these cardiac changes.
- Relying solely on fasting glucose or OGTT may miss individuals with prediabetes and associated cardiac risks.
Context:
Prediabetes is associated with subclinical cardiac changes associated with heart failure development.
Objective:
We investigated diastolic function and its association with markers of glycation and inflammation related to cardiovascular disease in patients with prediabetes. We focused on individuals with prediabetes identified only by glycated hemoglobin A1c [HbA1c; 5.7% to 6.4% and normal fasting glucose (NFG) and normal glucose tolerance (NGT) after an oral glucose tolerance test (OGTT)].
Design:
Cross-sectional study.
Setting:
Departments of Clinical and Experimental Medicine and Cardiology, University of Catania, Catania, Italy.
Main Outcome Measures:
HbA1c, OGTT, Doppler echocardiography, soluble receptor for advanced glycation end products (sRAGEs), and endogenous secretory RAGE (esRAGE) were evaluated.
Patients:
We recruited 167 subjects with NFG/NGT who were stratified according to HbA1c level: controls (HbA1c <5.7%) and HbA1c prediabetes (HbA1c 5.7% to 6.4%).
Results:
Patients with HbA1c prediabetes (n = 106) showed a lower peak mitral inflow in early diastole (E wave) to late diastolic atrial filling velocity (A wave) ratio (E/A ratio) than controls (n = 61) (1.10 ± 0.24 vs 1.18 ± 0.23; P < 0.05). They showed a higher left atrium volume (LAV) (28.4 ± 5 vs 22.1 ± 3; P < 0.05) and sphericity index (SI) (0.6 ± 0.06 vs 0.5 ± 0.05; P < 0.05). After multiple regression analyses, HbA1c, sRAGE, and esRAGE were the major determinants of E/A ratio, LAV, and SI.
Conclusions:
Subjects with HbA1c prediabetes exhibited subclinical cardiac alterations associated with sRAGE, esRAGE, and HbA1c. These subjects would not have been classified as having prediabetes on the basis of fasting glycemia or post-OGTT values.
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