Key result
The prevalence of abnormal ankle-brachial index was significantly higher in patients with established type 2 diabetes compared to newly diagnosed drug-naive patients (87% vs 60%, p<0.001).
Why the study?
Little is known regarding peripheral arterial disease evolution since diagnosis and its link with glycemic and lipid control in type 2 diabetes mellitus.
Does early glycemic and lipid control in newly diagnosed drug-naive T2DM patients improve or stabilize peripheral arterial disease assessed by ankle-brachial index?
Cohort (n=1,249)
No
Does early glycemic and lipid control in newly diagnosed drug-naive T2DM patients improve or stabilize peripheral arterial disease assessed by ankle-brachial index?
Absolute Event Rate: 87% vs 60%
p-value: p=<0.001
Universal screening for PAD using ABI at the time of T2DM diagnosis is warranted, as early glycemic and lipid control is associated with ABI stabilization and normalization.
Metabolic improvements associate with ABI stability in new T2DM; hypothesis-generating and should not yet change practice.
BACKGROUND: Little is known about the evolution of peripheral arterial disease (PAD) since diagnosis and its association with glycemic and lipid control in patients with Type 2 Diabetes Mellitus (T2DM). OBJECTIVE: Evaluate the actual criteria to start screening PAD with ankle-brachial index (ABI) in T2DM patients and assess its progression and relationship with glycemic and lipid control since diagnosis. METHODS: We performed a 3-year prospective cohort study with two groups: group 1 (978 individuals with T2DM undergoing drug treatment) and group 2 [221 newly diagnosed drug-naive (< 3 months) patients with T2DM]. PAD diagnosis was by ABI ≤ 0.90, regardless any symptoms. RESULTS: As expected, abnormal ABI prevalence was higher in group 1 vs. Group 2 (87% vs. 60%, p < 0.001). However, abnormal ABI prevalence did not differ between patients over and under 50 years in both groups. Our drug-naive group stabilizes ABI (0.9 ± 0.1 vs 0.9 ± 0.1, p = NS) and improved glycemic and lipid control during follow-up [glycated hemoglobin (HbA1c) = 8.9 ± 2.1 vs 8.4 ± 2.3%, p < 0.05; LDL = 132 ± 45 vs 113 ± 38 mg/dL, p < 0.01, respectively]. When compared, patients who evolved with normalization or maintained normal ABI levels at the end [Group A, N = 60 (42%)] with those who decreased ABI to abnormal levels (ABI basal 1.0 ± 0.1 vs final 0.85 ± 0.1, p < 0.001) [Group B, N = 26 (18%)], an improvement in HbA1c (9 ± 2 vs 8 ± 2%, p < 0.05) and a correlation between the final HbA1c with ABI (r = - 0.3, p = 0.01) was found only in the first. In addition, a correlation was found between albuminuria variation and ABI solely in group A (r = - 0.3; p < 0.05). CONCLUSION: Our study suggests that ABI should be measured at diagnosis in T2DM patients, indicating that current criteria to select patients to screen PAD with ABI must be simplified. An improvement in albuminuria and glycemic and lipid control could be related with ABI normalization in newly diagnosed T2DM drug-naive patients.
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Felício et al. (2022) conducted a cohort in Type 2 Diabetes Mellitus (n=1,249). Established Type 2 Diabetes (undergoing drug treatment) vs. Newly diagnosed drug-naive Type 2 Diabetes was evaluated on Prevalence of abnormal ankle-brachial index (ABI ≤ 0.90) (p=<0.001). The prevalence of abnormal ankle-brachial index was significantly higher in patients with established type 2 diabetes compared to newly diagnosed drug-naive patients (87% vs 60%, p<0.001).
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