What is the clinical evidence from this study?

Study design: Other. Population: Type I diabetes mellitus (n=17). Intervention: Enalaprilat and Enalapril vs. Pretreatment baseline. Primary outcome: Forearm blood flow response to acetylcholine (endothelium-dependent vasodilation) (p=<0.001).

August 1, 1997Open Access

Improvement in endothelial function by angiotensin converting enzyme inhibition in insulin-dependent diabetes mellitus.

Q: What are the key findings of this study?

Four weeks of oral enalapril therapy significantly improved endothelium-dependent vasodilation in type I diabetic patients, increasing forearm blood flow by 277% compared to 136% at baseline (P<0.001).

GOG. O’DriscollThe University of Notre Dame Australia DGDaniel J. GreenBrigham Young University JRJ. RankinThe University of Western Australia

Key Result

Four weeks of oral enalapril therapy significantly improved endothelium-dependent vasodilation in type I diabetic patients, increasing forearm blood flow by 277% compared to 136% at baseline (P<0.001).

Structured PICO

Does enalaprilat and enalapril improve endothelial function in patients with type I diabetes mellitus?

Population

17 male subjects, comprising 9 with uncomplicated type I diabetes and 8 healthy controls, evaluated for forearm endothelial function before and after ACE inhibition.

Intervention

Acute ACE inhibition with intrabrachial enalaprilat (8.3 µg/min) followed by 4 weeks of oral enalapril (10 mg twice daily).

Comparator

Pretreatment baseline and healthy control subjects.

Outcome

Nitric oxide (NO)-mediated endothelial function assessed by forearm blood flow (FBF) response to intraarterial infusion of endothelium-dependent (acetylcholine [ACh]) and endothelium-independent (sodium nitroprusside [SNP]) vasodilators using strain gauge plethysmography.surrogate

ACE inhibition with enalaprilat and enalapril significantly improves NO-mediated endothelial function in patients with type I diabetes mellitus.

Main Result

Absolute Event Rate: 277% vs 136%

p-value: p=<0.001

Limitations

Small sample size of only 9 diabetic patients and 8 healthy controls.
Only male subjects were included, limiting generalizability to females.
Healthy control subjects were significantly younger (mean age 28) than the diabetic patients (mean age 43).
Lack of a randomized, placebo-controlled design.

Abstract

We postulated that nitric oxide (NO)-mediated endothelial function would be improved by acute and short-term treatment with an angiotensin converting enzyme (ACE) inhibitor in patients with type I diabetes mellitus, in whom endothelial function is depressed. Nine type I diabetic patients and eight healthy subjects underwent forearm blood flow measurement using strain gauge plethysmography during intraarterial infusion of incremental doses of endothelium-dependent (acetylcholine ACh) and endothelium-independent (sodium nitroprusside SNP) vasodilators. Pretreatment ACh responses were depressed in diabetic patients relative to the normal subjects (P < 0.05). No difference between the groups was evident in response to SNP. Acute ACE inhibition (with intrabrachial enalaprilat) enhanced ACh responses in the diabetic patients (P < 0.005), with a further improvement evident after 1 mo of oral therapy with enalapril (P < 0.001) when ACh responses were normalized. ACE inhibition did not affect SNP responses. We conclude that acute administration of the ACE inhibitor, enalaprilat, enhances NO-mediated endothelial function in type I diabetic patients, with further improvement evident after 4 wk of enalapril therapy.

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