Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39

BMJ 1998;317:713-720 ( 12 September )

Papers

Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39

Editorials by Orchard and Mogensen Papers pp 703 , 720 This paper was prepared for publication by Rury Holman, Robert Turner, Irene Stratton, Carole Cull, Valeria Frighi, Susan Manley, David Matthews, Andrew Neil, Eva Kohner, David Wright, David Hadden, and Charles Fox.

UK Prospective Diabetes Study Group.

Correspondence to: Professor R Holman, UK Prospective Diabetes Study Group, Diabetes Research Laboratories, Radcliffe Infirmary, Oxford OX2 6HE

Objective: To determine whether tight control of blood pressure with either a $beta$ blocker or an angiotensin convertingenzyme inhibitor has a specific advantage or disadvantage in preventingthe macrovascular and microvascular complications of type 2diabetes.
Design: Randomised controlled trial comparing an angiotensin converting enzyme inhibitor (captopril) with a $beta$ blocker(atenolol) in patients with type 2 diabetes aiming at a bloodpressure of <150/<85 mmHg.
Setting: 20 hospital based clinics in England, Scotland, and NorthernIreland.
Subjects: 1148 hypertensive patients with type 2 diabetes (mean age 56 years, mean blood pressure 160/94 mm Hg). Ofthe 758 patients allocated to tight control of blood pressure,400 were allocated to captopril and 358 to atenolol. 390 patientswere allocated to less tight control of bloodpressure.
Main outcome measures: Predefined clinical end points, fatal and non-fatal, related to diabetes, death related to diabetes,and all cause mortality. Surrogate measures of microvascular andmacrovascular disease included urinary albumin excretion and retinopathyassessed by retinalphotography.
Results: Captopril and atenolol were equally effective in reducing blood pressure to a mean of 144/83 mm Hg and 143/81 mm Hgrespectively, with a similar proportion of patients (27% and 31%)requiring three or more antihypertensive treatments. More patientsin the captopril group than the atenolol group took the allocatedtreatment: at their last clinic visit, 78% of those allocatedcaptopril and 65% of those allocated atenolol were taking thedrug (P<0.0001). Captopril and atenolol were equally effectivein reducing the risk of macrovascular end points. Similar proportionsof patients in the two groups showed deterioration in retinopathyby two grades after nine years (31% in the captopril group and37% in the atenolol group) and developed clinical grade albuminuria $>=$ 300 mg/l (5% and 9%). The proportion of patients with hypoglycaemicattacks was not different between groups, but mean weight gainin the atenolol group was greater (3.4 kg v 1.6 kg).
Conclusion: Blood pressure lowering with captopril or atenolol was similarly effective in reducing the incidence ofdiabetic complications. This study provided no evidence that eitherdrug has any specific beneficial or deleterious effect, suggestingthat blood pressure reduction in itself may be more importantthan the treatment used.

Key messages

This study showed that an angiotensin converting enzyme inhibitor (captopril) or a $beta$ blocker (atenolol) gave similar reductions in blood pressure in hypertensive patients with type 2 diabetes
To achieve target blood pressures additional antihypertensive agents were often required
The two drugs were equally effective in reducing the risk of non-fatal and fatal diabetic complications, death related to diabetes, heart failure, and progression of retinopathy
Those given atenolol gained slightly more weight and showed a slightly greater increase in glycated haemoglobin concentrations, but this did not affect the reduction in clinical end points
The suggestion that angiotensin converting enzyme inhibitors have a specific renal protective effect in the treatment of type 2 diabetes is not supported

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