CLINICAL QUESTION
Does blood pressure (BP) control prevent diabetic retinopathy or slow its progression?
EVIDENCE-BASED ANSWER
More intensive BP control in patients with diabetes mellitus and hypertension decreases the incidence of diabetic retinopathy, especially among those with higher BP.1 There are many definitions for more intensive BP control, from a diastolic BP of less than 75 mm Hg to a BP target of less than 135/75 mm Hg or a systolic BP of less than 120 mm Hg; nonintensive control is typically a systolic BP of less than 140 mm Hg.1 (Strength of Recommendation [SOR]: A, consistent, good-quality patient-oriented evidence.)
More intensive BP control does not slow the progression of diabetic retinopathy once it has developed. Reduction of BP in normotensive people with diabetes does not prevent or slow diabetic retinopathy. (SOR: B, inconsistent or limited-quality patient-oriented evidence.) Treatment of hypertension increases the risk of hypotension (risk ratio [RR] = 2.04; 95% CI, 1.63 to 2.55).1 (SOR: A, consistent, good-quality patient-oriented evidence.)
PRACTICE POINTERS
Retinopathy is a common complication of diabetes that leads to visual impairment and blindness. In the United States, 4.1 million adults 40 years and older have diabetic retinopathy.2 Blood glucose control prevents the development and progression of the ocular complications of diabetes, including diabetic retinopathy.3,4 BP treatment has also been prescribed for this purpose, but individual studies on effectiveness have reported varying conclusions.1,5–8 The primary goal of this review was to summarize the effect of BP control interventions among patients with diabetes for the incidence and progression of diabetic retinopathy.1
This Cochrane review included 29 randomized controlled trials (RCTs) with 4,620 patients who had type 1 diabetes and 22,565 patients who had type 2 diabetes. RCTs were conducted in North America, Europe, Australia, Asia, Africa, and the Middle East. Settings included diabetes and ophthalmology clinics. Study designs, populations, interventions, lengths of follow-up (range = less than 1 year to 9 years), and BP targets varied among the trials. Study designs included assigning one group to one or more antihypertensive agents and the control group to placebo (in all seven RCTs for normotensive participants with type 1 diabetes, 8 of 12 RCTs for normotensive participants with type 2 diabetes, and 5 of 10 RCTs for hypertensive participants with type 2 diabetes). In the other studies, undefined methods of intense BP control were compared with usual care (four RCTs for normotensive participants with type 2 diabetes and five RCTs for hypertensive participants with type 2 diabetes).
In the trials conducted in the 2000s with participants who had type 1 diabetes, hypertension was defined as a systolic BP greater than 130 mm Hg or diastolic BP greater than 85 mm Hg in the absence of antihypertensive medication. This definition was noted to reflect lower BP values than for trials conducted earlier on the population of participants with type 1 diabetes. Among the participants with type 2 diabetes, the definitions of normotensive and hypertensive varied. More intensive BP control also had varied definitions among the trials. When looking at BP targets (lower diastolic or systolic BP targets for the intensive group), some trials used the same antihypertensive medication. Other trials compared antihypertensives with placebo or no treatment. Some trials compared different antihypertensives with each other, placebo, or no treatment. Other trials added BP control strategies, including behavioral home BP monitoring and a program for patient education and clinical management of hypertension.
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