Met-HeFT found no measurable cardiovascular benefit from metformin in heart failure
In the double-blind Met-HeFT study across 23 Danish centres, 940 people were assigned to metformin or placebo. Over a mean 3.7 years there was no significant difference on the primary endpoint of death, worsening heart failure, heart attack and stroke, and none on overall death or unplanned heart failure events. The result limits the hope that metformin protects the heart beyond lowering blood sugar.
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A double-blind comparison in 940 people
Observational work and small short trials had suggested that metformin protects the heart beyond lowering blood sugar. The Met-HeFT study, part of the Danish DANHEART programme, ran across 23 centres. 940 people with symptomatic chronic heart failure, a left ventricular ejection fraction of up to 40 per cent and type 2 diabetes, prediabetes or a raised risk of diabetes were assigned in a double-blind design to metformin or placebo. Mean follow-up lasted 3.7 years. The result was presented at the European Society of Cardiology Congress in Munich.[1], [2]
The primary endpoint showed no difference
No significant difference was reported on the primary endpoint of death, worsening heart failure, heart attack and stroke. The combined measure occurred in 25.1 per cent on metformin and 23.4 per cent on placebo. No significant difference appeared on overall death or unplanned heart failure events either. Secondary measures, including new diabetes cases, also showed no difference. The presentation stresses that metformin brought no measurable cardiovascular benefit in heart failure.[2], [1]
Glucose-lowering use stays separate
The trial found no harm from metformin, and its glucose-lowering use is unaffected. Only about 10 per cent of participants had type 2 diabetes when they entered, because joining required stopping metformin and few people or doctors were willing to do that; investigators name this as the reason enrolment stayed low in part. Mean age was 70 years and 16 per cent of participants were women. The observational hope for a heart-protective role did not find support at the level this large double-blind study could measure.[1]