One of the many exciting things about being in medicine for a long time is seeing how things change. It’s one of the things I love about science the most – the way knowledge builds incrementally, like a Jenga tower, but then new research can come along and just knock it down again. For example, when I qualified from med school in the 80s you would’ve failed finals if you’d said you would give beta blockers for heart failure or if you said that you wouldn’t give them after an MI. How things change!
There is no debate now of course that beta-blockers are a cornerstone of management for heart failure with reduced ejection fraction, one of the ‘four pillars’ of treatment along with renin-angiotensin drugs, MRA antagonists and SGLT2 inhibitors. Beta-blockers have also been a sacred pillar of CHD secondary prevention for decades; however, this was based on research from an era before coronary syndromes were diagnosed by sensitive biomarkers and ejection fraction assessed post event. It is likely that many of these patients would have had reduced ejection fraction post a large STEMI, so we would expect beta blockers to be effective in these cases as heart failure drugs. But what if ejection fraction is preserved post MI, as is now commonly the case, plus patients also receive the benefit of high intensity statins, anti-thrombotic and RAS drugs? Will beta blockers still give an added benefit?
This has been an important clinical uncertainty for some years now. The most recent NICE guideline NG185 recommends that all patients are offered (i.e. strong recommendation) a beta-blocker as soon as possible after an MI, then titrate to maximal tolerated dose and continue for a year. At 12 months, patients who have reduced ejection fraction should then continue the beta-blocker indefinitely (as heart failure drugs) and for those with preserved ejection fraction, we should ‘consider’ (i.e. less strong recommendation, based on weaker evidence) continuing based on clinical judgement and tolerability. This should be a specialist-led decision, but my suspicion is that there are a lot of patients discharged to primary care post-MI who just remain on beta-blockers indefinitely even if ejection fraction is preserved.
A very useful light has been shone on this clinical uncertainty by the REDUCE-AMI trial published last month. This trial examined patients (n=5,000) who had an acute MI and a preserved ejection fraction > 50% and they were randomised to beta-blocker (metoprolol or bisoprolol) or no treatment, and had a mean of 3.5 years of follow-up. Crucially, beta-blocker treatment did NOT improve outcomes compared to no treatment for a composite outcome of new MI or death from any cause. The conclusion therefore is that if ejection fraction is preserved, beta-blockers do not appear to give any secondary prevention benefit.
This is great research, examining an important clinical question, but as an associated editorial NEJM 2024 points out it’s not perfect as the trial was open-label and possibly underpowered to show a true difference. As ever, they say ‘more research is needed’ but in the meantime, we shouldn’t be surprised/alarmed if we see patients with preserved ejection fraction post-MI who are not started on beta-blockers by our cardiology colleagues, and for those who are on them for secondary prevention then we should at least examine at 12 months whether they should continue, as per current NICE guidance. We should check their post-MI echo result, and if we have confirmation that their ejection fraction is preserved this new research strengthens the case for stopping the beta-blockers. These patients already have to take a lot of meds, so knocking one off their list will make you very popular!
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