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Dr Deepak Bhatt: Empagliflozin Shows No Increased Kidney Risk After Acute Myocardial Infarction

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Deepak Bhatt, MD, Mount Sinai Heart, highlights the kidney-specific outcomes of the pivotal EMPACT-MI clinical trial in an interview at the 2024 European Society of Cardiology Congress.

At the 2024 European Society of Cardiology Congress, Deepak Bhatt, MD, MPH, MBA, the director of Mount Sinai Heart, presented pivotal new findings on the cardiorenal effects of empagliflozin following acute myocardial infarction (AMI). Building upon the earlier results of the EMPACT-MI trial, which were published in the New England Journal of Medicine, Bhatt highlighted the kidney-specific outcomes, shedding light on the safety and efficacy of sodium-glucose cotransporter 2 (SGLT2) inhibitors in high-risk patients post AMI.


This transcript was lightly edited for clarity.

Transcript

Can you discuss the results of your study evaluating the cardiorenal effects of empagliflozin after acute myocardial infarction?

It was really a pleasure for me to present here at the European Society of Cardiology 2024 in London on the kidney results from the EMPACT-MI trial as a late-breaking clinical trial. The overall EMPACT-MI trial was previously presented and published in the New England Journal of Medicine. It examined patients with a myocardial infarction who are at high risk of heart failure, either with or without diabetes, and randomized them to empagliflozin or to placebo. These patients were examined over the course of the next couple of years, and for the primary end point, there was no significant difference, but that primary end point included mortality. If one looked at just heart failure–related end points, as we did in a subsequent publication in Circulation, there was, in fact, a significant reduction in multiple different heart failure–related end points, similar to what other trials of SGLT2 inhibitors have shown. So overall, no reduction in mortality, but a reduction in heart failure–related events in this population that had previously been excluded from prior trials of SGLT2 inhibitors examining acute coronary syndrome. So, that's the overall EMPACT-MI trial.

What I presented here was the kidney-specific results from EMPACT-MI. A concern had been that perhaps SGLT2 inhibitors would be unsafe in sick patients, such as those coming in with a heart attack. And in the context of coming in with an acute coronary syndrome [ACS], patients most often get cardiac catheterization, stent procedures, intravenous contrast loads in addition to the contrast delivered during those procedures I mentioned and, therefore, might be at risk for kidney failure if SGLT2 inhibitors were started in this context. As well, patients coming in with an ACS, especially if they're at high risk for heart failure, are often getting other medicines, like ACE [angiotensin-converting enzyme] inhibitors or angiotensin receptor blockers, that can also affect kidney function.

So, perhaps adding an SGLT2 inhibitor into the mix could be unsafe for the kidney—that was the concern. What we found quite reassuringly, first of all, was that introducing SGLT2 inhibitors, specifically empagliflozin—though I think the results are generalizable to the class—that introduction of the SGLT2 inhibitor in this context was safe. That is, there was no increase in kidney-related events; in fact, the rate of events was lower, not statistically significantly lower, but wasn't higher. The concern was that it might be increasing kidney adverse events, but in fact, there was no increase. And as I just said, the rate was actually numerically lower, so very reassuring from a safety perspective that in patients without contraindications, it's safe to start an SGLT2 inhibitor if they've come in with an acute coronary syndrome. I will point out that patients with a GFR [glomerular filtration rate] less than 20 were excluded from the trial. So the number of patients with a GFR between 20 and 30 were rather small, but certainly, in all the other GFR categories, we had a large number of patients. We found consistent reductions in heart failure–related end points in all those different GFR categories and additionally found safety from a kidney perspective.

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