Understanding that there is a third type of heart failure will further our understanding of the disease, noted Clyde W. Yancy, MD, MSc, chief of cardiology and vice dean for diversity and inclusion at Northwestern University's Feinberg School of Medicine.
Understanding that there is a third type of heart failure—the intermediate-range ejection fraction phenotype—will further our understanding of the disease, be helpful for clinical trials, and inform how we can best position contemporary therapies appropriately, underscored Clyde W. Yancy, MD, MSc, professor of medicine, chief of cardiology, and vice dean for diversity and inclusion at Northwestern University’s Feinberg School of Medicine.
Yancy will be presenting “Evolving Understanding & Therapeutic Role of SGLT2i and ARNI in 3 Heart Failure Phenotypes: HFrEF, HFiEF & HFpEF” on day 1 of the American College of Cardiology's 70th Scientific Session, being held May 15-17.
Can you preview your conference discussion on sodium-glucose cotransporter-2 inhibitors and angiotensin receptor neprilysin inhibitors in 3 heart failure phenotypes?
I’m happy to do that, because it really is the crux of what’s new and exciting about heart failure. The first thing is that we really have officially declared that heart failure has 3 phenotypes. That’s actually important, because up until now we only discussed 2 specific phenotypes. One, clinical symptom with heart failure signs and symptoms and the ejection fraction that was associated was greater than 50%. And the more ordinary, the more usual syndrome, was that where the ejection fraction was less than 40%.
Intuitively, there is a space between 40% and 50%. Did we overlook it? Did we not understand it? Is it that much splay between the 2 different phenotypes and we could dismiss it? And the answer is, no, no, and no. We actually recognize that there is an intermediate-range ejection fraction phenotype, probably sourced from 2 directions. One, because some people simply have a heart muscle that expresses an ejection fraction between 40% and 50%. We think, in large measure, that that kind of muscle response is if it was heart failure with reduced ejection fraction. And our thresholds for normal are changing—that is, are higher—because we recognize that even numbers in the low 50s, high 40s still behave like reduced ejection fraction heart failure.
But the other thing that’s really, really intriguing: we’ve known all along there was a group of patients previously with very low ejection fraction, who when treated with effective evidence-based therapy improved sufficiently that the residual ejection fraction was greater than 40% and the number of ejection fraction over which the improvement occurred was at least 10. We call that heart failure with improved ejection fraction.
So the first thing to do is to say that in the information that we will be discussing at ACC.21, we are endorsing these 3 different phenotypes of heart failure. It’s helpful for our understanding, it’s helpful for clinical trials, and it’s helpful to understand how best to position contemporary therapies appropriately. Now, having said that, that’s where the conversation about the ARNIs and SGLT2 inhibitors becomes pretty important.