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Given the paucity of effective therapies for heart failure with preserved ejection fraction (HFpEF), any potential treatment is highly anticipated. There is one in the works at the moment: inter-atrial shunt therapy.

"It's really exciting that we have any therapy for HFpEF, which is a horrible problem clinically," says Ted Feldman, MD, of Evanston Hospital in Illinois, in this exclusive 番茄社区 video. His group is researching an inter-atrial shunt device they believe can relieve pressure overload and improve the prognosis of patients with a 50% ejection fraction.

Following is a transcript of his remarks:

We're going to talk today about inter-atrial shunt therapy for heart failure with preserved ejection fraction (or HFpEF). This is of tremendous interest because this is a clinical problem for which there is no effective therapy, and we have a glimmer of one now. HFpEF is similar in frequency and sadly, similar in prognosis to heart failure with reduced ejection fraction, and everybody thinks about the EF 20% or 30% patient as having a poor prognosis and doesn't realize that the EF 40% or 45% or 50% patient with clinical heart failure has the same prognosis.

HFpEF is growing in proportion to HFrEF, reduced EF heart failure, as the population ages. Pharmacotherapy has not been effective in this population. We observed the historical clinical scenario in which patients with mitral stenosis and elevated left atrial pressure, which is the genesis of HFpEF, if they had an ASD historically, this decompressed the left atrium and they presented much, much later in the course of the disease with any signs of heart failure. That begs the question if we create such an ASD in a patient with left atrial pressure overload, will we relieve their symptoms?

This led to the development of a inter-atrial shunt implant device and I'll call it IASD. It's like an ASD occluder, a little nitinol disc, but it has a hole in the middle. We did some baseline hemodynamic modeling using a simulator and calculated that we would get a small shunt with an eight millimeter opening, that that would be enough to reduce left atrial pressure overload during exercise without overloading the right side of the heart, without creating too big a shunt.

We've now studied this in two cohorts of patients. One a single-arm study which demonstrated that, in fact, we created a shunt, that people felt better, and that their exercise capacity improved (this is invasive exercise with a Swan catheter during bicycle ergometry). Then a small randomized study to really prove the mechanism, and we reported the early results of this at the American Heart Association a few months ago in which 40 patients were randomized to either medical therapy or a shunt, and then we looked at serial exercise studies. We found that peak exercise wedge pressure was significantly decreased in the patients with the device compared to those without a shunt. We found that the shunt ratio, the amount of flow across the shunt was a Qp:Qs, pulmonary to systemic flow ratio, of 1.2 preserved at 30 days and 6 months and that most of these patients feel better. We're going to have late results from this trial. We hope to present at the European Society of Cardiology, and we are in the midst of a 400-patient randomized pivotal trial to prove the therapy.

This is really very exciting that we have any therapy for HFpEF, which, again, is a horrible problem clinically. The mechanism, I think we've established, that we do decompress the left atrium with exertion and now we need to demonstrate that the clinical outcomes in a larger population are robust enough to carry this into practice.

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