Emerging mechanical therapy options have given life to a field which has gone under severe recharacterization in an era of increased obesity.
The burden of heart failure with preserved ejection fraction (HFpEF), and exactly what the subtype population is, has become better defined over the years. Unfortunately, it’s not an optimistic outlook—the public health struggle of obesity has led to younger HFpEF patients, with concerning comorbidities including diabetes and pulmonary hypertension.
But fortunately, therapeutic options may eventually become available.
In an interview with MD Magazine® while at the Heart Failure Society of America (HFSA) 2019 Scientific Sessions in Philadelphia, PA, Mark Dunlap, MD, director of the Heart Failure Program at MetroHealth System, and a professor at Case Western Reserve University, detailed the history of HFpEF assessment, and looked forward to mechanical therapy designed to target the pathopshysiology of the HF subtype.
MD Mag: How are emerging mechanical therapies benefitting patients with HFpEF?
Dunlap: This has been a space that there have been multiple, multiple failures previously. It's such an important patient population, because we all have patients that are symptomatic and admitted to the hospital, and have not only significant morbidity, but mortality. And we're still waiting for a winner—not the winner. I think we're a little more sophisticated than that.
But, the trials of left atrial decompression devices—one of the really exciting things I find about this is it's treating the underlying pathophysiology itself. What I mean by that is the pathognomic sign of preserved heart failure is an increase in pulmonary-capillary wedge pressure during exercise—during some activity. These patients often have no symptoms at rest, or even minimal symptoms with activity.
Well, this rather interesting experiment in nature in patients who happen to have an atrial septal defect in a setting with raised left atrial pressure, the observation has been that these patients actually do better when they can decompress that rise in left atrial pressure.
So now we're in an era where we're purposefully—at least, currently experimentally—trying ways to decompress that left atrial pressure with increased pressure during exercise to the right side of the heart.
Now, there may be some problems with that. We have to be careful with patients presenting with pulmonary vascular disease. But boy, we'd all love to see a therapy that could help to decrease this exercise-related rise in pressure.
MD Mag: What is the average patient with HFpEF? Are they generally older?
Dunlap: The patients of HFpEF, we have undergone a little bit of change in thinking about them. It used to be the older, thin lady who came in to offices and hospitals complaining of shortness of breath in any activity. They could have pulmonary edema.
But really, the phenotype's been changed over the past 20-30 years to more of a younger, more obese patient population with many comorbidities. Typically, they have some kind of pulmonary hypertension or sleep apnea—one of the consequences of obesity, as well as other problems with obesity which we think contribute to the HFpEF phenotype.
A large number of the patients have diabetes, pre-existing hypertension. And it is half the heart failure patient population.
We used to also think that the morbidity and mortality outcomes were less in that of HFpEF patients than in those with reduced ejection fraction. However, that's an amended hypothesis. These patients are admitted to the hospital frequently, they are very symptomatic, and their mortality may not be quite as high as patients with HFrEF, but it's a very close second.
It is both a morbid and mortal condition that as of yet, we have no way of preventing those hard outcomes of mortality.
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