Acute decompensated heart failure is a condition that clinicians want to prevent rather than treat.
The idea that patients hospitalized with acute decompensated heart failure can have a substantial change in their prognosis from an acute intervention given in the hospital seemed to finally hit a brick wall in November at the American Heart Association scientific sessions.
Treatment of acute heart failure patients with the vasodilating natriuretic peptide ularitide failed to cut long-term cardiovascular mortality or improve several other acute and mid-term outcomes in the TRUE-AHF trial. In a second report, ATHENA-HF , acute treatment with high-dose spironolactone during acute heart failure hospitalizations failed to improve a marker of heart failure severity, N-terminal pro B-type natriuretic peptide.
These two trials join what the discussant for TRUE-AHF, Clyde W. Yancy, MD , called a “litany” of half a dozen different types of interventions that all failed to produce clinically meaningful changes in the prognosis of patients with acute decompensated heart failure.
What alternative interventions are left? Dr. Yancy, as well as Milton Packer, MD , the cardiologist who led TRUE-HF, had somewhat similar answers.
In his discussion of TRUE-AHF, Dr. Yancy cited two possibilities: greater use of the relatively new drug formulation sacubitril plus valsartan (Entresto), which showed strong benefit treating patients with chronic heart failure with reduced ejection fraction (HFrEF); and expanded use of pulmonary-artery pressure (PAP) monitoring using an implanted device that gives clinicians early warning when a heart failure patient’s fluid volume moves into the danger zone that precedes by days or weeks the acute decompensation that produces dyspnea and drives a patient to the hospital.
Increasing experience with PAP monitoring “continues to endorse the notion that having early warning [of fluid overload] is important,” Dr. Yancy said in an interview. “The point of acuity in acute decompensated heart failure predates hospital admission, and this monitoring system allows us to catch this before it causes an emergency department visit. The data are very persuasive.”
This view of regular PAP monitoring to stop acute decompensation before it gets bad enough to cause hospitalization was echoed by Lynne W. Stevenson, MD , during a wrap-up session at the meeting.
“PAP usually rises 2-4 weeks before a heart failure hospitalization. Perhaps we need to focus more on long-term treatment rather than treatment in the hospital.” That’s especially true for patients with heart failure with preserved ejection fraction (HFpEF) because right now no treatment is clearly proven to improve HFpEF outcomes (although several experts make a persuasive case for spironolactone).
“Tight regulation of volume status is our best chance to improve outcomes in HFpEF,” said Dr. Stevenson, who helped pioneer the idea of PAP monitoring for heart failure patients. “Maintaining good volume is very important for HFpEF patients.”
But success with PAP monitoring requires more than gathering the pressure data. Producing benefit for patients “is predicated on having an infrastructure to accommodate the influx of PAP data, being nimble enough to respond to the data and being very precise about which patients you use this in,” cautioned Dr. Yancy. “The tool is not beneficial if the infrastructure is not there,”
The idea is still so new (the first implanted PAP monitor received U.S. approval in 2014) that at his institution, Northwestern Medicine in Chicago, about a dozen patients now have a monitor, he said.
“We’re looking to use it in patients with HFpEF, whom we can’t offer anything else. I’m intrigued by what I see,” in this first wave of Northwestern patients. Dr. Yancy’s anecdotal experience with PAP monitoring so far “helps endorse what the trial results suggested” about providing incremental benefit to heart failure patients.
Although Dr. Packer also supports broadening PAP monitoring, he sees heading off acute decompensations as primarily an issue of more diligently using existing guideline-directed therapies on advanced HFrEF patients: sacubitril plus valsartan, a beta-blocker, a mineralocorticoid receptor antagonist like spironolactone, and a diuretic.
“The solution is to prevent hospitalization in the first place with the medications we already have, but they’re not used. The medications we already have are enough, but they need to be used,” Dr. Packer told me in an interview during the meeting. He speculated that perhaps 10%-15% of HFrEF patients currently receive the full guideline-directed regimen of heart failure drugs. “That’s unbelievable,” he exclaimed. If clinicians diligently treated advanced HFrEF patients with these four agents, “you’d see a 60%, 70% drop in hospitalizations,” he suggested.
Dr. Packer put some of the blame for underuse of guideline-directed medications on the low financial incentive physicians have to vigorously apply this strategy.
He backed PAP monitoring as a good additional step for selected patients with unstable heart failure. “But as a general approach to managing patients with class III HFrEF, first put them on optimal medical therapy; then we can talk about an invasive procedure to place a PAP monitoring device.”
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