This transcript has been edited for clarity.
Hi. I'm April Stempien-Otero, associate professor of cardiology at the University of Washington, where I practice as an advanced heart failure transplant cardiologist and translational scientist. I'm here today to talk to you about new approaches in acute decompensated heart failure (ADHF) treatment.
I'm going to limit this discussion to the patient who comes in to the emergency room short of breath, with newly diagnosed heart failure, and is admitted — usually to the floor and not to the cardiac care unit. You're pretty sure that the patient is nonischemic, you're not working up coronary disease in them, and you just want to treat them and get them on the best medications possible.
Guideline-directed medical therapy (GDMT) of angiotensin-converting enzyme (ACE) inhibition, spironolactone, beta-blockade, and now the addition of sodium-glucose cotransporter-2 (SGLT2) inhibitors is our cornerstone of therapy. The question I want to address is, how do we get patients on this therapy when they've come in to the hospital acutely congested and decompensated in heart failure?
Some great studies have come out over the past 5 years that have really given us the data to guide our use of these medications and how to best treat patients who come in short of breath, congested, and decompensated.
The first priority is decongestion. We have a patient who comes in and they're obviously volume overloaded. Multiple studies have shown that the approach to decongestion, be it continuous infusion or direct bolus infusions of diuretics, doesn't make a difference. What's more important is that you get patients decongested, and that you get them decongested following their N-terminal pro-B-type natriuretic peptide (NT-proBNP) as a marker as opposed to their creatinine levels.
One thing I'm going to emphasize is that for years we've used creatinine as a stopping point in our uptitration of medications. The data show that this has not been the best approach for our patients. Recent studies show that patients who leave the hospital with a creatinine level higher than it was when they came in do better to avoid rehospitalizations than those who have normal creatinine levels or no change in renal function, likely because they were not adequately decongested during their hospitalization.
Put these patients on diuretics and keep it going until their weight goes down. Here at the University of Washington, we like to use Archimedes' principle: that no matter the intake and output of fluids charted, if the weight of the patient does not change, that means that the volume has not come off.
I highly encourage the use of a set diuretic protocol as we do here. We use the protocol that was used in the CARRESS study, and then have added on subsequently acetazolamide as an augmentation and boluses of 3% saline in certain patients. A protocol keeps the patient going even when the creatinine level may be increasing and the medical team may be getting nervous.
If the patient is not losing weight, then you are clearly in a situation that is more severe, and augmentation of therapy with loop diuretics plus metolazone or Diuril (chlorothiazide) is indicated. If you're really hitting a wall after 3-4 days, right heart catheterization to see if the patient is truly volume overloaded, or if cardiac index is low, is indicated.
Optimizing GDMT in ADHF Patients
Once you have your patient on decongestive therapy, it's time to get them on their heart failure therapies. I recommend that everyone read the STRONG-HF study, which came out recently in The Lancet. This study included patients who were selected right before hospital discharge and randomly assigned them to an aggressive therapy of uptitration of their heart failure GDMT drugs vs usual care.
I will admit that the protocol was very intensive for outpatient therapy. It's a challenge for all of us to get our patients in to see us, but the structure of the study made it such that the time they would need to spend in the outpatient clinic was brief.
Essentially, 2 days before discharge, they were randomly assigned to these two strategies. If they had not reached a half-dose of GDMT, they were put on a half-dose of GDMT — so that would be 100 mg/d of Toprol (metoprolol), about a 45/50 -mg dose of Entresto (sacubitril/valsartan), or equivalent doses of generic ACE inhibitors, angiotensin II receptor blockers (ARBs), or beta-blockers.
At the same time, spironolactone was added. Then patients were seen weekly for 3 weeks post-discharge, with a goal that they would be on full-dose therapy by 2 weeks post-discharge. The key to this trial was the safety monitoring. Patients had laboratory assessments done at 1, 2, 3, and 6 weeks post-discharge to ensure that their potassium and creatinine levels were stable.
As long as creatinine clearance or estimated glomerular filtration rate (eGFR) was > 30 mL/min/1.73 m² and potassium was < 5.0 mmol/L, patients continued to uptitrate medications. The blood pressure goal was ≥ 95 mm Hg systolic, which is also very liberal. With this, the patients who were able to get to full-dose therapy either by their first or sixth visit post-discharge had a dramatic decrease in rehospitalization rates and overall felt quite a bit better.
I think what's most encouraging about this study was the safety; it was very safe and effective to rapidly increase patients' ACE inhibitors and beta-blockers. When we have people sick in the hospital, lying around in bed and vasoplegic, it can be hard to push these drugs as their blood pressures sag a little bit and everybody gets nervous.
Similar to the HF-ACTION trial, which showed us that aggressive exercise is good, this shows us that aggressive uptitration of medications is safe and effective in patients, even with their first hospitalizations for decompensated heart failure.
I will say that the negative of the trial is that it didn't really specify what the decongestive regimen was or whether patients were defined as decongested prior to discharge. They all did have continued elevations in NT-proBNP levels. Of course, the interaction between uptitration of vasodilators and diuretics can be tricky at times.
I ask you to go back to that principle about the creatinine. As long as creatinine clearance is > 30 and you're watching potassium closely, you can be more aggressive with these therapies than you previously suspected, as long as you're watching laboratory assessments closely as outpatients.
The Benefits of Physical Rehabilitation
In regard to HF-ACTION, which I mentioned previously, that was the trial published a long time ago of aggressive exercise in patients. We've had a redux in that trial and the REHAB-HF trial, which showed in older adults that aggressive physical rehabilitation in the hospital, starting with their heart failure decongestion admission, was quite beneficial over the long term. These patients began a 3-day-a-week progressive exercise regimen, kind of a precardiac rehabilitation regimen, of walking around and doing exercises; it then continued at home 3 times a week with outpatient physical therapy. They had a dramatic improvement in their exercise tolerance and stamina by the 12-week end of the therapy.
Now, this was, again, an older group. Quite a few patients dropped out of the trial because they were unable to do the activities, but in those who could do the activities, researchers found a significant improvement.
I think that this combination of decongestion, aggressive uptitration of medications such that patients have reached their goal doses of GDMT as quickly as possible, along with this aggressive physical therapy and cardiac rehabilitation as soon as possible, is going to keep patients out of the hospital longer, and living longer and healthier lives. Thank you.
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Cite this: Upping the Pace in Acute Decompensated Heart Failure Therapy - Medscape - Aug 22, 2023.