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Heart failure high-wire act

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Karen Titus

July 2013—After weeks of bewilderment, W. Frank Peacock, MD, finally solved the mystery of one of his so-called frequent fliers in the Emergency Department.

At the time, Dr. Peacock was vice chair, Emergency Medicine, at the Cleveland Clinic. Every Monday morning, week after week, a local pastor would show up with symptoms of possible heart failure. It turned out that every Sunday evening, the pastor attended his church’s community dinner, where duty compelled him to try every last casserole. “He ended up with a salt load every Sunday night, and every Monday morning we’d see him,” recalls Dr. Peacock, who’s now professor, associate chair, and research director for Emergency Medicine at Baylor College of Medicine, Houston.

Would that all heart failure cases could be handled by telling patients to avoid Protestant potlucks. As it turns out, heart failure cases—never simple to begin with—now have a new, potentially costly wrinkle. Last fall, the CMS began cracking down on hospitals with higher than expected 30-day readmission rates for heart failure (as well as for acute myocardial infarction and pneumonia). That has launched among clinicians and administrators fresh scrutiny of how well HF is managed, from diagnosis to guiding therapy to risk stratification.

With heart failure readmission rates getting attention, biomarkers are too. Troponins and BNP/NT-proBNP are in wide use. “Now all we’re saying is just get a couple more, at least maybe one more, before they leave the hospital,” says Dr. Alan Maisel, above center, on rounds in the CCU at the San Diego VA. [Photo: Sandy Huffaker]

“It’s a topic of intense discussion just about anywhere you go, because it is a major cost center,” says Alan Wu, PhD. “I think in the very near future, with pay-for-performance in the new health care initiative, this is going to be even bigger. If you have really high readmission rates, your reimbursements might be affected,” says Dr. Wu, professor, laboratory medicine, University of California, San Francisco, and laboratory director, Clinical Chemistry Laboratory, San Francisco General Hospital.

While it may not be a lab issue right now, it will be in the very near future, says Dr. Peacock. “Every hospital administrator is scared to death of this,” he says. Their concern has trickled down to emergency medicine and cardiology physicians, with the lab not far behind.

Readmissions historically haven’t been closely tracked, explains Dr. Peacock, because no one felt personally responsible if a patient returned. Likewise, no one felt the sting financially.

That’s now changing. Readmission rates are now serious business, emphasis on the business. Some hospitals are turning with new enthusiasm to old measures, while others are looking at new measures to reduce rates. In both scenarios, biomarkers might be important, with clinicians looking at new uses for standard markers as well as searching for novel ones.

All these efforts come with a catch, however. With so little emphasis placed on heart failure readmissions in the past, physicians have precious little data to guide them. “We’ve never really looked at what predicts 30-day outcome,” Dr. Peacock says.

They’re starting to find out.

Even the number 30 is a little shaky. In general, readmission is worse than nonreadmission. But if a patient does return for care, it’s not always the fault of the hospital, says Adam Singer, MD, professor and vice chair for research, Department of Emergency Medicine, Stony Brook (NY) University. Heart patients can be notoriously hard to manage, and mortality rate for heart failure is high—almost 50 percent within two years. “These are sick patients,” says Dr. Singer.

Heart failure therapies haven’t advanced much in recent years, he continues. Yes, biomarkers have improved, as has physicians’ understanding of the disease. But treatments themselves are treading water. There have been plenty of hopefuls, says Dr. Singer, including nesiritide and other endothelial receptor antagonists as well as other novel therapies, but when tested they’ve failed to show clinical benefit. “It’s been disappointing. I’m not sure how we expect, all of a sudden, we’re going to do much better in managing heart failure patients, when the armamentarium hasn’t shifted much.”

Dr. Peacock sees 30 days as a marker of who’s sick. Patients who have more visits die at a higher rate than those who don’t, he says. “After your fourth revisit, you’re probably going to die really soon.” And the sickest people come back soonest, he says.

But why not 29 days, or 31 days, or even 60 days, when 58 percent of readmissions occur (O’Connor CM, et al. Am Heart J. 2010;159[5]:841–849)? “You have to pick something,” says Peter Pang, MD, associate chief and associate professor, emergency medicine, and associate professor, medicine, Northwestern University Feinberg School of Medicine, Chicago. “Do I think it’s the best? Not necessarily. Do I think it’s a place to start? I do.” Noting the lack of success in improving heart failure outcomes in the last decade, he says, “You can clearly see why they had to start somewhere.”

To Dr. Singer, the 30-day mark is arbitrary. “There’s no evidence that that means the patient was mismanaged and that there was an error. You could have patients who were managed well, but that’s the nature of the disease. Some people have severe disease and are very brittle.” In some cases, he posits, it might even be better for patients to have several one- or two-day admissions over a month than one two-week stay.

That lines up with the longstanding approach of focusing on shorter length of stay. DRGs, says Dr. Peacock, encourage hospitals to move sick people out the door. And if they came back, hospitals “simply bill them another DRG.” Little wonder, he says, that the CMS is now focusing on readmissions—it’s the next logical step financially.

But improving heart failure outcomes—or, to be precise, lowering readmission rates—is a problem without a clear answer. In fact, it’s hard to figure out where to start looking, the result of which is hospitals are looking almost everywhere.

Are readmissions the result of diagnostic failure? Treatment failure? Are patients being discharged at the right time? Are the right ones leaving the hospital? Is followup care adequate? Are the right ones staying hospitalized, for the right amount of time? Is this even a heart failure issue at all?

And where do biomarkers fit in?

If it were possible to improve care for heart failure patients by clinical means alone, says Dr. Peacock, “we’d already be doing it. For years we’ve been bad at this. The medical community cannot tell who is a low-risk patient. We send them all home, and a third of them come back.”

Enter biomarkers, which tend to be a fairly inexpensive, easy-to-use way to risk stratify patients. For years they’ve been used as diagnostic markers, but now physicians are looking at using them prior to discharge.

The reigning heart failure marker remains natriuretic peptide (NP), either B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP).

Alan Maisel, MD, professor of medicine and cardiology, University of California, San Diego School of Medicine, and director, coronary care unit and heart failure program, Veterans Affairs San Diego Healthcare System, is a big fan of using NPs in risk prediction algorithms. The usual tools for preventing 30-day readmissions (including medicine reconciliation with pharmacists, home nursing, telehealth monitoring) have not proved helpful. Not because they’re bad tools, Dr. Maisel says, but because not everyone is using the information they provide to make changes, which in turn might reduce readmission rates.

At the San Diego VA, policy recommends using NT-proBNP prior to discharge for two reasons: 1) it lets physicians know whether the patient’s NP level is as low as it should be, and 2) if it’s high, it might encourage physicians to continue monitoring the patient, because higher levels increase chances the patient will be readmitted.

Troponin also looks like a good marker of risk stratification in heart failure patients, Dr. Maisel says. If it’s high in a patient who’s sent home, it indicates lurking subendocardial ischemia. When high-sensitivity troponins become approved for clinical use in the United States, reliance on troponin for risk stratification will increase, he says.

Two other markers have already been approved. Dr. Maisel says he’s most familiar with galectin-3, having been involved in multiple research studies involving the marker. Galectin-3, a marker for fibrosis, runs high in 40 to 50 percent of heart failure patients, he says. When a heart failure exacerbation occurs, more collagen is secreted, related to the inflammatory insult. This will lead to slower recovery and prolong demise and likely is important in 30-day readmissions, he says.

Dr. Maisel says at least three published studies (plus data from other studies) suggest that levels above the 17.8 ng/mL cutpoint predict a two to three times higher readmission rate than levels below the cutpoint. It’s helpful, too, he says, that galectin-3 levels remain steady. Unlike BNP, which needs to be measured at discharge, rather than at admission, galectin-3 levels at admission can help physicians plan accordingly if the level is high.

If it’s high in the ED, he continues, it may indicate a patient should be admitted, rather than treated in an observation unit and then sent home. For inpatients, high galectin-3—along with a high NP or troponin, as well as other indicators of early readmission, such as older age and renal dysfunction—might suggest to physicians that a patient should receive home monitoring as well as quicker uptitration of cardiac medications, says Dr. Maisel. In fact, he adds, the REGAL study, scheduled to begin this summer, will measure galectin-3 in acute heart failure patients; if it’s high, they will be randomized either to a control or to spironolactone (an aldosterone blocking agent; aldosterone makes fibrosis through the galectin-3 pathway). “This furthers the notion that you can use a biomarker not just to risk stratify a patient, but to start them on a treatment,” says Dr. Maisel, who’s involved in the REGAL study.

Dr. Peacock

At Baylor, Dr. Peacock and his colleagues looked at galectin-3 for predicting 30-day outcome. Declining to provide details (they’ve submitted their work for publication), he says, “There’s a cutpoint on that molecule that says you will be alive, guaranteed, in 30 days, with five percent heart failure revisits. That’s what I need, because now I know who I can throw out of the hospital early and get my financial benefit from the DRG.”

The greatest need for new biomarkers, as Dr. Peacock sees it, is to identify low-risk patients, that is, those who can be sent home safely. Troponin takes care of the high-risk end of the spectrum. “Your troponin is positive, you usually go to the cath lab or you’re going to die,” as Dr. Peacock puts it.

High-risk markers aren’t useful in low-risk patients, Dr. Peacock continues. “When your creatinine is low, when your troponin is low, when your BNP is low, does that mean you’re not sick? No! You can drop dead with a normal troponin.”

ST2 is the other hopeful. It, too, is FDA approved. It interacts with IL-33, a vasodilator of the heart. High ST-2 levels are bad—it’s both a stretch marker as well as an inflammation marker, Dr. Maisel explains. Unlike IL-33, ST2 levels change with treatment. “So it’s quite possible—we’ve actually done this before—that you’d try to titrate down your treatment, both ST2 and BNP, during hospitalization, to make sure you have the best therapy to try to cut down the number of readmissions,” he says.

Not yet approved in the United States (though it is approved in Europe) is NGAL, a marker of kidney injury, which occurs about 30 percent of the time in heart failure patients. The GALLANT trial showed that if NGAL and BNP are high when a patient is released, the readmission rate is high, Dr. Maisel says.

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