Published in the December 2006 issue of Today’s Hospitalist
With heart failure the No. 1 admission diagnosis in the U.S. for patients over age 65, hospitalists know they’re on the line to improve care and reduce the disease’s spiraling costs.
Yet some standard therapies, like the use of diuretics, are adding to heart failure’s high costs and re-admission rates, according to Shashank Desai, MD, medical director of the heart failure/transplant program at Inova Fairfax Hospital in Falls Church, Va.
Take a look at our 2019 feature on managing heart failure patients: Tuning up your heart failure patients at discharge.
“We’re spending significant money on inpatient heart failure care, even though we know that inpatient therapies do not improve morbidity and mortality,” he said during his update on managing heart failure at the Fall 2006 Hospitalist CME Series meeting in Tampa, Fla. “Many therapies for acute decompensated heart failure, including inotropes and even loop diuretics, have the potential to worsen heart failure outcomes.”
Fortunately, he added, physicians now are much more focused on improving the quality of inpatient heart failure management. With the Centers for Medicare and Medicaid Services singling out heart failure as one of only a handful of diseases targeted by quality measures, “hospitals are going to be graded on how well they manage heart failure,” he said “and may see their revenues rise or fall for those efforts under a pay-for-performance program.
“Cardiologists have much less of an impact on those outcomes than internists and hospitalists,” Dr. Desai added, “because of the volume of heart failure patients they see.” During his update, he spelled out a new understanding of loop diuretics and pointed to looming liability concerns involving heart failure patients with few symptoms.
Diuretics: part of the problem
According to Dr. Desai, physicians are just now starting to recognize the implications of the fact that heart failure is not simply a cardiac disease, but a cardiorenal syndrome. That’s why therapies that target only the heart have not worked in acutely decompensated patients.
In fact, the diuretics that hospitalists routinely give to heart failure patients fuel a vicious cycle.
“Diuresis by loop diuretics squeezes the kidney and diminishes the amount of blood the kidney receives,” he said. As a result, the same neurohormones that physicians are trying to suppress with therapies like ACE inhibitors and beta-blockers are activated and eventually bring on the diuretic resistance that all inpatient physicians see.
“The IV furosemide on day one may work well, but by day four you’re not getting any fluid out by using the same dose,” Dr. Desai said. “Our natural response is to dose escalate, which makes the problem worse.” This is when hospitalists find that they’re not able to discharge patients, or they discharge them, only to see them bounce back to the hospital.
To break that cycle, said Dr. Desai, researchers are rushing to find novel diuretic therapies that would allow you to dump fluid while boosting renal blood flow.
Some trials focus on adenosine blockade or vasopressin antagonists. Others, including one with promising results presented at this fall’s Heart Failure Society of America meeting, target adenosine- receptor blockers.
And at the 2006 American College of Cardiology meeting, researchers presented findings on an ultrafiltration system used in the hospital that was able to remove fluid, maintain intravascular volume and reduce re-admission rates.
“Compared to the IV diuretics we now use,” Dr. Desai said, “this kind of approach to decompensated heart failure could actually lead to less re-hospitalization at 30 and 90 days.”
Still a place for nesiritide?
Just a few years ago, Dr. Desai continued, the prospect of reducing heart failure re-admissions was a big factor in physicians’ widespread adoption of the then-new drug nesiritide.
Data supporting the drug’s effectiveness came from studies in which the vasodilator went head-to-head against nitroglycerine and inotropes, and posted promising results in a select group of patients. When those results were combined with a muscular marketing drive, he said, “nesiritide got very wide use in this country.” Hospitalists embraced the drug to treat heart failure patients, while cardiologists started using it in the outpatient setting to try to improve refractory heart failure.
In 2005, however, two different meta-analyses published in Circulation and Journal of the American Medical Association put the brakes on nesiritide’s burgeoning use. One study found an association between the drug and impaired renal function, with a particular dose-base effect.
“The higher the dose, the worse off the renal function was,” said Dr. Desai. The other study linked the drug to higher mortality. Both were retrospective meta-analyses of only selected data, he added, which should have led to prospective studies.
Instead, nesiritide’s use fell off sharply. An article in the Oct. 18, 2006, issue of Journal of the American Medical Association, for instance, measured the impact those 2005 studies had on nesiritide prescriptions in close to 500 hospitals. Researchers found that in March 2005, the drug was being used in 16.6 percent of all hospital admissions. That rate had plunged to only 5.6 percent of admissions by December 2005.
According to Dr. Desai, such a steep dropoff “just like its sharp uptake when the drug was introduced “probably wasn’t warranted. At the same time, the renal and mortality findings underscore the need to use nesiritide only in appropriate patients.
“Nesiritide really needs to be focused on decompensated inpatient use,” he explained. Among patients presenting to the hospital or emergency room with dyspnea at rest or with minimal activity, IV nesiritide can reduce pulmonary capillary wedge pressure and improve their shortness of breath.
And for heart failure patients who are “warm and wet,” meaning they have good kidney perfusion but congestion, either nesiritide or other vasodilators, such as nitroprusside or nitroglycerin, “are probably reasonable therapies,” he said.
At the same time, nesiritide is “probably not an up-titratable drug.” he added. “If it doesn’t work at 0.01, the incremental benefit you’re going to get at 0.02 or 0.03 is probably not going to be that much greater.”
Nor is nesiritide recommended for intermittent outpatient infusion or for scheduled, repetitive use, or to improve renal function or enhance diuresis.
According to Dr. Desai, the drug is now being tested in an international trial that is enrolling 7,000 patients. “The question of higher mortality will eventually be answered,” he said, “but not for a couple of years.”
The need to consider ICDs
Finally, Dr. Desai turned from the issue of treatment to prevention, and to a growing liability concern for hospitalists.
He gave the example of a patient admitted and treated for pneumonia. “She previously had a heart attack and echocardiography reveals an ejection fraction that’s low, but she’s having few symptoms of heart failure at all,” he said. “Then she goes home and dies, and the hospitalist was the last physician to treat her.”
Unfortunately, it is patients with less severe heart failure, particularly those who don’t get a cardiology referral when they’re admitted for other diagnoses, who are more likely to die of sudden death, not pump failure.
“These patients never come to my heart failure clinic,” said Dr. Desai. “The young people who have had previous heart attacks and reduced ejection fractions, but are feeling well and jogging a mile “they’re the ones you have to worry about for sudden death.”
He presented findings from a 2002 trial that looked at patients who had a myocardial infarction at least four weeks before and whose left ventricular ejection fraction was 30 percent or less.
Researchers found a 31 percent reduction in overall mortality (and a 61 percent reduction in arrhythmic death) in patients given an implantable cardioverter defibrillator (ICD), compared to conventional medications.
Those kinds of results led the American College of Cardiology/ American Heart Association to issue revised guidelines in 2005 that recommended ICDs in the following cases:
“¢ as primary prevention in patients with ischemic heart disease who are at least 40 days post-MI, have an ejection fraction of less than or equal to 30 percent, and have New York Heart Association (NYHA) class II-III heart failure (class IA evidence);
“¢ as secondary prevention for patients who have low ejection fraction and have survived a cardiac arrest (class IA evidence);
“¢ as “reasonable” primary prevention in patients who are at least 40 days post-MI, have an ejection fraction of 30 percent or less, and NYHA class 1 heart failure (class IB evidence);
“¢ for primary prevention in patients with non-ischemic cardiomyopathy, an ejection fraction of 30 percent or less, and NYHA class II-III heart failure (class IB evidence); and
“¢ as primary prevention for any patient with an ejection fraction of between 30 and 35 percent and NYHA class II-III heart failure (class IIB evidence).
Hospitalists are not picking up on the patients whose ejection fractions are less than 30 percent, said Dr. Desai, when those patients may be admitted for an unrelated diagnosis. Instead, hospitalists need to recommend defibrillators for appropriate patients and refer them to a cardiologist or electrophysiologist.
“These are now the standard of care,” Dr. Desai warned. “All of us will be held up to these guidelines to prevent sudden death.”
Phyllis Maguire is the Executive Editor of Today’s Hospitalist.
BNP testing: Is it overused or a valid predictor?
Walk into any hospital and you’ll probably find standing admission orders to test heart failure patients for B-type natriuretic peptide (BNP).
“BNP testing has hit the market hard, and it’s being touted for having high predictive data in chronic heart failure patients,” said Shashank Desai, MD, medical director of the heart failure/transplant program at Inova Fairfax Hospital in Falls Church, Va. “That worries me because I don’t know what to make of single BNP results for any patient.” That’s because there are currently no strategies for how BNP should guide therapies.
During an update on heart failure management presented at the Fall 2006 Hospitalist CME Series meeting in Tampa, Fla., Dr. Desai cited one 2002 study in which investigators picked BNP-cutoff points at the time of discharge to predict long-term cardiac events.
“They picked 230 and 480,” he said, adding that such cutoffs are relevant only for large patient populations. “It doesn’t tell you what to do with the patient who’s sitting in front of you with a BNP of 486. That’s the problem with BNP.”
According to Dr. Desai, researchers still haven’t answered questions on how physicians should use BNP-test results to tailor treatments or gauge the efficacy of different interventions, such as bi-ventricular pacemakers or beta-blockers. But he did point to one big advantage of BNP testing that hospitalists should make use of: boosting the accuracy of a heart failure diagnosis on admission.
For patients presenting with dyspnea, for instance, a 2002 study found that physicians’ clinical judgment has “a 74 percent predictive value that the shortness of breath is coming from a heart issue, not a lung issue,” he said. Researchers in the same study found that plasma BNP levels boosted that diagnostic accuracy to just over 81 percent.
“Because BNP results predict a heart failure diagnosis better than clinical judgment alone, you combine the two and get incremental benefit,” he said. “That’s very useful when this is the first time you’re seeing these patients and don’t know what their shortness of breath actually is from.”