Care Pathways and Their Kin

Transitions of Care in Heart Failure, Circulation Heart Failure, January 2015

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-Wes

Preventing Hospital Readmissions for Heart Failure

"How are you feeling Ms. Jones?"

"Fine."

"Have you been more short of breath lately?"

"Not really, just when I exercise."

"How much exercise?"

"I dunno. But after I go to the mailbox and walk back up to the house, I’ve got to stop now where before I didn’t."

Exertional dyspnea. It conjures up a large differential of potential cardiovascular or pulmonary causes. And as the above commonly-encountered doctor-patient conversation demonstrates, the problem is a dynamic one: at rest things are often fine, on exertion or with recumbency less so.

Now imagine that the doctor then sees elevated neck veins, hears rales in the lower lung fields, and sees swollen ankles on their patient. Heart failure, right?

Perhaps. But we should recall that heart failure is not a disease, but a condition caused by an underlying pathology. So a slew of diagnotic studies are under taken and if no easily correctable cause identified, symptomatic therapy started. If it's caught early or the ause identified, perhaps an admission will be avoided. But if things progress, Admission Number 1 for "heart failure" is chalked up on the books.

Our new health care law requires (Page 8) doctors avoid expensive hospital readmissions by “intervening” on heart failure since this problem is one of the leading causes of readmissions to hospitals. These readmissions cost our health care system billions of dollars. To prove the point, millions upon millions of dollars have been spent to try to prevent heart failure admissions with the assumption that, surely, many readmissions are preventable and cost savings reflected to our health care system.

We should acknowledge that better compliance with medications, careful management of one’s diet, and avoidance or behaviors known to exacerbate heart failure could be better avoided. For the motivated and highly engaged patient, improvements in readmissions can be made, but I wonder how much so: after all, they’re already the Compliant Ones. It’s the Non-compliant Ones and the Medically Challenging Ones that are the problem for our health care system from a cost standpoint.

The Non-compliants are a particularly difficult bunch. They don’t want to think about their health. They want to think about this weekend’s football game, child’s graduation, their upcoming trip to Europe, or being able to pay this month’s bills. And there are many more Non-compliants than Compliants out there. They are not all Non-compliants because they mean to malign their doctor but rather because life gets in the way of dealing with daily health issues for them. And we’re not even talking about the problems inherent to people with severe shelter, social, education, family and economic challenges. Can we expect our health care system to impact all of these areas to prevent hospital readmissions?

And the Medically-Complex Ones have their own challenges: maybe it's heart failure this week, then maybe a bout with a COPD exacerbation the next. Are they a readmission, too?

You bet.

But this has not influenced attempts at expensive innovation in this area. This past week we saw the second clever innovation for measuring physiologic parameters to predict the development of heart failure suffer a devastating blow at the hands of the FDA:

An FDA advisory panel decided that CardioMEMS failed to prove that its wireless, implantable heart monitor's benefits outweigh its risks, casting a shadow on a potential $375 million acquisition by St. Jude Medical (NYSE:STJ) – which already owns nearly a fifth of CardioMEMS.

The watchdog agency's cardiovascular devices committee decided that a clinical trial of the device, designed to be the first permanent heart implant for a solely diagnostic purpose, was warped by the assiduous care given to its participants. (emphasis mine) That's because the clinicians administering the single-blind trial knew which patients were implanted with the device and made sure they got specialized care.

The panel voted 9-1 that the device is safe, but decided that the trial failed to prove its effectiveness on a 7-3 vote. The committee voted 4-6 that the benefits of the device, which measures pulmonary artery pressure, have been proven to outweigh its risks.

Recall that this is the same fate that Medtronic's earlier right ventricular hemodynamic pressure monitor, the Chronicle device, suffered in 2007.

But maybe we can make lemonade our of lemons when it comes to innovation to prevent heart failure. Maybe we can realize the importance of people interacting with people and the time necessary to assure better outcomes in heart failure. And maybe, just maybe, we should realize that even with all the technology in the world, expensive medications and expensive testing, that penalizing doctors and health care providers who spend the time with patients just because they present again to a hospital might be exactly the wrong approach to address our readmission issue.

And maybe we should acknowledge that a good portion of the problem with hospital readmissions starts outside hospitals, not in them.

-Wes

Thoracic Impedance Monitoring Fails to Limit Heart Failure Admissions

Imagine being able to detect heart failure before it happens. The potential to offer significant cost reductions in health care might be significant.

So device makers created a way that implantable defibrillators could measure a drop in impedance between the pulse generator can and the lead in the patient's heart. Lower impedance should mean more water in the chest, suggesting fluid overload.

It seemed, well, so logical.

But with today's release of the DOT-HF trial, it seems that all that thoracic impedance information contained in an ICD, when used to alert the patient to a fluid accumulation in their chest, has the potential to create more rather than fewer hospitalizations:

METHODS AND RESULTS: We studied 335 patients with chronic heart failure who had undergone implantation of an implantable cardioverter-defibrillator alone (18%) or with cardiac resynchronization therapy (82%). All devices featured a monitoring tool to track changes in intrathoracic impedance (OptiVol) and other diagnostic parameters. Patients were randomized to have information available to physicians and patients as an audible alert in case of preset threshold crossings (access arm) or not (control arm). The primary end point was a composite of all-cause mortality and heart failure hospitalizations. During 14.9+/-5.4 months, this occurred in 48 patients (29%) in the access arm and in 33 patients (20%) in the control arm (P=0.063; hazard ratio, 1.52; 95% confidence interval, 0.97–2.37). This was due mainly to more heart failure hospitalizations (hazard ratio, 1.79; 95% confidence interval, 1.08–2.95; P < 0.022), whereas the number of deaths was comparable (19 versus 15; P = 0.54). The number of outpatient visits was higher in the access arm (250 versus 84; P < 0.0001), with relatively more signs of heart failure among control patients during outpatient visits. Although the trial was terminated as a result of slow enrollment, a post hoc futility analysis indicated that a positive result would have been unlikely. CONCLUSION: Use of an implantable diagnostic tool to measure intrathoracic impedance with an audible patient alert did not improve outcome and increased heart failure hospitalizations and outpatient visits in heart failure patients.

Postulating why this unexpected result was seen, Dr. James E. Udelson in an accompanying editorial suggested several reasons:

In the DOT-HF trial, among the episodes of HF hospitalization, only 60% were preceded by an alert condition, where impedance readings fell below the prespecified threshold indicting risk. In other words, the sensitivity of the impedance alert to predict a HF episode was only modest. This is actually consistent with previous studies, and false-positives seem common, as well.

Almost half of the outpatient visits in the treatment group were a result solely of an alert, which may have resulted in a drive to more intervention and possibly hospitalization.

Moral of the story: more data from ICDs is not necessarily better when it comes to predicting heart failure exacerbations.

-Wes

References:

van Veldhuisen DJ, et al. "Intrathoracic Impedance Monitoring, Audible Patient Alerts, and Outcome in Patients With Heart Failure." Circulation 2011 http://circ.ahajournals.org/content/suppl/2011/09/18/CIRCULATIONAHA.111.043042.DC1.html

Udelson JE. "T.M.I. (Too Much Information)?" Circulation http://circ.ahajournals.org/content/early/2011/09/19/CIRCULATIONAHA.111.067819.citation

Life and Death With an LVAD

Left ventricular assist devices (LVADs) are dramatically altering the field of heart failure care. There are pros and cons with the use of these devices, and this Reuter's article does a good job exploring them in simple terms.

Cardiologists need to become more familiar with these devices' limitations, too:

We have to address what is the meaning of death on one of these pumps," said Dr. Valluvan Jeevanandam, chief of cardiac and thoracic surgery at the University of Chicago Medical Center and an investigator for Thoratec's clinical trials.

Roughly 70 percent of patients on the HeartMate II were alive after a year, and nearly 60 percent were alive after two years, according to the latest data.

"It's not hard to imagine a person who has had severe stroke that has impacted both sides of the brain, the kidneys are shutting down, he is on a respirator, but yet the LVAD just keeps churning along," said Martin Smith, a clinical ethicist at the Cleveland Clinic.

Under U.S. law, patients are allowed to ask that implanted devices be turned off. But Dr. Diane Meier, a professor in the department of geriatrics and palliative medicine at the Mount Sinai School of Medicine, said cardiologists are particularly bad at preparing patients for death, especially this kind of death.

Like pacemakers and ventillators, these devices intervene on the natural course of the dying process and when the quality of life declines sufficiently after their use, it is ethical for patients and family members to request such support be withdrawn.

The challenge, of course, is what to do when these members of the care team aren't there...

-Wes

Re-Learning Heart Failure Semantics

Thursday, Boston Scientific received word from the FDA, that three of their implantable cardiac defibrillators capable of cardiac resynchronization therapy (CRT-D), or biventricular pacing, have been approved for use in patients with "left bundle branch block who have either mild heart failure or heart failure with no apparent symptoms."

This is an interesting discovery - people can have heart failure without symptoms!

This, of course, flies in the face of most of the definitions of heart failure. Take, for instance, this definition from Mayo Clinic:

"Heart failure, also known as congestive heart failure (CHF), means your heart can't pump enough blood to meet your body's needs."

How is someone supposed to know that the blood flow needs from the heart are not met if the patient has no signs or symptoms? Saying it another way, does this mean that everyone with left bundle branch block and no symptoms might actually have heart failure?

*Sigh*

The lines of classifying the severity of heart failure have never been clear, despite what our medical coders and researchers would like us to believe.

In reality, in the upstream push to prevent heart failure, MADIT-CRT (the study the FDA cited to reach its approval of Boston Scientific's CRT and CRT-D devices) has demonstrated that intervening BEFORE symptoms occur in patients with weak heart muscles and left bundle branch block can improve mortality and reduce hospitalizations for heart failure. This a good thing.

But what we also have learned is that patient symptoms are immaterial for device implantation any longer in patients with weak heart muscles (EF <= 30%) and left bundle branch block (with QRS width of 130 msec or more) on their EKG. As such, classic symptoms of "heart failure" like shortness of breath, swollen legs, and the like, are also immaterial to qualify for a cardiac resynchronization device.

This makes me wonder if we should still be calling CRT devices "heart failure" devices or rather, "heart preserving" devices.

For now, they'll have to stay "heart failure" devices, despite all of the negative connotations. For whoa to the doctor that forgets to give the diagnosis of at least "Congestive heart failure, NYHA Class I" (or, "congestive heart failure without symptoms") when they ask, pretty please, for permission to implant one of these devices from our insurers in our new era of cardiovascular guidelines mandates.

Such are the billing and coding games we must continue to play.

-Wes

Reference: The NEJM publication of MADIT-CRT.

Why Did Dick Cheney Develop Heart Failure?

Years ago, when I was indoctrinated as a fellow in to American College of Cardiology, Dick Cheney - then a former secretary of state, was the keynote speaker at our commencement ceremony. His keynote speech reflected on what it was like to watch his father die following a massive heart attack, comforted only by morphine, oxygen, bed rest. By then, Mr. Cheney, already a recipient of two bypass operations, made a point to thank the cardiovascular community for helping him.

Many years later, Mr. Cheney's complicated yet remarkable cardiovascular history reads like a social studies timeline - one with heart attacks, arrhythmias, blood clots, and now, congestive heart failure. (Of course, political spin meisters want to make sure we call it "fluid retention" rather than congestive heart failure, since "failure" is not an option when speaking of all things political).

Congestive heart failure is nothing more than an insufficient pumping of blood to meet the body's needs. As a result, the kidneys detect the decreased perfusion pressure and trigger the release of a cascade of hormones to increase the blood pressure to maintain perfusion of the tissues. Some of the hormones help retain fluid in the vascular space. If this fluid becomes too excessive, the fluid can spill into the lung resulting in a sensation of shortness of breath, usually worse when lying flat. One of the main drugs used to fool the kidneys to release the accumulated fluid are diuretics - the most common being furosemide (Lasix).

There are a number of things that may have contributed to the development of Mr. Cheney's heart failure. Since HIPAA knows no bounds with disclosing Mr. Cheney's heart history, we can use this opportunity to tease apart a few possibilities.

First, dead meat don't beat.

It doesn't help that Mr. Cheney has had many heart attacks in the past. With the progressive loss of healthy muscle cells to to the heavy lifting of contraction, the ejection fraction falls. At first, the heart compensates by recruiting other, non-injured segments of heart muscle to take up the slack, but with each successive heart attack, the reserve heart muscle dwindles. Lose enough muscle and the heart must rely on increasing the rate at which if contracts to increase output, but for hearts already with limited blood flow this might lead to futher shortage of oxygen to the heart muscleto When this happens, the heart rate kicks up just a bit to increase cardiac output. If it kicks up too much, the heart can outstrip it's own oxygen supply, resulting in additional injury to the heart. This is part of the reason medication that slow the heart rate (beta blockers) can be helpful adjuncts to preserving heart muscle function and slowing the progression of worstened heart failure.

Second, Mr. Cheney's atrial fibrillation.

The loss of coordinated pumping of the top chambers (atria) just before the lower pumping chambers (ventricles) can lead to 10-20% drop in effective cardiac output in some patients. The irregularity of the heart's rhythm while in atrial fibrillation also causes a loss of coordinated closing of the normally one-way valves that direct the flow of blood through the heart, further compromising the heart's pumping ability. Rate control of atrial fibrillation or the restoration of normal sinus rhythm in the heart are often important adjuncts to the treatment of atrial fibrillation.

Third, is the presence of Mr. Cheney's defibrillator.

Although we do not know for sure, it would not be surprising if many of Mr. Cheney's heart beats are being supplied by his defibrillator's pacemaker feature. Excessive pacing the right ventricle can cause a dis coordinated beating of the lower pumping chambers, resulting in a subtle, but real, fall in cardiac function during paced heart beats compared to beats that are not paced and normally conducted from the top to bottom heart chambers. At some point in the future, Mr. Cheney might benefit, in appropriate circumstances, by adding extra pacing wire to his existing defibrillator system (so-called biventricular pacing) to re-coordinate the contraction process of his heart chambers above and beyond that which can be achieved with medications alone.

Finally, might he have new portions of heart muscle lacking sufficient oxygen?

Not all coronary arteries that might be partially blocked can be revascularized during surgeries or angioplasties. As a result, some segments of heart muscle might not have enough blood flow to maintain proper function, yet have just enough to survive intact. Many of our medications help lower blood pressure to decrease the work the heart has to perform on a beat-to-beat basis, dilate blood vessels to improve coronary blood flow, and work to decrease the negative affects that excessive adrenaline-like compounds can have on the heart's remaining muscle cells. The very fact that his doctors did not feel further invasive procedures were necessary suggests Mr. Cheney's revacularization options are limited at this point.

So given his current setback, what should we expect regarding his prognosis?

Hard to know. But given what I know about the successful management of heart failure these days, I wouldn't count him out quite yet.

-Wes

Wide and Thin or Narrow and Thick

Get your mind out of the gutter. We're talking about defibrillators here.

There's a great picture comparing the size of implantable defibrillators for the management of ventricular arrhythmias and heart failure (and a nice article on the not-so-new wireless telemetry features) over at the New York Times today.

Here's the question:

If you needed a new defibrillator and assuming all implantable devices had identicle capabilities, which would you rather have: (1) a wide and thin device (a la the "Cognis 100-D" device of Boston Scientific's), or (2) a thicker and slightly narrower device (sported by Medtronic's Consulta CRT-D and St. Jude's EPIC-HF devices)?

Go ahead and place your vote in the comments section.

For fairness, here's a side view of the three devices arranged left-to-right as in the prior picture:

(Click to enlarge)
Left: St. Jude; Middle: Boston Scientific; Right: Medtronic

(Industry reps needn't vote. Thanks.)

-Wes

Can an Electronic Pulmonary Embolic Device Help Heart Failure?

The news appeared yesterday, looking surprisingly like the company's press release: A new pressure sensor (CardioMEMS, Atlanta, GA) using the same technology as found in RFID sensors, reported favorable preliminary data after six months that suggested measuring pulmonary artery pressures can help prevent heart failure hospitalizations.

Awesome.

But I wonder, given the information on the lack of utility of more invasive Swan Ganz catheters to change patient outcomes and given the earlier failure of another implanted pressure sensor to reach a real-life significant clinical endpoint, if such a technology will develop. After all, pressure changes in the heart are very dynamic - varying with fluid loads, exercise loads, periods of hypoglycemia or other metabolic derangements, etc. And now this week we learn that kicking heart failure patients out of the hospital too soon once they are admitted might be just as harmful as keeping them a bit longer.

All this before any mention of what a foreign body implanted in the pulmonary artery in patients might bring if people's anticoagulation status were subtherapeutic, even if for a little while (think minor surgical procedure).

So while these preliminary results of the CardioMEMS device were encouraging, they should be taken with a grain of salt (or perhaps, for heart failure patients, a grain of caution).

-Wes

Reference: CARDIOMEMS Press release.

How You Can Help Heart Disease Researchers

... shoot a wild turkey.

-Wes

Waiting, and Hoping, For a Heart

A patient, recently listed for cardiac transplantation, tells his story about being rejected, then accepted, to the cardiac transplantation list:

Next week, I'll check into Mayo, one of the world's premier hospitals, to undergo additional treatment in preparation for receiving a new heart. Since my brain tumor turned out to be benign and my prostate cancer has responded to treatment, doctors there said those issues no longer should disqualify me as a candidate for a heart transplant.

Now that I'm on the list, I am on an around-the-clock standby alert. I have to be ready to be on the operating table within four hours once a compatible heart becomes available. The fact that Chicago is 331 miles from Mayo, in Rochester, Minn., complicates things since I don't have my own charter jet. But the Mayo Med Air charter service could assist me if a commercial flight can't get me there quickly enough.

The challenge now is the wait. The heart I need will become available only when the donor is declared brain-dead and his heart can be taken from him and implanted in me within four hours. I am told the fact my blood type is B positive increases the chances of me getting a transplant quicker, though there are other patients ahead of me.

I had wanted it all to happen at the University of Chicago Medical Center, where world-renowned Dr. Valluvan Jeevanandam, who performed a triple-bypass on me in 2001, has done more than 1,000 transplants. But that hospital takes a more conservative approach to the fact my prostate cancer still is in remission. They wouldn't put me on the transplant list until I had been using an implanted heart pump ''for several years.''

Fortunately, the Mayo Clinic and Northwestern Memorial Hospital feel I have progressed enough in my recovery from the slow-growing prostate cancer to be eligible for a heart now.

With the competetion for patients underway as the large health care system land-grab extends across state lines and overseas (See here and here), have the selection criteria for transplant patients remained a form of rationing or really become a form of marketing?

I wonder.

-Wes

The Rationer

Every cardiac electrophysiologist has been there: a relatively young individual in their 50’s presents to the Emergency Room short of breath, sitting bolt upright in bed and is found to be in congestive heart failure. This is not their first admission; several others have come before and each with a common theme: a positive urinary screen for cocaine.

The EKG shows left bundle branch block. Catheterizations occur, coronary disease absent or moderate, discussions held, patient recommended for defibrillator or biventricular pacing to improve their heart failure after medications have been ineffective for the past year. The person seems sincere – “No more drugs, doc, really” – a line uttered near the conclusion of every one of the patient’s prior hospitalizations, but this time, really, they mean it.

I wrestle with the ethics of the management of these patients every time I’m called to see them. Our guidelines state that ejection fractions of 15% should be treated with defibrillators, especially if no improvement on adequate, aggressive medical therapy. Our guidelines also say that patients with significant social or psychological disease that precludes careful follow-up of their device should not get a defibrillator. Outside the room the decision seems obvious; inside the room after a glance at the eyes of the desperate its another thing entirely - the suffocating feeling of heart failure having taken its toll. The family, at the patient's side, is concerned and wants to help, wondering if there’s anything that can be done.

Will the patient really quit using cocaine? My father’s voice whispers in my head: “What a person has done is an indication of what they will do.” Our business manager wonders why our volumes have slipped recently. What if they die shortly after leaving the hospital suddenly?

No matter what I decide, I will fail it seems. Is the patient sincere or playing me the fool? Can I tell? Put in the defibrillator or pacemaker perhaps it will help. But if I have guessed wrong, then resources are wasted and the patient is exposed to another risk, like infection. Don’t put in the defibrillator and I revoke a lifeline or effective therapy.

On the surface, these decisions should be easy. In reality, they are anything but.

-Wes

MADIT-CRT Meets Primary Endpoint

From a press release, just released:

Boston Scientific Corporation (NYSE: BSX) and the University of Rochester Medical Center today announced that the landmark MADIT-CRT trial has met its primary endpoint. Preliminary results show Boston Scientific cardiac resynchronization therapy defibrillators (CRT-Ds) to be associated with a significant 29 percent reduction (p=0.003) in death or heart failure interventions when compared to traditional implantable cardioverter defibrillators (ICDs). High risk(1), asymptomatic or mildly symptomatic, New York Heart Association (NYHA) Class I and II(2) patients were enrolled in MADIT-CRT. The MADIT-CRT Executive Committee expects to present and publish the trial's full results later this year.


MADIT-CRT, sponsored exclusively by Boston Scientific, demonstrates that early intervention with cardiac resynchronization therapy can slow the progression of heart failure. It is the world's largest randomized NYHA Class I/II CRT-D trial, with more than 1,800 patients enrolled at 110 centers in 14 countries. The trial is being conducted under the leadership of Principal Investigator Arthur J. Moss, M.D., Professor of Medicine at the University of Rochester Medical Center.

The MADIT-CRT trial was designed to determine if combined implantable cardiac defibrillator (ICD)-cardiac resynchronization therapy (CRT-D) would reduce the risk of mortality and heart failure (HF) events by approximately 25%, in subjects who were in New York Heart Association (NYHA) functional Class II with non-ischemic or ischemic cardiomyopathy and subjects who are in NYHA functional Class I with ischemic cardiomyopathy, left ventricular dysfunction (ejection fraction [EF] < or = 0.30), and prolonged intraventricular conduction (QRS duration > or = 130 ms). 60% of patients were randomized to CRT-D and 40% to ICD only.

This news could not come sooner to the medical device industry, but the fiscal realities before us make me wonder if soon we will dealing with medical device benefits managers, just like we're dealing with pharmaceutical benefits managers.

-Wes

Guidelines: Our New Health Care Derivatives Market?

I didn’t attend the American College of Cardiology meeting in Orlando, FL this year, mainly because I am concerned about my ability to pay for my son’s college. I do not quality for financial assistance for his tuition so I cannot afford the luxury of attending every cardiovascular meeting each year right now.

I’m sure many Americans feel the same way, particularly those who have seen their retirement savings evaporate in current economic mess we’re in. People are angry, frustrated, and dumbfounded that our political and financial leadership failed to realize the consequence of their actions when they permitted banks to lend more than they had assets to cover. I mean, who knew, right?

But back in the not-so-distant “glory days” of banking, it was all about “OPM:” other people’s money. You know: using other people’s money to buy a house. Using other people’s money to leverage a shopping center. Using other people’s money to buy some risky asset and sell it to another person so you could all reap some profit. OPM was the financial way to get ahead at almost no downside risk to you. What was not to like? If things went bad, well, it was other people’s money!

And now, in retrospect, we see it for what it was: a time of overindulgence; a time of greed…

… all on the backs of OPM.

Health care is kind of like that, unfortunately. We use OPM all the time when we pay for expensive treatments and procedures and don’t have a clue what it costs. Now, though, we get ridiculously inflated prices sent to us on our “Explanation of Benefits” from our insurer and are all too relieved, yes, relieved I tell you, that OPM has picked up so much of the tab for our health care.

That is, until the OPM goes away and we’re stuck paying the inflated price. Then we’re pissed. And maybe even bankrupt because, unlike the federal government, you and I can’t just print money. It doesn’t work that way. As the old Smith Barney commercial used to say in their thick British accent, “We have to earn it.”

So it was with some amazement and plenty of dismay that I read the very recently-released ”focused” 2009 Heart Failure Guidelines, guidelines that form the cornerstone of the American College of Cardiology and American Heart Association’s Hospital to Home (“H2H” as they call it) initiative to “reduce hospital heart failure re-admissions 20% by 2012.”

It’s a noble initiative, funded by OPM, to demonstrate our cardiology societies deep commitment to help President Barack Obama reduce health care costs.

But like most things with OPM, the details of the cost savings afforded by this initiative are quite vague: especially when the new guidelines include expensive medical devices to be used as therapy now, when in earlier guidelines, there were none.

Not to say that these devices may not have been shown to improve symptoms and longevity in heart failure. They certainly have. And to that extent, these guidelines are exceptional because they put the patient’s health first.

But at what cost?

When we use OPM, we don’t care about cost. OPM will pay for our guidelines’ implementation. Look how we’re helping our patients live longer! OPM will pay for the electronic medical record that will screen the chart for the patient’s ejection fraction and make sure the patient gets the proper test and therapy that is recommended by the guidelines. After all, our goal is to reduce heart failure readmissions by 20% in 2012! No need to worry what it will cost! What’s the risk? Hey, it’s OPM!

And unfortunately, just like the banking fiasco, this OPM will some day run out. The pot of gold is not limitless, but there are few doctors admitting this. We can’t. We are bound by ethics to preserve life that are in direct conflict with our duty to help our patients remain fiscally solvent.

And yet, with our children’s health care and our national economy on the brink, I wonder if we’re not being ethical to our future generations’ patients by not asking these tough questions right now.

-Wes

Helpful Severe Heart Failure Prognosticator

I attended a lecture on severe heart failure this morning by the folks at University of Chicago and they mentioned this helpful website from the University of Washington to determine 1-, 2-, and 5-year mortality in patients with severe heart failure. Plug in things like blood test results, functional class, presence of devices, etc. and it estimates prognosis.

It does not include outcomes in patients with left ventricular assist devices or after transplant, but for doctors seeing severe heart failure patients without these destination therapies, it might patients understand the effect of their medications and devices on their survival.

-Wes

Parsing Heart Failure Treatment Guidelines

Want to know how to treat heart failure? It seems there are plenty of subspecialty groups within our specialty eager to offer guidelines on the proper management of various aspects of heart failure. Consider recommendations for treating heart failure from:

• The Society of Chest Pain Centers


• The Heart Failure Society of America or


• The American College of Cardiology/American Heart Association

Can you venture any guess why so many organizations want to make sure we know how to treat heart failure? I wonder what it costs to create all these specialty societies and who funds their existence. Do all funds come from their members? Or might the pharmaceutical and device industries be supporting a significant portion of one or more of these societies?

Hmmm....

Now, let's see... which heart failure treatment guidelines should I choose?

Eenie, meenie, miney, moe....

-Wes

h/t to the Natrecor rep who visited my office today.

Managing Atrial Fibrillation in Heart Failure

When the number of authors on a paper approach the number of patients in one arm of a prospective, randomized trial... heads up.

I have just finished reading an article that appeared yesterday in the New England Journal of Medicine (Khan MN et al., "Pulmonary Vein Isolation for Atrial Fibrillation in Patients With Heart Failure" N Engl J Med 2008; 359: 1778-1785) regarding the PABA-CHF Trial (Pulmonary Vein Antrum Isolation versus AV Node Ablation with Biventricular Pacing for Treatment of Atrial Fibrillation in Patients With Congestive Heart Failure). It was an ambitious trial that compared atrial fibrillation ablation to biventricular pacing with AV nodal ablation for the treatment of heart failure. At least 29 investigators from 17 different centers randomized a mere 81 heart failure patients with weak heart muscles (ejection fractions <40%) into two treatment groups: 41 for atrial fibrillation ablation and 40 for AV nodal ablation and implantation of a biventricular pacemaker. The pre-specified endpoint was a composite one: improvement on a 6-minute hall walk, improvement on the Minnesota Living with Heart Failure Score, and improvement in ejection fraction. After showing remarkable results favoring ablation in terms of these three measures, the authors concluded that "pulmonary vein isolation was superior to atrioventricular-node ablation with biventricular pacing with heart failure who had drug-refractory atrial fibrillation."

Those are powerful words, especially when they are published in the New England Journal of Medicine.

Given that atrial fibrillation is the most common arrhythmia in man and occurs in probably 10% of the population over 80 years of age and heart failure, too, is an incredibly common disorder, we have to ask ourselves why so few patients were enrolled in this important trial? Was it tough to find appropriate patients willing to submit to the trial? Why were so many centers involved? Might the results have been skewed by sampling error or selection bias?

These are not small questions, especially for a trial studying such an economically and therapeutically important topic.

There are important distinctions between the two procedures studied that were conveniently ignored by the authors. First, atrial fibrillation often requires the use of an anesthesiologist and an impressive array of personnel and equipment (3D mapping systems, ablation equipment, etc) to perform. The average procedure time in many centers averages 4-5 hours and is labor-intensive. Further, earlier studies reporting on the world-wide experience of atrial fibrillation ablation in a much larger group of over 8000 patients demonstrated that 27.3% of patients required more than one procedure to render patients "cured" of their atrial fibrillation and only 52% of patients were rendered free of antiarrhythmic drugs. Further, there was a 6% incidence of major complications from atrial fibrillation ablation when performed in a larger cohort of presumably healthier patients.

Not to say that pacing and AV junctional ablation isn't potentially expensive, too. It is. But usually only one procedure is required. Further, the use of a biventricular pacemaker in these patients with ejection fraction under 40%, rather than a defibrillator, is puzzling since several trials have demonstrated a survival advantage for biventricular defibrillator therapy over biventricular pacing therapy in similar heart failure patients (SCD-HeFT, COMPANION). Were these patient's not really as sick as the authors suggest? Further, was 6 months' follow-up really enough? Why were there no deaths in such a sick patient population in either arm of the trial? Are the data reported in the new trial representative of a more representative population of patients with atrial fibrillation in heart failure?

I worry about studies like this that fail to drill down on such important issues and are published front and center in journals with the impact factor of the New England Journal. While this trial might have profound implications that urge us to delve further into catheter ablation as a means to treat heart failure, to claim that catheter ablation of atrial fibrillation is "superior" to biventricular pacing and AV nodal ablation with such limited data and only 6-months of follow-up is overreaching and might miss important morbidity and mortality endpoints.

-Wes

ICD Shocks - A Blessing or a Curse?

It's all across the media: ICD shocks predict impending death!

Thanks. My patients appreciated these headlines, I'm sure.

But if we're going to tell the 234,000 people who have implantable cardiac defirillators (ICDs) that they're going to die in less than a year after their first shock, shouldn't the media attempt to exercise even a modicum of discernment before going public with these headlines?

First, these findings come from analysis of the Sudden Death in Heart Failure trial (SCD-HeFT) - a well-designed prospective multicenter randomized trial in adults over age 18 which randomized over two thousand patients between three therapeutic treatments for heart failure: (1) conventional medical therapy, (2) converntional medical therapy plus Amiodarone, and (3) conventional medical therapy plus a single chamber, shock-only ICD therapy. The main finding of the SCD-HeFT Trial, in its original form, was that medical therapy (be it with o without Amiodarone), mortality in this group of patients was 7.2% annually. In other words, our best antiarrhythmic at the time, Amiodarone, failed to effect patient mortality. The addition of an ICD for primary prevention of sudden death is this sick population, actually reduced mortality (to 5.5% per year in patients followed for 5 years - a 23% reduction in mortality compared to medical therapies).

So now, is it any wonder that patients who have received an ICD to prevent death on a preventative bases, might just get a shock as their condition deteriorates?

When you can take fairly sick individuals and implant an ICD in them as primary prevention (i.e., they never had an arrhythmia before) and then look at those who develop arrhythmias suddenly, it seems intuitive to me that those patients would be sicker or have had a change in their clinical situation.

The data from the study support this theory. Therefore, evaluating for the development of worsened heart failure or additional ischemic burden might be prudent in these patients, since these causes seemed to be the largest culprits resulting in ICD shocks. Additionally, the study found that patients with either appropriate (shocks for ventricular arrhythmias) or "inappropriate" (shocks for rapid heart rates from non-ventricular causes, like atrial fibrillation onset) have a poorer prognosis compared to those who did not receive shocks, but this also might be a way to risk-stratify the sicker patients of the overall implant population. Does this mean the patients should not receive devices to live longer? Of course not. But there has to be balance to recommending ICDs in the sickest patients, since recurrent shocks can impact the patient's quality of life if they occur frequently. Infrequent shocks, interestingly, did not seem to convey a worse quality of life in this same group as reported (ironically) in the same issue of the New England Journal of Medicine.

Remember that all mortality curves of different therapies that divert favorably from one therapy, will again meet with the alternate therapy some time in the future, since none of us are immortal. ICD's reduce mortality in sick patients with heart failure, but an ICD shock might suggest that, of the group implanted, those patients with shocks have a better indication for the device, since their mortality is higher. It is important, however, to keep in mind who was NOT studied in this paper:

The patient population studied did not include children.

The patients studied did not have cardiac resynchronization devices.

The devices were not programmed for antitachycardia pacing and did not have dual chamber devices which are better capable of detecting atrial arrhythmias.

So before our patients go out to buy funeral plots, let's keep the issues of the risks and benefits of ICD therapy, and the benefit or curse of their shocks, in perspective.

-Wes


Reference: Poole, JE et al, "Prognostic Importance of Defibrillator Shocks in Patients with Heart Failure," New England Journal of Medicine Sep 4, 2008 Vol 359(10):1009-1017.

CMS-Mandated Mortality Data: Whoop Dee Do

I wonder how much money was spent to collect, collate, process and puree the hosptial mortality rates of heart attacks, pneumonia and heart failure in our nation's hospitals, and plotting these data nice little graphs on a website?

I looked at data from most of the hospitals near our facility and was not surprised to find that there was really no big difference in mortality between centers.

So I guess what this data tells us is this: all hospitals are pretty good at collecting data. Whoop dee do.

Now, can we get back to treating patients?

-Wes

Reverse Medical Tourism

There has been a lot of buzz about losing patients overseas to other cheaper venues to deliver care, but we must not lose sight that America still has significant expertise in areas where world leaders come to gain access to our healthcare system, especially when it involves expensive devices or therapies.

Lech Walesa, Poland's former President and Nobel Peace Prize winner who was instrumental at struggling against communism, has sought treatment at Houston's Methodist Hospital for congestive heart failure. The Houston Chronicle reports:

Former Polish President and Nobel Peace Prize winner Lech Walesa is scheduled to be fitted with a pacemaker at a Houston hospital today, a day after tests left doctors hopeful he won't need a heart transplant anytime soon.

Walesa, 64, underwent tests at The Methodist Hospital on Tuesday for advanced heart failure. He traveled to Houston from Mexico, suffering from shortness of breath and fatigue that had caused some doctors to suggest he might need a transplant.

"The struggle with communism took a lot out of my health," said Walesa, speaking through a translator. "But to be part of the discussion regarding remaining questions, I need to be healthy."

Walesa also has significant lung disease, Methodist doctors said.

They didn't rule out that Walesa might eventually need a heart transplant but said such a scenario isn't on the horizon now. Emphasizing that they think Walesa's heart can be strengthened, they said most patients who get a pacemaker don't go on to need a transplant. Only if his heart worsens will they evaluate whether he needs a new heart, they said.

The doctors said they hope Walesa can be discharged from Methodist early next week.

My bet is he won't receive just a pacemaker, but a biventricular implantable cardiac defibrillator in hopes that he'll gain benefit in his left ventricular function and shortness of breath. Data from the MIRACLE trial using biventricular pacing for severe heart failure in patients with markedly reduced ejection fractions and widened QRS complexes demonstrated symptomatic improvement in about 66% of patients. The CARE-HF trial also demonstrated a mortality benefit with biventricular pacing alone, while the COMPANION trial demonstrated superior mortality benefit to biventricular pacing coupled with a defibrillator when compared to beventricular pacing or drug therapies alone.

Who'll pay for this device and his care is another question: will it be former-President Walesa, the State Department, or Methodist Hospital? Will his device be donated by a device company for PR purposes?

I wonder how this is handled in these cases? Should VIP healthcare be different than that received by the average Joe here in the States?

-Wes

UPDATE: 1 Mar 08: An ICD it was.

HeartNet for Heart Failure

Heart failure occurs then the heart pump is unable to meet the body's metabolic needs. It typically occurs from two basic pathologies: (1) dilated cardiomyopathy, where the force of contraction of the pump is diminished and the wall tension stretches the chamber dimensions of the heart or (2) restrictive cardiomopathy, where is heart pump works normally, but the heart is restricted from receiving blood, either because it's muscles don't relax to fill adequately or because the heart is encased in a non-compliant shell that restricts filling.

To me, I just don't see how the HeartNet device, a nitinol wire mesh that encases the heart and will ultimately be surrounded in fibrous tissue, won't just convert the pathophysiology of a dilated cardiomyopathy into that of a restrictive cardiomyopathy...

A 6-month trial seems much too short to test the long-term safety of this device. After all, the wire mesh puts a whole new meaning to "a porcelain heart."

-Wes

Reference: Early, industry-sponsored results.