What New Pacemakers that Can Be Used with MRIs Mean for Consumers

This week Medtronic will begin shipping to hospitals in the United States the first pacemaker approved by the FDA as safe for most MRI scans.  For consumers, it is a significant step in what is expected to be a wave of new MRI-compatible implanted cardiac devices. 

But this is an example of one technology chasing another and the one being chased, the MRI scanner, is changing and is a step ahead of the new line of pacemakers.  The pacemaker approved for U.S. distribution is Medtronic’s first-generation pacemaker with certain limitations, while its second-generation MRI-compatible pacemaker is already in use in Europe where approval for medical devices is not as demanding as it is in the U.S.  So let’s check out what this is all about — what it means now for current and future heart patients and where it may be headed.

We are all born with a natural pacemaker that directs our heart to beat 60 to 100 times a minute at rest.  The pacemaker is a little mass of muscle fibers the size and shape of an almond known medically as the sinoatrial node located in the right atrium, one of four chambers of the heart.  The natural pacemaker can last a lifetime.  Or it can become defective.  And even if it keeps working normally, some points may not function well along the electrical pathway from the pacemaker to the heart’s ventricles which contract to force blood out to the body.  

Pacemakers

Millions of people in the world whose hearts beat too fast, too slow, or out of sync because their own pacemaker is not able to do the job right, follow their doctors’ recommendation to get an artificial pacemaker connected to their heart to direct its beating.  The battery-run pacemaker in a titanium or titanium alloy case the size of a small cell phone, (why can’t it be the size of an almond?) is implanted in the upper left chest, just under the skin, with one or two insulated wire leads connecting to the heart.  It can be programmed to run 24/7 or to only operate when the heart reaches a certain state of irregular beating.

With some rare exceptions, there are few drawbacks to having a pacemaker.  But you need to avoid powerful magnets.  No problem being around your microwave or computer and when you talk on a cell phone, just hold it on the opposite side of your body from the pacemaker. But it’s best not to walk through airport security scanners, and instead submit to a body search and hand-held scanner.  The biggest “no” that accompanied your pacemaker is to avoid any magnetic resonance imaging (MRI) exam. That may not have seemed like a problem at the time you agreed to get a pacemaker implanted.  But we never know what turn our health may take.  And there are many conditions for which doctors seek to learn more through an MRI scan that uses a very strong magnet, radio frequencies, and a computer to produce images of soft tissue, bone, and blood vessels.  Because it produces such detailed images of soft tissue, it is frequently used for organs of the body such as the liver, bowel, pancreas, kidneys, brain, and spinal cord. The MRI, which does not require ionizing radiation, is also used in diagnosing and staging cancers and pinpointing heart problems.

But, only a few medical centers in the United States and maybe 10 worldwide have the ability to perform MRIs on patients with the pacemakers now in use. Most people wearing pacemakers who need an MRI have been unable to get one.  Pacemaker companies advise against it and the American Heart Association issued a statement in 2007 that discouraged doctors from performing MRIs on pacemaker patients unless the need for the MRI was compelling enough to warrant the risk of the exam.  Medicare will not pay for an MRI done on a patient who has a pacemaker.  There have been a few reported deaths of pacemaker patients who got an MRI and the risks include movement of the pacemaker and re-setting of the beating pattern. The wire leads are insulated except for the exposed metal tips that screw into the heart and under the tremendous vibrating of an MRI scanner that goes on for 30 minutes to an hour and a half during the course of an exam, the tips can heat up to the point that they can burn the flesh.

So getting a pacemaker that is safe to use during an MRI is a big deal for heart patients. “This is an important step in the right direction,” says Dr. Bruce Wilkoff, president-elect of the Heart Rhythm Society and Director of Cardiac Pacing and Tachyarrhythmia Devices at the Cleveland Clinic.  Wilkoff was the primary investigator for the EnRhythm MRI clinical trial that was the basis for the FDA’s approval of the first U.S. MRI-compatible pacemaker and he presented the study’s findings to the FDA.  The study involved 464 patients in an international multicenter trial. Changes were made to the pacemaker, its leads, and the programming system, Wilkoff said, to address the potential for interfering with the device’s pacing, overstimulating the patient, and overheating the tip of the leads.     

Revo’s Limitations

However, this Medtronic first-generation Revo MRI SureScan Pacing System has some significant limitations.  

1.  The MRI-pacemaker is for new heart patients.  Patients who already have a pacemaker can not get this new model unless they undergo the risky procedure of having their old pacemaker completely removed. Usually, when it comes time to replace the battery in a pacemaker (about 5-7 years), the metal case containing battery and circuitry is detached from the leads, and a new model device is hooked up to the leads.  But doctors generally consider it too risky to remove the old leads from the heart for fear of tearing the heart or the veins through which the leads are inserted into the heart. Part of the design of the Revo pacemaker is its new leads and so they must be the leads that connect the pacemaker to the patient’s heart.

2.  Patients must have the Revo pacemaker implanted for 6 weeks before receiving an MRI.

3.  The Revo pacemaker requires a certain position of the patient inside the MRI tube so as to avoid most chest scans.  This is to prevent overheating the metal tips of the leads that are attached to the heart. So heart scans are forbidden with this first-generation model.

 4.  And Owen Faris, senior scientific reviewer for the FDA, explains that the new pacemaker won’t work for all types of MRI scans and won’t work in all MRI scanners.  In his words:In addition to the chest scan exclusion, there is a restriction on how much radio-frequency energy can be deposited into the body by the scanner. MRI scanners have two operating modes for most clinical applications. ‘Normal operating mode’ is how the scanner is normally programmed and that mode restricts the scanner to lower-energy scans (less than 2 Watts per kilogram). This is sufficient energy for most clinical MRI scans. However, for some patients and for certain scans, more power is needed. In those cases, the MRI scanner is placed in ‘First level control’ mode, which allows for greater energy deposition (up to 4 Watts per kilogram). For patients implanted with the REVO MRI pacemaker, those patients are not allowed to have these higher energy scans. 

MRIs for these patients are also restricted to only allow use of 1.5 tesla MRI systems. “Tesla” is a measure of the strength of the magnetic field.

5.  Medicare does not now pay for MRI scans on a patient who has a pacemaker.  Medtronic spokesperson Wendy Dougherty says that Medtronic will not speculate on whether Medicare will cover MRIs done on patients wearing the new Revo pacemaker.  The federal agency is considering a petition from a physician to cover MRIs done during an investigational study to determine the risk of MRIs involving pacemakers already in use.  During the comment period for this request, Medtronic asked Medicare to restrict MRI payment to patients wearing pacemakers approved by the FDA for use with MRIs.  Medicare’s decision is due by March 1.  Patients on Medicare would be wise to check on whether Medicare will pay for their MRI before getting the test which costs between $1,600 and $3,500 at different medical centers and offices.

What to Expect for the Future?

Approximately 1.5 million Americans have cardiac pacemakers. Worldwide, 5 million people are implanted with a pacemaker or implantable cardioverter-defibrillator (ICD) that shocks a chaotic shaking heart into normal working order. 

Europe, where the approval process of medical devices is less strict than in the U.S., began using Advisa, the Medtronic second-generation MRI-compatible pacemaker, early last year.  The Advisa has no restrictions on chest scans and Medtronic says this model is in clinical trials in the U.S.  

The cost of a pacemaker is $5,000 to $10,000 (just for the device, not counting the much larger charge by hospitals and physicians for implanting it) and Medtronic says the Revo pacemaker will be in that range.  Tao Levy, Collins Stewart market analyst, says that the Revo will cost about $1,000 more than a standard pacemaker and will boost Medtronic’s revenue in the U.S. by $50 to $60 million.  Boston Scientific and St. Jude Medical are developing MRI-compatible pacemakers and other implanted devices and as other companies bring these products to market, the use is expected to grow.  

But “not over the near-term,” says Levy.   “In a recent survey of electrophysiologists (who put pacemakers into people), the expectation is that Medtronic’s MRI-conditional pacemaker would comprise around 20% of the pacemaker implants. So the vast majority will still be regular pacemakers. Over time this might change.”

“Expense and the need for proprietary leads and the coordination of personnel may prohibit widespread adoption,” says electrophysiologist Dr. Westby Fisher, clinical associate professor of medicine at the University of Chicago’s Pritzker School of Medicine.  He is a member of the Speaker’s Bureau for both Medtronics and Boston Scientific.  “Monitoring in the MRI by EKG (an electrocardiogram of the heart) is required and not all MRI machines are equipped for this feature.”  Using a scanner that does not have EKG capability will call for scheduling a technician or a company representative to be present when the lengthy MRI test is performed, he says, which will mean “scheduling challenges due to logistics of having the right people in the right place at the right time.” 

The technology of pacemakers is chasing the technology of MRI scanners.  “Right now the issue is that Medtronic’s device is designed only for 1.5T powered MRI systems and there is a move to higher-powered MRI machines (3T) for which the Revo is not indicated,” Levy says. The 3T MRI scanners produce clearer images in less time.

Nevertheless, cardiologists and electrophysiologists, and market analysts think that MRI safety will spread beyond standard pacemakers.  “I think eventually all implanted cardiac devices will be MRI compatible,”  says Dr. Henry Halperin, a Johns Hopkins professor of medicine who is Director of the Cardiology Bioengineering Laboratory.  Not that Hopkins is in any hurry.  It is one of the very few centers in the United States and in the world to run MRIs on patients with standard pacemakers and has done over 800 with no complications, Halperin says.  

To accomplish this, he says they re-program the patient’s pacemaker into a “safe mode” so that the force of the MRI can’t make the pacemaker send out electrical impulses that are too fast or too slow, and they reduce the MRI scanner’s power by about half.  But he acknowledges that “there are still risks” and each decision to perform an MRI on a patient with a pacemaker comes down to this point:  “The risk of doing the scan vs the risk of not doing the scan.” That’s why Halperin says “All pacemakers should be MRI-compatible and I think they will be.”

“I expect MRI compatibility will become more commonplace in implantable cardiac devices and may become the standard,” agrees Dr. Thomas Callahan, an electrophysiologist at the Cleveland Clinic.  “A lot of people are hoping an MRI-compatible ICD will come along.” 

“That is the plan,” Levy says, both for ICDs and for a special kind of pacemaker used for cardiac resynchronization therapy (CRT) which resynchronizes a left ventricle that is not beating normally.  “But in order to be successful, they will need to avoid any disadvantages (like a stiffer lead) and not have restrictions that might be confusing (having an MRI-safe pacemaker, but not realizing that you are getting scanned in a more powerful machine than the pacemaker was originally tested in, designed for.”)

So, it seems, a good start, but there is lots of technical development to go.  Will  MRI-safe pacemakers eventually replace all other pacemakers? 

“Most likely,” says Wilkoff.  “But the transition will take up to 10 years or so.” 

Note:  A Medtronic spokesperson who initially said clinical trials for the Advisa pacemaker are underway in the U.S. now says, “Medtronic does not have any FDA-approved clinical trials in the U.S. for Advisa.” 

Heart Sense Helpathon: Sixth in a Series

Mini Exercises(Beware of Sitting for Too Long at One Time)

I can’t leave our discussion of exercise without talking about mini exercises throughout the day to counteract our terribly sedentary lifestyles.  I confess I sit far too long every day.  I, like Peter Janiszewski, have to make a plan to change that.  And so do you.  Almost all of us sit too long.  Think about it.  We sit at our computers to write, do research, communicate by e-mail, Twitter, Facebook, and more, and play games.  We sit to eat.  We sit to read.  We sit driving in our cars and on other transportation. We sit to chat on the telephone and when friends come over to visit.  We sit to watch movies and TV shows.  I am a writer and so I sit a lot at the computer.  When I was writing the heart failure book with Edward Kasper, both of us considered investing in a stand-up desk because, frankly, the part of your body you sit on for long times can start to go numb, and it is just not good for your circulation to sit for long periods.  But the health effects of being sedentary go farther.

Who is Peter Janiszewski, you may ask?  He is co-author with Travis Saunders of a delightfully written and highly informative and helpful blog called Obesity Panacea which you can find here at the PLoS (Public Library of Science) blogging network.  Please read their series of excellent blog posts about how sitting long periods harms your health and may cut short your life.  Break up your sitting pattern, they urge, by frequently getting up and doing mini exercises and other activities.  

Helpathon

This get-you-to-your-feet set of articles begins with a five-part series on sedentary physiology by Travis Saunders. In Part 1, Travis really got my attention with this simple fact: “sitting too much is not the same as exercising too little.”  He says he borrows this line from Marc Hamilton, one of the leading researchers in sedentary physiology.  But I heard it on Obesity Panacea. 

In Part 2, he reports that a study of over 17,000 Canadians found that “individuals who sat the most were roughly 50% more likely to die during the follow-up period than individuals who sat the least, even after controlling for age, smoking, and physical activity levels.”

In Part 3 Travis discusses the benefits of taking breaks from sitting.  He reports on another study that found “The greater the number of breaks taken from sedentary behavior, the lower the waist circumference, body mass index, as well as blood lipids and glucose tolerance.”

Some readers responding to this popular series wondered how much sitting time was too much and whether it helped enough just to get up and go do some chore or whether you need to exercise every so often throughout the day.

Peter Janiszewski responded to his blogging partner with a not-to-be-missed post My Home-Based Mini-Exercise Regimen.  

“Essentially, I decided (completely arbitrarily) that I would do mini exercise breaks throughout my workday, with the daily goal of reaching 450 repetitions of whatever random movement popped into my head at each break.”Peter got an enormous reader response to that blog post and followed up by sharing suggestions from readers.  For instance, reader Dirk Hanson said this:  “I’ve started arranging things in a way that requires me to bounce up from my desk at various intervals for 15-minute chore breaks–watering all the house plants, filling the bird feeders, vacuuming one room, making coffee, getting something out of the garage, taking a brief walk, whatever.”I am so impressed with this fine blog and its authors.  Here, reprinted from their PLoS blog site, are bios for Travis and Peter.  Please visit them often. A good prescription for your health.

As for me, I will break up my long sitting periods.  But, I warn you, it’s hard to do, at least at first.  I want to turn now to finishing the syllabus for the spring writing course I teach.  But I would need to keep sitting here to do that and I can’t because now it’s time to get up and do marching exercises or use my leg press or go play with the dog or walk through the house looking at the ceilings to see if there are any cobwebs in the corners.  Jeez, I’ve got to work on the balance of all this. Up, down.  Concentrating, distraction.  Writing, not writing.  But, otherwise: Better health, not health?

Hey, it’s cheating to get up from sitting and go to the fridge.

Heart Disease Deaths Decline 27.8% — Now let’s do our part and commit to healthy living

Heart Disease Deaths

 We are continuing to put ourselves at risk for getting heart and circulatory diseases through improper diets, lack of exercise, and even the continuation of smoking. “As risk factors for coronary disease increase in a population, we also expect the future incidence of coronary disease to increase within the population. Control of risk factors is critical in the prevention of coronary disease,” said Edward K. Kasper, clinical director of cardiology at Johns Hopkins Hospital and co-author with me of Living Well with Heart Failure, the Misnamed, Misunderstood Condition. And Daniel Levy, director of the Framingham Heart Study says that with regard to heart failure, “in the majority of cases, it is preventable.”  That is an amazing statement.
Dr. Roger urges people to take responsibility for their risk of getting cardiovascular diseases through personal “risk factor management.”

Most of us know what to do.  We just need to start doing it. 

We need to lose weight. Two out of three of us should lose weight! Even losing a little weight can improve your chance of avoiding heart disease. We need to control our blood pressure and cholesterol.  One-third of adults have high blood pressure but only 48% of those aware of their condition have their blood pressure controlled to a safe level. We need to eat less sodium, less saturated fats, and NO trans fats. We need to eat whole grains, fruits, vegetables, and unsaturated fats. We need to exercise regularly, and some of that exercise should be vigorous enough to give our hearts a workout, which means breaking into a sweat or increasing our heart rate and starting to breathe faster and heavier. Stop smoking and if you have not started, don’t smoke.

I am going to renew my commitment to heart-healthy daily habits and I ask you to join me.  A colleague on Twitter got in touch just yesterday to say she has put on some weight and do I have advice.  Well, I have put on some weight, too.  I need to do better at eating right every day and doing the right exercises every day.  Let’s make this commitment together.  As winter approaches, it is all the easier to fall into bad habits of not exercising, sitting too much, and eating too much.  In the coming weeks, I’ll discuss our goals in more detail.  Adopting these healthy daily habits is the best present you could give your loved ones this holiday season.

Heart Failure a scary name that doesn’t make sense

For the last week, I have been mulling over the name heart failure, questioning why the collective conditions that bear its name ever got such a name, and looking into the very murky area of heart failure death statistics.  , many of us who were shocked to get the frightening diagnosis of “heart failure” do not have hearts that have failed.  We got treated, some more quickly than others, and went right on with our lives.  Others are not so lucky and die of heart failure, sometimes suddenly and sometimes after years.  Trying to discuss what heart failure is getting very difficult because it is not a disease, it is a syndrome brought on by many different underlying causes including coronary artery disease, disease of the heart muscle, high blood pressure, valve malfunction, poor artery connection, alcoholism or drug abuse, and certain chemotherapies, to name just a few.  And heart failure affects the heart in different ways. 

The term heart failure covers conditions ranging from no symptoms to severe shortness of breath from fluid collecting in the lungs, swelling of the abdomen, ankles, and feet, and fatigue even at rest — see American College of Cardiology/American Heart Association Stages of Heart Failure and New York Heart Association Classification of the stages of heart failure here.

Somehow the field of medicine has allowed so much under the same umbrella of heart failure that discussing heart failure becomes confusing for physicians and patients.  “Skilled clinicians have difficulty with this and most fumble around,” James B. Young,  Professor of Medicine & Executive Dean, Cleveland Clinic Lerner College of Medicine, told me in an e-mail. So trying to write about what medicine calls heart failure, what’s wrong with the name, and what, if anything, to do about it is challenging. 

Then yesterday something happened that clarified the picture for me.  I knew when I got a pit bull from a rescue organization a year ago that he had a kidney problem and I agreed to take him because he had a terrible earlier life that included months spent in a cage that nearly drove him insane.  I wanted to give him a loving home for whatever time he had, a year or two.  He arrived with skin hung over his skeleton, but he had a great appetite and put on weight, filling out very normally, enjoyed his walks, and loved to play catch-me-if-you-can with a nylon bone or an old house shoe in his mouth every time one of us who had been out during the day returned home.

Heart Failure a scary name

Then in the last week, things changed.  He started throwing up and for the last four days he could not keep anything down.  He was noticeably losing weight.  His very thick neck thinned in a matter of days and his spinal column began protruding.  He would only go one block on a walk before turning to come home.  He quit playing catch-me.  He lay constantly on his bed or, at night, my bed.  Monday we took him to the vet and yesterday morning we got the results of his blood tests.  His blood urea nitrogen (BUN) was 237, the highest my vet said he had ever seen. 

A normal BUN level in a dog is 6 to 31, the vet said.  A high BUN level indicates that toxins are not being removed by the kidneys.  My dog was in kidney failure, my vet told me.  That was the first time I was told he was in kidney failure.  And those words made a lot of sense.  Teddy was not in kidney failure for the last year, only for the last few days.  His kidneys indeed had failed.  If he were a person, he would have to either go on dialysis or get a kidney transplant in order to live.  Teddy was miserable, had noticeably lost weight quickly, and also had grown a tumor which I would have wanted the vet to operate on, were it not for the kidney failure.  The dog doctor said that the anesthesia itself could be so toxic on the kidneys that it might kill Teddy.  And so at noon, with tears and heavy heart, to end his suffering, we had him put to sleep. 

Yesterday afternoon in a house far too quiet, I tried to return to writing.  And then I got to thinking.  Kidney failure.  Heart failure.  The two terms sound alike but are used by doctors for very different health problems.  But why?  In kidney failure, the kidneys don’t work anymore.  It’s so obvious you hardly need a blood test to prove it.  As with heart failure, many different things may have caused it, and the kidney failure may have come on gradually or acutely, but kidney failure is kidney failure.  It means what it says.  Contrast that with heart failure, where most of the time the diagnosis is made, the heart is still working. 

It has not failed, although something about the heart is not normal and may have begun causing symptoms.  But if the heart had failed, an analogy to kidney failure would mean that a person with heart failure would have to regularly be on a machine that circulates blood throughout his system or get an implanted device that takes over at least partial function of the heart or get a heart transplant in order to live.

Heart failure is an appropriate name for patients who are now said to be in “end-stage heart failure” in which they have only months or less to live unless they get mechanical aid to take over part or all of their heart function as in a ventricular assist device ((VAD) or get a heart transplant.  But I submit that this is the only true heart failure.  Just drop the first two words, because “end-stage heart failure” is redundant.

Heart failure is not an appropriate diagnosis for people who have no symptoms or who have symptoms that can be improved or even disappear under treatment.  

Why does it matter what conditions are called heart failure?  Why does it matter how many people hear their diagnosis is heart failure?  Shouldn’t I just leave the naming of medical conditions and diseases to doctors and mind my own business?  What’s in a name?  

Here’s why it matters.  As I consider the words heart failure, and the effect those two words can have on the person diagnosed with it, I am reminded of an event that happened to me while I was in college.

Occasionally someone can say something to you that is so scary it seems it might scare you to death.  Near final exam time, I quite suddenly came down with a paralyzing illness, transverse myelitis, and had the misfortune of being hospitalized where doctors had never seen a case of transverse myelitis, did not recognize it, and decided to operate on this viral illness, looking for an obstruction they did not find. While inside me for “a look-see”, the general surgeon cut into inflamed tissue to take out my healthy appendix.  Already very sick and rapidly becoming paralyzed, I nearly hemorrhaged to death from the surgery and was placed on the hospital’s “critical list” of patients who may die.

While I knew how terrible I felt, neither doctors nor family had let me know how very sick I was.  The sight of my 8-year-old blonde cherub-faced nephew cheered me. This was his first visit and I could tell he was excited about something and wanted to share it with me.  How sweet.  He came right up to my bedside. 

“Hey, Aunt Mary,” he gushed, “Do you know you’re on the CRITICAL LIST?”  

AAAAAAhhhhhh!  Terror hijacked my entire body. 

No, Gary, nobody had told me I’m on the CRITICAL LIST.  Who let this kid in the room?  There’s a reason why children shouldn’t be allowed in hospitals.  I couldn’t speak.  A numbness began in my feet and crept up my legs. 

This story, still so vividly recalled, comes to mind as I write about the diagnosis of heart failure because like those other two words critical list the term heart failure is very frightening to hear.  And much of the time heart failure is an unnecessarily scary diagnosis.  Every day thousands of people are frightened to learn they have heart failure.  I was.  

Never having had any known heart problem, I sat in shock when a cardiologist told me in 2003 that I had HEART FAILURE.  When a doctor tells you that, it’s like being told you have end-stage cancer. You know nothing about heart failure, probably have never heard of it, and it sounds quite fatal.  I went home and made out a will, then spent several months educating myself about heart failure and going from doctor to doctor, searching for the right treatment, afraid that I could drop dead at any moment. 

It’s one thing for an 8-year-old kid to scare a sick patient, quite another for a grown-up doctor to do it.   I realize that there are many times when a doctor has to give a diagnosis to a patient that is frightening and I appreciate that this is emotionally hard on many caring doctors. 

But, doctors, do you ever wince when you tell a patient she has heart failure when you believe that proper medications may make a big change in her symptoms?  I ask doctors to be more aware that a diagnosis is a two-way act of communication:  It words the physician says and it is worded the patient hears. One is just as important as the other.  Your diagnosis is not complete, doctors until the patient has heard it.

I was not able to find out who originated the term heart failure as a diagnosis.  Renowned cardiologist historian Arnold M. Katz, who is the most likely source, told me “It will be hard to find out who (first) used the term heart failure as most of the early texts were written in Latin, a language I do not speak.”  But the name got into the medical literature long ago before modern therapies were available.  

I wish the medical community would find a new term — how about Heart Flux or Heart Fatigue or Heart Stress Syndrome — or multiple terms for diagnosing this condition that now wears one inappropriate label disturbing and confusing for the person diagnosed and those in the labeled person’s close circle at home and at work. How much easier and more exact to tell your patient and for him to hear the words, “Your heart is in a state of flux/or fatigue/or stress/ and I have some medications to give you that have a good chance of helping it a lot” instead of “You have heart failure.”  

Until then, I hope that, when pronouncing the scary words “heart failure” to a new patient, doctors will take the time to explain that, much of the time, it’s not what it sounds like.  

Heart Failure Death Statistics: Don’t believe what you read on the internet

In its website section on heart failure facts, the Heart Failure Society of America directly faces the question all people with heart failure and their loved ones desperately want to know:

“Q: What is the prognosis for a patient with heart failure?

A: Less than 50 percent of patients are living five years after their initial diagnosis and less than 25 percent are alive at 10 years. Poor prognosis can be attributed to a limited understanding of how the heart weakens and insufficient private and government funding.”  

I was startled to see those grim statistics on the HFSA website, given that clinical studies published in peer-reviewed journals have shown that ACE inhibitors and beta-blockers prolong the lives of people with heart failure and in the last decade those medicines have become standard recommended therapy.  Implanted defibrillators known as ICDs that prevent sudden death by shocking the heart when the heart goes into a chaotic rhythm, cardiac resynchronization therapy (CRT) which corrects abnormal beating of the left ventricle, and other effective treatments have also grown in use in the last decade.  

I also felt uneasy reading the HFSA answer that tied “poor prognosis” to “insufficient private and government funding.”  That seemed to have a political tinge to it, out of place in an answer directed to worried patients and family members about how long someone can live with a diagnosis of heart failure.  Many conditions can cause heart failure in which the heart is not pumping out enough blood to meet the needs of the body. 

When a patient with heart failure has a poor prognosis, there can be any number of reasons, including these:  the doctor did not order the most effective medications that could have prevented progression of the heart failure, the patient didn’t faithfully take the correctly prescribed medications either because she couldn’t afford them or was not reliable, the patient didn’t observe a low-sodium, low-fat diet and get regular exercise, and, frequently, the patient has other significant health problems. 

Also, despite excellent care, a patient may have a heart too damaged from a heart attack or from a genetic malfunction to be able to successfully pull out of heart failure.  But I doubt any doctor ever tells a patient’s family, “Your husband and father is in late-stage heart failure and has only a few months to live because the government didn’t fund enough grant money for heart failure research.”

Working on the assumption that a journalist or a person with heart failure or, for that matter, any member of the public could ask what HFSA’s source is for its grim prognosis and get an answer, I contacted HFSA.  I sent an e-mail to Cheryl Yano, HFSA longtime executive director, explaining that I was writing this blog report on heart failure death statistics, and then a second e-mail, but did not get a reply, so I called.  She would not talk to me. 

Loreen Anderza, HFSA administrative assistant who answered the phone, said there is no specific source for the HFSA statement on how long people with heart failure can expect to live.  It is “a consensus of experts in the field.  They have no source for it,” she said, after putting me on hold to speak to Cheryl Yano.  I asked if Ms.

Yano would talk to me about whether or not heart failure is becoming more of a chronic condition that can, for most people be managed, and Ms. Anderza said that Ms. Yano is not the right person to talk to because she is not an MD.  I asked who at HFSA I could talk to and she said Ms. Yano had no one to recommend.  Ms. Anderza said that everyone uses the same numbers and suggested that I ask the American Heart Association if they know what the source is for the scary prognosis that is on the HFSA website.

Instead, I contacted the president of HFSA, Barrie M. Massie MD, Chief of the Cardiology Division at the San Francisco Veterans Affairs Medical Center who responded in an e-mail:

“This is out of date.  It is based on Framingham data and several trials largely dating back 10-20 years.” 

The Framingham Heart Study

The Framingham Heart Study supported by the National Heart Lung and Blood Institute, part of the National Institutes of Health, is an ongoing project begun in 1948 that has enrolled over 14,000 members of three generations and periodically issues reports about the risk factors for developing heart disease.  The study here has provided many important findings including the risk of cigarette smoking, cholesterol, high blood pressure, and much more.  But the study is set up to find information on all forms of heart disease and its ability to track heart failure patients is quite limited. 

Original Framingham participants are seen at a clinical visit every two years and their offspring are seen every four years. “Participants with heart failure often undergo treatment between a clinic visit and before death and these interventions are not captured in our clinic visits,” said Daniel Levy MD, director of the Framingham Heart Study. Therefore his report did not have information on what treatments heart failure patients who died were using.

Many sites on the internet including HFSA that offer a prognosis for heart failure base their projections on a Framingham study published in 2002 in the New England Journal of Medicine that used data going back 15 to 20 years ago.  Even the American Heart Association’s Heart Disease and Stroke Statistics 2010 Update quotes the Framingham death rates for heart failure. 

I examined the Framingham report on heart failure and found that the prognosis the study gives is based on a very small number of deaths — 86 deaths of men and 80 deaths of women.  This study occurred before the modern therapy of ACE inhibitors and beta-blockers which are proven to prolong life in heart failure.

The Framingham study followed 323 people (145 men and 178 women) who developed heart failure between 1990 and 1999.  Dead in five years were 59% ( 86) of the men and 45% (80) women.  The study did not learn whether these men and women died of their heart failure or of some other cause, said Dr. Levy, lead author of the report that appeared October 31, 2002, in the New England Journal of Medicine.            

The Framingham study on heart failure deaths also looked at deaths in  decades going back to the 1950s and said that “Overall, there was an improvement in the survival rate after the onset of heart failure of 12 percent per decade.” 

In the decade since the Framingham study of the 1990s, “there is optimistic evidence that we have improved treatment for people with heart failure,” Dr. Levy said in a telephone interview, though he would not estimate by how much.

Other Clues to Heart Failure Prognosis

I talked to eight nationally known cardiologists in preparing this article, to get a sense of where heart failure stands as a treatable condition vs a progressively fatal condition.  Not all are quoted.  One cardiologist who asked not to be identified because he knew what he was saying was “controversial” commented on the annual AHA Heart Disease and Stroke Statistics Update:  “These are not really current data.  They are estimates extrapolated from NHANES (National Health and Nutrition Examination Survey) … with changes based on changing size and age of the population. 

Hence, they are unlikely to be accurate and will not reflect real or measured changes.  Consider them propaganda for those that thrive on high event rates. These data are useful for those seeking investment in development programs for heart failure treatment.”  NHANES, a part of the Centers for Disease Control (CDC) surveys about 5,000 people in the United States a year and estimates results for the national population. The AHA Heart Disease and Stroke Statistics 2010 Update here bases its estimated incidence of heart failure and prognosis of life expectancy largely on NHANES and the Framingham Heart Study of the 1990s.

One clue to how long people with heart failure live comes from clinical studies that try to prove a new drug or device is better than standard care at prolonging lives.  Both Dr. Massie and Alice Macette MD, chief of the National Heart Lung and Blood Institute’s Heart Failure and Arrhythmias Branch, point to the improving life expectancy for people in the placebo group of these trials — those who are on the existing standard therapy against which the new treatment is being tested.  

“For instance in the SOLVD study of 1991 which first showed the benefit of ACE-inhibitor drugs,  the three-year survival rate was about 65% in the group receiving placebo, whereas three-year survival rates were approximately 80% (or greater) in two studies (one on eplerenone and one on use of CRT for mild to moderate heart failure)reported this week at the American Heart Association here and here dealing with heart failure patients of varying degrees of severity,” said Dr. Macette.  In fact, the improvement of heart failure outcomes has helped set the bar higher for any new therapy being tested,” she said.

Dr. Massie agreed.  “If you compare the placebo groups over time there is a substantial decline in the placebo group mortalities,” he said.  “Used to be up to 20% per year and now is close to 8% per year.  This low (death) event rate has made the conduct of clinical trials hugely expensive, which is why there are far fewer of these and even fewer positive ones.”

I also asked cardiologists to judge from their own experience how treatable heart failure has become.  Edward K. Kasper MD, director of clinical cardiology at Johns Hopkins Hospital and a specialist in heart failure, (disclosure:  I co-authored Living Well with Heart Failure, the Misnamed, Misunderstood Condition with him) said “I expect most to improve with modern therapy for at least some period of time – say 75%.”

“Indeed there have been great advances and people do live longer, but progress has been slow and we need to do better,” said Dr. Massie.

I asked Mariell Jessup MD, chair of the American College of Cardiology/American Heart Association Guidelines for the Diagnosis and Management of Heart Failure in Adults found here if heart failure has become more of a chronic condition:  

Question:  “From your own patient experience, do you find that most people diagnosed with heart failure will be able to manage their condition, keeping it from advancing, or even improve with the right treatments?”

“I agree,” she replied. She pointed to a study of 2,029  people taken from the general population in Olmsted County, Minnesota.  Study participants were classified according to how sick they were.  Since this was a random sample, it included healthy people called stage 0.  Stage A had risk factors for heart failure, stage B showed cardiac structural or functional abnormalities found by testing but were not experiencing symptoms, stage C had symptoms of heart failure, and stage D had end-stage heart failure.  Survival at 5 years was 99% in stage 0, 97% in stage A, 96% in stage B, 75% in stage C, and dropped to 20% in stage D, by far the smallest group with only 5 people. The study published March 12, 2007 online in Circulation can be found here.  “It is only those patients who present with intractable symptoms that do poorly,” Dr. Jessup said.

Needed:  A Huge National Prospective Study or a National Registry

The Minnesota study, though still small numbers, gives some window into a more accurate prognosis for heart failure.

But the only way doctors and patients and their families will get a really accurate handle on prognosis with current therapies is if a huge prospective study is undertaken or at least a national registry that includes tens of thousands of patients seen at many academic centers and those seen in the community by both cardiologists and general practitioners. The study or registry should include a variety of races and ethnic backgrounds, male and female.  Much could be learned by such a study, including this information:

  • modern survival rates and deaths due to heart failure and not some other cause
  • percent of people with heart failure who die suddenly from ventricular fibrillation
  • possible geographic differences in death rates
  • treatments patients were on up to and at the time of death
  • a library of data on the genetics of heart failure

Such a study or registry should have no funding from pharmaceutical companies.

Just before publishing this article, I checked the website of the Heart Failure Society of America.  The unnecessarily scary prognosis for heart failure is still there with not even an asterisk explaining how old and outdated the data are on which it is based.

Heart Sense Helpathon: Fifth in a Series

In earlier posts in this blog we have discussed stretching exercises, aerobic exercises such as walking, biking, running, and balance exercises.  A fourth type of exercise that many people diagnosed with heart failure as well as those in good health can do safely is resistance exercises which build muscle endurance by challenging targeted muscles through a certain number of repetitions.  

But be sure to avoid straining. 

You are not the candidate to crouch and stand while hoisting heavy barbells over your head.  Before you start, look at these tables of contraindications established by the American Heart Association Science Advisory Committee which are at the end of this blog post.  I suggest you take them to your cardiologist and also show them to the rehabilitation specialist or trainer who will devise your exercise routine. The full article is in the medical journal Circulation here.

Usually, you will start with one set of repetitions, then in future sessions go to two sets with a brief rest in between the two sets.  Some examples of resistance exercises:

  • knee extensions and hamstring curls done with weights strapped to your ankles
  • knee extensions and hamstring curls done sitting on a machine such as a home gym
  • lifting your hips up off a training table or a mat on the floor while squeezing a ball between your knees and again with a ball under your legs
  • lying down on a training table or mat and opening and closing your knees with an elastic theraband around your thighs for resistance
  • Rotating the trunk of your body and doing rowing exercises with resistance bands 
  • Squats and lunges are practical exercises that help prepare your body to get out of a chair or up off the floor.

If you use a machine such as a leg press, as I do, the resistance comes from the weights stacked on the leg press as, sitting down or lying on your back, you push a heavy bar down with your feet, until your knees are almost straightened out, and then bring your knees back up.  The amount of resistance is easy to control because you can add weights to the machine or take them off, making the pushing exercise more difficult or easier.  Typically you don’t have to physically lift weights onto the machine and take them back off.  The machine is made with a column of weights and you simply insert a metal pin into the weight level that is correct for you.

To determine the appropriate weight you should use in doing an exercise, the American Heart Association Science Advisory Committee says to first find out the maximum amount of weight you can push when doing that exercise.  Then take only a percentage of that maximum.  Starting out, that would be 30 percent to 40 percent for the upper body and 50 percent to 60 percent for the hips and legs.  “Most studies of previously sedentary adults with and without heart disease, including those with heart failure, reported training workloads of 50 percent to 80 percent” of maximum weight the person could tolerate, the advisory committee reported. 

If you or your trainer or therapist have any doubts about your ability to test your maximum weight-bearing strength for an exercise, don’t do a test.  Just approximate your maximum based on what weight you comfortably handle, the committee advises. 

“For most people, if they can lift a weight 12 to 15 times before having to stop, that weight corresponds to about 50 percent of their maximum capacity,” says  Kerry J. Stewart Ed.D., director of clinical and research exercise physiology, Johns Hopkins University School of Medicine.  Dr. Stewart works with heart patients and is co-author of the guidelines for resistance training adopted in 2007 by the American Heart Association. 

It is very important for people with heart problems to use the correct breathing pattern while doing resistance exercises. To avoid putting strain on your heart, exhale on the part of the exercise that takes exertion and inhales on the part that does not as you return to your normal position.

Heart Sense Helpathon
Woman Making Heart Shape with Hands

Times to Exhale

  • when you push the leg press down with your feet
  • when you push up from a squat
  • as you do an ab crunch
  • as you move your legs up in a leg curl
  • as you curl your arm upward in a bicep curl

By using this breathing pattern, instructs my trainer Randy Rocha, who is a certified athletic trainer and strength and conditioning coach,  you don’t build pressure.  He explains:  “That’s one of the biggest concerns with people with heart trouble — that they’ll get on a machine and they’ll try to do a certain amount of weight and they’ll hold their breath and everything builds up inside, their blood pressure increases and that’s where they get into a lot of trouble and that’s why people with heart conditions may think that exercise is bad.”

Breathing correctly while doing strength training is not automatic with me.  I have to think about my breathing and remember when to exhale and when to inhale.  As I began doing resistance exercises, Randy continually prompted me to exhale when exerting myself, even though I was not aware of holding my breath.

Never hold your breath deliberately when straining.  But it may happen briefly.  “Some breath-holding is unavoidable,” Dr. Stewart says, “but try to avoid extended holding and strain.  Too much strain can raise the blood pressure to very high levels which put unnecessary strain on the heart.” 

I hope you find you are healthy enough to engage in resistance exercises to build your strength and endurance.  I enjoy this strength training.  Please be sure to get your individual program structured at a heart rehabilitation center or by a certified trainer.

Recommendations for the Initial Prescription of Resistance Training

Resistance training should be performed 

  • in a rhythmical manner at a moderate-to-slow controlled speed, 
  • through a full range of motion, avoiding breath holding and straining (Valsalva maneuver) by exhaling during the contraction or exertion phase of the lift and inhaling during the relaxation phase, and 
  • alternating between upper and lower body work, to allow for adequate rest between exercises. 

The initial resistance or weight load should 

  • allow for, and be limited, to 8 to12 repetitions/set for healthy sedentary adults, or 10 to 15 repetitions at a low level of resistance, for example, <40% of 1 repetition maximum, for older (>50-60 years of age), more frail persons, or cardiac patients 
  • be limited to a single set, performed 2 days per week, and
  • involve the major muscle groups of the upper and lower extremities, eg, chest press, shoulder press, triceps extension, biceps curl, pull-down (upper back), lower back extension, abdominal crunch/curl-up, quadriceps extension or leg press, leg curls (hamstrings), and calf raise.

[Source:  American Heart Association Science Advisory, Resistance Exercise in Individuals With and Without Cardiovascular Disease:  2007 Update] 

Absolute and Relative Contraindications to Resistance Training 

Absolute Contraindications:

If you have any of these conditions, do not do resistance exercises:

  • Unstable (Active) coronary heart disease. This means you are having symptoms of chest pain or shortness of breath even though you are on treatment.
  • Decompensated heart failure. You are having symptoms of heart failure such as shortness of breath, fatigue, and fluid retention even though you are being treated for heart failure. 
  • Uncontrolled arrhythmias
  • Severe pulmonary hypertension (mean pulmonary arterial pressure >55 mmHg) 
  • Severe and symptomatic aortic stenosis
  • Acute myocarditis, endocarditis or pericarditis
  • Uncontrolled high blood pressure (>180/110 mmHg). If your blood pressure is this high or higher, do not do resistance exercise until you get more treatment and your blood pressure falls below 160/100.  
  • Aortic dissection
  • Marfan syndrome
  • Avoid high-intensity resistance training (80 to 100% of 1-RM (one repetition maximum) if you have active proliferative retinopathy or moderate or worse nonproliferative diabetic retinopathy. 

Relative Contraindications:

If you have any of these conditions, consult a doctor before participating in resistance exercise:

  • Major risk factors for coronary heart disease (diabetes, smoking, high blood pressure, high cholesterol)   
  • Diabetes at any age. If diabetes is controlled, resistance exercise is okay and even recommended by the American Diabetes Association.  
  • Uncontrolled high blood pressure (>160/>100 mmHg). You can exercise if your blood pressure is below this level, even while taking medications to control blood pressure.
  • Low functional capacity (<4 METs). Mets are a measurement of exercise capacity
  • Musculoskeletal limitations – If the problem is so severe that it severely limits walking.
  • Implanted pacemaker or defibrillator 

My Journey with Heart Failure

I got to know something about heart failure the hard way, by having it.  I also happen to be a health journalist.  So when I got the stunning diagnosis in 2003, I began researching this condition that sounded so fatal.  Not only was my diagnosis overwhelming, but my first encounters with the health care system were dismal.  It took me three and a half months to find good care.   My story is worth sharing because it illustrates how important it can be for a patient to become knowledgeable about an illness and get involved in her own treatment plan.

Heart failure is a condition in which the heart can no longer perform well enough to get adequate blood and oxygen to the body.  With 6 million people living with heart failure in the United States alone, it is already a huge medical problem and will get bigger as baby boomers continue to hit their fifties and sixties.  Heart failure is a serious condition that can be fatal, but I would learn that it often can be managed with the right treatments.  My own research about heart failure changed my life.

In December 2002, I found myself getting fatigued and easily out of breath, with swollen ankles and abdomen. My asthma was normally under control, but I turned to my asthma specialist because of the shortness of breath.  He noticed my swollen ankles and said he didn’t think my problem was asthma.  I had begun to think the same thing.   He told me to see my internist right away who referred me to a cardiologist who gave me a diagnosis in words that roll off the tongue of a heart specialist but shock the patient who hears them:  “idiopathic dilated cardiomyopathy and biventricular congestive heart failure.”  It was those last two words that got my attention. 

I tried to get over my shock and digest the big words of the diagnosis,  searching the internet to make some sense of what had happened to me.  Cardiomyopathy, I learned, is a disease of the heart muscle, and dilated cardiomyopathy means that the heart is enlarged.  When a heart stretches, it is trying to work harder, but an enlarged heart actually functions more poorly.  The “idiopathic” in my diagnosis means doctors don’t know what caused my cardiomyopathy.  Half of the people who are told they have dilated cardiomyopathy have no known reason why it developed.  An echocardiogram that uses sound waves to show the heart beating on a monitor revealed that the amount of blood my heart pumped out to my body with each beat was only 15-20% instead of the normal 55 to 65%.  The left side of my heart was enlarged, the result of struggling to work harder.

My search to understand my condition led me to national treatment guidelines for heart failure developed by expert panels of the American College of Cardiology and the American Heart Association.  I recommend every person with heart failure and their loved ones read these guidelines.  To my dismay,  I saw that I was not on two of the basic medicines proven in clinical trials to treat heart failure and prolong life, an ACE inhibitor, and a beta-blocker.   I turned to a second cardiologist.   He insisted I have an angiogram in which a catheter is threaded through an artery in the groin up to the heart to see if the heart’s main arteries are blocked by fatty buildups that could prevent blood from getting through.  The question he wanted to answer did I have severe coronary artery disease that could cause a heart attack.  I didn’t agree to the angiogram immediately. I didn’t want to have this test because  I am extremely allergic to the dye used in the exam.  So he suggested I see a heart failure specialist, which I did. 

My Journey with Heart Failure

The specialist blew me away with his advice: I needed a heart transplant.  He ordered a stress echocardiogram, the same sound-wave test I had gotten before in a cardiology group practice center, but this time, it would show how my heart functioned when challenged by activity. However, the doctor running the test stopped before getting to the stress part.  “We found what we need to know,” he said.  The specialist would come in to talk to me.

I waited for about half an hour wondering what the heck.   The specialist arrived, sat down beside me, and drew a rough outline of my heart on a piece of paper, shading an area from the left side down and around the bottom.

 “This part of your heart is dead,” he said.  “You have either had one large heart attack or several small ones.”

I felt shocked to my bones because this was news to me and, next, oddly, I felt a deep embarrassment, almost shame.  I was a veteran health journalist and I had not known when I was having a heart attack?  How incompetent of me.

The specialist agreed that I must have an angiogram and said he could give it to me.  The test would take 30 minutes and would likely find several very occluded arteries, he said.  The second cardiologist I had seen, the one who referred me to the specialist, had told me he could do the angiogram in 20 minutes and held out more hope than the specialist did that he could perform some intervention during the angiogram to open the dangerously occluded arteries he expected to find.  I chose the 20-minute man, reluctantly agreeing to this dreaded test.  

I warned this doctor who would perform the angiogram that I am very allergic to the dye he would use in the test.  I had never had an angiogram, but the same iodine-based dye is used in CAT scans as a contrast medium, and years earlier during a CAT scan I suddenly couldn’t breathe.  The doctor assured me he could give me medicines before the procedure that would prevent any allergic reaction.  I took the medicines, the procedure began, and I thought this isn’t so bad, piece of cake.

Then a technician called out “Mary, how do you feel?”  

“I feel strange,” I said.  I had no pain or heaviness in my chest but felt a very abnormal and unsettling sensation in my heart.  “Very strange.” 

The next thing I knew the procedure was over and the doctor who administered my angiogram was hurrying out of the room.  “But I have questions to ask you,” I said to the back of the departing cardiologist.  “You won’t remember the answers,” he said over his shoulder.

As soon as the doctor left the procedure room, a technician who had helped with the test spoke up.  “We had to shock you,” she said.    

 I was dumbfounded.  “I didn’t feel anything.”

“It’s a good thing you didn’t.  It would have been very uncomfortable.” 

I looked down and saw three burn marks on my chest and later found one on my left ribs.  I had died on the exam table and been resuscitated with four electric shocks.  But we found the answer to the doctor’s question, which I would soon learn. 

My accidental worldly departure during the angiogram led the doctor who gave it to admit me for an overnight stay in the hospital for observation; but, although I asked to see him, he would not visit me. He turned my care over to the third cardiologist, the heart failure specialist.  I’m a big believer in all’s well that ends well and was glad to be alive. 

The specialist came to my room and told me what the angiogram had revealed:  my arteries were not at all blocked. I did not have coronary artery disease.  Therefore, reversing what he had told me days earlier, he said I could not have had a heart attack.  My face lit up with a huge smile. “That’s great!” I nearly shouted.

“Not really,” he said, no smile on his face.  “We could have fixed that.”

“So where do we go from here?”  I asked, feeling deflated that he did not share my joy.

“Heart transplant,” he responded.

None of the three cardiologists I had seen, including this one, had put me on the two major recommended medicines for heart failure, an ACE inhibitor, and a beta-blocker.  Yet, without seeing what these drugs could do to improve my own heart’s function, the specialist wanted to take my heart out of my body and sew in a new one.

No, no, no!  You’re jumping the gun, fellah. I was so surprised that after getting such good news from a test that nearly cost me my life he would want to proceed with the same plan as before the test.  I knew I had to get away from this doctor and look once again for good care.  It was now three months since my diagnosis of heart failure and the clock was ticking.  Without proper treatment, heart failure progresses and is deadly.  And one aspect of heart failure is that a person who has it can experience sudden death, dropping dead in an instant unless someone can get to them with a defibrillator to shock their heart back to work.

Frightened and very stressed, I asked myself, “Who do I trust?”  That’s not grammatically correct, but it was what my brain was asking.  The answer came to me:  a neurologist I had seen many years ago at Johns Hopkins Hospital.  I contacted him and explained my situation.  He contacted a colleague who was a senior cardiologist at Hopkins who told me the person to see was Edward Kasper, then director of the Heart Failure and Transplant Service.  Uh, oh, I thought, concerned about the “transplant” part of his title.  But a doctor I trusted was sending me here and I felt this was the right thing to do.

Dr. Kasper listened to my story and then said that he would not consider a heart transplant.  The first thing to do, he said, was to see how I did on an ACE inhibitor and a beta-blocker, along with some other medicines for heart failure.  And if those didn’t work well enough, there were other things to try such as implanted devices to help the heart work better.  A heart transplant was only a last resort.  I was scheduled to begin teaching a university writing course in a few weeks.  Would I be able to do that?  Yes, he said, he was sure I would be feeling much better soon.  I thought he seemed almost nonchalant about my situation, which, actually made me feel relieved.  He expected me to get better.  

I took my new medicines faithfully and began improving. My attitude toward heart failure changed as I relegated it to the background of my life and got back to teaching writing and co-editing a book.  We decided I should get a biventricular pacemaker to correct an electrical timing problem that made my left ventricle beat out of sync.  This problem called a left bundle branch block was not the cause of my heart failure.  But the uneven beating of my left ventricle caused my heart to work harder.  I recovered from heart failure.  I still have my own heart which returned to normal size and is pumping blood out at a very normal 65%.   I continue to take low doses of an ACE inhibitor and beta-blocker, avoid high-sodium foods, and exercise.   Since we don’t know what caused my cardiomyopathy which caused the heart failure, I want to do all I can to avoid its returning.  

My experience with heart failure and the health care system made me realize just how important we, the patients, can be in deciding a treatment plan.  The patient must truly be a partner with her doctor and not passively accept whatever any doctor says to do.  In order to be a strong partner,  you will need to educate yourself to become informed and then get involved in planning your treatment.

What turn might my life have taken if I had not done some research and continued looking for the best care?  Getting the gift of a new heart is a miraculous second chance for those people with severe heart failure who have not responded to medicines and devices to help their hearts work better.  But a heart transplant also means a lifetime of taking many medications, having some serious side effects, and getting tested repeatedly.  Let’s be sure those who get this precious gift need it.  I, thankfully, did not.

What is Mitral Valve Regurgitation that led to Elizabeth Taylor’s Heart Failure?

I am saddened that Elizabeth Taylor died today of heart failure.  In his appreciation of her, film critic Roger Ebert said in the Chicago Sun-Times, “Of few deaths can it be said that they end an era, but hers does.” 

She is a star that many of us felt we knew.  She was a great actress and a woman of great beauty who was a hard-working champion of people with AIDS and always seemed to be a determined person who knew herself. Yet she always had a vulnerable side.  So many marriages, so many illnesses, so many, many surgeries, over 40, I’ve read.  And then her heart problem developed.  This leads me to talk a little about that problem, mitral valve leakage.

The heart’s mitral valve

The heart has four chambers and four valves that open to let blood through to the next chamber of the heart and on out to the body and back.  The valves, acting as gates, then immediately close to prevent the blood from running back where it just came from. The mitral valve looks like a mouth with leaflets that look like lips that open and close.  When I saw it in action on an echocardiogram, a test that uses sound waves to show moving pictures of the heart, I thought it looked like a very sensuous mouth.  Each of the valves looks different.  But because it looks like a mouth, the mitral valve stands out.  Blood has just left the lungs carrying oxygen and arrives at the left atrium of the heart.  The mitral valve’s mouth opens to let the blood pour through into the left ventricle.  As the left ventricle contracts, the mitral valve closes and the aortic valve opens to allow blood to leave the heart and get out to the body. 

Heart Failure

A mitral valve can start to leak.  This can range anywhere from a condition that is minor and does not need treatment to a serious problem that leads to a weakened heart and heart failure.  In Elizabeth Taylor’s case, it led to heart failure and her symptoms must have included difficulty breathing and fatigue.

I asked Edward K. Kasper, M.D., director of clinical cardiology at Johns Hopkins Hospital, to talk a little about what can go wrong with a mitral valve.  I should mention for disclosure that Ed is my cardiologist and co-author with me the book Living Well with Heart Failure, the Misnamed, Misunderstood Condition:

A leaky mitral valve – mitral regurgitation, is common and has many causes. Most people tolerate a leaky valve well, but some need surgery to correct the leak. Repair is preferred to replacement. The MitraClip (which was used for Elizabeth Taylor) is a new technique to try and fix mitral regurgitation in the cath lab rather than in the operating room. There are no long-term comparison studies of this technique compared to standard OR repair – that I know of. Repair is currently the gold standard for those who have severe mitral regurgitation and symptoms of heart failure.  Outcomes are better including improvement in symptoms and survival in patients with the repair rather than replacement.

What makes a person from a leaking mitral valve to heart failure?

The leakage back into the left atrium increases the pressure in the left atrium. This increased pressure in the left atrium is passed back to the lungs, causing fluid to leak into the lungs, leading to heart failure. With time, the demands of severe mitral regurgitation on the left ventricle will lead to a weakened left ventricle, a dilated cardiomyopathy (disease of the heart muscle). We try to prevent this by operating before it gets to that point.

Mitral regurgitation can also be a consequence of dilated cardiomyopathy – the orifice of the mitral valve enlarges as the left ventricle enlarges. The leaflets of the mitral valve do not enlarge. Therefore, they no longer close correctly, leading to mitral regurgitation. 

It’s easy to see why anyone would want to opt for the Evolve MitraClip over open-heart surgery.  The MitraClip is a little different from a common test known as an angiogram in which a catheter is passed through the femoral vein in the groin up to the heart.  In this repair procedure, however, the catheter guides a clip to the mitral valve where the metal clip covered with polyester fabric is positioned over the leakage and brought down below the open flaps and back up, fastening the valve’s open leaflets together.  The manufacturer, Abbott, shows in a video here how blood still is able to pass through on either side of the fastening. 

Elizabeth Taylor got her MitraClip repair a year and a half ago, so it must have worked for a while.  Then about six weeks ago she was hospitalized with heart failure at Cedars-Sinai Medical Center in Los Angeles where she died with her family at her bedside.  For more on mitral regurgitation, see this NIH site.

Heart failure has many other causes.  High blood pressure can damage the lining of blood vessels leading to deposits of cholesterol.  Coronary artery disease causes heart attacks.  A heart attack kills part of the heart muscle, forcing the rest of the heart to work harder and in doing so, get large and weak. Only about half the people who develop heart failure have a weak heart.  In another cause of heart failure, the left ventricle becomes stiff and the heart does not fill properly.  And in some heart failure, the heart itself is normal but connecting blood vessels are not or a valve may be too narrow.  In all of these cases, a person is said to have heart failure because the heart and vascular system are not able to provide the body with the blood and oxygen it needs. 

The HeartSense Helpathon: Second in a series

Helping Each Other to Good Health:  Preventing Heart Disease

Brian Mossop trained to be a neuroscientist but then decided that writing about science was more fun and quickly became a well-known science writer.  If there is a genetic predisposition to athletic pursuits, Brian must have one because he started competing in sports as a preschooler and is a self-described “exercise fanatic”.  Whether or not he has a genetic drive to pursue athletics, he also has days when that motivation to exercise is just not there.  But with a family history of heart disease and experiencing what can happen to your body when you don’t exercise and eat right, he pushed forward with an intense exercise program, choosing running and Crossfit to keep his heart healthy. 

Running, biking and walking are all forms of aerobic exercise that increase your heart rate, build your heart’s endurance, and help muscle function in your legs and arms.  Crossfit is a program that includes resistance exercises and strength training that target muscles, building muscle endurance and the ability to respond quickly and more powerfully.  People with controlled heart failure can benefit from both aerobic and resistance exercise, but please avoid straining with heavyweight lifts and learn correct breathing patterns when doing resistance exercises. We will discuss in more detail strength training for people with heart problems in a future article in this series.

I am delighted to bring you this adventurous, disciplined commitment to healthy living in Brian Mossop’s guest blog post below. 

Why I Run

I’ve been a competitive athlete for as long as I can remember.  Um, wait, scratch that.  See, there was this period during the end of grad school and the start of my first postdoc, when I was completely burned out, and fell into some bad habits.  But let’s start at the beginning.

I started participating in organized sports at an early age, around age 4 or 5, according to my very proud mother, who beams with excitement when I ask her to recall sports stories from my childhood.  Personally, I think my parents just got tired of my incessantly asking them if I could play tee-ball, so they signed me up thinking my interest wouldn’t last very long.  But the trend continued, all the way through college, where I was a short distance sprinter – 50m, 100m, 4×100 relay – at Lafayette College.   

I stayed fairly active for my first years of grad school, but soon the humdrum of lab life caught up with me.  It started innocently enough, bailing out on a workout or two during the week when I just couldn’t muster the energy to change into exercise clothes.  Next thing I knew I was about 30 pounds overweight and none of my clothes fit.  I forgot where the gym was located.  My LDL cholesterol and blood pressure were in bad shape, both on the verge of requiring pharmaceutical intervention.

But the depressing blood work results, not to mention my expanding mid-section, lit the fire under me.  Several of my maternal uncles had multiple heart attacks – one of them was at the tender age of 35 when the first one hit – and this was one family tradition I didn’t care to follow.  

Instead of drowning my sorrows in pints of Ben & Jerry’s – an all-too-familiar trend during those times – I decided to start doing something crazy: road racing.

Being a sprinter, I had never done much long-distance work.  In the past, making it around the 400m track just once was an accomplishment for me.  Plus, my closest friends from college are hard-core distance runners.  And by that, I mean they are really, really fast.  Like a 2:30ish marathon fast.  Top 50 in the Boston Marathon fast.  Fast fast.  You get the point.  So getting into this road racing business was a bit intimidating.  I didn’t even tell my best friends what I was doing until shortly before my first race.  

I started out slow, running just twice per week, a sluggish mile or two at a time.  Week by week runs became easier, and I found myself starting to push myself to go further, and faster.  I started watching what I ate, making smarter choices on trips to the refrigerator.  As the months passed, I began feeling better than ever and had wrangled my waistline back to its proper diameter.  My annual physical revealed more good news, as my cholesterol and blood pressure were now held in check.

As I got into better shape, I once again started feeling the familiar, competitive itch.  I was then running about 25+ miles per week, and I thought signing up for an organized event would be a great way to feed my enduring desire to race.  Several half-marathons later, I still was unable to quell my inner adrenaline junkie.  No matter what kind of running workouts I did – 800m repeats, tempo runs, fartlek, you name it – I still couldn’t feel that rush of blood and emotion that is a sprinter’s life force.  

A co-worker told me about a new workout program she had gotten hooked on, called Crossfit.  Though I was reluctant to shelve the free-weight routines I’d been relying on since high school for what seemed to be just another fad, I decided to give it a fair chance.  

The Crossfit idea was simple enough: go to the website to find out the Workout of the Day, and do it.  The exercises were a mix of things like plyometrics, Olympic lifts, and bodyweight exercises (pushups, pullups, etc).  The amount of weight to use and the number of repetitions to perform were prescribed on the website for each exercise.  Contrary to most weight training methodologies, you got “better” by completing the workout faster, instead of boosting the amount of weight used, which gave a nice cardio burn throughout the session.  

At the time, Crossfit gyms were springing up all over San Francisco.  A new breed of trainers had turned old, converted warehouses into places where people could meet and work out together, making weight training into a team sport.  

For me, exercise has been a way to actively battle my family history of heart disease, while simultaneously holding my stress levels, and possibly even my cognitive ability, in check, as studies have shown the immense value of voluntary exercise on the brain.

It took quite a bit of trial and error for me to find the exercise routine that worked for me.  In the months before I got hooked on road racing and Crossfit, I tried it all: racquetball, swimming, the list goes on.  And so when I hear people become quickly discouraged with their New Year’s resolutions to get in shape, I try to help them discover the many, many ways to get the heart rate up.  

Getting back into a regular exercise routine was not easy.  I struggled quite often.  And I still have days where I don’t feel like going for a run.  But one thing to remember on the dark and dreary days: you’re not alone.  Every athlete, from newbies all the way up the chain to the elites, struggles with motivation from time to time.  

When my motivation tank is running on fumes, I usually do one of two things.  First, I’ll call up a friend and schedule some time for a nice, slow run with a running buddy.  Whether it’s a quick lunchtime trot, or a long weekend run, the small talk with your running buddy will make the time, and distance goes by much faster.  Second, I’ll start tracking my runs online using an exercise log like Running AHEAD, now in beta testing, or a cool gadget like Nike+.  These are relatively inexpensive, and provide a great way to keep tabs on my progress, and see how I’m improving each week.

Finding the exercise that’s right for you trigger those dopamine reward circuits in your brain, and will, eventually (I promise you!) turn exercise from a measly chore into your favorite hobby.

Follow the Money

I’ve been working for a couple of months on an in-depth article on personal defibrillators that are implanted beneath the skin of a person’s chest to shock a heart that starts shaking, thereby restoring its normal beating and preventing sudden death.  Discussing these

I’ve been working for a couple of months on an in-depth article on personal defibrillators that are implanted beneath the skin of a person’s chest to shock a heart that starts shaking, thereby restoring its normal beating and preventing sudden death.  Discussing these defibrillators is extremely complex, which is why I am spending so much time on researching and writing the article intended to help patients and their families make an informed decision by learning the truth about the devices known as implantable cardioverter defibrillators (ICDs) — the good and the bad, your life saved vs nothing happening or the accompanying risks and harm you may receive.  So when I heard that a new study would be presented at the annual scientific meeting this week of the Heart Rhythm Society, a professional organization of cardiologists and electrophysiologists who use cardiac devices in their patients, I made sure to get an advance copy of what would be presented and interview the lead author.

Potentially such a study would be of interest to physicians and to patients considering getting an ICD because it looked at all shocks the defibrillators gave the heart in patients who took part in the clinical trial, including those sent for life-threatening rhythms and in error.  For several reasons, I felt the study is not ready to report to the public.  It is only an abstract.  The full study has not yet been written, let alone published in a peer-reviewed journal or even accepted for publication.  Patients with defibrillators who received shocks were matched to only one other patient who was not shocked, but the two patients were not matched for what other illnesses or poor quality of health they had.  Yet they were matched to see who lived the longest and the study looked at death for all causes, not just heart-related. One critical question the study sought to answer was this:  Do the shocks themselves cause a shortened life (even if they temporarily save it) or is a shortened life the result of the types of heart rhythms a person experiences?

defibrillators

But the thing that really slapped me in the face and gave me pause was the exchange of money.  In all stories I write on drugs or medical devices, I have begun asking the sources I quote for any conflicts of interest they have with pharmaceutical companies that make these products and I list the conflicts within or at the end of the story.

Nowadays with the spread of COVID-19, it is of utmost importance that these patients take extra care about their health, as COVID get more severe where patients are suffering from other illnesses like sugar, asthma, and heart issues, these patients should regularly test themselves against COVID by rapid antigen test kits, now easily available in the market.

This study was funded by Boston Scientific, a pharmaceutical company that makes defibrillators.  And all eight authors of the study from different medical centers had financial ties to Boston Scientific.  All of them?

Would I be surprised if the study found that it was not the defibrillator’s shock that shortened life?  In the few write-ups that I’ve seen on this study presented Thursday, the lead author is quoted as saying that not the shock, but rather the type of rhythm is what was associated with a shortened life. 

This study that was able to look at shocks sent for a variety of heart rhythms and for other reasons may be a valuable study.  But I can’t help wonder, both as a journalist and as a potential patient, if the study would have been designed differently and reached any different conclusions if no money exchanged hands between a company that makes defibrillators and the eight physicians who designed the study and wrote its conclusions.  I am not making any accusation here. 

I simply am saying that I am made to feel uncomfortable by the financial association of the doctors and big pharma.  Why do doctors do this? Should organized medicine and university medical centers forbid doctors who have any financial ties to a company from participating in a clinical trial of a product that the company makes? 

Especially if the company is funding the clinical trial?  That would eliminate a lot of doctors.  But the tide is changing and some financial arrangements once commonplace between doctors and industry are no longer allowed at some major university medical centers and everything is under more scrutiny than before.  We were discussing this matter of conflicts of interest Tuesday in a university class I teach to doctors who want to write for the public.

Both doctors and journalists should be truth seekers, and seeking the truth is best done independently.  Would the public be able to trust my long-researched piece on the truth about defibrillators if it turned out that I am being paid to write press releases for one or more of the companies that make these defibrillators?  Or if I wrote speeches for executives of these companies?  Or if I served as a consultant to the companies on public relations?  As a journalist, I could not consider receiving money from groups I write about. Why should doctors be allowed to receive money from companies who make a product they are using on patients in a clinical trial that purports to provide answers to serious questions about the product?

As I was wrestling with this issue and whether to write about why I am not writing about that study, journalists with Pro Publica published several articles on their website and with USA Today on money ties between big pharma and the Heart Rhythm Society. 

When I first began attending various cardiology organizations’ scientific meetings I was taken aback by the number of physician speakers who would begin their talks with a conflict of interest slide that stayed visible only for what seemed like one second before the speaker clicked to the next slide, visible just long enough for the audience to see there was a long list of financial ties to industry, but not long enough to read what they were.  The slides were there because the doctor organizations were requiring transparency.  But what was happening was not transparent because nobody could read what was on those slides.  How rare but heartening it was when a speaker began a talk by saying “I have no conflicts of interest.”  That is changing and more doctors are able to say they have no conflicts. But much more needs to change.

I was also amazed to see the large numbers of “non-official” scientific sessions sponsored by individual pharmaceutical companies and listed in the official scientific programs — with leading cardiologists as presenters and well attended by conference-goers — that preceded the official program at these major cardiology meetings. What portion of these presentations used company slides and drove home company messages?  After seeing all this, I remember holding my breath as I asked the cardiologist I had invited to co-author a book with me about heart failure if he had any financial conflicts of interest with the industry.  I felt that if he did have, I could not write the book with him.  How relieved I was when he said he did not.  

Pharmaceutical industry financial relationships with individual doctors and with organizations of doctors are important to the public welfare because these relationships can influence judgment and decisions, can influence what is said and not said in writing about medical products, and in speaking to and advising patients.  And that is why these relationships are important to journalists who are servants of the public. 

As for my long-researched piece on defibrillators, I have found more studies to read and a couple of new interviews to do.  I believe that this examination of the truth about defibrillators that I am writing for a well-known magazine’s website will be worth reading, and once it is published there, I will reprint it here. 

is extremely complex, which is why I am spending so much time on researching and writing the article intended to help patients and their families make an informed decision by learning the truth about the devices known as implantable cardioverter defibrillators (ICDs) — the good and the bad, your life saved vs nothing happening or the accompanying risks and harm you may receive. 

So when I heard that a new study would be presented at the annual scientific meeting this week of the Heart Rhythm Society, a professional organization of cardiologists and electrophysiologists who use cardiac devices in their patients, I made sure to get an advance copy of what would be presented and interview the lead author.

heart

Potentially such a study would be of interest to physicians and to patients considering getting an ICD because it looked at all shocks the defibrillators gave the heart in patients who took part in the clinical trial, including those sent for life-threatening rhythms and in error.  For several reasons, I felt the study is not ready to report to the public.  It is only an abstract. 

The full study has not yet been written, let alone published in a peer-reviewed journal or even accepted for publication.  Patients with defibrillators who received shocks were matched to only one other patient who was not shocked, but the two patients were not matched for what other illnesses or poor quality of health they had.  Yet they were matched to see who lived the longest and the study looked at death for all causes, not just heart-related. One critical question the study sought to answer was this:  Do the shocks themselves cause a shortened life (even if they temporarily save it) or is a shortened life the result of the types of heart rhythms a person experiences?

But the thing that really slapped me in the face and gave me pause was the exchange of money.  In all stories I write on drugs or medical devices, I have begun asking the sources I quote for any conflicts of interest they have with pharmaceutical companies that make these products and I list the conflicts within or at the end of the story.

This study was funded by Boston Scientific, a pharmaceutical company that makes defibrillators.  And all eight authors of the study from different medical centers had financial ties to Boston Scientific.  All of them?

Would I be surprised if the study found that it was not the defibrillator’s shock that shortened life?  In the few write-ups that I’ve seen on this study presented Thursday, the lead author is quoted as saying that not the shock, but rather the type of rhythm is what was associated with shortened life.  This study that was able to look at shocks sent for a variety of heart rhythms and for other reasons may be a valuable study.  But I can’t help wonder, both as a journalist and as a potential patient, if the study would have been designed differently and reached any different conclusions if no money exchanged hands between a company that makes defibrillators and the eight physicians who designed the study and wrote its conclusions.  I am not making any accusation here.  I simply am saying that I am made to feel uncomfortable by the financial association of the doctors and big pharma.  Why do doctors do this? Should organized medicine and university medical centers forbid doctors who have any financial ties to a company from participating in a clinical trial of a product that company makes?  Especially if the company is funding the clinical trial?  That would eliminate a lot of doctors.  But the tide is changing and some financial arrangements once commonplace between doctors and industry are no longer allowed at some major university medical centers and everything is under more scrutiny than before.  We were discussing this matter of conflicts of interest Tuesday in a university class I teach to doctors who want to write for the public.

Both doctors and journalists should be truth seekers, and seeking the truth is best done independently.  Would the public be able to trust my long-researched piece on the truth about defibrillators if it turned out that I am being paid to write press releases for one or more of the companies that make these defibrillators?  Or if I wrote speeches for executives of these companies?  Or if I served as a consultant to the companies on public relations?  As a journalist, I could not consider receiving money from groups I write about. Why should doctors be allowed to receive money from companies who make a product they are using on patients in a clinical trial that purports to provide answers to serious questions about the product?

As I was wrestling with this issue and whether to write about why I am not writing about that study, journalists with Pro Publica published several articles on their website and with USA Today on money ties between big pharma and the Heart Rhythm Society.  See  here, here, here and here

When I first began attending various cardiology organizations’ scientific meetings I was taken aback by the numbers of physician speakers who would begin their talks with a conflict of interest slide that stayed visible only for what seemed like one second before the speaker clicked to the next slide, visible just long enough for the audience to see there was a long list of financial ties to industry, but not long enough to read what they were.  The slides were there because the doctor organizations were requiring transparency.  But what was happening was not transparent because nobody could read what was on those slides.  How rare but heartening it was when a speaker began a talk by saying “I have no conflicts of interest.”  That is changing and more doctors are able to say they have no conflicts. But much more needs to change.

I was also amazed to see the large numbers of “non-official” scientific sessions sponsored by individual pharmaceutical companies and listed in the official scientific programs — with leading cardiologists as presenters and well attended by conference goers — that preceded the official program at these major cardiology meetings. What portion of these presentations used company slides and drove home company messages?  After seeing all this, I remember holding my breath as I asked the cardiologist I had invited to co-author a book with me about heart failure if he had any financial conflicts of interest with industry.  I felt that if he did have, I could not write the book with him.  How relieved I was when he said he did not.  

Pharmaceutical industry financial relationships with individual doctors and with organizations of doctors are important to the public welfare because these relationships can influence judgment and decisions, can influence what is said and not said in writing about medical products and in speaking to and advising patients.  And that is why these relationships are important to journalists who are servants of the public. 

As for my long-researched piece on defibrillators, I have found more studies to read and  a couple of new interviews to do.  I believe that this examination of the truth about defibrillators that I am writing for a well known magazine’s website will be worth reading, and once it is published there, I will reprint it here.