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Sudden Death in Young Athletes

John Mandrola MD is a cardiac electrophysiologist practicing in Louisville, Ky who blogs as Dr. John M.  Below is his insightful discussion about why cardiac screening may not be possible to prevent sudden death in young athletes.  Yet it is so distressing each time a young athlete falls dead during or after a game because he and his family did not know that he had a serious heart problem that could have been identified in a test.  For some heart defects, if only the family were aware of the defect, it would be appropriate for the young athlete to wear an implanted defibrillator that would save his life either through extra pacing as the disturbance began or through electric shocks if his heart suddenly went into a wild shaking known as ventricular fibrillation.  

I understand John’s concern about the high cost of making electrocardiograms and echocardiograms, heart tests that could pick up significant heart defects, a required part of sports physical in schools and colleges.  Aside from the cost is the important issue that screening can pick up false positives and “shadows and innocent blips” that lead to further invasive testing.  Yet, I could see parents springing for these cardiac exams themselves, but then being very cautious about doing any further testing.

It is unforgivable not to have an automatic external defibrillator at all sporting events, close to the court or the field, and more than one athletic staff member trained to use it. Every minute counts when a person’s heart stops working.  Realizing what has happened, then calling an ambulance and waiting for the paramedics to arrive, may take up too much time to save a young athlete’s life.  When an athlete falls to the ground and is not moving, the trainer or other staffer should immediately have the defibrillator or crash cart ready so that the shocks could be applied to the athlete’s heart within one to two minutes. 

It’s heart-wrenching when young athletes die of sudden cardiac death (SCD). This week, the death of Wes Leonard, a Michigan high school star athlete, was especially poignant since he collapsed right after hitting the game-winning shot.  This sort of tragedy occurs about one hundred times each year in America. That’s a lot of sadness.

Sudden Death in Young Athletes

The obvious question is: Could these deaths be prevented?

Let’s start with what actually happens.

Most cases of sudden death in young people occur as a result of either hypertrophic cardiomyopathy (HCM), an abnormal thickening of heart muscle, or long QT-Syndrome, a mostly inherited disease of the heart’s electrical system. Both HCM and Long-QT syndrome predispose the heart to ventricular fibrillation–electrical chaos of the pumping chamber of the heart. The adrenaline surges of athletic competition increase the odds of this chaos. Unfortunately, like heart disease often does, both these ailments can strike without warning.

Sudden death is sad enough by itself, but what makes it even worse for doctors (and patients) is that both these ailments are mostly detectable with two simple painless tests: the ECG and Echocardiogram (heart ultrasound).

Let’s get these kids ECGs and Echos then. Git-r-done, you might say.

On the surface the solution seems simple: implement universal cardiac screening of all young athletes. And you wouldn’t be alone in thinking this way. You could even boast the support of Dr Manny Alvarez of Fox News, and the entire country of Italy–where all athletes get ECGs and Echos before competing.

But America is not Italy and things aren’t as simple as Fox News likes to suggest.

There are three major flaws with Dr Manny’s simplistic proclamation that all (American) athletes should have pre-participation ECGs and Echocardiograms.

The Economic:

The estimated cost–in our current health care system–for adding an ECG and Echo to the sport’s exam is about $1000. That’s a bunch more than $19.99–the advertised price of the sports physical at my local grocery store’s walk-in clinic. Parents may be amendable to charging $19.99 to their credit card, but even when the safety of their teen is at stake, few can afford the current-day costs of ECGs and Echos.

Now, you could make the argument that 1000$ is ridiculously high. And you would own a valid point. But that argument goes to the heart of the healthcare debate.

Let’s consider this notion for a moment: I could listen to your teen’s heart, look at their ECG, place a hand-held ultrasound probe on their chest, and in a matter of five minutes I could clear them for competition. The ECG would exclude long-QT syndrome, and the Echo would exclude excessive thickening of the heart muscle. The reason why I could do this are threefold:

  1. My entire medical career revolves around understanding ECGs.
  2. I look at Echos nearly every day, and was schooled by one of its pioneers, Dr Harvey Feigenbaum.
  3. In general, I waffle a lot less than the average reader of subjective cardiac tests. (That trait might not be valuable at the Mayo Clinic, but it would be good for screening thousands of young people, who are normal 99.999% of the time.)

Ah, but that’s not how things work in our present health care model. Obviously.

You can’t just deliver quality care that easy. There’s got to be a certified technician and machine to do the studies–portable Echos will not work. Calling an Echo normal these days is totally insufficient, fraudulent even. There has to be a three page report documenting each section of the heart. And of course, I can’t officially read an Echo because I am not board-certified in Echocardiography, I am just board-certified in Cardiology and Electrophysiology.

It’s not just the high costs that make screening athletes problematic.

It’s the Math:

Why don’t the numbers support widespread cardiac screening of athletes?

Again, it isn’t as simple as Dr Manny suggests. He portrays ECGs and Echos as black and white, yes or no, high or low kinds of tests. That’s not even close to accurate. They are both highly subjective tests that require mastery of nuance, including the ability guts to call something “normal.”  When a young person’s life is at stake, shadows and innocent blips look much more sinister. Before guaranteeing the invincibility of a young athlete, doctors often see things on ECGs and Echos that “might be something.” Radiologists sometimes call these shadows “incidentalomas.”

That’s the rub with screening that Dr Manny omits. For every life saved by the screening test, there will be hundreds (perhaps thousands) of patients sent for more (and often highly invasive) testing. Doctors are not going to be wrong about sudden death in a young person. No way. No how. There will be more tests, not just because of defensive medicine, but also in the name of quality.

To the numbers: Rare diseases like HCM and Long-QT kill athletes at a frequency of about 0.01%. That’s the left side of the equation. On the right side of the equation are the risks of all the cardiac caths, electrophysiology (EP) studies and dye-requiring CT scans ordered as a result of the screening tests. Though an individual cardiac cath, EP-study or CT are low-risk, the cumulative risk of doing these on thousands of normal people surely approach the 0.01% chance of sudden death in an athlete. Said more simply, with made up numbers to make my point, if screening saves 50 of the 100 teens who die each year, but 50 die from complications that occur from chasing down incidentalomas, than it’s an expensive statistical wash.

The Reality of the Athletic Ethos:

The third major flaw with the idea that mandated cardiac screening will save lives is that making the diagnosis of heart disease doesn’t always equate to preventing sudden death. The athlete has to accept the treatment, which for them, like it was for Boston Celtic great Reggie Lewis, is often untenable.

Gosh, I wish we could save all the young athletes that die suddenly.

But the paradox of our present health care system is that awash in all its fury of available technology (the MRIs, the robots, the GPS-navigational-systems) is our inability to do simple things for the many.

That’s too bad.

JMM

P.S.: One thing that Dr Manny was spot on about was that more AEDs (Automatic External Defibrillator) in athletic arenas are surely a good thing. In the case of AEDs, there exists strong science to show that increasing their availability saves lives.

Heart Sense Helpathon: Third in a Series

Exercising Basics: Getting Started  

In the previous two guest posts on exercise, Jody Schoger and Brian Mossop inspired us with their stories of building and sustaining a rigorous exercise program.  Both promised that if you exercise regularly, you will never want to go back to being a couch potato. Exercise makes you feel better and has many health benefits.  For those of us who have experienced heart failure, the main reasons to exercise are to strengthen our hearts and the muscles in our legs, arms, and core of our bodies.

But the idea of walking, running, or biking for miles if you are unsteady on your feet or still get fatigued easily, may seem out of the question.  So let’s talk about how to get started and what types of exercise to do.  Please be sure to get your doctor’s approval before you begin exercising.  Much of the following is excerpted from Chapter 13 “Exercise:  How Much and What Kind” in Living Well with Heart Failure, the Misnamed, Misunderstood Condition the book I co-authored with Edward K. Kasper MD.  While the entire book was a collaboration, the exercise chapter was one I researched and wrote and the main references are listed below.  

If you are not already exercising regularly, why not start today.  Let’s make 2011 a year we build our strength and fitness.

Why Exercise?

To keep from turning into a statue; gain more freedom of movement; ease your heart’s workload; strengthen your core body, legs, arms, heart, and lungs; and become more active.  The main symptom of heart failure is an inability to exercise for long, or even do normal activities such as walking or bathing without feeling fatigued or short of breath.  Heart failure doesn’t just affect your heart.  It also affects many of the muscles in your body, and muscle weakness is often most noticeable in your legs. 

At least three things contribute to your muscle weakness:  As your heart labors to send oxygen to your body, your skeletal muscles receive less oxygen, certain damaging chemical changes occur, and using the muscles makes them tire easily.  Your symptoms of heart failure – your general fatigue, shortness of breath, and muscle fatigue —  often lead to your becoming less active.    Randy Rocha, strength and conditioning coach who has worked with me, explains that with inactivity, as can happen when people first develop heart failure or have moderate to severe heart failure,  muscle tightening and muscle atrophy set in.  “You atrophy so much that you don’t have the strength to get from Point A to Point B,” he says. “Not only is everything atrophying, everything’s tightening up and it’s slowly getting tighter and tighter.”  Then when you try to get up from a chair or off the toilet or walk upstairs or even walk on a flat surface, your shrunken muscles can’t meet the demands you ask of them.  So you may find yourself hobbling along, stopping to rest your hands on the back of a chair, or leaning against a wall.  Not the shape you want to be in?  Regular stretching and strengthening exercises will help you get up more naturally and walk more normally with better posture for longer periods. 

Heart Sense Helpathon

Most heart failure occurs in people who are over 55 and so, aside from your heart failure, you also may have gotten out of shape, overweight, and have some arthritis, diabetes, COVID, or other medical problems.  Now it has become very important for heart patients to test themself regularly against COVID, this can be done at home with the use of the rapid test, learn more about the rapid tests at https://clinicalsupplies.com.au/collections/rapid-antigen-tests

I was fortunate enough to get through my bout with heart failure and come out with a heart that is working normally.  But separately from heart failure, I’ve developed a neuromuscular problem that makes walking challenging.  Like me, you may have multiple reasons to exercise. When you plan your exercise routine, treat your heart failure, but also take care of your whole body’s needs.  Besides gaining the ability to be more active and do more things, benefits from exercising include lower blood pressure and improved ability of the blood vessels to expand and contract.

Types of Exercise

If your doctor says you are healthy enough to exercise and have no particular exercise restrictions, choose a combination of these four types of exercise:

1.  Stretching exercises will isolate individual muscles, lengthen them, and keep them and your joints flexible.

2.  Aerobic exercise, also called cardiovascular exercise, such as biking, walking, or running will build the heart’s endurance and improve muscle function in your legs and arms, depending on the exercise you do. 

3.  If you are strong enough, balance exercises such as standing on a balance board or wobble board will improve your body’s awareness in space.  

4.  Resistance exercises or strength training can strengthen muscles throughout your body, increase muscle endurance, and improve balance and posture.  Increasing muscle endurance can increase the body’s ability to burn fat throughout the day.

We will discuss stretching, aerobic, and balance exercises in this post and save resistance exercises for the next one because there is much to understand about how to safely do resistance exercises.

If you still have an active heart condition, the safest and most effective way to start your exercise program is to learn exactly what to do at a cardiovascular rehabilitation program or exercise center.  If your heart problem is resolved or if you don’t have a heart condition and are exercising to be healthy, you may want to go to a sports therapy center to learn how to build your personal exercise program.  Please get instructions on how to do stretching exercises.  Once you’ve learned what to do, you can work out on your own at home or you may choose to make regular visits to an exercise center.

These are some basic questions to ask a therapist or trainer:    

What exercises should I do?

In what order should I do them?  

How long should each exercise last? (How many repetitions?)

How frequently should I do each exercise?  (More than once a day?  Every day?  Two or three days a week?)

How long do I need to rest between exercises or between exercise sessions?  The right workout/rest ratio is important for people with active heart failure.  Start with short exercises and progress as you get stronger.

How will I know when to progress to more intensity with my exercises?

Stretching exercises. Before doing your stretching exercises, ride your stationary bike or walk for five minutes.  After a short warmup, you will get more benefits from stretching your muscles.  Stretching your calf muscles in your lower leg, your quadriceps — the major muscles in the front of the thigh, and hamstrings in the back of the thigh is important for walking well and not tiring easily.  Stretching the muscles surrounding the hips – glutes, hamstrings, and the iliotibial band — can help reduce back pain and improve posture.  You will hold each stretch for 20 to 30 seconds. 

Aerobic (cardiovascular) exercise. Examples are biking outdoors or riding a stationary bike, walking outdoors or on a treadmill, running or jogging, and using an elliptical trainer. These exercises, which you’ll spend the most time at, get your heart rate up. They also burn fat and help you lose weight. A recent study found that aerobic exercise helps remodel an enlarged left ventricle to more normal size.

Walking 20 to 30 minutes a day is a great aerobic exercise if you can manage it.  You may want to have a regular time each day to walk outside with a friend.  Walking in a grocery store is a good way to get started.  If you need some support when you walk, pushing a grocery cart acts as a great walker on wheels. 

If walking is difficult for you because your legs are weak, your balance is not as good as it used to be and you may fall, your knees are painful, or it’s too hot, too cold, or even icy out or the air quality is poor, there are aerobic exercises that you can do at home.  Riding a stationary bike is a good one.  Stationary bicycles and elliptical trainers are non-impact machines because there’s no pounding on the ankles, knees, hip joints, or spine. 

You can monitor your heart rate by wearing a heart rate monitor.  Some exercise machines have built-in heart rate monitors. You can also use the old-fashioned, low-tech method of counting your heart rate at your pulse.  Your target heart rate for aerobic exercise should be set by your doctor or an exercise specialist who communicates with your doctor. Your rate will relate to your medical condition and the type of shape you’re in.

Biking requires a lot of lower extremity strength, especially the quadriceps.  As you exercise targeted muscles, the heart sends blood and therefore oxygen to that muscle group.  Aerobic exercise also decreases your resting heart rate and your blood pressure.  Exercising your heart challenges it which helps it do a lot better when it’s not challenged.

Balance exercises.  Exercises such as standing on a balance board or wobble board are important because balance plays a role in stability and strength.  If you don’t have a good balance, something needs to assist you.  You’re going to focus more and use muscles a lot harder than a person who has good balance, or you will hold on to something such as a cane, a crutch, or a walker to take the stress off.  Randy says that, unless you have an injury, if you use a walking aid, what you are doing is making up for your lack of balance and strength. 

If you use a balance board or wobble board, please place it very close to a railing or other sturdy structure that you can grip to keep from falling.  You should also place the board on a rubber mat or rubber floor to help keep the board from slipping.

You can do balance exercises without using a balance board or wobble board.  Stand close to something you can hold onto such as a railing or the back of a sturdy chair in case you start to fall.  Try standing on one foot, standing on one or both feet with your eyes closed (but hold on to something or have someone stand next to you if you close your eyes), or practice marching, lifting one leg at a time, eyes open.

Start with short exercises and build to longer ones. Just get started.  Do a little each day and I think you’ll want to do more.  

Sources:

  1. Kerry J. Stewart Ed.D, Director of Clinical and Research Exercise Physiology, Johns Hopkins University School of Medicine.
  2. Randy W. Rocha, Director of Sports Medicine, Metro Orthopedics and Sports Therapy Centers, Maryland.
  3. American Heart Association Science Advisory, Resistance Exercises in Individuals with and without Cardiovascular Disease: 2007 Update.
  4. ExTraMATCH. “Exercise Training Meta-Analysis of Trials in Patients with Chronic Heart Failure,” British Medical Journal 328 (2004): 189.
  5. Stewart, K.J. “Cardiac Rehabilitation Following Percutaneous Revascularization, Heart Transplant, Heart Valve Surgery, and for Chronic Heart Failure.” CHEST 123 (2003): 2104-2111.
  6. HF-ACTION.  “Efficacy and Safety of Exercise Training in Patients with Chronic Heart Failure,” JAMA 301(2009): 1439-1450. 

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.

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.

Cardiologists comment on Heart Failure Death Statistics blog post

Some of my HeartSense blog posts are picked up and published on CardioExchange, a social network run by the New England Journal of Medicine which, as I write this, has 2,572 members.  The site was established as a safe environment for cardiologists to exchange views candidly and learn of breaking cardiovascular news quickly. I thank CardioExchange for extending an invitation to me, a journalist, to join its site and for finding some of my posts worth their time to read.  I learned yesterday that the public can see blog posts at the site but can not see comments.  And so with permission from Harlan Krumholz, editor of CardioExchange, I reprint comments made to my post “Heart Failure Death Statistics: Don’t believe what you read on the internet”.  I reprint only those comments made by doctors who also gave me permission to publish their comments here.  

Some commenters agreed that there are glaringly wrong statistics about life expectancy with heart failure on the internet and some expressed strong beliefs about the need to pursue the prevention of heart disease.  

To read the blog post that drew these responses, please scroll down to the post titled “Heart Failure Death Statistics”. 

Below are comments reprinted from CardioExchange:

Mark Dayer, PhD MRCP Physician, Taunton, , GB
Competing interests: none

I could not agree more. I now have to advise patients to be a little wary of the statistics quoted on many reputable websites. Although mortality for patients with intractable and unstable symptoms remains high, for many the annual mortality is much lower. I would hope that organizations such as Kaiser Permanente which collects a lot of data on patients electronically will be able to answer this question in time. In the UK more and more hospitals are routinely collecting data on all heart failure admissions and mortality data will follow from this.

Heart Failure Death

Mary Knudson, Health Journalist Other, Silver Spring, MD
Competing interests: none

So glad to hear you say this. Thank you for telling patients that much of the time heart failure is not what it sounds like and that life expectancy for people with heart failure is increasing. I recognize that mortality remains high for patients with intractable symptoms, and for some others, there is the possibility of sudden death. But I wish all reputable websites would take the responsibility of publishing prognosis statistics they can gather from experienced cardiologists who see many heart failure patients or else just not address the subject at all. What is not right is to frighten newly diagnosed patients who are seeking information about their condition and read these terribly outdated death statistics. 

I applaud what the UK hospitals are doing. I wish in the U.S. we could create a national registry or a huge prospective study in which information is collected uniformly and patients’ doctors would give out the information on the cause of death for the registry rather than have a third party try to ascertain from death certificates who died of heart failure. In addition to accurate death rates of people dying from heart failure itself and those experiencing sudden death, we could learn what medical regimens those who died were on and see if there is a pattern of people dying who didn’t get the best treatments. We not only want to know how many people die of heart failure. We want to know why they die. We could also gather a trove of genetic data that one day could be very helpful.
Thank you very much for commenting.

Barry M. Massie, BA (Harvard), MD (Columbia P&S) Physician, San Francisco, CA
Competing interests: none

I remember talking to Mary Knudson some time ago. I made the point that there is no one mortality rate for heart failure patients. Patients hospitalized for their first episode of heart failure have a poor prognosis, especially if it is caused by myocardial infarction, and the 50% 50-60% year mortality rates reported from the Framingham study in the late 1990s were astonishing. As noted by other commentators, these deaths often are not caused by heart failure or even related to cardiovascular disease. In a follow-up study from Framingham published in 2002, however, there was these rates had declined by 31% and 32% in men and women, respectively. Most of this improvement occurred between 1980 and 2000 and probably reflected the impact of ACE inhibitor and beta-blocker therapy. 
But numbers don’t tell the whole story.

Framingham MA, a relatively homogenous, middle-income town is not reflective of the United States. Nor is Olmstead County MN, mentioned by Ms. Knudson. By and large, residents of these communities have good access to health care. Another source of statistics is the data generated from large clinical trials. Compared to epidemiological studies, these patients uniformly have a much better prognosis. Why? They are carefully selected for the absence of other serious comorbid conditions and for their adherence to treatment. Their follow-up in the trial is frequent and rigorous. In these, mortality rates often fall below 5-8%/year, even in the control groups.

Despite what impresses me as a dramatic improvement in the outcomes of heart failure patients in the more than 30 years I have worked in this field, we still have a long way to go. Unfortunately, the attention focuses on the dramatic treatments that make it to TV—transplants, left ventricular assist devices, implantable defibrillators, stem cells. Yes, these work, but the costs are high, and the numbers of appropriate candidates for these are relatively small and will remain limited.

Hence, my plea would be that we shift our focus to prevention. Heart failure is relatively easy to prevent but will take a shift in our behavior. Early detection and effective treatment of hypertension can prevent up to 50% of all new heart failure cases. Prevention of heart attacks with changes in diet, life style, and smoking cessation will prevent another large number of heart failure cases. Changing diets can have a similar effect.  A decrease of 1 to 3 grams of daily salt would save more lives than all of these high-tech interventions taken together

Those of us who work in the field and keep up with the basic research advances in our understanding of the potential mechanisms causing heart failure and novel treatment targets are aware of the large number of potential therapies that have not been developed because the large pharmaceutical companies prefer to develop “me-too” drugs where the path to approval is more straightforward and the risk is less. Research is risky, but marketing works. In the end, they seem more interested in winning the marketing war than investing in “finding the cure”.  

Using the usual sports adages, if we want to win the war on heart failure, we have to invest. We need to change behaviors, emphasize prevention, and build on the great success of the decades of neurohormonal-directed interventions with novel and complementary approaches. 

This should be the role of the NHLBI. It needs to invest in the next generation of novel therapies, perhaps in partnership with the industry. It should use its prestige and resources to educate the public. As a recent seminal analysis by Bibbins-Domingo in the February 18 issue of the NEJM demonstrated, just a moderate reduction in salt intake (largely driven by intake of processed foods and fast-food restaurants) would have a major impact on cardiovascular outcomes including heart failure. It would be much more cost-effective and save many more lives if we direct our research toward the prevention of heart failure or early diagnosis and modification of the process in its early stages. Wouldn’t this be a wiser way forward investing enormous resources on developing high-tech interventions for the tip of the iceberg of patients with advanced heart failure?