Heart Failure

For Those Living with Heart Disease

White Hearts in a circle image

Learning that you or a loved one has heart disease changes your life. However, educating yourself about this disease is the first step toward feeling better and making choices that can help you live a longer and healthier life.

According to the Centers for Disease Control and Prevention (CDC), approximately 11.5 percent of Americans have been diagnosed with heart disease. February is American Heart Month and the National Institues of Health offer the following suggestions to help navigate treatment if you or a loved one has been diagnosed:

•Making lifestyle changes. Not smoking, following a heart healthy eating plan, maintaining a healthier weight and becoming more physically active can go a long way in helping to keep your heart disease from worsening. 

•Taking medication. Medications are often used to treat high cholesterol, high blood pressure or heart disease itself. Be sure to take your medication exactly as your doctor prescribes. If you have uncomfortable side effects, let your doctor know. 

•Following doctor’s orders. Your doctor may recommend procedures to open an artery and improve blood flow. These are usually done to ease severe chest pain or to clear blockages in blood vessels.

As you know, having a primary care physician (PCP) who can coordinate your care is vital to your good health. If you don’t have a PCP, finding one is easy! Just visit your insurance carrier’s website, look for the “find a doctor” area and follow the instructions.

When you’re being treated for a disease or condition, it may not always be easy to decide where to go for care. For anything that is considered a life-threatening situation (like chest pain, major injuries or sudden and severe pain) it’s best to go to the emergency room. 

For less severe matters that still require immediate attention, if you can’t get in to see your PCP, going to an urgent care facility can save you time and money. 

As your trusted health partner for life, Holy Cross Hospital is committed to helping you Live Your Whole Life by nurturing well-being through body, mind and spirit.

 

It’s not just about taking out the garbage

Two recently published studies highlighted what the authors think is an emerging problem.  They seem to have the data to document it.  The problem seems to be loneliness over the age of 60. The two studies are published in the Archives of Internal Medicine (Arch Intern Med 2012; DOI:10.1001/archinternmed.2012.2782).  They used two data bases and are observational which means that no intervention or grouping took place.  The first database was the Reduction of Atherothrombosis for Continued Health or REACH and the second was the Health and Retirement Study. Basically, loneliness was established by living alone.  This is much more common than it was, given the chances of remaining married have fallen below 50%.  Further, the sole survivor of long-term marriages now can live many years alone.  I see many patients who are married 60 years or more.  I believe this will be a tough act to follow given the trends of marrying later in life and divorce. I also see many patients who are now alone and live with an army of full-time aides.  I wonder if that will count.   Is loneliness worse than constant bickering among two people?  I don't know, and this study doesn't provide that insight, but I see interactions in my office that if they extend into the home -- and I see no reason why the behavior would be different -- are not conducive to happiness.  At least in my mind. The studies report that if you are >60 years old and live alone, you had a 59% decline in your ability to take care of yourself.  There was a 45% increase in mortality compared to having a companion.  Mind you, not necessarily a spouse, just someone who lived with you. In the REACH study, 44,573 patients were enrolled, and 19.3% were living alone.  After four years, the mortality difference was 14.1% vs. 11.1%.  This is a 27% increase in death and a 25% increase in cardiovascular death.  Of note, the increase in death occurred in those patients 45-65 years of age even though the risk of living alone triples after 80 years old. Why this occurs is not known and is clearly a risk factor that needs further evaluation.  There are differences in the nature of early coronary disease than later coronary disease.  If you live alone and are male you may not be impelled to improve your habits like smoking if you have no one to "remind" you all the time. Family is often an important motivator to improving health as mile post events are often present.  A graduation, a wedding, etc. that provide an impetus to improve your health, take you medications and so forth that might not be present in those that live alone. It is not reported whether an animal serves as a "stand in" for another person, but it is well-appreciated that having a pet can improve depression symptoms and bring happiness to people. We live in an age of instant and constant communication.  You cannot have a meeting or even a conversation lately without a text or call interruption.  This communication is wonderful, but it has also gotten woefully out of hand.  The plane lands, and 100 people all call and announce the landing. It's too bad that cell phones or computers don't stand as replacement for humans.  No one would die.

Even if they pay us, it doesn’t matter

Medicine is changing.  Everyday in the media there is another story as to the problems in medical care and the multiple ways that it is going to be fixed.  What doesn't get a lot of coverage or discussion is that none of the proposals currently being promoted to "fix" our healthcare system actually work.  I can say that because that is what the evidence shows. Flying under the radar is an article published recently in the NEJM.  A major reason I write this blog is to make sure that what is off the radar gets noticed.  Titled "The Long-Term Effect of Premier Pay for Performance on Patient Outcomes" and published on March 28, 2012 (10.1056/NEJMsa1112351), this article deals which one such concept. I have blogged about this before.  I find it difficult to understand the concept of paying me more to practice what is considered, at least at the time, "best medicine."  On a daily basis, I endeavor to practice medicine the same way, for the benefit of my patients, using all my knowledge and experience.  Can you really pay me more so that I will do better?  Is this really a concept? It turns out that it doesn't even work.  What's more, this study isn't about one year; it is six years.  We couldn't even get it right over time. What did they try to do?  Over six years ago, CMS or the Centers for Medicare and Medicaid started a pilot study know as HQID or the Premier Hospital Quality Incentive Demonstration.  Two studies after, and three years into the study, they failed to show any effect on mortality.  Nonetheless, this policy was placed in the Affordable Care Act to expand to all hospitals in 2012.  This article demonstrates the six-year data. The hospitals in Premier were generally larger, teaching hospitals and nonprofit, than the comparison hospitals.  Four conditions were examined.  These were acute myocardial infarction, congestive heart failure, pneumonia and coronary artery bypass surgery.  At baseline there was no mortality difference in these conditions  between the hospitals.  At the end of six years, there was still no difference in mortality among these conditions.  One small but insignificant difference was that the mortality to CABG was slightly higher at the Premier hospitals 4.12% vs. 3.34%. After six years, there was no evidence that you can pay to increase the quality of care and to decrease mortality.  As the authors state, "These findings are sobering for policymakers who hope to use incentives to decrease mortality."  Sobering perhaps, but it will not stop them from continuing to try.  Let me explain why this is a problem.  A considerable amount of time, effort and cost goes in to collecting the data required for these analysis at each hospital.  These data are required by law and must be done.  I am a firm believer in data because if you don't figure out where you are, you can't improve upon it.  All this costs money.  When the resources go to collecting data for poor uses, then the same resources can't be used to collect and analyze data which might be useful to patient care.  Some of this is hospital specific, and some is generalized. The Feds must stop trying to entice us to do better with money and just pay us a fair amount for the excellent work which is being done.  We all want the same thing: excellent outcomes for all patients.  It is not always possible, but it is always our goal.

The best drug you never heard about (Part II)

Why do we care about the resting heart rate?  Our bodies are made up of checks and balances.  One of these pathways is that when the cardiac function falls, the kidneys sense it and produce signals and substances that make the heart go faster to increase the cardiac output.  Back in olden times, the most common reason for low cardiac output was blood loss.  Making the heart go faster supported the body, and those that could support the blood loss lived another day.  This compensatory mechanism is good for sword fights but not very useful for poor heart function. When the SHIFT study was analyzed further, it showed that if you were on the usual meds and still had a resting heart rate >75, you had a 39% improvement in heart failure mortality if you received the drug.  Total mortality was reduced 17%.  Both numbers are very impressive for a little over $2 a day.  It is felt that roughly 15% of those patients with systolic dysfunction would qualify for this drug.  The higher your resting heart rate was to start, the greater the benefit. In the British system, an Institute known as the  National Institute for Health and Clinical Excellence, or as it is known NICE, reviews all the drugs and devices in the UK to see if they are cost effective.  Novel concept right?  The NICE evaluation of Ivabradine is to be released in December of this year, but in the system of the UK, patients are under the control of the General Practitioner.  Each GP has a roll and is responsible for those patients.  Each GP does not have many patients that fit this problem, so this drug is already receiving wide use before it was approved for this new indication as it is not that expensive. Another interesting point is that although used for the treatment of angina, the drug Ivabradine had no effect on cardiovascular death, new myocardial infarction of new or worsening heart failure.  The real use of the drug may well be the new indication. Now let's talk about why this drug is not here.  The answer is I don't know, but here are some guesses.  The company that made and paid for the study, Servier, is a privately owned French company.  It is the largest independent pharmaceutical company and the second largest French pharmaceutical company worldwide with revenue of Euro 3.5 billion in 2006.  Its largest drug to date is an ACE-I known as perindopril.  To bring this drug to market in the US, they would need a partner to sell it as they have no employees here.  They would need to do a study over again that shows that the drug is useful.  The work already done is interesting to the FDA but is not evaluable for the per poses of drug approval in the United States.  As I have blogged about in the past, most studies are now done worldwide so they generate approval data worldwide.  The cost of redoing this study would likely be over $300  million, and it's just not worth it to the company.  Unless an American company has an interest in doing it, the likelihood of our seeing or using this drug here is nil. Is this right?  Is it really necessary to do everything over and over again to approve a drug?  If we spend so much money on approval, how come we screw it up so many times?  Doesn't anyone care about the patients?  Doesn't anyone have the ability to make sense out of this mess?

The best drug you have never heard about (Part I)

Would you believe me if I told you that there is a drug that reduces a condition's mortality by 39%, and we don't have it here in the United States? By this time you, my readers, know that it is probably true. Now I will tell you who and what. I can't tell you why because like much of what we do here in the U.S., I have no idea what we are doing. I have blogged about the condition of lung congestion caused by a heart that is either stronger than normal, diastolic dysfunction, or weaker than normal, systolic dysfunction. The heart dysfunction causes the pressure in the heart to increase, and this increase is transmitted to the generally low pressure lungs so patients develop shortness of breath and fluid in their lungs. This leads to admission to the hospital. These health costs in 2008 were north of $35 billion. A common term for this is heart failure. I grew up in a system that "hated" that term as it was felt by my teachers that it was too frightening a term for patients and too loaded with baggage. Most people use it, however, and I continue to walk around with that nails on a chalk board sound in my ears. This illness accounts for 550,000 new cases a year and 300,000 deaths. One would think that we would use every available means at our disposal to combat it. That doesn't seem to be the case. I will make it worse. What if this drug cost $2.21 a day? What is this drug? The drug is called Ivabradine and was approved in Europe in 2005 for the treatment of angina. In Europe it is known as Procoralan. It is not a beta blocker like metoprolol, and it is not a calcium channel blocker like Cardizem. What does it do? Ivarbradine lowers the heart rate independently of those drugs, so it can be added to them or used instead of them. For instance, some patients can't take beta blockers because of asthma or other side effects. This drug is then used instead of beta blockers, or in addition to them, to promote a slower heart rate, and the patient has less angina. A study was done known as SHIFT or Systolic Heart Failure Treatment with the IF Inhibitor Ivabradine Trial. It was published in Lancet 2010;DOI:10.1016/S01406736(10)61198-1. This study was done at 677 centers in 37 countries and enrolled over 6,500 with NYHA class 2-4 heart failure with an LVEF70. One percent of the patients withdrew from the study because of a slow heart rate. It was not done in the United States. These patients were being treated with the standard drugs we use. 90% were on beta blockers, 91% on ACE-I or ARB drugs, 60% on aldosterone antagonists. Only 26% were at "target doses" of beta blocker. The target dose of a beta blocker would be a dose that achieved a resting heart rate of 60. These doses closely mirror the "real world" of the practice of medicine (remember we are "practicing"in the hope of one day getting it right). Next...what they found and why it matters.

The next big advance (Part II)

In my previous blog, I outlined the problem with resistant hypertension and its treatment. Now let me explain where medicine may be heading. Published in J Am Coll Cardiol, 2012; 59:901-909 and titled "Renal Sympathetic Denervation Reduces Left Ventricular Hypertrophy and Improves Cardiac Function in Patients With Resistant Hypertension" (Catchy title; we do know how to drag the readers in), this article relates the effect of this new device to ablate the renal nerves. Although predicted, this article reveals the stunning short term effects of this powerful treatment. In this relatively small study of 46 patients and 18 controls, the procedure resulted in a 27.8 mm drop in blood pressure at six months. LV mass was significantly reduced; diastolic and systolic function was significantly improved. A trifecta. Further, and perhaps most surprisingly, even those patients that "failed" the treatment defined as having blood pressure drops of < 10% still had a marked reduction of LV mass at six months. This reduction of LV mass may continue over time. This cohort is being studied in an ongoing manner. This technique is going to compete with several other techniques that are being developed to modulate sympathetic activity. The other techniques are much more invasive and leave hardware behind. They include carotid baroceptor manipulation by a coil around the carotid and a pacemaker like device implanted in the chest, spinal cord implanted stimulator and vagus nerve stimulator. Like Presidential candidates, each has its supporters or detractors. Indeed like Presidential candidates, one will win this race. The technique described is simple and a one shot deal. It does not need any patient compliance, and it will reduce the cost of treatment longterm. It is a winner on all fronts. In the form of full disclosure, this would be a technique that my skills would allow me to easily do if available. These kinds of advances are critical to reducing the cost of medical care and improving patient well-being. Admissions to the hospital setting because of systolic and diastolic dysfunction are a major drain on our healthcare dollars. These admissions are often not the fault of patients or providers, however, they are viewed as failure by the system, and soon Medicare will not reimburse for them. This will leave both hospitals and doctors at a disadvantage. This procedure will have a cost, but it is not nearly as much as the benefit, which will then extended far beyond the initial procedure. It represents the best that innovation can provide. One further note that you will read about here in more depth throughout the year: physicians' understanding of systolic heart failure and the causes of it are slowly changing. The gospel now is that weight gain through dietary and fluid noncompliance leads to increased congestion in the lungs and swelling and fluid collection in the legs. New information however is now pointing some physicians in a new direction. This direction is closely linked to evidence that the increase in lung pressure that starts off the cycle takes place at least a week before the symptoms occur. What if I told you that the sympathetic nervous system seems to be involved? More to come.

We are still batting zero (Part II)

What is the FDA’s problem?  In short, for this or any other heart failure device to be approved, it needs to reduce “heart failure” in some way.  Since the causes of heart failure are generally permanent, the one way that counts is to document that it prevents hospitalizations for heart failure by using the device.

An interesting aside 

Medtronic has a feature on pacemakers that are capable of pacing both sides of the heart and on ICD’s or as they are known, implanted cardiac defibrillators.  This feature is known as Opitivol, and it is a measurement of thoracic impedance through the wires that run through the heart and chest. The impedance goes down when the fluid in the chest cavity goes up, and so, it is a measure of volume overload not on daily basis but over time.  Much like the hemoglobin A1C measurement for diabetes.

This measurement is plotted on a graph and serves as a warning sign to physicians that a heart failure episode may occur.  This feature is accepted by Medicare, and reviewing it is a billable item for physicians.  The theory went that if the device would sound an alarm when the Opitivol threshold was crossed, patients might be able to avoid an episode of heart failure. 

This alert feature is allowed in Europe and Canada.  When it was tested in the SENSE-HF Trial, all the alert did was increase outpatient visits and hospitalizations without changing its effect on episodes of heart failure (Circ 2011;124:1719-1726).

Back to Cardiomems

On December 8, 2011, the panel known as the Circulatory System Devices Panel met and rejected the device.  Although not binding on the FDA, it usually follows the panel’s recommendations.  The 10 panel members voted 9-1 that the device was safe but then voted 7-3 that the device was not effective in preventing heart failure episodes.  The vote was 6-4 that the benefits did not outweigh the risks.

Much of the problem seemed to occur because of what was felt to be additional help to the treatment group that may have been over and above the protocol demands.

Since the device does work (i.e. it gives beat-to-beat measurements of the pulmonary artery pressure, which to this point is only available invasively), I suspect that we have not seen the last of it.  The company that makes this device was purchased by St. Jude, a large medical device company.  I do not know the status of that sale, but I suspect that other studies will be planned, and as St. Jude has both the resources and the expertise to run these studies, the result may be different the next time around.

As I have written, it is not clear to me why we can’t crack this nut.  As in most issues that are complex, it may be that we are not asking the right questions.  We may not be setting the right goals and so we are forever doomed to failure.  It is entirely possible that some episodes of heart failure cannot be prevented.

Perhaps we should concentrate on another method of caring for these patients.  This is getting some consideration in the Medical Home approach and the outpatient CHF clinic approach.  If we never admit these patients, have we succeeded?

Are our goals wrong?  Is this a Kobayashi Maru?

We are still batting zero (Part I)

I have blogged about the challenges of heart failure in the past.   It will continue to be a topic blogged about often because of the many unique challenges associated with this condition.

Heart failure is the collective term used to describe a situation and not an illness.  Dr.  J. Willis Hurst who was one of the founding fathers of modern cardiology, and one of my teachers for many years, would chastise any physician or caregiver who would use the term “heart failure." He felt, and I believe rightly so, that the term was freighted with difficulty for both patients and care providers.  To this day, I still can’t hear the term without it provoking anxiety in me.  I recall him shaking his head in disgust and chewing out whoever said it as if it was yesterday.

Patients in particular are bothered by it and rightly so.  What would you think if someone told you you have heart failure? What are you supposed to do about it?  This is not the same thing as being honest with patients.  How you present the same facts and the words you use can make a huge difference in someone’s understanding and cooperation.

You can have heart function which is normal but have lost the heart’s normal elasticity (diastolic) or have a heart that doesn’t contract properly (systolic) because of myocardial infarction, infection, drug toxicity, alcohol toxicity, etc.  These situations both produce a syndrome of fluid collection in the body and lungs which leads eventually to inability to breath, which leads to hospitalizations and enormous expense.

No matter what we do, we have not yet cracked how to manage this.  We can’t even invent a way of monitoring it without an invasive strategy of placing a catheter directly into a patient’s lung through a vein.  Many have tried, none have succeeded.

Now comes word that the next victim became the Cardiomems device.  Let’s understand one thing.  These devices all do what they say they will do.  They monitor the pressure in the lungs through various mechanisms.  The Cardiomems device is an elegant, small device that has no moving parts and no battery, so it would never wear out.  The device is inserted into the lung vasculature through the veins in the leg and released.  It settles in the lung vasculature and provides no damage to the lungs.   It responds to an outside the body stimulus, and the pressures in the lung are received.

These pressures are important, and they signal difficulty before symptoms appear.  This occurs roughly 5-7 days before the patients gain weight or leg edema occurs.  If we knew the pressures, we could adjust a patient's medication to prevent an episode of fluid overload, causing  shortness of breath and eventual hospitalization.

That is the theory.  The FDA is not interested in whether the device “works."  Much like they are not interested in the fact that drug X lowers cholesterol.  The FDA wants to know whether there is any clinical benefit, and does it reduce heart failure admissions.

Next...why they said no.

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How are “real” doctors doing?

As I have mentioned before, the practice of cardiology has led the way in codifying the results of clinical trials to formulate guidelines which, if one cares to read them, points a reasonable way to care for patients.

Physicians may disagree with some of the guidelines, and some guidelines do not have enough data from large trials and are “best guess” opinions, but in general, they represent years of work that I and others like me have participated in the past.

Cardiologists and cardiac surgeons also led the way in databasing their results in cath lab, angioplasty, electrophysiology and surgical procedures.  They are known as the NCDR or National Cardiovascular Disease Registry and the STS or Society of Thoracic Surgery registry.

Now a new database has been constructed known as PINNACLE.  PINNACLE is run by the American College of Cardiology and is an acronym for Practice Innovation and Clinical Excellence.  This database was launched in 2008 and now is beginning to bear witness to how we take care of patients.  In other words, do we follow directions?

30 large practices across the country are enrolled in PINNACLE.  PINNACLE uses a standard data collection tool to assess longitudinal patient care.  Symptoms, vital signs, lab values and hospitalizations are gathered and reported.

Published in Circulation at Circ 2011;124:2405-2410 is a study titled Coronary Heart Disease Statin Use in Outpatients with Obstructive Coronary Disease.  It details the results of 38,775 patients as to who was prescribed statins and who reached the prescribed guideline goal.

Repeat after me: if you have had a myocardial infarction, angioplasty or coronary artery bypass surgery, your LDL levels should be below 70 mg/dl.  The use of statins here is for secondary prevention not primary prevention, which is the treatment of patients without evidence of disease.  Primary prevention has been covered in other blogs.  Of the 38,775 patients, 77.8% were on statins.  5.3% were on nonstatin lipid lowering medication such as Zetia, and 17% were untreated.  In those patients who were untreated and had lipid values available about half just didn’t get any, and half had LDL’s less than 100 mg/dl.

Two points should be noted.  The first is that I often hear patients tell me that their lipid numbers are great.  The point is missed.  If your lipid numbers are so good, why do you have coronary disease?  Numbers don’t mean anything.  The atherogenicity of the lipid is what matters.  This can sometimes be teased out by extensive and expensive testing, but I usually avoid it.  Studies show that if you have an LDL less than 100 and coronary disease, guess what?  You need statins as much as the next guy sitting next to you with an LDL greater than 140.  You must drive your LDL as low as possible.

Second, the database does not allow for an understanding of why these patients go untreated.  It just documents the numbers that are.

Close to 25% of the patients in these highly motivated practices are not being treated with statins.  This represents a tragic loss of life and a waste of resources as events can be prevented.  I can only imagine what the  numbers look like in the general practice population, but of course, they are worse.

Databases like this will help us define best practice in the future.  We are trying to improve.  We need to improve.

P.S.  Lipitor is now generic.  In 180 days it will be very inexpensive to get one of the greatest drugs ever created.