Heart Failure

Well…Something the Democrats and Republicans can finally agree upon

It’s been a difficult couple of weeks for Uncle Sam.  We truly have had a spectacle in our nation’s capital, and for the average American, the news is all bad.  Somehow in the midst of all the work that our representatives should have been doing, a bill arose in the Senate and was passed unanimously.  Was this to endorse apple pie as our national dessert?  Was this to increase their pay?  Better parking at the Capitol building?  Give up?  It was Senate resolution 243 endorsing a campaign against Atrial Fibrillation.

Say what?  I’m not kidding. Unfortunately, I wish I was kidding about much of what I blog about, but you can’t make this stuff up.  What did this landmark bill say, and why was it promulgated?  This bill was introduced by Senator Crapo (I swear I’m not making this up) and co-introduced  by Senator Casey, Senator Inouye, Senator Akaka, Senator Rubio (yes ours) and Senator Toomey. In the House, a corresponding resolution House 295 has been introduced and is being supported by the Heart Rhythm Society, which has recently been in the news as being to cozy with industry and StopAfib.org -- a patient advocacy site which is heavily endowed by drug and device company money. I urge you to read the bill in it’s entirety as it is short.  It provides some facts such as the cost burcden of atrial fibrillation to the United States, which is estimated at $15.7 billion a year, that it affects about 2.5 million patients and that it is common over the age of 65. The Senate wants the Secretary of Health and Human Services to work with medical leaders “to explore ways to improve medical research, screening and prevention methods, and surveillance efforts in order to prevent and appropriately manage Atrial Fibrillation.” The resolution goes on to tell of all the wonderful ways we need to improve this problem, but guess what?  I knew you knew.  No money was appropriated in the making of this piece of information.  It’s just a resolution telling us, the populace, what our Senators would like us to know and do.  These are the same characters that voted along party lines whether or not to create a new healthcare act.  These are some of the same characters that are trying to dismantle the same said healthcare act because the insurance companies are doing such a great job. This is a great idea and a great need.  What we have, however, is a disingenuous ploy of doing something while doing nothing.  When the elected officials in Washington get serious about healthcare instead of worrying about who gives me a free pen, maybe we will get things done.  Until that time, all we have is the “war on cancer,” and we all know how that is going.

Another question about Pradaxa

A question was posted on my blog concerning Pradaxa pacemakers and dosing.  It brings up several good points and some information readers and -- judging from the question -- doctors need to know.

The writer asked whether Pradaxa interferes with a pacemaker.  Pacemakers and patients with defibrillators are common in patients who have atrial fibrillation because of the many pathways that lead to the condition.  Pacemakers are not affected in anyway by Pradaxa.  Pacemakers are not effected in anyway by anything we do unless specific instructions are given to it.  The only way to affect a pacemaker or defibrillator is to expose it to magnetic forces as that drives the device to a preprogrammed mode and inactivates some functionality of the device.  There are drugs that can affect the heart and its conduction system, and this might make the device do either wanted or unwanted actions.

The question poses two more issues which are more concerning.  The writer states that her mother was placed on the 75mg dose so that it would cause “less bleeding.”  First, many patients on anticoagulation have retinopathy secondary to diabetes and have had retinal bleeds.  Medicine has risks and balances.  There are choices.  Most patients would prefer losing vision in one eye to a debilitating stroke.  The option is of course theirs but that is what the ophthalmologists say.  You cannot adjust the intensity of Pradaxa by lowering the dose.  The only factor regarding the dose that counts is your kidney function.  If you have normal kidney function and take 75 mgs as a dose, you are not going to be affected by the drug.  If you have poor kidney function and take a dose of 150 mgs, you are going to be at severe risk of bleeding.  You must take the proper dose if you want the effect of the drug.

So the answer to the question is depending on her renal function and whether the patient wants a stroke or an eye bleed.  In the vast majority of cases it’s neither.

But, is 75 mgs a “real dose?”  How did we get to this point?  Pradaxa was approved based on the data from a study known as RE-LY.  The doses used in that study were 150 mg twice a day and 110 mg twice a day.  Huh?  Where did the 75mg dose come from?

The data in the study showed that the 150 mg dose was superior to the 110 mg dose in preventing strokes but caused more bleeding.  The bleeding with the 150 mg dose was similar to warfarin but still lower.  The FDA made the decision to accept more bleeding and less strokes as the better choice for the United States.  In particular, the data for those patients 75 years old or greater provided important information as these patients are very common.  Stroke with the 150 mg dose was 1.3 per 100 patient years and with the 110 mg dose, 2.4 per 100 patient years.  Bleeding was 5.3 vs. 5.7 with the lower dose.  In English, this means that the stroke rate was better but the bleeding the same, so don’t let people choose to have a stroke.

The 75mg dose was “made up” by the FDA using real data concerning the pharmacokinetic and pharmacodynamic modeling.  It was not in their words “based on efficacy and safety data” N Engl J Med 2011; 364:1788-1790.

So there we have it.  The FDA made these choices for us, and this is what we have to go on.  I do not know of a plan to test the 75 mg dose for “safety and efficacy."  Why would the company do it?

One last word today.  I received a troubling e-mail from a reader regarding her husband who was on Pradaxa.  He was to have a cardiac transplant, was on Pradaxa and received the call for the operation.  This operation is very time sensitive and must be done immediately.  As I have blogged about before, you cannot reverse Pradaxa’s effect.  The transplant took place on Pradaxa and the patient eventually died from the complications of managing the bleeding.

This serves as a warning.  If you have a time sensitive condition, it is probably best to be on warfarin.  It works and can be reversed.  My sympathies are with her.

A bad week for Cardiology Part III

We now come to the worst part of this week’s news.  This issue I have blogged about before on 04/07, 04/12 and 04/14, and will become an ever increasing issue for us.  Once the infrastructure is in place to track and understand this data, physician’s behavior will have to change or they will not get paid for the work that they do because it has failed the “appropriate use criteria."

As published in JAMA. 2011; 306(1)53-61 almost half of all non acute angioplasties maybe uncalled for.  This article queried the “oracle” our database from July 1, 2001 to September 30, 2010.  During that time 500,154 angioplasties were performed.  71% of these angioplasties were performed on patient populations who are deemed acute.  Any patient who is acute is automatically appropriate given our guidelines.  The acute categories are:
STEMI: 103,245 (20.6%)
NON-STEMI: 105,708 (21.1%)
High risk unstable angina 146 (29.3%)

They total 355,417.  That’s an awful number of patients that still suffer from an acute cardiac process.  Our identification of these individuals has improved but clearly we, as a nation, still have a great deal of work to do on primary prevention.

144,737 angioplasties, or 29%, were performed for non acute indications.  Here is where the problem lies.  As I have blogged about extensively, optimal medical management equals or surpasses angioplasty in the treatment of STABLE angina.  Angioplasty only plays a part in patients who fail medical management.  The COURAGE trial showed us this as well as other examples that I have written about. The stable patients broke out as:
No angina 53.8%
Low risk ischemia on noninvasive testing 71.6%
Patients taking less than 2 anti angina medications 95.8%

Angioplasty and cath are two different procedures.  It maybe appropriate to cath someone who has a low risk stress test because those tests are not infallible and an exact knowledge of the coronary anatomy helps in many ways to educate and reassure patients.  All of the patients in COURAGE underwent cardiac catheterization prior to enrollment.  In other words, you can cath, but if you want to do an angioplasty, you better have a good reason and it better be explicitly documented and recorded for our database. This issue will become an ever expanding issue for hospitals and cardiologists.  If the procedure is denied for insurance purposes, then the hospital payments will also be denied.  If a hospital is found lacking in oversight of its staff then regulatory agencies will respond.  It will not be pretty.

This is probably a good place for one final shout out.  It maybe time for cardiologists to perform the necessary paperwork for the data entry into the database.  This is often left to data abstracters who, although they give the work their best effort, are not the same as the physician who has an exact knowledge of the patient, the clinical situation, the decision making issues and the results.  If we as physicians don’t take more care of our results, then we will have no one to blame but ourselves when it blows up on us.

I can guarantee that it will.  Consider yourself warned.

An answer to a question

I received a question about a recent blog post about Pradaxa.  One of my goals when I started the blog was to provide an interactive forum with my readers about cardiac issues that interest you.  I urge you to comment or send me issues that you would like to see more thoroughly discussed.  The question that was sent me raises an important point and here is the answer.

The question was in regards to whether Pradaxa can be reversed?  The short answer is not at all.  This is the first time an anticoagulant was allowed on the market that can not be reversed.  We at JMHVRI were involved in the work of a novel anticoagulant that had a specific reversal agent but that work has been put on hold.  Heparin has protamine which at times can provoke life threatening and fatal reactions.  Warfarin (Coumadin) can be reversed with the replacement of the missing factors by administering Vitamin K or oral Vitamin K.

We presently use the powerful antiplatelet agents Reopro and Integrilin that also are difficult to reverse.  Integrilin can not be reversed and the effect must “wear off” which takes about six hours.  Reopro can be reversed with blood products.

If someone is injured or needs emergent surgery the only option is to deal with it.  We have multiple methods to insure what we call hemostasis and the replacement of many units of blood may be necessary.  The effect of the drug will wear off in several hours and the blood clotting parameters will return to normal.  If someone is bleeding on Pradaxa the mantra will be support, support, and support.

Patients ask “why can’t we measure the effect of the drug?”  We can measure the presence of the drug but the measurement is a simple yes or no.  We can draw a test known as an aPTT or activated partial thromboplastin time, and if normal, no drug effect is present.  If the test is positive, it does not tell you what the strength of the effect is just that the drug is active.

A limited availability test known as an Ecarin Clotting Time can tell in a linear relationship how strong that effect of Pradaxa is on the clotting ability and may be more widely available in the future.

Why would the FDA allow a drug on the market that can’t be reversed?  The large studies done did not reveal that this was a large enough problem to interfere with the benefit of the drug.  There was no increase in major or fatal bleeding with Pradaxa.  Across all spectrums, Pradaxa was more effective and safer than warfarin.

All drugs have risks which must be balanced with the benefits.  People can’t live and we can’t practice always worrying about the rare scenarios.  If you need this drug you will in all probability benefit from it.  It represents a remarkable advance in our ability to practice medicine.

A bad week in Cardiology Part II

Now let’s talk about why we keep doing things to patients even though no clinical benefit is derived, and the most recent guidelines state that it is a Class III event i.e. of no  clinical benefit and possibly harmful.

When angioplasty started we were so proud of ourselves that we invented a whole scenario as to how beneficial “an open artery” was.  All sorts of benefits were attributed to it.  An open artery improves LV function, may prevent left ventricular remodeling and may prevent the late development of arrhythmias.

The trouble was, and is, that this almost doesn’t exist anymore.  With the advent of early invasive management for myocardial infarction, both STElevationMI and NonSTElevationMI arteries are opened immediately, or if significantly blocked, opened at that time.  It is quite unusual to cath some 24 or more hours later and find a closed artery.  What should we do at that point?  The answer was derived in 2006 and published in N Engl J Med 2006; 355(23):2395-2407.  In the population studied, the opening of the artery vs. medical management did not lead to any benefit four years later.  In 2007, the opening of these arteries were deemed a Class III event.  It was made crystal clear: don’t do it anymore.

Well it looks like this is another message that didn’t get across.  Do we not read?  Does anyone read my blogs?  Published this week in Arch Intern Med Doi: 10.1001/archinternmed. 2011.315 is an article which queried our infamous data base -- the NCRCathPCI registry -- from 2005 to 2008.  They found 28,780 patients who qualified by having an occluded artery 24 or more hours later.  The authors found no difference in rates of angioplasty suggesting that, like small children, we still do what we want when we want.

This study has problems with it but is probably the best we are going to do short of another study to prove the same thing we already proved.  The only way to stop some behavior is to stop the root cause which is to not pay for it.  This, however, would actually take enormous resources to do and may in fact be more expensive than just paying.  A mechanism could be employed in which you have to submit data to get paid for an angioplasty but that would then require someone to read the data, understand the data and defend the data when payment is denied.  No easy task in the best of circumstances.

Patients differ and problems differ, but some issues are always the same.  An area of myocardial infarction that can not be shown to be viable will not by wishful thinking make it so.  We now have a way of knowing this foolproof, but of course it involves money and expertise.  MR scanning with Gadolinium enhancement will document viability of myocardial muscle and should make this decision more “scientific” in the future, but it is the future.

This community and I lost a great friend and doctor when Carroll Moody died this past December after practicing here for almost 40 years.  Carroll taught me the greatest lesson that I learned after training.  "Alan," he would say, as he looked at me after I showed him a set of films and gave him the information, “sometimes the best thing to do is nothing.”  I didn’t understand it at first but the older I have become, and the more I did, I realized that it was good advice to follow.

I wish more people would have gotten the same advice.  He would not be happy about this article.  I miss him daily.  Medicine misses him.

Next…even worse news to come.

A bad week for Cardiology Part I

At times, in the process of writing this blog, I am forced to confront the limitations of education and humanity.  This past week is a prime example.  An article has been published stating that 50% of all angioplasties done are unnecessary, that we continue to perform angioplasties’ on arteries that have been shown to be of no value and the revocation of Dr. Mark Midei’s  Maryland medical license. Who is Dr. Mark Midei and why should we care?  I will give you the brief version of this sordid affair.  Dr. Midei was hired away from his original group to lead the cardiology program at St. Joseph Medical Center in Towson Maryland a suburb of Baltimore.  He performed about 2000 angioplasty procedures over a two year period and stands accused of implanting “unneeded stents” in 585 of those patients. This case dates back to a patient complaint in April 2009, which then led to an investigation and the removal of his privileges to practice at St. Joseph.  Hundreds of law suits have now been filed on behalf of the patients who were affected, and the incident received congressional evaluation and drew in the American College of Cardiology and others to testify. The congressional committee released a scathing report calling it “a clear example of potential fraud, waste and abuse.”  On one day, Midei implanted 30 stents.  It is estimated that $6.6 million was billed for these procedures, and Medicare paid half.  The recoup by Medicare alone will bankrupt anyone, and if fraud is found, jail time will follow. The stent maker Abbott was drawn in as they frequently “rewarded” Midei as a high volume physician and paid him more than $30,000 as a consultant. This past week, after a seven day hearing in front of an administrative law judge, a 77 page decision revoked his medical license, and he can not reapply for it for two years.  At the hearing, which involved five cases that were not part of the original complaint, the “experts” found that he was found to have: -Unprofessional conduct in the practice of medicine. -Willfully making a false record in the practice of medicine. -Gross overutilization of services. -Violations of the standard of quality care. -Failure to keep adequate records. Among the “findings” was the conclusion that Midei implanted six stents in 4 patients in which he claimed that the lesions were 80% of the lumen, and the findings were that the % stenosis was much less.  One of Midei’s experts is a prominent local Cardiologist. This is to some degree a slippery slope.  The practice of medicine changes, and treatments change.  This, in most cases, is progress.  As I have stated many times, the use of angioplasty is to relieve angina that is not relieved by medication.  Appropriate use criteria now state that two anti-angina medications in appropriate doses should be utilized before angioplasty is performed (more on this later).  Chart documentation is required before proceeding, and a full knowledge of a patient's care is required.  In addition, we have mechanisms to provide exact answers in those borderline cases.   I can tell you that in general it is not difficult to tell which lesions are severe and which are not. Patients have been harmed in these cases.  The act of stenting a coronary artery is permanent and provides a long term follow up challenge for doctors and patients.  Stenting is not a benign procedure.  This unfortunately is a representation of the worst of medical care. Next…why do we keep opening the closed artery?

What TAVI is and isn’t

Edwards Sapien Valve on Balloon

There has been enormous interest generated by TAVI or Transcatheter Aortic Valve Implantation.  I have blogged about it before, and it represents the dawning of a new era in valvular heart disease. As with any paradigm change, there are good parts and bad parts.  Perhaps the most important part is keeping control of the genie once we let it out of the bottle.  This technology has been available overseas and in Canada for some time now, and we have already seen some of the cohesiveness and divisiveness that arise from it. As I have mentioned, this technology will allow us to place a new aortic valve in patients who ARE NOT CANDIDATES FOR REGULAR AORTIC VALVE SURGERY.  I emphasize that because those will be the regulations.  This will not be a doctor/patient choice; this will be decided by a committee, internet based, who will review candidates and allow procedures to take place.  The truth of the matter is that my surgical colleagues can operate on the vast majority of patients, and just because you want a valve in this way does not mean you will get it in the United States. In those patients that do qualify, TAVI will lead to a better lifestyle and less long term mortality.  Patients get to this point in a multitude of ways.  The disease of Aortic Stenosis (aortic valve restriction) goes on for many years, but patients are often reluctant to subject themselves to an operation when they don’t feel poorly.  When they finally do, their multiple co-morbidities often overwhelm them and their doctors.  Some patients present at a late stage because of a failure of the medical system in which they live.  Some patients just say no until they realize they are going to die. The busiest people these days are the folks from Edwards who will hand out the “keys to the kingdom” when the valves are released from FDA purgatory in the near future.  As written about in the Expert Consensus Document published jointly by the American College of Cardiology and the Society for Thoracic Surgery in J Am Coll Cardiol (doi:10.1016/j.jacc.2011.05.007), the components of this program are daunting, and only a few of the eligible programs will receive permission to start up. The components include the requisite surgical and interventional cardiology expertise.  It will include imagining expertise and a dedicated heart team.  It also requires a large capital expense of building or retrofitting an operating theater to perform the procedures in.  It will require ancillary personnel for database entry and management and an ongoing learning and training environment.

We at Holy Cross are privileged to have these components in place.  We have a Board of Trustees and a CEO who are foresighted and are building a brand new hybrid OR that you can see going up in the area in front of the Emergency Room entrance (sorry fellas).  It will be attached to the present Operating Rooms on the third floor of the hospital so it will be seamlessly integrated into our system. We have surgeons who are as good as any in the country, and we are presently among the largest valve programs in the state of Florida. Whether we achieve our goal of being awarded a key is unknown, but I want the community to know that we are working to bring this technology and opportunity to a broader reach of patients here in South Florida.  We will continue to improve our cardiovascular programs for you our community and neighbors.

More fun with statins

In keeping with the topic of statins, we have another piece of foolishness that was fussed over this past week in the lay press.  It involves the interaction that statins have with diabetes.  For some time now there has been a belief in some quarters that high dose statin therapy can lead to diabetes.  This signal originally showed up in the JUPITER study of Crestor that I have blogged about in the past.  Obviously, if true, we would like to know this.

Published in JAMA 2011; 305:2556-2564, this damned-if-I-don’t-and-damned-if-I-do study shows that the use of high dose statins to achieve target LDL levels of 70 is associated with a 12% increase in diabetes when compared to more moderate doses.

How did these individuals arrive at this information?  They used a total of five studies in a meta-analysis which contained a total of 32,752 patients who did not have diabetes at baseline.  These patients were followed from 2 to 5 years.

As in most of my blogs, there is a kicker -- a moment where the unreality of what I do on a daily basis kicks in.  Although it has been heralded in the press that now “statins cause diabetes,” here is the point of the paper that the press missed.  Your risk of developing diabetes from high dose statin is one in 498Your risk of not having a cardiovascular event is one in 155.  In English, it means that your benefit of not having a heart attack, stroke, or revascularization is far greater than your risk of developing diabetes.

Remember Austin Powers?  “What will it be MI or diabetes?”  Most people when presented with the facts will choose to take the high dose and eat less.  The numbers clearly favor that approach.

One other factoid  relates to my last blog.  When simvastatin 80 mg was compared to atorvastatin (Lipitor) 80 mg,  the risk of diabetes was the same but the benefit was a 22% vs. 5% risk reduction for cardiovascular events favoring Lipitor.  You maybe getting what you pay for with the statins.

This whole problem of cost vs. benefit will diminish when Lipitor becomes generic later this year.  Talk with your doctor to make certain you are on the proper statin at the proper dose for your condition.

Where there is smoke there is fire

For some time now, there has been a low rumble concerning the highest dose of simvastatin which is known by it’s trade name as Zocor.  This low rumble has now emerged as a full throated roar as the FDA has effectively halted the use of the 80 mg dose in new patients. How did we get to this point, and why did it take so long?  Zocor was originally approved in November 1997 and was approved as a generic in June 2006.  Really.  It took us 14 years to decide that a dose of a medicine was toxic?  We are on the ball.  This result was actually published on November 9, 2008 in England, but I guess the boat over from England took some extra stops along the way. The information that the FDA used is from a study known as SEARCH.  This study stands for the Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine.  It was done by the Clinical Trial Service Unit of the University of Oxford by individuals who are quite talented.  In fact, these are the individuals that I blogged about recently regarding the HRS-PREVENT study. The study was simple.  They took 12,000 men and women who had a heart attack gave half of  them 80 mg of simvastatin and half of them 20 mg of simvastatin.  These patients were then followed an average of 6.7 years.  The high dose was associated with a reduction of 6% in the number of heart attacks, strokes or revascularization procedures.  At the time a meta-analysis with three other studies showed that the reductions were at the 15% level. These studies are one reason that I urge my patients to take as much statin as they can tolerate. 

The second part of the study was to see if lowering homocysteine with folic acid would help and sadly it did not. Here is the “money shot."  In the 6,000 patients who took the 80 mg dose, 53 developed a myopathy as compared with 3 in the 6,000 group.  This works out to about 1 in 1,000 compared to about 1 in 10,000. None of this relates to other drug interactions that occur with simvastatin.  The FDA is clear at this point that no one should be started on the 80 mg dose and that if you are on it, it is possible that you need to be switched.  I will not review the drug interactions here, but they are multiple and are with common cardiovascular drugs. Now lets get to the real problem.  In today’s practice of medicine, at least once a day I get a notice from some pencil head at an Insurance company that I need to change the statin someone is on to simvastatin .  This is being done solely because it is “cheaper” and has no bearing on the effectiveness of the patients present therapy.  As simvastatin is 1/2 as strong as Lipitor and 1/4 as strong as Crestor this interchange is problematic at best and seriously impossible at worse.  The combined goal of lowering the LDL to 70 that is the target in this patient population can not easily be obtained in the  most part by simvastatin. To paraphrase Austin Powers, “what will it be, cost or effectiveness?”  When will the FDA stop telling me what to do and begin to tell the Insurance companies?  I will let you know how I and my patients do.  In the mean time if you are on the 80 mg dose of simvastatin you may want to discuss it with your doctor.

An answer to a question

I received a question on a recent blog from a 67 year old woman.  She wanted to know what a calcium score of 44 meant.  Hers happened to be in the left anterior descending, but it could be anywhere in the coronary tree.

The answer is unfortunately poor in that we don’t quite know, and likely never will, because it would take a large randomized clinical trial, and no one will pay for it.  The reason being is that there is no money in it and no money to be made from it.  Although this answer is not a very satisfying answer, it is nonetheless the truth.  As I mentioned in my recent blog, this is the job of the NHLBI or the new Medicare center for applying best practices if it doesn’t get gutted by the Republicans.  I will be blogging about this more soon.

Another reason that it won’t get done is that the powers that be in Medicine (yes there are such people) who adjudicate whether study A or study B should be funded often have preconceived opinions about these issues and will not approve the studies to come forward.

We do know some things, and I will share them with you.  First and foremost, we as doctors need to know whether you had the test as screening or whether you had the test because you have symptoms.  If you have symptoms and you had the test, it is possible that this would need to be worked up further, particularly if you are on medication.  If you are not on medication, then all you may need is to start medication and see if you feel better.  If you did not have symptoms, then many physicians, including me, believe that you should be started on a program to reduce your risk.  The mantra is the same.  Stop smoking, eat better, lose weight, exercise and take statins.

Can we use calcium scoring to assess risk?  That is the real question that needs an answer.  As published in JACC 2003;41:1475-9, the Framingham risk score and the NCEP-III guidelines turn out to be poor predictors of myocardial infarction risk in men< 55 and women <65.  This method utilizes a CT scan and one spin of the gantry.  The score is derived from a combination of the density of the calcification and the number of pixels in which it appears.  The higher the score, the worse it is.  Recently, this has been improved upon by utilizing individual scores for each of the coronaries instead of the whole heart method.  The original method was developed at the University of Miami by Drs Janowitz and Agaston (The South Beach Diet).  The calcium is there on the outside of the artery because of the cholesterol damage.  It is a marker of atherosclerotic disease and can even at times be seen on a plain chest x-ray.  We often get results about this phenomenon when patients have CT scans of their chest for other reasons.

Recently, an article was published in Arch Intern Med 2011;DOI:10.1001/archinternmed.2011.204 which touches on this issue.  They used full CT angiography of the coronaries which is different then calcium scoring.  These patients were asymptomatic, and a control group comparison after 18 months found no difference if you had disease or not.  The study is flawed but hypothesis generating.  Again, it is unlikely that this concept will be put to the test.  The one thing we don’t want is to keep adding tests that lead to greater expense and radiation exposure for no benefit.  Maximal medical therapy, as I have described, is the treatment for coronary disease that is symptomatic.  If you have calcium in your coronary tree but are asymptomatic you need treatment and not more tests, aspirin and statin at a minimum.

I hope that answers the question.