LOWER THE HEART RATE, LONGER THE LIFE. TRUE?

When I first started private practice, I was given a desk calender by one of the pharmas, which had these sayings " Humans are predetermined to have almost 3 billion heart beats / lifetime. ", and another one which says, " The Galapagos tortoise has a heart rate of 6 beats / minute, and so it should live 177 years ". Does that mean that a reduction in mean daily heart rate be expected to prolong life?
Are these sayings true. I am not so sure. Perhaps a bit exaggerated. Maybe there is some element of truth.
Recently, there were a couple of clinical studies which seem to imply that slowing the heart rate reduces cardiac events. Prime of which are the studies using the drug, Ivabradine. In fact, the good old CASS study of bypass surgery in the good old days, seemed to suggest this.
Well, at the just concluded Canadian Cardiovascular Congress 2010, Dr Sherryn Remihar and colleagues from the McMaster University, Hamilton, Ontario, presented a paper linking CV mortality and morbidity, with increase in basal heart rate. They actually when into the TRANSCEND and ONTARGET data base, of about 30,000 patients. These were patients with stable CAD who were on treatment for hypertension. They were deemed the high risk group. Dr Sherryn and colleagues looked into their baseline heart rate each time they came for follow-up over 56 months, and related it to CV mortality, strokes, MIs, and heart failure admissions. They found that if you suffer from stable CAD, and your baseline heart rate is in excess of 70 /min, you have a40-50 % increase risk of developing one of these CVS complications, namely CV death, strokes, heart attacks and heart failure. That is very significant. You cannot argue with a cohort of 30,000 patients. In fact, the risk starts to go up from a mean baseline heart rate of 50 / min. They observed an increasing trend from a HR of 50/min. Whats important, this trend seemed to be more important for those 65years or younger. It seemed to be less significant for those above 65 years.
These findings are important. Whether increase heart rates in stable CAD means that these patients had more stress, or poorer heart functions, or inadequate medications, is not certain. We also do not know if lowering heart rates artificially with beta-blockers or Ivabradine, will help. Looks like Ivabradine, helped those patients in heart failure, if SHIFT is to be believed, although BEAUTIFUL did not show the same ( both studies by Servier ).
At the end of the day, maybe it is true, that we each are pre-determined to have 2 billion heart beats per lifetime, so we must use it wisely, otherwise, the heart beats may run out and so may we. So treasure each day and each heart beat. We may live longer and better that way.

THE LATE Mr NESTOR KIRSCHNER - SUDDEN CARDIAC DEATH. ? DES STENT THROMBOSIS

The whole of Argentina, the whole of South America and I believe also the whole world is surprise at the sudden demise of the immediate past Argentinian president, Mr Nestor Kirschner, on Wednesday. My condolences to his family and love ones. Officially, he died from sudden cardiac death. I believe that there are some lessons that we can learn, so that his death is not in vain.
The late Mr Nestor has multiple coronary risk factors, including stress +++, cigarette smoking, and probably hypertension. In February 2010, he had undergone carotid ultrasound which picked up a carotid artery stenosis, and he choose to undergo carotid endartrectomy. It may be that at that time, he was also found to have coronary artery disease. In early September 2010, he underwent coronary angioplasty and had a DES implanted ( we are not sure which artery ). It was uneventful, and it was alleged that he had gone for a political meeting, upon discharge from the Argentinian hospital. 6 weeks later, on Tuesday, he complained of flu-like symptoms, and on wednesday morning, he felt some chest pains and collapsed before he could reach the hospital. Technically, this is sudden cardiac death. But surely, for those of us who are interventionist,unfortunately, he had suffered a subacute stent thrombosis, on his DES. By ARC definition, this would be a probably stent thrombosis, and if it is autopsy proven, a definite stent thrombosis. I am sure that his interventionist must have given him dual anti-platelet therapy, be it clopidogrel + aspirin or Prasugrel + aspirin. There is of course the small possibility that he may have taken some PPI ( proton pump inhibitor ), for some previous gastric pproblem ( we are not sure ), or he may be " clopidogrel resisitant ".
Whatever the exact situation, we can learn that we must respect PCI and DES implantation. Sometimes, because, the devises are so good and success rates are so high, we implant them with impunity, and take short cuts. We do not spend time explaining the serious need for anti-platelet therapy ( with religious vigor ). We allow them back to stressful activity too quickly. Maybe CABG, brings about more patient respect and compliance with medical advice, because there is a painful scar to remind them of the severe disease, for a few months at least. We also learn that stent thrombosis kills, and can kill quickly.
I have often express the view that perhaps, angioplasty equipment should be difficult to use and the stents difficult to get down. Then less physician will dare try and thereby ensuring that only the most experience, with healthy respect for the procedure would dare undertake it, and so maintain good standards and success rates.
We are not sure, which Argentinian interventionist undertook the procedure, but I am sure that he/she is well qualified. I must say that there are some very good interventional centers in Brazil. In fact the " first-in-man" experience with the first DES - the Cypher stent, was in Sao Paulo, Brazil.
Again, my condolences to Mr Kirschner's family and love ones.

SODAS, SUGARY DRINKS AND DIABETES RISK

We have always said that the fast food culture is mainly to blame for the increase risk of obesity, diabetes and metabolic syndrome in the younger generation. The combination of cheese burgers, ( quarter pound ) and sodas is a killer ( silent killer ). Well it is not silent anymore.
The Nov issue of Diabetes Care carried a piece of work ny the researchers in the Harvard School of Public Health, Boston, led by Dr Vasanti Malik and Dr Frank Hu. They did a meta-analysis on the relationship between sugary drinks and diabetes and the metabolic syndrome. They found that the consumption of 1-2 sugary drinks is associated with a 26% increase in the incidence of type 2 diabetes and a 20% increase in the incidence of the metabolic syndrome ( the more cardiac deadly form of type 2 Diabetes. This risk is proportional to the amount of sugary drinks that you take. To put it in perspective. Smoking 1 pack of cigarette daily, is associated with a 30-40 % increase in the risk of developing type 2 diabetes. So that drinking 2-3 sodas a day could carry the same risk as smoking a pack of cigarettes. I use to tell my obese patient who consume coca cola, to just spill some on the table and run their finger through it, and feel the sugary stickiness. Some of the carbonated drinks contain as much as 6-8 table spoonful of sugar. No wonder the young ones love them.
Does consuming " diet sodas " make a difference. We do not know. The jury is still out on this one. Does artificial sweeteners help to lessen the risk. The data here seems conflicting. We need more data.
What then can be done? Action to be taken must be by the health authorities, if they are serious on reducing obesity and diabetes, both of which are serious health problems that consume alot of our healthcare expenditure.
Well, we have proposed before for the ministry of health to carry out mandatory food labelling, detailing how much calories there is in each drink or food substance, so that the public knows what they are ingesting. Then we physicians can take a detailed diet history, to try and ascertain the amount of calories, our young ones are consuming. Removing sugar subsidy is a good idea. In fact, making sugars more expensive is a good idea. That should cut down usage. If all these soft steps fail, we could of course take the more drastic step to sell sugar and sodas by sugar / soda coupons. Certain people are not allowed to buy sodas, and you can only buy so much sugars per month. This is being tried in some states in the USA.
No one will like the last step. But can I say that " It is for your own good ", now that we have evidence.

SOME SCIENTIFIC EVIDENCE ON RED YEAST RICE

Red Yeast rice is sold over the counter ( OTC ), in many countries, including Malaysia and Singapore, as a traditional herbal treatment for dyslipidemia ( commonly called high cholesterol ). It is cheaper then " statins " and there is some evidence to show that it works like Lovastatin. There were some small studies which showed that it was helpful in people with "statin" intolerance.
The recent, 25th October, issue of the Archives of Internal Medicine, carried an article by Dr Ram Gordon, from the University of Pennsylvania Health System, Philadelphia, on an a piece of research that they have done on Red Yeast. They took 12 brands of Red Yeast, and send them to an independent chemist to find the composition. The chemist was blinded to the brands and told to analyse the compound.
They found that 60mgs of red yeast contain varying amounts of Monacolin K, which is the active ingredients. The concentration of Monacolin K, in red yeast could could vary by as much as 2-3 times, so that their effects become difficult to predict. They also found upon analysis, that red yeast also contain some bacteria, aspergillus, and penicillium, and even worse, contain some nephrotoxic substances, like citrinin. These may be contaminants from the manufacturing process, or may be from the yeast itself.
Looks like there is more in red yeast then Monacolin K ( lovastatin like ). The contaminants is cause for concern, and certainly the nephro-toxicity, is bad.
I would advise that physicians do not recommend red yeast to their patients, until the manufacturing process is cleaner and more standardised. By then, it may cost as much as a "statin".
At least we are beginning to get more data out of herbal traditional therapies. Such work should be encouraged.

EXERCISE AND THE HEART FOR SENIORS

Cardiologists are always advocating the importance of fitness and exercise, advising that these activities are good for the heart. In all aspects, yes. Sedentary lifestyle is a coronary risk factor. We want our patients to be active and exercise. Although that advice is true, we must learn to distinguish what benefits exercise confers on the senior citizens ( many of us, myself included are near that stage of our lives ).
Firstly, regular moderate exercise, as we advocate for all people, is about brisk walking, 15 Km a week, in divided portions. Basically, 5 Km of brisk walking ( or its equivalent ) daily, 3 times a week. For those seniors, who do not wish to measure and be exact, I always tell them, 3 times a week of walking, until you break out into a good sweat. For some of them, at 75 years, this is reasonable advice. If you do this, you should be able to contain your weight, or even lose some weight, and improve your fitness. It may reduce your cardiac risk profile, keep away obesity, diabetes and hypertension ( the 3 sisters of CAD ). That is all true, but it may not make your heart younger.
To get your heart younger, is that possible?
The 18th October on-line edition of Circulation carries an article by Dr Naoki Fujimoto of Texas, USA, who examined the issue of exercise and cardiac muscle stiffness and fitness. He studied 12 males above 65 years, to see if 12 months of intensive exercise can regress the stiffness of the heart. These senior citizens were asked to exercise 6 days a week. After 12 months, all their cardiac performance indices were measured, in particular the cardiac muscle stiffness factors and also the arterial stiffness factors. These were compared with 12 elite athletes above 65 years. These elite athletes had been training 6 days a week all their life and had been taking part in competitive sports. He found that that although the arterial stiffness factors improved, and the major blood vessels became less stiff, it made no difference to the cardiac stiffness. Meaning that once you age, if you have been seriously exercising all your life, your heart remain less stiff, for longer. If you have not been exercising vigorously all your life, intensive exercises at 65 years or more, only helps you to keep fit and relaxes your arteries, but not your heart. This is obvious, because as we age, the heart muscle loses its tensile strength gradually and the muscular fibers get replaced by collagen fibers and amyloid ( we call this aging ), and it slowly becomes stiff.
The researches are now studying if drugs can help to stop this change and slow down the replacement of muscle fibers with collagen fibers. Studies have shown that the cut off point seem to be when we are 45-65 years when the cardiac muscles begin to be replaced, and any attempt to improve and reverse it may have to be undertaken at or before 45 years. I have my doubts. I do not think that you can fight against aging. Maybe we can delay it for a while. All cells are program to die, given time.
So, we learn that we cannot fight against aging. When you exercise, do so in moderation, 3 times a week and break out a good sweat. Especially if you are 65 years or more.
Keep fit, keep healthy and enjoy your age.

hS-CRP, IS IT DEPENDENT ON RACE?

There is an article circulating in the internet, purportedly written by a retired cardiac surgeon, saying that coronary artery disease ( CAD ) is not the result of raised cholesterol levels, but from inflammation. That statement is partly true, but it certainly is not as simple as that. Inflammation causing CAD is what I thought I will discuss here, since I am asked to explain what the retired cardiac surgeon meant.
Since the 60s, large population studies have shown conclusively, that raised cholesterol levels was associated with an increased incidence of CAD. As a portion of the blood ( serum ) cholesterol comes from food, it made alot of sense that we should educate our patients to take less cholesterol rich food, in an attempt to lower or blood cholesterol and so our risk of heart disease. Blood cholesterol, in the medical eyes, is just one amongst many risk factors for CAD. The rest being cigarette smoking, hypertension, diabetes mellitus, obesity. The minor risk factors are gout, sedentary lifestyle, stress, etc, etc. No body is saying that cholesterol is the only risk factor for heart disease. The pharmaceutical industry, sensing an opportunity, had gone ahead to find drugs that will lower cholesterol effectively ( and they have with the "statins" ). With their high powered marketing, send out the message that cholesterol is all important and that we must reduce our cholesterol till it reaches ground zero ( or as low as possible ). They obviously have much to gain, if all of us do that. What is often not said , is the significant risk associated with too low a serum cholesterol level for that individual. Afterall, God did give us serum cholesterol for a purpose. Anyway, I am digressing.
So it became that serum cholesterol was almost made synonymous with the presence or absence of CAD. That is wrong. Afterall, almost 50% of people with heart attacks have a normal or below normal serum cholesterol level.
In the 80s, researchers began looking into this issue of inflammation as a cause of CAD. They looked at bacterial and virus infections as a cause of inflammation causing CAD, and came out blank, except for some association of dental infections and CAD. Bad oral hygiene can be associated with CAD. They were also trying to associate Rheumatoid Arthritis ( an inflammatory joint disease ) with CAD, and there is some association. Some research workers in USA, especially the group working around the Boston area, found that LDL-cholesterol, was itself a toxic agent in the artery wall, and it excites inflammation. This was easily shown in basic science research. The inflammation, under the microscope was obvious, and easily demonstrated. What we did not have in the 80s was a bedside way of identifying who was having inflammation and who was not.
Since the 80s, there was a blood test available for us to monitor our patients suffering for inflammatory joint disease call the C-Reactive Protein ( CRP ). When the C-Reactive Protein level was elevated, it meant that the joint condition ( be it SLE or Rheumatoid Athritis ), was flaring up and a relapse was coming. This allowed us to increase the steroid doses to lessen the inflammation and control the joint inflammation. So C-Reactive protein became a blood maker for inflammation. But CAD is not joint disease, although inflamed joint can trigger CAD.
The workers around the Boston area ( led by a researcher call Dr Paul Ridker ) is credited with measuring micro levels of CRP, in patients with CAD, without joint inflammation, and associated it with CAD. Infact his work was mainly to associate miro-CRP or what highly selective or highly sensitive CRP ( hS-CRP ), with heart disease and postulated that hS-CRP was another risk factor for heart disease.
Needles to say, waiting by the side are the pharmas, who have a drug to lower hS-CRP, and so lower heart disease. ( Remember my earlier article in this blog about the close relationship between physicians and pharmas ). So convenient. This was studied in a large clinical trial sponsored by Astra Zeneca, called the " JUPITER study ". On the basis of this study, they convince the FDA ( who I think did not need much convincing, with Pharmas behind prompting ), to add their indication that Rosuvastatin, the AZ drug that lowers serum cholesterol and hS-CRP, is indicated to lower hS-CRP.
What prompted this blog is a study, published in the September 28th issue of Circulation CVS Genetics, by a group of workers across the pond, namely University College, London UK, who showed that hS-CRP was variable and their baseline values varied according to race and ethnicity. You see, the background is that although the Boston group from this side of the pond believed heavily in hS-CRP, their colleagues on the other side of the pond, UK and Europe, do not quite share their enthusiasm. Yes, hS-CRP may have some association with CAD but not quite the same importance as stated by the Boston boys. It is just another risk factor, like cigarette smoking, not anymore important.
So the controversy goes on.
In our own experience, we see clinical kit out commercially, and every Tom, Dick and Harry is measuring hS-CRP, with varying degrees of accuracy. The results are so variable, that I could not rely on them for decision making. So in a way, I am on the side of the pond that says that hS-CRP is another risk factor and not the "critical " risk factor that some would like to make it out to be. It is so variable.
Maybe, it again raises the whole bigger issue of too close a relationship between physician and pharmas. Certainly, the conclusions of the " JUPITER study " was questioned and some differ strongly. Well, we are small fry, so will just conclude that hS-CRP makes inflammation and many things else, and is just another risk factor for CAD. By the way, all statins lower hS-CRP, to varying degrees.
And the controversies continues.

MEDICAL / HEALTH TOURISM. THE PROS AND CONS FOR MALAYSIAN HEALTHCARE

Lately, we have been hearing much about Tourism and in particular Medical / Health tourism. It may be because we have a very active Minister of Tourism, trying to make more money for the government coffers. This is of course not wrong. It helps our country's bank account. But are there any downside? What are the pros and cons?
Let me share with you the perspective from a private medical practitioner, quite senior in service. Firstly, let me begin by differentiating between health tourism and medical tourism. Health tourism is providing healthcare to foreigners who are not " SICK ". These are all part of wellness. A good example is cosmetic surgery ( lifts, nips and tugs ). Medical tourism on the other hand is giving medical therapy to a foreign patient. These are people who are not well ( patients ) who either find the waiting list is their respective countries unacceptable ( e.g UK ), or find the cost of treatment too high ( e.g USA )., or both. Labour cost being cheaper in developing countries, we can hopefully provide "equivalent " healthcare or medical care at perhaps half the cost. Why do I put " equivalent " in inverted commas? Because it is perceived that way. The so called equivalent standards of care is all marketing and market driven. Private hospitals will pay money ( quite alot ) for certain international companies, for example JIC, to come and evaluate their hospital. Should they pass, they are awarded a JIC certificate and this allow them to go to USA and UK and advertise that they have good facilities and good doctors. But wait a minute. All that JIC or equivalent bodies do is to evaluate the standard operating procedures ( SOP ) of a hospital, and their facilities. As for the medical personnel ( which is one third medical care ), they only ask for a list of the medical personnel on staff and their CVs. Everything is on paper, not on expertise and experience. So, if you have a fresh FRCS, he is on paper as good a surgeon as an FRCS practising for the last 20 years. Hospitals are always recruiting new graduates, so that their hospital is full of " specialist ", of whatever calibre. Medicine has become a business, and doctors are also beginning to feel that they are a pair of hands in this business cycle, and so some of them are also beginning to behave like businessmen, and can you blame them.
One of the good thing coming out of this push to medical / health tourism, is that doctors will get an increase in fees. I could not understand why the MOH ( ministry of Health, Malaysia ), wish to enact a bill to control doctors fees. In the light of health tourism, and the government attempt to encourage our own doctors working or training overseas to return. They have to increase doctors pay and fees. Which doctor, with a cushy job overseas, will wish to come back, go on call and take off a gallbladder at 1am in the morning for 600 UK pounds? or USD 1,000? We have always asked the government to remove the fees schedule, and this push towards medical tourism, may just help us to do just that. Maybe that is why, at the last fees schedule Task Force, committee meeting, we were told that the PM feels that doctors fees must be increase quickly.
The other problem with medical / health tourism is that, there may come about two standards of care. One for the full paying foreigner and one for the locals. Hospitals will become 6-7 stars, and charge 6-7 star fees, where the average locals will not dare to tread. All the specialist, who feels that they are 6-7 stars will gravitate there, is it a business mah, so who will be left to care for the deserving locals in their own country?
Of course doctors / specialists are also worried. Should they do a procedure on an American, and the procedure goes sour ( patient suffers a complication ), he can be sued in US courts and be awarded damages in US courts. That will be a small catastrophy for the specialist. His whole life work could be wiped out in one go, so he will buy more medical indemnity insurance to protect himself. Medical indemnity fees will climb till US proportions, and the cost will be passed on to the patients. So cost of care will go up.
Yes, the Thais, especially the Bumrungrad hospital I am told is doing very well, so everyone here would like to imitate them. Not so easy. That can form another story.
Finally, the government has announced that they wish to have a Public-Private Partnership to start an Academic Medical Center? I suppose it is a private corporation ( probably GLC ), forming a partnership with John Hopkins - College of Surgeons, Ireland. We have heard painfully little about this. Nice idea. As usual, it is the working out that is the more difficult part. I must say, the tune has changed. Last February, when we were gathered together for three days to hear the Minister ( MOH ) launch the 10th Malaysia Plan Healthcare Transformation and Re-structuring, we were given briefings by all the DG and Deputy DGs on this subject, and there was no mention anywhere of an Academic Medical Center. I suppose, should it come about, we should see many retired overseas " experts ", here partly for the " Malaysia my second home - silver hair " program and also to teach some courses. Well lets see what happens? Is it another flash in the pan idea, or are there any substance in it. They lend their names. It is always nice to say that John Hopkins is here ( borrowing their name ). I hope it does not lead to them testing ( ideas / drugs / procedures ) what they cannot test in USA, here. That would be a shame.
Interesting what the future holds? As for me, it is cardiology as usual.

TRANSMYOCARDIAL LASER REVASCULARISATION. TMR / TMLR : IS THIS THE END?

Transmyocardial laser revascularisation is a technique of using laser catheters to punch micro-holes in the myocardium of the left ventricule, in an attempt to improve the blood supply, directly to the heart muscle. This technique was invented to try and help those patients who could not be revascularised either percutaneously ( PCI ) or surgically ( CABG ). This technique was extensively studied in the mid 90s, with many clinical trials done, some showing that it helped, and others showing that it was essentially a placebo effect and that it did not help.
Well ( re-hashing old news that I just discovered), NICE has just stopped re-imbursement for TMR / TMLR in UK, saying that the cost does not justify the benefit, and quoting severe lack of data to suport its continual use. As we all know, NICE stands for the National Institute for Health and Clinical Excellence.
Just to recap, TMR / TMLR was quite popular in the late 90s and early part of the 21st century. In fact, some US centers are still using it. I see some advert promoting it in the Cleveland clinic website.
The concept is really quite attractive. There are sophisticated equipment invented to map out ( in 3-D ) the ischemic regions of the myocardium. These are patients who had 3-VD, had undergone CABG previously and also PCI, until it is no longer possible to PCI and no more vessels to graft, or maybe CABG is too risky for too little gain. With the 3-D mapping ti guide, a laser catheter is introduced percutaneously, and manipulated to the ischemic region and burst of laser ( usually CO2 laser ), is applied, to create micro-holes. Some patients feel better, and their grade 3-4 angina got better ( maybe to grade 2-3 ). This clinical improvement was thought to be due to improvement in direct blood flow to the myocardium ( something like the Vineberg techniqe ). There was also a theory that making small holes in the myocardium, may stimulate angiogenesis, so that new blood vessels are formed and so myocardial blood supply is improved. Remember that these are class 3-4 angina patients who have no other choice. Of course, the effect is only temporary and repeated courses are necessary. At the height, in 1999, many centers were buying the machines and the technique was shown at live demo courses.
Well, further research revealed that the micro-holes barely lasted 2 weeks before they close off
And also, no consistent pattern of angiogenesis was noted. Patients symptoms invariable recurred and the process had to be repeated with less and less effects. So NICE put a stop to it.
I think Malaysia also need some kind of NICE or NICE equivalent. Of course, UK has a social health system to deliver healthcare. Through taxes ( rather high ) UK citizens are looked after by the NHS ( National Health System ). NICE is a very respected body who look into treatment and treatment modalities. They study clinical trial materials and drugs and see if certain drugs or procedures help more then harm. Those that harm, does not help enough ( cost effectiveness ) will not be recommended for re-imbursement by NHS. Which means that that drug or technique will lose its main payer, which usually means that it will slowly fade away. The payer controls the use.
I suppose with rising cost of healthcare, we do need this type of body, to adjudicate, what should and should not be used. All specialist have their favourate hobby horses, some of which do not add significantly to quality or quantity of life. We need a " NICE-like " body to say, enough is enough.
I suppose, in away, it does ask the question, how much is life worth? Especially when society have to pay for it. Would you spend RM 50K per course for 3 courses to prolong life for 9 months in a patient with incurable cancer. Such a difficult question to answer, when emotions get in the way. Is this money better spend helping more patients with hypertension better treated. That is where NICE play their part.
As for TMR / TMLR, NICE has decided in May 2009, enough is enough. And I think it is fair.

CARDIONCOLOGY, A NEW MEDICAL DISCIPLINE

Over the weekend in my reading, I came across an article telling us that since last year, a new medical discipline has been born, called CARDIONCOLOGY. This idea was first formulated at a meeting of oncologist last year in Milan Italy. The scientist there found that there is a great need for oncologist to be familiar with the workings of the cardiovascular system, as many of the oncologist drugs have cardiac side effects, which ultimately limit their use. In the good old days, it was only adriamycin. I remember those days, whenever " hematologist " ( in those days, there were no oncologist yet ) were going to use adriamycin, they will let one of us know, and we will get an ECG and echocardiogram done, before they started their adriamycin, so that we can monitor them. Every now and then, one of the patients will go into heart failure, or develop some ECG changes, while on adriamycin, and we would have to try and get them stabilised.
Obviously, now adays, cancers are very common and oncologist are in great demand. ( By the way, they are one of the highest earners. They are not cheap ). With good treatment, cancer victims survive much longer and better now. That gives them time to develop cardio-toxicity, and so the need for cardioncologist. I dare say, most, if not all the inti-cancer drugs have cardiac side-effects, either primarily, on their own, or because of accelerated atherosclerosis, which may be an unintended side effects of chemotherapy.
However, although we are good at creating names and disciplines, there are yet no training program for these specialist, so it is very much, learning on the job, ( with some guidance from seniors, I suppose ). In the end, I hope that the founding of this new specialty will help patients live longer and better. Of course, there is a cost to pay. As I keep saying, modern healthcare cannot be cheap. Living longer and better has a price.

BASIC LIFE SUPPORT - BYSTANDER CPR MADE EASIER

Part of the new Private Healthcare Facilities and Services Act 1998, and accompanying Regulations ( 2006 ) mandates that doctors must attend to all emergencies brought to their clinic and no one in need of help should be turned away for whatever reason. We spend many hours meeting at Putrajaya, Ministry of Health to help define what is adequate "emergency help ". There were views expressed that required medical GP clinics to be furnished and staff like a " MASH " field hospital, able to perform all kinds of emergencies. We protested that this was ridiculous and that some have been influence too much by MASH and Chicago Hope, and Hollywood. We instead propose that all GPs should be able to resuscitate and help anyone collapsed. We also advised the MOH to go on a nationwide campaign to educate the public, so that our public have knowledge of CPR ( cardio-pulmonary resuscitation ) and less fear of it. To this, MOH finally agreed and we have gone of nationwide ( a few states ) to conduct talks and CPR courses for layperson, often in co-operation with the St John's Ambulance.
We advised the standard BLS ( Basic Life Support ) technique that is advocated by the British Resuscitation Council, basically 1. Identify the problem and call for help. 2. Maintain airway. 3. Cardiac compression of 30 compressions and one mouth-to-mouth breathe. 4. If an external defibrillator is available ( this is the program of St.John Ambulance, which we do not advocate ), to defibrillate. And to keep doing this until BP and Pulse returns or until professional help arrives. This is all standard in any emergency medical textbook.
I am very happy to note that studies have been done on out of hospital cardiac arrest and the technique have been simplified with some medical evidence to backup.
In the last 3 months, 3 studies have been published. Two studies were published in the July 29th issue of the NEJM ( New England Journal of Medicine ), and one in the Oct 6th issue of the Journal of the American Medical Association. Two of the studies were from USA ( one from Seattle, the resuscitation capital of the world, and the other from Pheonix, Arizona ). The third study was from Sweden. All three studies showed that, 1. It is important to have public education for out of hospital cardiac arrest, and that this increases survival. 2. That all that is needed is to compress the chest ( no need for mouth-to-mouth breathing ), to improve the chances.
In the study by Dr Bobrow of Pheonix, he prospectively studied 5,272 patients with out of hospital cardiac arrest, over a five year period. He followed the survivors till hospital discharge. He found that in Pheonix, after a program of public education, 2,900 of the 5,272 with out of hospital cardiac arrest, were not helped. Of these 5.2% survived till hospital discharge ( so you can survive without help, by the grace of God ). 666 patients had conventional CPR ( compression + mouth-to-mouth ) and 7.8% survive. 849 patients had only chest compression CPR, and 13.3% survive till hospital discharge. These numbers were basically similar to the other two studies in NEJM.
Now we have some fairly good medical evidence that if you see someone collapsed, first identify the problem. If he is no longer breathing and there is no pulse, call for help, and begin chest compression. And keep doing until help arrives. You could save 13.3% of collapse patients ( or 1 in 10 ).
Of course trying to help could have consequences, When we were discussing this emergency medicine regulations for GPs, we also advise the MOH that it must come with a " Good Samaritan " clause to protect the GP, or whoever Good Samaritan, who try to help. Otherwise, he may not get paid for his kindness, and yet end up having to defend himself ' herself from charges of causing hurt and even worse, the death of the patient.
We have along way to go, but if the Government is serious about 2020 and NEW with high income economy, and the status of a developed nation, all these things become important and necessary.

CONFLICTS OF INTEREST. TOO CLOSE A RELATIONSHIP BETWEEN PHYSICIANS AND INDUSTRY.

One of the new features in many American medical meetings ( present in AHA 2009, ACC 2010, and TCT 2010, is a discussion of new health regulations governing relationships between medical industries and physicians. In spring 2010, the Obama administration, passed through the US Congress something called the Physicians Payments Sunshine Act. Amongst all the tiny details, it, and I quote, " requires yearly reporting by manufacturers of drugs, devices, and biological and medical supplies of all payments to physicians or physician-owned organizations over a cumulative value of $100. Under the act, these reports would be then made available to the public ".
This has become the topic for discussions at medical meetings, the last was at the just concluded TCT 2010. It is of particular importance because TCT is where industry show-pieces their latest devices and products to get market awareness. We all know that key physicians are always approached to develop new ideas, and innovate. Sometimes the ideas come from the physician and the industry is sold the idea and they help develop. Many devices, including stents came this way. Physicians buy stocks is these companies, before the breakthrough device is announced and so make " tons" of money when the share rises. In the pharma industry, some physicians ( the big guns " are paid to speak at meetings about certain products and in a way become a marketing agent for the drugs. They are paid hefty fees for that. Some " famous physicians " are paid to write good articles in famous journal to influence practice patterns. Sometimes clinical trials are reported in such away as to help certain drugs. We have also heard, last year of " ghost writers ". These are some famous physicians, who never took part in the clinical trial, but write findings for famous journals so as to influence practice patterns. All these practices, I am sure are unethical and lead us to be wrongly influenced in our choice of therapy, be it drugs or devices.
Of course, in Malaysia too, we have some of the above. We do not yet ( to the best of my knowledge ) have innovators who invented devices which has greatly impacted on clinical practice internationally. I do not think that we have " ghost writers ". We do have physicians, paid by pharmas to speak good about their products. We do have physicians, particularly in government service, who have pharma paid holidays, so that they can " put in a good word " to the relevant authorities, to influence the inclusion of certain drugs from certain companies, into the government " blue book ". The " blue book " has items that the government purchase for use in public healthcare facilities. The government is the largest single purchaser of drugs in this country and if your product ( drug or devices or prosthesis ), get into the blue book, you are assured of alot of sales for the period of the contract. So companies will " take care " of key government senior physicians well ( almost at their back and call ) so that their product can get into the " blue book ". I have seen how they " take care" of these doctors. Believe me, the companies are prepared to spend big.
In a more controversial way, is the present system of organising CMEs ( continual medical education ) meetings for doctors. Doctors who graduated in 1995, will need to be refreshed and updated. Being very stingy people ( they certainly are not poor, but have just got use to free lunches ), they would not pay, to attend CMEs to update. They will only attend if the medical meetings are free ( sponsored ), and if possible with door gifts and leather bags, before they will consider attending. If the meetings charge a fee, the doctors will ( shamelessly ) ask the pharmas to pay for them. Such is our legacy. So we have always depended on pharmas and device companies ( the industry ), for our continual education.
I have laboured the points enough. The US authorities are beginning to take action. What then is the solution for us?
I organise two big CMEs annually, with sponsorship from the industry. I have discussed these issues with the organising committee.
One of our strategy is to raise sponsorship money, from all the competing pharmas and device companies, into a common pool, under the treasurer-ship of a registered medical association, and have the organising committee draw up the scientific program for the meeting. We were hoping that by so doing, we can avoid, in large part, " conflict of interest issues ". All the therapies ( drugs and devices " will be discussed openly, pertaining to the treatment of the certain condition, and leave it to the expert physician to follow clinical trial results and guidelines in their presentation. This has worked well for us, and by and large, the meetings so far have been very successful. But of course, pharmas will only sponsor " small money " if they have no exclusivity. They will be prepared to pay more for sponsorship, if their product is highlighted. So we have to operate with tight budgets.
In the US nowadays, all presenters at meetings, must begin their talk by declaring their conflict of interest statements. I have seen many of my rich and famous colleagues " hide " their conflicts in vague statements.
Is the Obama administrations " Physicians Payments Sunshine Act " the solution? Will it hamper innovations? Locally, will CMEs be able to be conducted without industry help. Not to forget that anything above USD 100 have to be declared and there is not much that you can do for less then USD 100. There are more and more physician organisation being formed annually ( so many experts around ), and they all wish to have their expert conferences. What to do? What is the solution.
I suppose the MACC ( locally ), can begin by looking into these senior physicians who are very " cushy / pally " with industry. Maybe that would be a good first step. Then that riases the whole issue of MACC and their partiality or impartiality?
Looks like doctors, can we stick to being just doctors?

UPDATES ON DES FOLLOWING TCT 2010

Last weekend saw the conclusion of TCT 2010 at Washington. TCT stands for Transcatheter Therapeutics a meeting organised ( very successfully ) by the Cardiovascular Research Foundation of USA. It showpieces all the latest advances in the field of interventional cardiology, and now even beyond that into the field of percutaneous valve replacement ( TAVI ), percutaneous peripheral vascular angioplasty, and also cerebral artery and carotid artery interventions. This TCT 2010 meeting saw many papers and presentations on the latest in Drug Eluting Stents ( DES ) clinical data. So I thought that I should do an update on this, having seen the scene evolved so rapidly over 33 years from a simple balloon angioplasty done using a balloon made in a kitchen, to bioabsorbable stents ( 2 year followup data ).
It may be good ( especially for those not initiated, or not in this line ), for me to step back and recall the events from September 1977 till now.

September 1977 saw the first attempt by Dr A. Greuntzig of Zurich, Switzerland, to successfully treat a proximal LAD stenosis in a middle age dentist. That procedure lasted him 20years, till the dentist developed re-stenosis and required a second procedure when a bare metal stent was implanted, which lasted 6 months ( to the embarassment of the interventional cardiologist, who was also the assistant to Dr Greutzig at the first balloon angioplasty ). Anyway, from the 1977 experience, we saw the birth of a new branch of cardiology called interventional cardiology and we all became "bal-lunatics" ( balloon lunatics). It also saw the establishment of " live demo" courses to quickly teach this new branch of medicine so that it can benefit cardiac patients ( or did it benefit cardiac doctors ). The whole discipline mushroomed and the procedure became immensely popular ( not to forget that the alternative was either medical therapy or the traumatic by-pass surgery ). Then we learned that however good or careful you are, there is a 40-50% chance of the dilated lesion re-narrowing again, and a 4% chance that during the procedure, you may dissect the artery and result in an acute heart attack and the need for emergency bypass surgery. We use to have to keep an open heart theater waiting, a cardio-surgical team on standby, while we work in the angio suite. This went on until we developed the stents. These were basically surgical grade stainless steel, bare-metal scaffoldings that could prop up artery walls and prevent them from collapsing ( in the event of a major dissection ) and because of them we dare to open the artery bigger and more aggressively, thereby reducing the chance for re-narrowing ( from 40-50% to 15-20%, on an average ). Re-narrowing following stenting with bare-metal stents was a result of tissue overgrowth ( scar tissue ), in those patients who were proned ( not everyone, only 20-30% of patients treated ). Also with the advent of the stents, acute closure ( acute heart attacks ) was a thing of the past and we could work without having an open heart theater on the ready ( although it would be nice if there is an open heart theater in the same facility ).
We then realise that a 20% re-narrowing rate was still not good enough and innovators worked feverishly to try and lessen this problem of re-narrowing following ballooning and stenting ( bare-metal ). Taking a page out of cancer chemotherapy, the innovators discovered that coating the bare metal stent, with a layer of chemotherapy ( cytotoxic paclitaxel or cytostatic sirolimus ) was practical, safe and effective, to limit tissue over-growth, and so limit or prevent re-narrowing. To allow the drug coated on to be released in a controlled predictable manner ( just like with oral tablets ingested ), the drug has to be coated with a polymer ( to control its release ). So now, with drug eluting stents ( DES ), you have the drug, coated on the stent ( bare metal ), and covered by a thin polymer coating. This was the first generation DES, as exemplified by the CYPHER stent and the TAXUS stent. Because the chemotherapy drug was delaying the tissue healing ( which is a protective mechanism by the body, to protect the integrity of the artery wall ), patients after DES had to take dual blood-thinning, anti-platelet agents. Initially, we were recommending dual anti-platelet medications for 3-6months. In September 2006, at the European Society of Cardiology Congress, it was reported that some patients were getting heart attacks following implantation of DES, months or even years after the procedure. Further research found that this was because, the artery wall healing was incomplete and the patients had stopped their blood thinning to early. Researchers also discovered that this delayed tissue healing was partly due to the drug effect ( the purpose of the drug ) and partly due to artery wall allergic reaction to the polymer coating. The search then began, to try and develop a technology of having a drug coated on the stent, either without the polymer, or with a polymer that can be absorbed back into the body ( and disposed by the body's scavenging system ). Some companies are so smart that they can coat the drug on the stent, with an absorbable polymer only on the vessel wall side of the stent ( where the action for the drug is ). These formed the second generation DES, as exemplified by Endeavour, Endeavour Resolute, Xience V. Xience Prime, Biomatrix Flex, Taxus Promus, Taxus Element. One company actually tried to harness the body's own healing cells and tried to encourage a natural ( or artificially natural ) healing of the vessel wall after the injury with the stent implantation. The evidence released in TCT 2010 on this Genous stent, showed that this did not work well. The clinical trial data ( TRIAS HR ) comparing the Genous stent with the Taxus stent showed that the Genous stent was inferior to the Taxus stent. Obviously much more work needed to be done with the Genous stent. It is not so easy to imitate God's healing process.
So TCT 2010 revealed many comparative clinical trial data, comparing many of the DES. I sat down and looked through the numbers and came out with the " DES-O-Meter " which I believe is a simple way to illustrate where each of the well studied DES stand. Obviously there are many other DES that are not in the chart. It also means that the good reliable data on them is sparse, or very sparse and so using them is at one's own risk. This big 5, are well studied, proven safe and good. Maybe cost a bit more. If your doctor has used a stent for you that is not on the list, you know what it means. The stent with many arrows pointing towards it, is obviously very popular and many like to compare against them ( bench-marking ). The words in the arrow refer to the clinical trials which arrived at the conclusion, and the positive sign at the end of the arrow shows that that stent is proven superior by those trials. Stents with few arrows involving it shows that there is a lack of good evidence. We all hope that it is not a one off?

Nonetheless, this is not the end of the story. TCT 2010 also saw the presentation ( on Friday ) of the early pilot trial data on the ABSORB. This is a biodegradable DES, owned by Abbott Vascular. The early data seem promising, but still not quite good enough. Suffice to say that this 3rd generation DES is under serious study and I am sure that we will soon ( next 5 years ) see the use of a DES that is biodegradable and totally absorbed back in to the body's scavenging system, after 6 months, so that there is no stent left. The stent and drug just do their work in 6 months and disappear. How nice? The 2 years data on the first cohort, is so so. The 6 months data on the 2nd cohort is so, so, so we have to wait for more corrections and more work.

Interventional cardiology marches on, to give better treatment options to our patients. They are all good, when properly applied, but are they all good? In away, only time will tell. Needless to say, there is a cost to pay.

We live longer and better, at a cost. Is it worth it? Each of us must answer for yourself.