DIABETIC DRUG. NEW KID ON THE BLOCK : LIRAGLUTIDE OR VICTOZA

Over the weekend, I had to sit in a company ( in this case, Novo Nordisk ) cardiac advisory board meeting on their new drug, Liraglutide / Victoza, for the management of diabetes. As we all know Liraglutide, is a GLP-1 human analogue, meaning that although it is made from recombinant genes, it works like the human GLP ( Glucagon like peptide )hormone. With this new tool of recombinant genes, we can do that now with many products ( meaning that we can copy nature ).
I suppose, the current group of drugs coming into the market for management of diabetes, tries to mimick the body's natural feedback loop, in the sense that the drug only works when there is glucose to reduced. They are no longer secretogogues ( drugs that stimulate the pancreas to product more insulin ), but they are insulin sensitisers or insulin assist agents. This principle overcomes one of the biggest problem in diabetic management, and that is hypoglycemia. We now know that management of diabetes is often plague by the complication of hypoglycemia when one is using the older generation secretogogues. Basically, secretogogues are out, medically, but because they are very cheap ( when compared to the newer agents ), they are in commercially.
Anyway, this liraglutide looks like an interesting agent. I think the fact that it lowers blood sugar effectively is not in doubt. What I was concerned about, at the presentation, was the fact that there are extra blood sugar lowering effects. The human body is very complex and so not compartmentalised. Liraglutide also acts centrally to make one lose appetitie and also acts on the renal tubules to make one lose salt and water ( in that case, it also lowers blood pressures ). On the surface, that looks good. Now we have an agent ( given by injection, subcutaneously ) that can lower blood sugar ( for use in diabetes ), that can also make one lose weight ( maybe open to abuse by non diabetics ), and which may upset the body's fluid balance ( losing salt and water has other consequences ). Obviously, these pleotrophic effects of liraglutide, can be harness for good by doctors, but there is also a great potential for it to be abused, by others.
All things said and done, I think there is a role, but I did express my concern at the meeting, that it is an injectable ( and most patients here equate injectable to insulin ) and this is a drawback, and also the pricing? Is it going to be affordable, given that it may be lifelong therapy. I am also a little concerned, that since it also acts centrally ( at the brain level ), to reduce satiety ( appetite ), will it also have other CNS actions that may lead to depression and suicides, as we have seen with some other weight losing, appetite surpressing drugs. For which reason, I also express concern that long term data ( their longest is 2 years ), may be necessary for all of us, clinicians, to feel comfortable.
Basically a nice meeting. The drug looks promising, although there may be a few more questions to be answered.
It also gave me another occasion to use to LRT to get to Le Meridien, where the meeting was held. Always in support of efficient public transport.

TRIGGERS FOR HEART ATTACKS. COMMUNITY FACTORS

Cardiologist , and I am sure the general population as well, is very interested in what triggers a heart attack. How come patients with severe coronary artery disease, some get a heart attack and maybe die, while others with similar blockages have nothing happen to them and they live to good old age and die from a motor vehicle accident?
What triggers a heart attack?
I remember when I was a young cardiologist, about 20years ago, I did a coronary angiogram on a young man, in his 50s for evaluation of a positive stress ECG. It revealed that he had 3 vessel CAD. So I referred him for coronary artery bypass surgery. Those were the days before PTCA in Malaysia. About 10 years later, another man cam to see me. He also had 3 vessel disease CAD. When I suggested that he goes for CABG, he declined saying that he wanted medical therapy and showed my angiogram report and diagram, of the previous patient who had 3 vessel disease, refused CABG, and was still surviving, and well. The point is that, there are many out there with 3 vessel disease, some discovered and some undiscovered, who go along in life, apparently well. The difference is that some 3 vessel ( or even 1 vessel ) disease may meet a trigger and result in a heart attack, while others have no triggers and so live to good old age.
What then triggers a heart attack?
This has been the subject of extensive medical research, as it may hold the key to who is most at risk and who is not.
In the 23rd Feb issue of Lancet, there is an article by Dr Tim Nawrot et al, ( from Belgium ) on the subject. In a paper entitled "Public health importance of triggers of myocardial infarction: A comparative risk assessment. " Dr Nawrot and colleagues collected epidermiological data from 36 large epidermiological studies on this subject. They concluded that while on an individual basis, cocaine is probably the most important trigger for a heart attack. On a community base, air pollution and traffic exposure, is probably the most important. They figured that air pollution and traffic exposure forms 5-7% the risk of triggering a heart attack. Of course the other triggers in the community / population includes, heavy meals, anger, negative and positive emtions, alcohol, coffee and physical exercise.
From a cardiac standpoint, what this means is that for those of us with some coronary artery cholesterol blockages, the blockages are stable and remain silent, or cause us occasional exertional chest pains. But should we meet a trigger / trigger event, that stable cholesterol plaque, may rupture, exposing the underlying cholesterol accumulation, to blood following pass it ( it is exposed to the blood because the plaque has ruptured ). And when blood meets cholesterol, blood clots instantly. The blood clot obstructs the whole artery lumen, so blood can no longer flow downstream, and the heart muscle beyond the obstruction dies, as they become devoid of oxygen and nutrients. The death of the heart muscle, constitutes a heart attack.
All this sequence of events are because something has triggered the plaque to rupture. So when you are in a polluted environment, with some alcohol and positive or negative emotions, becareful. Whats more, this situation may follow a heavy meal. Add to it, a bit of sex. Then we are just asking for it.
Of course medical science is working very hard to see if we can be a bit more specific, and whether there could be other warnings to allow us to prevent. So far, we are still not sure.
I suppose asking us all to avoid traffic exposure, pollution, emotional upsets, heavy meals, sex etc, is impossible. Better not live then, as some of my patients tell me.
Some even believe that a massive heart attack is a "good" death.
You have been warned.

DRONEDARONE / MULTAQ LAUNCH. 19th Feb. 2011

Last Saturday, I was invited to the launch of a new anti-arrhythmic agent ( there has been so few anti-arrhythmic agents produced since the CAST study ), dronedarone. Sanofi-Aventis, the maker of dronedarone, touted it as an important launch and a paradigm shift. It was a rather low key, muted launch, quite unlike the launch of rimanobant, not so long ago. Yes, the staff were dressed in Greek outfit ( to reflect their landmark study of ATHENA ), the food was good and the speaker, Prof John Camm of UK ( St Georges Hospital, London ), was excellent, as usual. Missing was the fan -fare ( dancing and entertainment ) and wine for the occasion.
Actually, I am in full agreement that drug launches should be for good, pure medical reasons and not a commercial launch like iPhone 3 or iPad.
Anyway, Prof Camm gave a good overall review of Dronedarone, in the management of atrial fibrillation, based primarily on his understanding of ATHENA, which showed that in patients with atrial fibrillation and other coronary risk factors, dronedarone, reduces the primary end-point of mortality and repeat hospitalisation. The p value here was 0.001. This primery end-point however was driven mainly by a mark reduction in repeat hospitalisation ( which to many of us was a rather soft end-point. The mortality reduction, especially cardiac mortality reduction was only modest, and just about made the significance level. I think cardiac mortality reduction p value was 0.02. Whatever it is, I was more intrigued by the fact that dronedarone as an anti-arrhythmic works at all 4 levels of the electric cardiac cycle, as taught to us by Vaungh-Williams. If we had to classify dronedarone using the old Vaungh-Williams classifiaction,, then dronedarone will be a weak class 1, class 2, class 3 and also a weak class 4 ( calcium channel blocker ). Thereby, it will have many other potential uses. Being a weak class 1 agent, it may have ability to reduce ventricular arrhythmias. In fact, the reduction of cardiac mortality in ATHENA was driven mainly by a reduction in sudden cardiac death. Being a class 2 agent, it is a beta blocker of some sort. In fact, as an anti-arrhythmic agent, it has significant Heart Rate lowering effect. The slowing of A.Fib rate was significant. Being a class 4 agent, it does have coronary vasodilatation effects, meaning that it could reduce angina and maybe blood pressure ( through systemic vasodilation like amolodipine ). Interesting, interesting.
I am a little concern about the hepatic toxicity, which were reported, with 2 patients having to undergo liver transplantation. It is also metabolised through the cytochrome P450 system, thereby giving the potential of drug-drug interaction. Of particular importance is the interaction with warfarin, statins and maybe clopidogrel.
Nonetheless, after so many years, we see that anti-arrhythmic agents are still being investigated and being brought to the marketplace. Many of us thought that with the landmark CAST study, showing that anti-arrhythmic agents are potentially pro-arrhythmogenic, anti-arrhythmic agents will be w thing of the past, what with the ICD becoming more popular.
All in all, it was an interseting evening on 19th Feb, very educational and of course, lets see how this new agent for management of atrial fibrillation pan out. Does it have a useful role. Afterall, it does cost about RM 15 a day. It is not cheap. Warfarin and beta-blockers ( the current alternative ) only cost a dollar or so.

US HEALTH STATISTICS, LESSONS FOR US

The US Center for disease control and prevention has just released their 2010 report on Health Statistics from the National Center for health statistics. A few trends are worth noting to see what lessons we can learn.
It would appear that since the 80s till 2009, age adjusted death rates have come down, meaning that people live longer and better. Their CVS mortality has also declined by about 20% Their national cholesterol levels have declined but only 30% are lowered to guideline levels. Of course the use of statins have increased by 10 fold. The rate of obesity has continued to increase and the prevalence of hypertension has plateaued.
CVD remains the leading cause of death in the US.
What lessons can we learn. It looks like the US, that spends 14% of their GDP is still very much on to curative medicine., which remains good but very expensive. Their efforts at prevention of chronic lifestyle diseases has met with some success, but the effect after 20 years is still largely small. Obesity is becoming a very serious problem, negating some of the improvements in CVS mortality and morbidity. Hypertension remains very much an issue. Americans would rather take statins then change their lifestyle, and they do not quite believe their guidelines, as only a third have been treated to target.
We Malaysians must see what we can do and how to spend our healthcare dollar. in 2006, we spend 4.2 % of GDP. Lets hope that we can spend more, particularly on prevention of chronic lifestyle diseases.

AMENDMENTS TO THE 13 th FEES SCHEDULE - FINAL WORKSHOP

Starting form tomorrow, we will be housed in The Grand BlueWave Hotel in Shah Alam for the weekend, to finalise the amendments to the 13th Fees schedule. When I received the invitation to attend, I was very disappointed that a whole host of specialist and MOH officers invited to the meeting. Many have never participated in any of our previous discussions.
I am very concern that we will be wasting precious time, going over the basic rules and term of reference again, the whole weekend ends with no conclusion and the MOH will exercise their right of final say, because we cannot agree amongst ourselves. I also see new items and Fees proposal just submitted.
So, I am afraid that I have just wasted another weekend of my life.
Anyway, if we should agree on a final amendment to the 13th Fees schedule, then the final draft will be submitted to the minister by 1st march for him to make present to the cabinet and thereafter to make a press statement / announcement in March 2011. It then becomes a part of law.

Wish us luck, patience and energy.

ACUTE LOWERING OF BP IN STROKE PATIENTS

We are seeing an increase in strokes, probably resulting from a concomitant increase in the incidence of hypertension and what the minister calls, chronic lifestyle disease.
A stroke occurs when a blood vessel to the brain suffers a brain attack ( neurologist borrowing a phrase from the cardiologist ). As in a heart attack, a brain attack is when an area of the brain is suddenly deprive of blood, oxygen and other nutrients, due a sudden blockage or rupture of a brain blood vessel. The neurological deficits in a stroke ( brain attack ), usually last for 24 hours or more and may be permanent. If the stroke ( brain attack ) is due to a complete blockage of a brain artery, we call it an ischemic stroke, and if it is due to a blood artery rupture, we call it a hemorrhagic stroke. Hemorrhagic strokes are mainly triggered by sudden rises in blood pressure and ischemic strokes are triggered by sudden blood clots forming in the brain blood vessels.
Invariably, following a stroke, the blood pressure will rise, as a compensatory mechanism, and sometimes the rise in blood pressure could be due to the sudden increase in brain pressure due to brain swellings following a stroke. It has been a medical delimma since my training days, as to whether we should lower the acute BP rise following strokes and if so, how quickly and to what degree.
Well, at the recent International Stroke Conference 2011 held in Los Angeles, the workers from Norway, led by Dr Eivind Berge, studied 2029 patients who had suffered a stroke ( ischemic and hemmorhagic ) and had BP > 140 mmHg systolic. Half of them were given Candesartan to lower their BP and the other half had placebo. The trial is called, " Scandinavian Candesartan Acute Stroke Trial " ( SCAST ). After 6 months followup, they found that lowering BP did not help in the recovery. Those on treatment did no better then those on placebo. In fact there is a trend ( non significant trend ) that lowering BP may aggravate the CNS deficits. Their recommendations was that in patients with acute rises of blood pressure, take good care of the stroke and CNS deficit and do not be too aggressive in lowering the BP. They usually do not use anti-hypertensives in the first 7 days.
So now we have some data to help us.
The same meeting also had numerous papers on the early ( less then 4.5 hrs ), use of IV thrombolytics in the management of acute ( white - ischemic ), strokes.
Stroke is a big issue in the developing and developed world. It kills, and in those who do not die, it incapacitates, and steals away your quality of life so much so that ultimately ( in those severely affected ), they would rather die, then be a living vegetable. And yet it is an illness that can be effectively prevented. Eat less salt ( no added salt ), is a very effective way of reducing hypertension and strokes.
No added salt in your food please. No soya sauce and no salt. Live longer and better.

HYPERTROPHIC CARDIOMYOPATHY, A UNCOMMON DEADLY PROBLEM.

This morning when I open my newspaper, I read of the sudden, dramatic demise of Master Wong ( 10 yrs old ), who suddenly collapsed in his school at Kulai.
A form of cardiomyopathy was first described by Dr Robert Teare some 50 years ago. He noticed that in one of his patients who die, autopsy showed some swelling in the heart muscle. He at first called it a cardiac tumour. That was probably the first description of hypertrophic cardiomyopathy ( HOCM ) as we know it today. The British did extensive research on this. Similarly, across the Atlantic ( the big pond ), the Americans were also researching this peculiar disease, that seemed to run in families and that often kills suddenly, young fit men at the peak of their career. I was first introduced to this disease by my consultant in UHKL ( this was in mid 70s ), Dr KT Singham and Dr HO Wong. They both were had worked at the Royal Hammersmith Hospital with Prof John Goodwin, who had a special interest in HOCM. Prof Goodwin had a research unit on this, and much work was published by him and his assistant Dr McKenna. Those were the days.
When HOCM first came on the scene, we did not understand the etiology, and it was a disease called by many names. It was just one form of heart muscle disease. The others being dilated cardiomyopathy ( COCM ) and restrictive cardiomyopathy ( RCM ). Over across the pond, the Americans ( arguably led by Dr Barry Maron ) liked to call it " Idiopathic subacortic stenosis ( IHSS ) ". Those of us who were training and who subscribed to NEJM will find many case discussions on IHSS. That seemed to be the American variety. Across in UK, they called it hypertrophic cardiomyopathy either with obstruction, or without obstruction. There is also an Asian ( Japanese variety ) first described by Dr Yamaguichi. He called the Japanese variety : Apical HOCM". We have a few families ( if I am not wrong, 20+ ) in Malaysia with this type of " Apical HOCM ). I currently have 3 cases of HOCM under my care. They are non-familial, and all doing well, two into their seventies and one in her sixties.
The names are confusing, but they all described severe heart muscle thickening ( Hypertrophy ) for no medical reason. So HOCM is just Hypertrophy ( thickening ) cardiomyopathy ( heart muscle disease ). This condition is usually genetically linked and so run in families. Ms Wong has 2 other sibs. They should both be examined. The inheritance is autosomal dorminant. Some are as a result of genetic mutation. It is one of the commonest causes of young, fit, athletes who collapsed suddenly. If you exclude blunt trauma to the chest or contact sports injuries, HOCM will be the most common cause of sudden cardiac death in young, fit athletes.
The cause of death is invariably primary ventricular fibrillation. A good medical examination, with a high index of clinical suspicion can diagnose the disorder. The ECG can give a valuable clue and of course the transthoracic echocardiogram invariably is diagnostic. In the American variety ( IHSS ), there bulging of the hypertrophy into the LV outflow tract thereby partially obstructing it. This too can cause sudden collapse in these patients when they are under stress. The diagnosis is quite straight forward once there is a high index of suspicion.
Symptoms are few and may be non-specific. Those with significant LVOT can complain of syncope or near syncope. Sometimes these symptoms are potentiated by medications given for other unrelated conditions. Other symptoms may include palpitations, and sometimes non-specific chest pains.
In Master Wong's case, I was a little upset, that he was picked up ( they said that he had a hole-in-the-heart ). That must mean that he had seen a medical doctor ( unless the story is wrong ). I wonder if an echocardiogram was done. Certainly, I hope that they will do an echocardiogram on the brother, and the other sib. It is stated in the newspaper that his brother also has heart disease.
Treatment has proven difficult. Once upon a time, when the Americans felt that the IHSS variety had significant LVOT obstruction, they advocated surgical removal ( myomectomy ) of the obstructing LVOT muscle bulge. The British, on this side, have pioneered the use of alcohol ablation of the LV septum as a means of infarcting the LVOT obstruction. This work of alcohol ablation was pioneered by a friend of mind, Dr Sigwart, a Swiss working in Hammersmith, and has been proven to be quite successful. In fact, it is probably the treatment of choice now, for HOCM with significant LVOT obstruction ( a gradient across the subaortic area on cardiac catherisation ).
There are simpler medical management for those patients who have no significant outflow obstruction. I like the use of beta-blockers, that seemed to be able to reduce sudden cardiac death. Cordarone have also been used with limited effectiveness, against V. Fib. At one time, we used ventricular pacing as a means of reducing LVOT obstruction. Some common drugs, esp GTN, are contra-indicated as they potentiates the LVOT obstruction.
There are of course genetic markers that can pick out families with this HOCM trait.
I hope that Master Wong did not die in vain. We can learn a few lessons from his unfortunate demise. Firstly we can improve our diagnostic capability. HOCM is a far cry from hole-in-the-heart ( granted they both have murmurs ). Secondly, I hope that the siblings of Master Wong will go for a thorough checkup, so that they will not meet with this unfortunate sudden cardiac death.
My condolences to Master Wong's family.

MEETING WITH DG of MOH. 8th Feb 2011

It is still Chinese New Year. My clinic is still not open. My staff are still away.
, so I spend an hour this morning meeting with the DG of Health on issues affecting GPs and private practice doctors. We did make some headway trying to improve the current working conditions of GPs and private doctors.
One of the most important points that we made was the issue of "kickbacks" and "fees-splitting". The DG is very categorical that THERE MUST BE NO KICKBACKS OR FEES SPLITTING. This also includes, no contracts by the hospitals-doctors to force doctors to split their fees. This also includes no blacklisting of doctors who did not agree to kickbacks. No more contracts by hospitals to force doctors to cover for the hospitals in the event of litigation by patients. We have asked the DG to crack the whip. we are prepared to give evidence of one sided contracts force upon doctors, we are prepared to give him names of doctors who have been blacklisted. We are prepared to give him evidence of MCOs asking for feedback. He knows of the situation in Adventist Hospitals, Penang. He has send his senior officer to go and talk to the Adventist Hospital management. We were quite forceful, asking him to crack the whip, or else the hospitals will continue to make doctors sign, one sided contracts, including kickback clauses. However, the DG has also informed us that the private hospitals and MCOs have asked for another meeting with the Minister of Health, to re-discuss this issue. We have asked to be invited to this meeting. Let us see if they will.
The DG also informed us that there will soon be a fees schedule for private hospitals. They are still working on it. So our work last year is not all in vain.
He also informed us that the country is not yet ready for a separation of dispensing and prescribing. There are still not enough pharmacist in the country. He did say that it will eventually come about. That doctors will soon not be allowed to dispense. They however will be allowed to employ pharmacist to work at their clinic.
There were some other minor issues discussed, like doctors changing clinic location can apply for an amendment to their registration, thus not requiring re-registration.
By and large, it was a good meeting, with much fruitful discussion. We shall wait and see the outcomes, and see if the discussions bear fruit. That afterall, is most important, the outcome. we wait patiently.

CARDIAC ADAPTATIONS AT EVEREST.

Sometimes humans do irrational things, just because it is thrilling. Climbing mount Everest is one of those irrational things that people do for not-so-cheap thrill. Costing about USD 1000,000 per attempt ( rough estimate ), as till June 2007, 11,000 climbers have attempted Everest, 3,304 have made it, and 209 have lost their lives trying. A mortality rate of about 1:15.
A few of my colleagues have tried to reach Everest base camp ( not foolish enough to try Everest itself ), and return safely, although there were episodes of altitude sickness.
In my reading this week, I came across an article detailing the experience of 14 doctors ( mostly anaethetist ), who studied the effects of Everest base camp, on cardiac function. Led by Dr Cameron Holloway, and funded by University of London CASE, the 14 doctors, had a baseline MRI and echocardiogram. They then flew to Katmandu ( 1,300M ), and then fly to Lukla ( 2,850M ). From Lukla, they trek 11 days with 2 days rest to Everest base camp ( 5,300 M ). They spend 3 days at Everest base camp, and then return down, and flew back to London where they had their MRI and echocardiogram again, and again at 6 months. Of course, they wanted to document, as scientifically as possible, the cardiovascular changes to low oxygen concentration.
At base camp, the O2 saturation was about 70-80% average. They found ( for all our benefit ), that 11 days trek and 3 days at basecamp, does not change cardiac output, stroke volume, or LV ejection fraction. It however does reduce LV mass ( reduce by about 11% ), and also LV diastolic function. Total body weight also reduces by about 3%. All these adaptive changes are reversible and at 6 months, they all return to normal. Among these 14 healthy doctors, there were no clinically significant complications. I had a patient a long time ago ( an old professor of cardiac surgery ) who went to Everest base camp, and developed acute pulmonary edema, and had to be evacuated from Everest base camp.
I think these information is important for all preparing to climb high altitudes, and also help us to understand physiological changes in people suffering from low O2 concentration, as perhaps in COPD.
Interesting piece of work, documented in the February issue of the Journal of Federation of American Societies for Experimental biology.

GongXiFaCai

PHCFS REGULATIONS ; AMENDMENTS TO THE 13th SCHEDULE. UPDATES

As you are all aware, I get invited to the Task Force for amendments to the 13th Fees schedule of the Private Healthcare Facilities and Services Regulations 2006. We had our final; meeting on the 27th Jan. 2011 ( I almost forgot to post, in the midst of all the festivities and golf ). The final meeting was chaired by Dato Dr Nor Hisham ( deputy DG - medical services division ). Looks like all the proposal has passed the first round. I must confess that some of the fees asked for is outrageous. Doctors sometimes are unrealistic and do not know market sentiments and consumer concerns. One party even asked that post operative cardio-surgical ICU care professional fees be RM 500 per hour or a maximal of RM 5,000 per day. !!!! Can you imagine? When we all objected, he was trying to justify. One member of the committee asked, then if the patient stays in ICU 1 month, the post op fees is RM 150,000??
Anyway, I learned through this exercise, that doctors ( I wont say all ) are inherently greedy. They all ( not all ) feel that they are God's gift to mankind. And I mean, these are not poor specialist. Not by any stretch of imagination. For one, they are all obviously richer than me.
Anyway, the chairman made a few points which I must pass on.
1. The amended fees schedule will be a Ministry of Health amended 13th Fees schedule.
2. The proposed 30% across the board increase is accepted for all procedures currently listed in the 13th Fees schedule. All procedures current not listed, will be derived from a compromised fees between the College of Surgeons' proposal and the MMA 5th schedule. we will have to meet to combine the two into a reasonable one.
3. After office hours will be allowed a 50% increase in fees. He hopes that this will not be mis-used. Bilateral operations will be allowed two separate full fees. Ad hoc angioplasty will be allowed a separate full fees from the angiogram fees. The anaesthetist fees will be revamped totally, based on anatomical sites, degree of difficulty and also time. Time will be from skin to skin and for 15 mins portion of RM 100.
4. Other related business - the MOH will look to have full private hospital fees disclosure. The public hospital full fee paying will be 20% full fees. They will work out full fees for case related fees, so that we will know what is reasonable fees for procedures. This is an initial attempt to control private hospital fees. Doctors are also asked to come out with justification for their fees. I was asked, " why do you charge RM 1,250 for angiogram fees?" How do I breakdown my fees? All these seem to be in preparation for the eventual health insurance that may be coming.

Anyway, please note that this is not all cast in stone. There will be a weekend workshop ( bengkel ) from the 18th - 20th Feb to finalise the complete amendments. ( No golf on that weekend ). This will then be passed to the minister, who will present it to the cabinet for approval, before the minister make the press announcement, sometime in March 2011.
There are heavy rumours that GE 14 maybe in April 2011.

MECHANICAL VALVES Vs BIOPROSTHETIC VALVES IN THE AORTIC POSITION. LATEST DATA

I have seldom written about valve surgery as I did not consider it in the realm of interventional cardiology, until the recent trends at live demo meetings to showcase " Transcatheter Aortic Valve Implantation " or TAVI. It looks like coronary interventional cardiology has reached a plateau and interventional cardiologist ( those jack of all trades ) have gone onto start a new frontier, as it were. So I began to keep an eye on what is happening there. Over this week, the Society of Thoracic Surgeons are holding their 2011 annual scientific meeting at San Diego. One of the papers presented was a piece of work by the cardio-thoracic team at University of Berne, led by Dr Alberto Weber. They studied the 10 year outcome of bioprosthetic aortic valve replacement ( in this case the Carpentier Edwards valve ) against the mechanical aortic valve ( the St Judes valve ) in a relatively young population ( less than 60years ). They found in their series, that both the valves performed equally well in terms of MACE, but the patients who had the bioprosthetic valves had significantly less 10years survival. This reduce 10 years survival was not due to re-do operations. In a way, this was surprising. We are puzzled.
Sometimes, young people, still full of athleticism, will op for a bioprosthetic valve to avoid the long term use of anticoagulations like warfarin. Now they can even reason that should I need a re-do, I can op for a TAVI ( at the moment, no such indication). We were always taught that a mechanicxal valve last much longer, and the St Judes, bi-leaflet, mechanical valve is durable and performs well mechanically. When the Swiss team measure the indices of function between the two groups, they found no significant difference between the two groups. Why then did the bioprosthetic group lived shorter? I suppose it may be because, the cardiac surgeons may have selected the younger patients with more co-morbidities to implant the bioprosthetic valves, knowing that the other co-morbidities will limit their lifespan. Afterall, this is not a prospective randomised trial but a propensity score, comparison trial.
I think it is also fair to say that the Carpentier Edwards valve by Edward Lifesciences, is not the lastest in bioprosthetic valve technology. I understand that there is a second generation Hancock's by Medtronic, that is theorectically superior, in terms of hemodynamics.
It is therefore understandable that Edward Lifesciences and Medtronic International is also heading the march to produce valves for TAVI.
Fiinally, a word about anti-coagulation. It used to be that warfarin was standard anti-coagulation for all mechanical valve replacements. Then we learned that in the aortic position, the warfarin need not be lifelong. Being in a high flow situation, even for mechanical valves, warfarin for 1-2 years may suffice and in many of my patients, I have successfully switched them to aspirin and they are still doing well. Nowadays, we have dabigatran ( a factor 10 inhibitor ) as a safer ( but much costlier ) anti-coagulant.
There have been some advances in cardiac valve surgery, but obviously not as much as was in interventional cardiology, over the last 20 years.
But know that I am of course bias, since I am an interventionist.