THE MIDEI, McCLEAN, DeMAIO SYNDROME

When I arrived back from Phuket, and opened my internet connection ( the wifi connections in Phuket were limited and all for a fee ), I was rather upset to read about another interventionist in USA, this time in El Paso, Texas, having to appear before a board of Complaints about unnecesary stents and procedures being done by interventionist. This will be the 3rd interventionist that I know of, in USA being sued for misconduct from unnecessary stenting and angioplasty and other procedures.
I have coined a new term called the Midei, McClean, DeMaio syndrome. I am not saying that they are guilty. I do not know, and I hope that they are not. I hope that they will be given a full and fair hearing. Let the truth prevail.
But I am very concern that we are getting more and more such complaints. There semed to be a pattern, and that is also very worrying. In all three cases ( 2 in Maryland ) and this one in Texas, the hospital where they practice, have been the whistle blower, writing to patients, asking for them to complain. So that besides the breakdown in doctor-patient relationship, there is also this very worrying issue of breakdown in doctor-medical center relationship. The medical center of course have all our notes, and can use it to instigate patients to complain. This usually happens when the doctor ( or interventionist ) have outlive his/her usefullness. I have noticed more and more that a doctor in private practice have three phases in their private practice career. ALL OF YOU OUT THERE IN PRIVATE PRACTICE BETTER TAKE NOTE. Phase one is when the Medical Center wants you, for whatever reason ( including to dilute a popular doctor, on their staff. ( lets say that a certain female gynae is very popular and commands 50% or more of the gynae case load. That becomes a problem She can then dictate terms to the center, so the center will bring in more gynaes ( female ones ) to take her case load away ). In phase one, the medical center will be very nice to you. ( Remember, I was invited to have dinner by the poolside of the CEO house, when they first approach me to join the medical center ). You will get your reasonable wishes. Phase 2 is the growing phase, where you work hard to built your career and they also want to see you grow, as they also benefit. They will tolerate you, as you are of great use to them, especially when you have a good case load. Phase 3 ( usually when you are thinking of slowing down ) is when you are most vulnerable. You would like to slow down, and you cutdown your case load and decline to go on call. The medical center will then find all kinds of reason, either to sideline you, or replace you.
In the 3 American Interventionist, the center obviously see them as a threat ( either because they are moving out to a rival, or starting their own center, in the same locality ). They all had smear campaigns, to tarnish their reputation, and they all made phonecalls to patients, instigating patients to complain and sue. They will get other interventionist from the center ( there are no shortage of ...licking traitors ) to look through and find fault with you.
I fear that what is happening in USA will soon come to our shores ( if not already here ). We are hearing more and more of doctors being terminate " without just cause ".
I only wish that they will all get a fair hearing ( is that possible in Malaysia ), and they have deep pockets to fight the large corporations who sack them
Let me tell you, from personal experience, it is very difficult. With their deep pockets, the whole Malaysian system, is vulnerable.
I hope that the Midei, McClean, DeMaio syndrome, will not arrive here. I hope that they will resolve it amicably if possible. I hope that the truth will prevail.

ICF 2010, MOVENPICK HOTEL, PHUKET. 26-28th Nov 2010.

I returned last night from Phuket, having successfully conducted, the 6th ICF. ICF stands for " Interventional Cardiovascular Forum ". We started in 2005, under the umbrella of the Federation of Private Medical Practitioners Association of Malaysia. We subsequently included University Malaysia Medical Centre and University Kebangsaan Medical Center as sponsoring bodies.
Over the 2 days ( half day meeting and half day fellowship ), we were able to cramp in 4 didactic lectures, and 7 hours of cine case reviews. We must have discussed ( to various degrees ) about 40-50 cases. The meeting was attended by about 21 interventionist from Thailand and 31 interventionist from Malaysia. ( This is a closed door, interventionist only meeting ). There were about 10-15 sponsors there to fellowship with us and mix with their clients.
The weather was kind and we had plenty of sunshine. It did rain, right after our gala dinner ( set in the lawn at the hotel compound, amongst some trees ).
The feedback ( by way of survey forms ), showed that all the interventionist were happy with the weekend and all replied that they will be happy to tell their friends and return again next year for ICF 2011. They suggested that the program must be more structured ( esp the cine reviews ), so that we can be more time efficient. Something that the organising committee have taken note of.
Dr Wasan ( Thailand ), and Dr Kirti ( Mumbai ) were our faculty. They came along to share their wealth of experience in all aspects of Interventional Cardiology, and they mixed very well with all present. I was particularly pleased that there were many young ( next generation ) interventionist with us, and they were prepared to show their cases, and accept suggestions. There were so many cases, that I had to extend cine review sessions by another 100 mins, and had to turn down ( felt so bad ), more cases, in the interest of time.
We had about 11 sponsors, but I must say that the budget is very tight this year. I hope that we can make ends meet. If there are too many claims, I may end up in the red, for the first time.
We have always felt that small, budget conscious weekend sessions of cine case reviews was the way to go, to help improve the standard of interventional cardiology in Malaysia, so that our patients can have better trained and better informed doctors. A small price to pay, for a large improvement in practice standards. We also made many new friends on the way.
I would like to express my thanks and appreciation to Dr Kirti, Dr Wasan, the Thai delegation, the Malaysian doctors, and to all our sponsors. I hope that you have all enjoyed it as much as I do. " Terima Kaseh ", thank you so much, for making this meeting such a success.
Everyone is looking forward to ICF 2011, if we can find the money and the time.
We will remember Phuket ICF 2010 as a successful meeting, a good time of learning, relaxation and friendship.

ICF 2010, Movenpick Hotel, Phuket

Tomorrow, I fly out to Phuket to chair the sixth ICF meeting, ICF 2010. There will be some update lectures and plenty of cine cases to help all of us interventionist, to learn from each other. If the last 5 ICF meetings are anything to go by, there should be 50 interventionist there from Malaysia and Thailand, and about 20 industry staff to interact with us. It has always been a good time to share and discuss cases, and share experience. hoping that it will shorten the younger interventionist learning curve, and so help patient care. It is so nice to hear views from interventionist from Penang to Johore Bahru, Ipoh to Kuching, Kuala Lumpur to Alor Star. All of us speaking the same language ( interventionist language ).
I hope to God that the weather will be good for us. Movenpick, I am told is a nice hotel with comfortable facilities.
I firmly believe that Cine forum discussions is a more beneficial and cost effective way to learn interventional cardiology.
Please wish us happy learning and sharing.

PREDICTING HEART ATTACKS, A SMALL BREAK THROUGH

One of the interesting papers presented at the recently concluded 2010 Annual Scientific Session of the American Heart Association at Chicago, was a paper by the researchers in Mayo Clinic. They studied 1262 well individuals with no history of heart disease. They used the standard Framingham Risk Score, to predict the individuals risk of heart attacks in the next 10 years. As you may know, we also use the Framingham's Risk score, which includes risk factors like cigarette smoking, lipid levels, the presence of diabetes and hypertension, obesity, etc. Having risk stratify them, they then took blood specimens from these individuals and looked for 11 gene variants known to be related to called " single nucleotide polymorphism " or SNP, including the 9P21 gene variant, well-known to be related to increase risk of heart attacks. About one third of those risk stratified using the FRS ( Framingham Risk Score ), had to be reclassified, some from low risk to intermediate risk, or even to intermediate high risk.
Of course this is an important step forward, to try to identify those at high risk of a heart attack, especially in those in the intermediate risk group, who may otherwise, have nothing done to prevent the heart attack. The day may not be far off when we can take a sample of blood and accurately predict your risk of heart attack. That will certainly save many lives, and also many healthcare dollars on unnecessary angiograms and angioplasties.

HEALTH WARNING, ON PROPOXYPHENE

Propoxyphene is a mild narcotic based pain killer, sometimes used in combination with paracetamol. I do not think that it is commonly used in Malaysia.
Anyway, the FDA has just issued a warning that propoxyphene should be withdrawn with immediate effect, citing the dangers of fatal cardiac arrhythmia as the reason. The Europeans have already withdrawn the use of this drug earlier. Being a potassium ion channel blocker, there is always the potential for ventricular arrhythmias.
Please be warned.
If you are one of those who are taking pills containing propoxyphene, I think you should contact your doctor urgently and consult him / her.

hS-CRP, WHAT DOES IT MEAN FOR CAD PATIENTS?

When I was in medical school, we were always taught that Coronary Heart Disease ( CAD ) was a degenerative condition, where artery walls accumulate cholesterol and harden with age. This we called atherosclerosis. Then came along the findings that seemed to suggest that atherosclerosis seemed to also be a response to inflammation. There were inflammatory cells found at the sites of the vulnerable plaque. These findings gave rise to the current theory, that atherosclerosis may also be an inflammatory response. Some even suggest that the vulnerability of the plaque, may be due to the inflammation. In fact, there was much work to suggest that " inflammation ", may not be infection, but a response to injury with LDL-Cholesterol. It may be the oxidised LDL-Cholesterol in the plaque that is the cause of the inflammatory response that was noted by the pathologist. Researchers search high and low, to see how they could mark out plaque inflammation. Many of our usual clinical inflammatory markers, like ESR, C reactive proteins, etc, did not quite provide an accurate enough marker. C reactive protein is something we found in patients with SLE, as a marker for the state of activity in SLE and their potential for renal involvement in lupus.
Someone then stumbled on hS-CRP as a marker. hS-CRP stands for highly sensitive, or highly selective C reactive protein. It was essentially micro levels of C reactive protein that can only be detected by very sensitive assay techniques.
" Statins ", a group of drugs very effective in lowering cholesterol, especially LDL-Cholesterol, also seemed to lower hS-CRP.
There in comes the difficulty. Some researchers seemed to feel that hS-CRP is an important risk marker for CAD, while others feel that it is not. The cardiac community seemed rather divided on this. After the publication of the JUPITER trial ( led by the Amercans ) results, suggesting that hS-CRP was very important as a CAD marker and lowering it confers significant benefit on our patients, the FDA review their guidelines and adviced that hS-CRP should be measured to ascertain risk for CAD and that the indication for Rosuvastatin ( the statin used in the JUPITER trial ), should include its ability to lower hS-CRP.
At the recent AHA 2010 meeting in Chicago, Dr Peter Sever presented a re-analysis of the ASCOT trial ( led by the Europeans ) on CAD with the use of Lipitor, and found little benefit in measuring hS-CRP and found that lowering it with Lipitor, did not confer much benefit. They argued that using LDL-cholesterol as a guide to treatment was much better ( what we have always taught ).
So the debate goes on. What is the role of hS-CRP in the management of CAD? Is it useful? Must it be measured in risk assessment? Does lowering hS-CRP alone confer benefit, or is lowering LDL-cholesterol the important thing?
I do not know the answer. But I do know that most labs do not measure hS-CRP well, and the results are so varied that is was difficult to aplly clinically ( at least in my experience in Malaysia ). Measurement of LDL-cholesterol was more consistent, and clinically useful.
Whatever it is, it does look like atherosclerosis is partly a degenerative process, with an inflammatory component, very likely to be due to oxidised LDL-cholesterol as the cause of the inflammation.
I am sure that the debate will go on, between the cardiologist on both sides of the pond.

MORE NEWS FROM AHA 2010 CHICAGO. WILL ANACETRAPID WORK?

Back in 2006, Pfizer felt strongly that they had a blockbuster drug that will take the company for the next decade. That drug was Torcetrapid, and the clinical was Illuminate. Torcetrapid belong to a new class of drug called " Cholesteryl Ester Transfer protein inhibitor or CETP inhibitor. By inhibiting the CETP, we increase HDL-C ( the good cholesterol ), thereby protecting all of us from nasty CAD, and saving lives. So we thought. Well, 5years later, we know that Torcetrapid is removed from the market. The Illuminate study was terminated and withdrawn. Although the theory seemed straightforward and good, unexpectedly ( that is what clinical trials are for ), torcetrapid did increase HDL-C, but it also increase blood pressure and worse still, it also increase CV events including CV deaths and heart attacks. That was the end of torcetrapid. Pfizer's coffers took a big hit and they are still recovering, even as they see their lipitor and norvasc patency expire without another block-buster to fill the void.
Well, at this just concluded AHA, at their 17th Nov late breaking trial session in Chicago, Dr Christopher Cannon of Bringham and Women's hospital, Boston, presented the results of the DEFINE trial. Define stands for " Determining the Efficacy and tolerability of CETP inhibition with Anacetrapid. This trial is sponsored by MSD, on their CETP drug Anacetrapid. Well Dr Cannon ( a very senior researcher ) and colleagues studied 1,623 patients ( a modest number ), with CAD. As usual, half the patients were on placebo and the other half were on Anacetrapid. They wanted to know the effect of anacetrapid on LDL-C lowering ( primary end-point ) and HDL-C increase ( secondary end-point ). They were also observing for any adverse reaction ( having learned the lesson from ILLUMINATE ). They modest number I suppose was to limit the lost, in case it tuns out wrong again.
Well, the good news is that after 24 and 76 weeks of anacetrapid, LDL-C was reduced by about 36% and HDL-C was increased by about 138%. They were also no significant increase in blood pressure and no incrase with CV events. So yes, it is a CETP inhibitor, but without the bad CV effects of torcetrapid. This is very much a biochemistry mandated trial on surrogate CV endpoints of LDL-C and HDL-C, not truly a CVS trial on hard CV end-points of CV death, heart attacks and need for revascularisation.
Following DEFINE, MSD is planning the next big trial called " REVEAL HPS-3 TIMI-55 " to study the effects of anacetrapid on CV end-points, besides their effect on blood lipids. This will be keenly watched.
We are keen on HDL-C raisers, as this will afford CV protection, which is better then CV mitigation with lowering of LDL-C. At the moment, the only effective HDL-C raisers are the naicin group of drugs, and even with this, you have to go to high doses of naicin ( running the risk of side effects ), before you can see appreciable HDL-C increase.
Well DEFINE is certainly one of the more important clinical trials presented at AHA 2010 Chicago. Needless to say, MSD has also timed the presentation to coincide with the publication of DEFINE in the Nov 17th issue of NEJM.

FROM AHA, CHICAGO 2010. THE LATEST IN HEART FAILURE THERAPY

The Annual Scientific meeting of the American Heart Association, is happening now at Chicago, till late this week. Amongst the many papers, there will be many presentations on heart failure, especially acute systolic heart failure. I have picked out one of them for mention.
Eplerenone, is a new aldosterone antagonist ( the old member being spironolactone ). We were thought to use spironolactone in the 1980s as a diuretic, together with frusemide, in an attempt to control salt and water retention, thereby lessening water-log symptoms like breathlessness, and leg swelling. Little did we know in then that, future studies will show to us that the major benefit of aldosterone antagonist, will be to increase survival, and lessen hospitalisation from heart failure. In this role, it has proven to be much better then ACE-I, and ARBs. This was very well shown in large clinical trials like " RALES " and " EPHESUS". These drugs ( ACE-I, ARBs and aldosterone antagonist, all act via the RAS system, which is deranged in systolic heart failure ). Looks like aldosterone antagonist, which works at the end of the pathway, reduces mortality the most. Interesting.
The latest study to be presented at AHA 2010, and also published on-line in New England J of Medicine 14th Nov., is the EMPHASIS-HF trial. The lead investigator is Dr Faiez Zannard of Nancy France, together with Dr Bertram Pitt of Chicago ( who also led the RALES study ). They studied 2737 patients with class 2 ( mild ) heart failure. These patients all have low LV systolic function ( LVEF <35% ). After 21 months of follow-up ( prematurely discontinued ), they found a 24 % reduction in CV mortality, 42% reduction in Heart failure hospitalisation, and a combined 37% reduction in CV death and HF hospitalisation. This is very significant. If this is true, all patients with systolic HF should get aldosterone antagonist. Of course, spironolactone is cheap, but Eplerenone is expensive.
Another Heart Failure study to be presented at AHA 2010, Chicago, is the ASCEND-HF study, with the use of a vaso-dilator, nesiritide, , in acute systolic heart failure. This study came out negative again, like the previous study on nesiritide. Looks like this expensive vaso-dilator, nesiritide, even if it makes it to the market, will only have very limited, use, as the cost does not justify, the lack of good clinical evidence.
Lets see what else AHA 2010 will bring. As far as I can see, nothing much.
I wish them a very successful AHA 2010 meeting, but.....................

EXERCISE AND DIABETES CONTROL, AND CV HEALTH.

It is World Diabetes Day ( WDD ) , this weekend, so I thought that I should post a diabetes / cardiac topic. Afterall, as I am going to emphasize at tomorrow's talk, diabetes is actually a cardiovascular disease. After the advent of insulin injections, all the dangers of chronic high blood sugars are in the arteries of the body. Diabetes is a cardiovascular disease.
The Nov 8 issue of Arch. Int Med carried an article by Dr Stefano Balducci of La Sapeinza U of Rome on the effects of structured ( supervised ) exercise on HbA1c and cardiovascular health. They studied 606 patients over 1 year. Half of the patients had exercise counselling ( told to exercise ) twice weekly ( control group ), and the other half had supervised exercise ( study group ), 75 mins each time, twice weekly. After 12 months, they found that the study group had lower HbA1c, lower fasting serum triglycerides, lower LDL-C, higher HDL-C, better CV fitness, and lower BP. Better BMI. Basically all the good things.
I suppose we knew this all along, but now we have data for it.
Put it another way, exercise will lower weight ( lower BMI ), give greater fitness, and improve your CV risk profile. Therefore, we expect lesser CV mortality and morbidity.
We may each not have a exercise supervisor ( I suppose the many gyms around us, may promote and market this ), but I think it will sure help, if we can park our cars abit further on ( not to double park in front of our destination ) and walk to our destinations, use the stairs, when you have a choice of the stairs or escalator, over 1 floor ( except for personal safety issues ), and do our regular 15 kilometers a week of brisk walking, culminating in the weekly measurement of our weight. I think that should be reasonable. Of course the difference in just counselling and supervised exercise is commitment and discipline. It also works out in greater cost. If only we are committed enough and disciplined, exercise counselling may be just as good, and more affordable to more people.
This is World Diabetes Day, and so we should all make an effort to learn more about Diabetes and put to practice what we have learned, whether we are diabetic or hope to avoid diabetes. Then WHO's effort to bring greater awareness through World Diabetes Day, would have achieve its objective.

WORLD DIABETES DAY

All are welcomed

FOR CPR, IT SHOULD BE CAB, INSTEAD OF ABC

The 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, has just be published in the November 2 supplemental issue of Circulation: Journal of the American Heart Association. This new guidelines incorporates the latest data from all the recently published clinical trials on cardio-pulmonary resuscitation ( CPR ). The clinical trials that I highlighted in the 10th August blog has also been part of the data source.
Basically, what the AHA guidelines are advocating is that, instead of the traditional ( almost 40years of teaching ) ABC ( Airways-Breathing - Circulation ) for CPR, we should now teach CAB ( compression or circulation - Airways - Breathing ). What this means essentially is that when we identify someone who has had a cardiac arrest, call for help, and begin with chest compression, as deep a c ompression as you can get ( without breaking the ribs is possible, although it is common to ), airways should be cleared, but ventilatory support and mouth-mouth, is not so crucial ( what a relief ). More people survive, if we practice CAB.
This weekend, on the 13th Nov, I shall be speaking at a public forum in USJ 19, and the organisers have included a video demonstration on CPR.
I shall be speaking on " Diabetes and Heart disease ". This meeting is organised by the resident's association of USJ19.
Please, should you see someone collapsed, render help. The least you could do is call for help. It would be better if you can also perform CAB. This would be inline with a developed country status.

VITAMIN E AND STROKES

There are many of my patients who take vitamins and food supplements, thinking that these drugs ( they do not think these are drugs ), enhance their health and give them vitality, and some may even think that these supplements may be anti-aging and also a mild aphrodisiac. There are so many claims. I always put it down to good marketing by these companies, to get their direct selling agents to push their product and yes, many of them push it so well. In fact, almost half of our health expenditure is on health supplements and OTC ( over the counter ) drugs.
Anyway, to day, I would like to comment on a piece of medical research done and published in the Nov 4th issue of the British Medical Journal. This work was led by Dr Markus Schuks from the Bringham and Woman's Hospital, Boston. The researchers studied the effect of Vitamin E on Strokes. The meta-analyse 9 randomised clinical trials ( RCT ) on Vitamin E and strokes. They choosed the 9 RCT which directly compared vitamin E against placebo, in their effects on strokes. All those dealing with multivits or who had other vitamins, were excluded. At one time, there were many such trial because Vit E was thought to have anti-oxidant effects. Anyway, from the 9 RCT, they found a total of 118,765 patients ( this is a very large number of patients ), half on Vit E and half on placebo. At the end of the study, they found that there were equal number of strokes in the Vit E and placebo arm, showing that overall, vitamin E did not reduce the incidence of strokes. They however, further sub- analyse the effects on the two main type of strokes, viz, the hemorrhagic stroke ( stroke due to active bleeding with blood clot in the brain ) and ischemic strokes ( strokes due to loss of blood supply to the brain ). When they did this, they found that vit E did reduce the chance of getting an ischemic stroke by some 10% but it also increase the chance of getting a hemorrhagic stroke by 22%. In other words, the authors worked out that for every 476 person taking Vit E, you prevent 1 ischemic stroke, but for every 1250 person taking Vit E, you may cause 1 hemorrhagic stroke. Overall, Vit E may do more harm then good, as far as stroke is concern.
I suppose all those people who like taking supplements, should be aware, that these supplements, like Vit E, is not as innocent as you think. Stroke is a very serious matter. Do not fool around with it. Once you get it, your whole life changes.
Their meta-analysis also revealed that life-style modification and blood pressure control, remain the most important strategy to prevent strokes, whether it be ischemic or hemorrhagic.

SOUTH ASIANS AND HEART DISEASE

We are still largely dependent on the West to produce medical data for us, or put another way, the data about Asians from the West seemed to be better highlighted in the established medical journals and congresses. Whatever it is, we need data, credible data. We need credible data to plan, we need data to understand clinical trial results and how to advise patients and how to understand risks.
Be that as it may, I picked up a study, done in Canada, and presented at the Canadian Cardiovascular Congress 2010, on South Asians in Ontario, Canada. The study was led by Dr Milan Gupta from the McMaster U, Hamilton, Ontario. He took from the his registry, a cohort of 514 patients, 199 of whom were South Asians ( meaning Indians ) and 315 Whites. He studied their cardiovascular risk factors, which were essentially the same in both groups. Followed them for 5 years, and compare the outcomes in both groups after 5 years. The primary endpoint was cardiovascular death, non-fatal MI, non-fatal strokes and need for re-vascularisation ( basically all the cardiac indices ), and found that in the 5 years, 25.1% of South Asians and 19.7% of Whites met the primary endpoint. Although it did not meet statistical significance ( p was 0.15 ), I am sure it would have been significant if the numbers enrolled were larger. It does appear that South Asians, have a higher CV risk then Whites.
They subsequently studied " Why ? ", and found that their South Asians had a higher PAI ( Plasminogen Activator Inhibitor ) level, or as the locals will say " their blood was thicker ", then the whites, and also there was a higher incidence of the Metabolic Syndrome. Could it be that the higher PAI levels were genetically related and the Metabolic Syndrome and high CVS event rates were due to the high PAI levels? Interesting.
Obviously, we need larger numbers to be sure, but it does give room for more research and also more work to be done, hopefully by us Asians.
Let us all hope that this John Hopkins / College of Surgeons Ireland / Academic University thing that the present government is talking about, will contribute to this end, when or if it comes about.
South Asians, be aware, you are at higher risk for CV events, should you have Metabolic Syndrome and CAD.