THE SILENT DIABETIC EPIDERMIC. THE RISING DANGER

The June 25th issue of Lancet carried a very revealing article about the silent epidermic of diabetes. The authors were Dr Goodarz Danaei leading the group from the Harvard School of Public Health and the co-authors, led by Dr Majid Ezzati from Imperial College, UK. They did a population survey, across 370 countries, involving 2.7 million adults age above 25 years. They measured their fasting blood glucose level. They found that from 1980 - 2008, the incidence of diabetes has increased 18% in males and 23% in females. The number of diabetics in 1980 was 153M and the number in 2008 was 347M. This was attributed to age, population expansion and also, about 30% could be attributed to the rising incidence of obesity. The increase in diabetics was worse in Oceania, South Asia, Central Asia, the Caribbean, Latin America, Middle East and North Africa. Basically, everyone. Amongst the developed countries the worse was USA, Greenland, Malta, New Zealand, Spain. The best was Holland, Austria and France. England is somewhere in between.
I suppose, the numbers speak for themselves.
Now what to do? I suppose reducing obesity must be our first objective. The Ministry of Health is moving in the right direction, by removing sugar subsidy ( health amongst one of many reasons ), food labelling, less junkfood in schools, and more exercises.
I think we all know what to do, but doing it seems a different matter.
I suppose, I am just highlighting the issue again, and hope that along the way, some will take note, and the incidence of diabetes will plateau off, before coming down.

STANDARD OF CARE ; CHEST PAINS

To continue with the Monday series, let us consider the issue of chest pains, a very common complain to a family practice clinic or cardiac clinic.
Of course, chest pains frighten the patient because of the fear of death, knowing that people with chest pains may be suffering from a heart attack, and so may die.
When face with chest pains, a patient must try his / her best to remember the events surrounding the onset of chest pains ( what brings it on, what relieves it ), the duration of chest pains and any other associated discomforts with the chest pains.
It is always good to remember that over the chest, there are about 5 important organ systems, viz the musculoskeletal ( muscle and bones and joints ) system, the nervous systemm ( the nerves and nervous, emotional disorders ), the pulmonary ( lung system ), the gastro-intestinal system ( stomach, gullet, gallbladder ), and of course the heart and great vessels. Anyone of these organs can cause chest pains. I usually tell my patients that it is often impossible to completely diagnose the chest pains, because we have no means of accurately pin pointing the cause of the chest pains. Sometimes, the pains may have dual cause, for example, the monir gastritis could trigger a severe emotional response because his office colleague have just collapsed and died following a squash game. In fact the most important clue to the diagnosis of chest pains is the history. Chest pains that come on effort, and is relieved within 5-10 mins by rest, maybe due to heart artery blockage. We call this angina. We sometimes add that besides being relieved by rest, it can also be relieved by sublingual GTN. The other chest pains without those cardinal features ( chest pains on talking, chest pains on hunger, chest pains on stretching the muscle, chest pains on deep breathing, chest pains following a blow to the chest ) are unlikely to be from heart artery disease. Chest pains not from heart artery disease, invariably do well long term and are seldom the cause of death. So always remember if there is a pattern. What brings the pain on, and what relieves it, is a great help to us. Chest pains on effort ( like climbing stairs, jogging, cleaning the windows, playing badminton, etc ), and relieved once you stop, rest, that one, please take note and visit your friendly GP.
We also give weightage if chest pains occur in the context of someone likely to have heart artery disease. Chest pains in someone with two or three coronary risk factors, must never be ignored, even if the features are not characteristic. As we all know, coronary risk factors include cigarette smoking, diabetes, hypertension, dyslipidemia, family history of coronary artery disease. Of course, patients with previous established coronary artery disease ( previous angioplasty, previous CABG, previous heart attacks, previous angina ), must have their chest pains thoroughly investigated.
Generally speaking, if the chest pains have any of the possible features of angina, and in the context of someone, who is likely to have angina, that chest pains must receive full attention.
Check ups for someone who may have heart artery disease, should include, an ECG, a full blood profile and a stress ECG. In patients who are unable to stress, perhaps a stress echo, or othe forms of nuclear imaging. These are the standard test.
The stress ECG, does two things for us. Firstly, it helps us to find out the reason for the chest pains, including excluding important heart artery disease ( should the chest pains be negative ). Yes, you can still have heart artery blockage without it showing on the stress ECG, but those heart artery disease are usually relatively minor and not life threatening. So, a stress ECG also helps us to separate out those heart artery blockages that is potentially deadly, and those that can be managed medically. In fact, many of us will not do an coronary angiogram to delineate the coronary anatomy, unless there is inducible ischemia ( stress ECG positive ), unless the reason to do an angiogram is so compelling ( and cash from angiogram, is not a compelling reason ).
I suppose, I should say a word about the CTA ( CT scan with angiogram ). In 2011, at the present stage of our understanding, and present stage of the machines available, there is no role for the use of the CT angiogram, to screening the population for heart artery disease. Besides the cost ( about RM 2,700 ), there is the radiation risk ( 500 chest X-ray equivalent ), and the rpesence of false positives ( thereby ending up with many unnecessary angiograms, and maybe even unnecessary angioplasties. Heart artery disease, when they are assymptomatic ( not giving chest pains ), and are stress ECG negative, do very well with medical therapy, like life style modifications and stains, and aspirin. In this category of people, all the evidence seem to suggest that medical therapy is as good as angioplasty or bypass surgery. CT angiogram, should be used to exclude heart artery disease, meaning that if my CT angiogram is normal, it is very, very unlikely that I have any heart artery disease. It is NOT a good tool to diagnose heart artery disease. It is true that with time ( over the last 10 years, we are seeing better and better scan machines coming into the market, so that eventually we will have machines with a high degree of accuracy, and low level of radiation. Eventually.
Lastly, I must mention that we advocate a strategy, where males above 40 yrs and females above 50 yrs ( post menopausal ), should go for a routine medical check-up, including ECG and stress ECG, in a n attempt to pick out occult, important heart artery disease. This is because, the majority of patients with important heart artery disease, do not know that they have it. It is silent, and so we depend on ischemia producing test to pick it up. Non-ischemia producing test have a high level of false positives. Patients with no symptoms, and a negative stress ECG are either normal, of does not have any high risk heart artery disease.
Well, keep a healthy cardiac lifestyle. Not to smoke, eat wisely, exercise regularly and maintain your ideal body weight. The old cliche is true, prevention is much better than cure.

MORE BAD NEWS FOR HIGH DOSE STATINS. INCREASE IN T2DM

I have reported earlier, that high dose simvastatin, should be used with caution, as advised by the US FDA. Read June 9th, Dangers of simvastatin 80mg. Well, in the 22nd June issue of the Journal of the American Medical Association, Dr Kansik Ray and colleagues from the St Georges University, London, reported their results of a meta-analysis of 5 major clinical trials on high dose versus medium dose statins, and its cardiovascular effects and benefits. They also measured fasting glucose and in some of them, HbA1c. Well, these 5 mega trials, had 32,752 who were not diabetic to start. After an average of 2-5 years of followup ( not so long ), they found, on the average, a 12% increase in the incidence of T2DM, diagnosed in the usual way. High dose statins, would be Atorvastatin 80mg simvastatin 80 mg and rosuvastatin 80mg. Actually this current meta-analysis did not include rosuvastatin.
The effects of high dose rosuvastatin, increasing the incidence of T2DM, was first noted folowing the JUPITER study, in 2009. In 2010, there was a paper in Lancet which showed that high dose statins was associated with an increase incidence of T2DM. This recent paper just serves to confirm it.
They worked out that if you use high dose statins, you would need to treat 155 patients at risk, to reduce 1 incidence of major adverse cardiac events, whereas you would need to treat 498 patients with high dose statins, to inccur one case of T2DM. So they concluded that it was still worthwhile using high dose statins.
I must say that, personally, I do not believe in lowering LDL-C to super low levels, despite the "alleged" evidence. I believe that some of the evidence is massaged by big pharmas to push the sales of their drugs. I would lower LDL-C significantly, using diet and medium doses of statins.
This recent spate of articles on the dangers of high dose statins, just serves to re-inforce my view, that taken all the adverse effects of high dose statins, together, the risk may outweigh the benefit, or the alleged benefit, of super low LDL-C.
I suppose there is a price to pay, for trying to be perfect. God did give us LDL-C for a reason, and so abolishing it totally, may be against the order of nature. Reducing it so that our CV risk is reduced, makes sense.
Anyway, I do not wish to be preachy. Each of us must decide, which part of the spectrum, we wish to be. Just be warned that high dose simvastatin has muscle problems, and high dose statins ( lipitor and zocor ), has the potential of inducing T2DM. The mechanism and the reason why, has not been clearly worked out yet.

PUBLIC WARNING. SCARLET FEVER IN HONG KONG

I just pick-up an announcement by the health authorities in Hong Kong of an outbreak of scarlet fever in Hong Kong. There are almost 400 cases reported this year in the small island state. There is usually some cases reported, but these year, the HK Health Authorities say, the cases are more then usual. They think that the bacteria has mutated, and is now more contagious, and perhaps more virulent.
We in Malaysia, should be more vigilant, as scarlet fever is very contagious, as it is spread by droplet spread, meaning that talking, coughing, sneezing, especially in a close environment can easily spread the disease, especially to the immune compromised ( the very young and the very old )..
Scarlet fever is an infection by the Streptococcus Pyogenes. As spread is by droplet spread, the portal of entry is usually the nose and throat. So scarlet fever presents as fever followed followed by sorethroat and a strawberry tongue. There is also a red rash, which characteriscally comes 1-2 days following the fever. If untreated, the patient may develop complications like nephritis ( inflammation of the kidneys ), or carditis and valvulitis ( inflammation of the heart muscle and valves ). The second may lead on to acute and chronic Rheumatic heart disease.
Treatment is easy. A 10 day course of antibiotics ( it should be sentive to penicillin group antibiotics ) should eradicate the infection, useless this mutated strain, develops resistance to the antibiotics.
Our Hong Kong colleagues reported two deaths.
It is good to be aware. The infection can be easily diagnosed, when there is an index of suspicion and the treatment is easy.
Hong Kong to KL is just 4 hours by plane and many Malaysians travel to Kong Kong and back for work or holiday, so that what affects HK may soon also affect Malaysia.
Just to let you know.

STANDARD OF CARE ; ACUTE HEART FAILURE

Continuing in our Monday series, I would like to discuss the standard of care expected when a patient has acute heart failure. This is to allow the lay public to know what is and what is not reasonable, so that they do not misunderstand what the doctor is trying to do.
Acute heart failure, unfortunately is quite common. Heart failure is defined as the inability of the heart to maintain an adequate circulation, to meet the body's metabolic demands. In short, the heart cannot maintain adequate cardiac output, to circulate enough blood for the body to use. When this happens, the patient usually presents with acute breathlessness, and begins to sweat profusely, cold sweat, Incessant coughing is also a symptom, as well as rapid heart beat or irregular heart beat. By nature of the definition, acute means that it comes on rapidly over days or even hours and minutes, as oppose to chronic ambulatory heart failure which may take days, or weeks to evolve. Of course patients with chronic heart failure could also suddenly become acute.
Keeping to the issue of acute heart failure, making the diagnosis is usually fairly easy. The patient or relatives tells the doctor that he suddenly notice that he is short of breath, can no longer talk in full sentences, seems to be sweating cold sweat, and he keeps coughing and the heart feels very fast. The physical examination by the doctor will reveal that there is tachycardia, cold sweat, and also signs of water in the lungs, on listening to the lungs.
These signs and symptoms are easy to explain. As the heart decompensates ( for whatever reasons that we should come to later ), it cannot generate enough output, and so the circulation slows down. The organs begin to tell the brain, that they are not receiving enough oxygen and nutrition, so the brain will respond. Initially by having the heart pump faster, hoping that a faster rate will mean more blood flow. This works for minutes and then the heart cannot cope, and tells the brain, this first response is not sustainable and is harmful. So the brain initiates the second response, which is to cut down all the circulation to the not so useful organs of the body, like the skin. When the circulation to the skin shuts down ( to conserve blood flow so that blood flow can go to more vital organs like the brain, the heart, the kidneys and the liver ), the skin begins to cool down and sweat cold sweat. The skin at the extremities, may also become bluish or dusky in colour. If that is still inadequate to maintain a central circulation, the heart pump being so inefficient, then blood begins to well up in the lungs, as the forward pumping action of the heart begins to get less and less efficient. In circulation terms, the lungs are the organs just before the heart, so that when the heart is unable to pump, the blood can not circulate forward, so it gets dam backwards, almost like a drain that cannot flow out to empty. When the blood dams into the lungs, the air sacs in the lungs, which should contain air, now begins to well up with water and gets heavy, as water is heavier then air. So there is now, increase work of respiration. The patient notice this as breathlessness or dyspnea. On listening to the lungs, we can hear fluid in the lungs.
Once you reach a doctor, he / she should be able to make this diagnosis. Sometimes, in the initial stages, when the signs are not so obvious, there may be some delay in diagnosis.
For the doctor, the challenge may be to know why? What has cause the heart to fail suddenly? In the older age group, above 40 years of age, acute heart attacks must be excluded. Sometimes a heart attack can happen without chest pains, or sometimes with so much breathing distress, the chest pains is forgotten. An ECG done and some blood test for cardiac enzymes, should be able to help make the diagnosis. Sometimes, patients can be so overloaded with fluids that the heart cannot cope. This may be due to IV fluids given too aggressively by the attending physician, not realising that the patient's heart cannot take it, or more often, this can happen with end stage renal failure. Too high a blood pressure can also be a cause of acute heart failure. There are some heart muscle diseases that can cause acute on chronic heart failure. Certain viruses can sometimes affect the heart muscle to cause it to fail, so we hear of a flu-like illness followed by acute heart failure. Sometimes, lung infections, or other serious infection can push an elder patient into heart failure.
In an emergency situation, the attending physician ( all acute heart failures should be attended to, as far as possible, in a hospital, as things can turn bad suddenly ) should perform the basic blood tests, looking at the kidney function, blood count and cardiac enzymes, do an ECG and CXRay. These should suffice in the immediate emergency context. There is always time for the echocardiogram to be done, when the patient is more stable and better.
Often, patient may have to be monitored in the intensive care, as a failure of the heart is a serious matter, and can result in death. Oxygen therapy by mask or nasal prong, is mandatory. The first priority in management, is to get the extra fluids out or the lungs. This will alleviate the acute distress, cut down the panic ( which stresses the heart more ), and make the circulation better. We can usually achieve good diuresis ( passing urine ), with IV diuretics like frusemide. making the patient calm and restful also helps alot. We sometimes achieve this with a small guarded dose of IV morphine. Once the patient calms down, and begins to pour out urine, by the litres literally, he will improve over minutes and hours. In patients with chronic renal failure, this may take a longtime, and sometimes, we need to use the dialysis machine to extract out the extra fluid, so as to off-load the heart. There are certain drugs that can also offload the heart like ACE-I or ARBs, or the good old, nitrates, and calcium channel blockers. When I am meet a severe heart failure, I am one of the few, who like to use a small, carefully monitored, dose of IV sodium nitroprusside. I find that it takes away the strain on the heart very effectively and quickly.
You can almost know that you are getting out of the acute heart crisis, when the hands and feet warm up, the colour returns, and the urine is pouring. Soon the patient can talk to you in full sentences, and he calms down.
If the investigations carried out suggest a heart attack as the cause, then the management should be as with a heart attack, complicated by heart failure ( this usually mean a big heart attack and the prognosis is not as good. Mortality can be 50% ).
Once things are stable, management then becomes management of what cause the heart attack. You have now reverted the patient back to his status before whatever trigger this heart failure happened. Control of poor controlled hypertension is important. Treatment for chronic renal failure is important. Viral infections usually recover, sometimes, leaving behind chronic heart condition and chronic heart failure.
Generally, if you have acute heart failure once, you can have it again, so great care must be taken in the long term. Chronic heart failure will form the basis for another chapter.
As least now you all know what to expect, should someone suffer from acute heart failure.

DIAGNOSTIC ACCURACY OF CCTA

The June 13 issue of Arch in Internal medicine carried an article by Dr Benjamin Chow from University of Ottawa, Canada, studying the accuracy of CT coronary angiogram ( CCTA ), across different medical facilities. Are all CT angiogram interpretation reliable and the same? The answer is NO.
They studied 169 subjects of intermediate cardiac risk group from across 4 centers in Canada. These subjects all had their CCTA done and were agreeable to have their invasive coronary angiogram done within 10 days of their CCTA. The CCTA and coronary angiogram were read, in a blinded fashion by independent observers.
Well, the centers failed badly. Their sensitivity is only about 81.3%, specificity about 93.3%, positive predictive value was 91.6% and negative predictive value was 84.7%. All these numbers were way below those published by specialised centers in the initial papers. Whats even more upsetting is the spread of accuracy across different centers. See the table below.

Diagnostic accuracy ranges across centers

Statistical measure of CCTA accuracy	Lowest value achieved by any center (%)	Highest value achieved by any center (%)	p
Sensitivity	50	93.2	<0.001
Specificity	92	100	<0.001
Positive predictive value	84.6	100	<0.001
Negative predictive value	42.9	94.7	<0.001

The numbers were varying so much, how can one draw a conclusion. Obviously, the experience in individual centers vary alot. Therein lies the need for constant quality assurances from these centers. Afterall, the CCTAs are not cheap, and they carry a significant radiation risk, although I am told that the later machines, have much less radiation. Couple with these risk, if the CCTA varies so widely in their accuracy across centers, it may increase the need for invasive coronary angiogram, thereby negating the need for the CCTA isn the first place.
As more an more data comes out with the older 64slice MSCT, we know that that technology is just not good enough.
As for the newer 256 slice MSCT, or the dual source, or multi-detector MSCT, supposedly better, we need much more data. It looks like in all these Xray technics where we interpret a mixture of gray ( from white to black ), nothing is really black or white. It is all in different shades of gray, and so observer experience is of paramount importance.
As one of my old physician colleague use to say, when we discuss Xrays, the eye sees not, what the mind knows not.
In CCTA, nothing is really black and white. It is all a mixture of gray. Oh yes, you get significant radiation, not as much as Fukushima, but about 500 CXRays.

BREAKING NEWS. JnJ CORDIS CLOSE DOWN STENT DIVISION

I read with great surprise this morning that Johnson and Johnson Cordis is getting out of the coronary stent business and has also stopped development of its latest NEVO stent. The timing is a real surprise, although those of us in this line, knew that things were not well in JnJ Cordis for awhile.
I first became associated with Johnson and Johnson Interventional way back in 1991 when I first saw the PS153 bare metal stent in Toulouse, and wanted to have it for our Malaysian patients. JnJ Interventional at that time arranged for me to be proctored and as an FDA co-investigator, began to use the stent. At that time, it was just JnJ. They later acquired a rival company, Cordis Niche ( Hong Kong based ) as Cordis were making good balloons and guidewires. Remember, JnJ had a stent and no balloon or guidewire. Maybe the bosses felt that with the Cordis acquisition they will have their own patented balloon. This marriage got on quite well, and JnJ Interventional became JnJ Cordis. I was a bit upset that all mt friends in JnJ one by one began to leave JnJ, and I also found that the business philosophy of Cordis, was quite different from that of JnJ. I had some very good friends in JnJ who took me into their confidence, when I was starting on this road.
Anyway, JnJ Cordis did well at the beginning. They brought out the first Drug Eluting stent ( Cypher ) in 2001 ( FDA approved in 2002 ), and that was market leader for quite a few years In many head to head trials of Cypher and Taxus ( the other DES out after Cypher ), they consistently bettered Taxus. However, many companies innovated much faster then JnJ Cordis. We saw the release of the second generation thin strut cobalt chromium DES from Medtronic and Abbott Vascular which were just as good, if not better then the cypher.
Cordis decided to buy a company called Conors Medsystems in 2007. Conors had the patent to the multi-pit stent technology. That acquisition ( on hind sight ) was not profitable. The Conors results ( bare metal stent ) which was released soon after the purchase, was poor. Cordis decided to put their sirolimus drug into the Conors stent ( now called the NEVO stent ). The NEVO I results were so so at 8 months. After 8 months, we hear nothing. All was quiet on the NEVO stent, so I suspected that things were not going right. I kept asking the Cordis boys here in Malaysia what had happened. They too had no information. I thought that that was a bad sign. Now Cordis has halted work on their NEVO III trial, and have in fact stop all work on the NEVO stent. I can only conclude that either the results are poor, or that there is a manufacturing problem.
Cordis also was affected by numerous patent suits, on their balloons. I think that their Cypher stents all these while was mounted on a balloon under license from Abbott Vascular, and that license runs out in 2011.
We began to get bad feelings about Cordis, when they began laying of staff in USA, and of course the silence over their NEVO program. I knew then that things were not going well.
I also had occasions to work with many JnJ, and JnJ Cordis management as they have always been very supportive of all the CMEs that we organise, to help GPs and also Interventionist.
Anyway, we now see the end of an era, in the history of interventional cardiology. JnJ gave the world the PS 153, which launched the era of coronary stenting, and JnJ Cordis gave us the Cypher stent, which launched the era of Drug Eluting Stents.
I must make it clear that the Cordis division of JnJ is still functioning, concentrating on their peripheral devices and also their electro-physiology division. I will still be able to use their guide-wires, balloons, guiding catheters and sheaths.
Thank you Cordis, for giving us the Cypher stent. There are many grateful patients out there because of you.

WATCHING TV ( >2hrs ) IS BAD FOR HEALTH

There is a small interesting paper, published in the June 15th issue of the Journal of the American Medical Association, syudying the effects of watching TV on diabetes and heart disease. Dr Frank Hu ( Harvard School of Public Health ) and associates did a meta-analysis on 8 studies, studying the ill effects of TV watching on health. With the 8 studies, there were a total of 175,000 subjects, from US and Europe. They were asked how many hours they watch TV a day and this was correlated with the incidence of type 2 diabetes, heart disease and all cause mortality. They found that for every 2 hours of TV time, there is a 20% increase in the incidence of type 2 diabetes, 15% increase in incidence of heart disease and a 13% increase in all cause mortality.
Whether this is due to the sedentary activity ( couch potato ), or the associated use of junk food, it is difficult to know. Somehow, working on the computer, was found to have no correlation.
Actually, this information we already know. What I was interested were the numbers. 13-20% in high. The average of us must be watching TV 2 hours a day ( also depend on your age. The younger ones less, and the seniors more ). In Europe ( especially in winter ), one could be watching TV for 4-8 hours, if not the whole night. TV watching is ranked the third most common daily activity after work and sleep.
There is a move to see how we could exercise while watching TV, or some exercise in between watching TV. Of course, cutting of junk food helps ( I am quite certain). It would appear the the invention of the remote control is bad for health, taking away even the little activity that our fathers and grand fathers use to do, in the good old days.
But then, today is the days of the "instant" culture.

STANDARD OF CARE : STROKE

Stroke is a devastating disease. Not only does it kill, but for those who survive, it can leave behind severe disabilities, including inability to move ( bed-ridden ), inability to talk, inability to eat, inability to respond, all of the above, or some of the above. It is therefore a dreaded disease. It usually occurs in patients suffering from hypertension and diabetes. Of course, it is also more common in the older age group. In stroke ( or what some may now call, an acute brain attack ), the brain is suddenly deprived of blood flow, and so the brain cells die from lack of oxygen and nutrition. ( almost like what happens in the heart during a heart attack, therefore the name brain attack )
There are two main kinds of stroke. We call them hemorraghic stroke, when the artery supplyoing that area of the brain ruptures ( usually from a sudden rise in blood pressure ), and so the blood flows out of the blood vessel into the surrounding tissues, and cause pressure effects on the surrounding normal brain tissue, causing it also not to get enough blood flow as the surrounding tissues become compressed. ( The brain after all is enclosed in the bony skull that cannot expand to accommodate the blood leaking out from the ruptured brain artery. The other kind of stroke, is what we term the ischemic stroke. Ischemia is lack of blood supply. This form of stroke is due to blood clots, blocking off the artery preventing blood from flowing, like what happens in a heart attack. There are essentially two kinds of ischemic stroke. When the blockage is due to a small clot, sometimes that small blood clot can flow away, and so the blockage is acute but transient. We call this a minor stroke ( as if like a warning ). Sometimes the blockage is by a large blood clot and so the clot stays and cause a massive loss of blood supply to the brain tissue that it supplies. This is called an major ischemic stroke.
When a stroke presents, the most important thing is to recognise it and seek medical care. Again here, TIME IS BRAIN CELLS. Every minute that we waste, more brain cells are destroyed, and so worse is the outcome. Fortunately, when a major stroke occurs, it is easily recognisable. The patient will stop doing whatever he / she is doing as there is a sudden loss of brain function. If they are standing, they may collapse. If they are eating, they will drop whatever they are holding and cannot eat. If they are talking, they will suddenly lose their speech, of they will have difficulty finding the right words, or they will begin to slur. There will be sudden loss of brain function. The unfortunate ones are those patients who suffered a stroke while sleeping. No one knows, and so treatment can be delayed.
Quickly take him / her to the nearest medical center. There the doctors will quickly assess him, and confirm that a stroke has occurred. The blood pressure will be measured, the ECG done and the blood sugar measured, as these are all important pieces of information. Usually the medical center will alert the neurologist on call, and if there is a brain attack team, the brain attack team will be alerted. A CT scan, or MRI brain scan should be done. This will confirm the diagnosis, distinquish between a hemorraghic stroke and an ischemic stroke, and decide on the treatment strategy.
If this is a hemorraghic stroke ( red infarct ), the outcome is grave. A large bleeding and blood clot in the brain may necessitate brain surgery to remove the blood clot, which is compressing the normal brain tissue. In the acute phase, this can be very hazardous. Some times, when the brain is so swollen, after removing the blood clot, the brain wound cannot be safely closed, and so either the brain is left partially open, only for the wound to be closed later, or sometimes part of the brain may have to be sacrificed and removed, to make enough space to close the brain. All of these measures, are, in one word ugly and the outcome is usually bad ( as least those that I have seen ).
If the stroke is an ischemic stroke ( white infarct ), then the neurologist may advise treatment with thrombolytic agent ( clot buster like in a heart attack ). The time window for reperfusion ( re-establishing blood flow ) is about 3 hours from onset of symptoms. The neurological fraternity is studying if this time window could be extended to 4.5 hours? With the successful use of the IV thrombolytic agent, blood flow is re-established and blood will flow again, hopefully allowing the brain issue to recover, thereby reducing the brain deficit. In fact, this has been found to be so. With successful use of the IV thrombolytic agent, we see a 30% reduction in neurological deficit, over the next 3 months, when compared to those not given IV thrombolytics. But it is wellknown that IV thrombolytics may not improve survival.
In the meantime, the blood sugar should be optimised, and the BP controlled, not too low, and not too high.
After successful medical treatment, the patient should be rehabilitated, with physiotherapy, stroke counselling and medical therapy, including the use of anti-platelet agents idf it is an ischemic stroke.
Patients who have suffered a minor stroke, must know that it is a warning stroke, and will usually be followed by a major stroke so they must seek proper medical therapy to prevent a major stroke, including the use of anti-platelet agents, and good control of hypertension and diabetes.
Remember, recognise a stroke, and seek medical help as soon as possible. TIME IS BRAIN TISSUE.

PUBLIC WARNING

I was just send this post. I must confess that in the past, I have taken some of these. I never realised that Aspartame breakdowns to Formaldehyde when heated.
Anyway, I thought that I should highlight these facts, and warn all of you. Of course, I will not take these again.




ASPARTAME - THE SILENT KILLER
For those who take
Ricola & Fisherman , please note that they both contain Aspartame - the silent killer.


This website shows the adverse effects of ASPARTAME:
http://www.nexusmagazine.com/articles/aspartame.html

Fisherman Sweets
FOR THOSE WHO LIKE TO EAT FISHERMAN SWEETS BE CAREFUL: Sugar free products contain ASPARTAME .. So don't consume Sugar free product esp. 'fisherman sweets' ASPARTAME - THE SILENT KILLER (by Ron Harder)

To those who prefer to consume artificial flavouring:

There is an epidemic across North America today of Multiple Sclerosis and Lupus. Most people do not understand why this epidemic is happening, and they do not know why these diseases are so rampant. I would like to share with you the main reason we are having this very serious problem. Many people today use artificial sweeteners in their tea or coffee.

They do this because the ads they see on TV tell them that sugar is bad for their health. This is absolutely true. Sugar is toxic to us , but what most people use as a replacement for sugar is much more deadly. I am talking about ASPARTAME. It is the cause of the epidemic that was mentioned above. ASPARTAME is an extremely toxic chemical that is produced by a chemical company called Monsanto.

ASPARTAME is being marketed around the world as a sugar substitute and is found in all diet soft drinks, such as Diet Coke and Diet Pepsi . It is also found in artificial sweeteners such as NutraSweet, Equal, and Spoonful; and it is used in many other products as a sugar replacement.

ASPARTAME is marketed as a diet product, but it is not a diet product at all. In fact, it will cause you to GAIN weight because it makes you crave carbohydrates. Causing you to gain weight is only a very small part of what ASPARTAME does. It is a toxic chemical that changes the brain's chemistry. It can and does cause severe seizures.

This chemical changes the dopamine level in the brain, and it is particularly deadly for anyone suffering from Parkinson's disease.

ASPARTAME is extremely poisonous, and here is why one of the toxic ingredients of it is wood alcohol. When the temperature of

ASPARTAME exceeds 86 degrees F, the wood alcohol in it is converted to Formaldehyde, and then to formic acid, which in turn causes folic acidosis.

FORMALDEHYDE is grouped in the same class of poisons as Cyanide and Arsenic which are very deadly toxins. The only difference is, Formaldehyde kills quietly, and it takes a little longer. And, in the process of killing people, it causes all kinds of neurological problems. There are 92 documented symptoms of Aspartame Poisoning leading to coma and death.

The majority of these symptoms are neurological, because the ASPARTAME attacks and destroys the nervous system. One of these symptoms is Lupus, which has become almost as rampant as Multiple Sclerosis, especially with Diet Coke and Diet Pepsi drinkers.


You have been warned.

THE PROBLEM WITH DIABETES, CARDIOVASCULAR - WISE THAT IS?

It has been known for a long time that though we understand that diabetes is a "sugar" disease, due to the inability of the body to handle a glucose load, diabetes is actually a cardiovascular disease, because patients with diabetes dies from cardiovascular complications or heart attacks, strokes, peripheral vascular disease, renal vascular disease and eye vasculopathies. Yes, before the days of insulin, some diabetics die from high blood sugar with coma. True, nowadays, some patients, treated over aggressively die from low blood sugar. But the majority of diabetics nowadays, die from cardiovascular complications. If fact, in our circle, it is commonly debated that diabetes is a cardiovascular disease and diabetologist should be a part-time cardiologist. many of our cardiac meetings will spend a large portion of our time discussing diabetes and its effect on patients.
In the May 26 issue of Diabetes ( the journal ), Dr Naila Rabbani explains why, in a paper published by her group from the University of Warwick, UK. We all know about total cholesterol and LDL-cholesterol ( bad cholesterol ). We also know that there are many forms of bad cholesterol, some rather aggressive and some more benign. The aggressive LDL-Cholesterol, are usually small and dense. Dr Naila and group found that in diabetics, particularly the poorly controlled ones, the circulating LDL-cholesterol is easily glucated ( attached with glycine-like molecule to change its structure ), by methylglyoxal. This glycated LDL-Cholesterol, becomes small, dense and sticks very easily to the arterial wall, thereby initiating the process of atherosclerosis, or furthering the process of atherosclerosis.
They also found that the diabetic drug, metformin ( good, old and cheap) reduces the glycation of LDL-cholesterol, meaning that patients on metformin, is likely to have less of the small dense LDL-cholesterol.
This kind of basic science discovery is very useful, as it allows us to understand the disease process better and also to manage it better. This will explain in large part why metformin did so well as a drug in reducing major adverse cardiac events, in diabetics, like in UKPDS.
So, not all LDL-C are the same. The small ones are more aggressive and sticks to arterial walls causing trouble. Metformin, if tolerated, is a good drug to counter this.

DANGERS OF SIMVASTATIN 80mg

Yesterday, the US FDA issued a safety communication regarding the use of high dose simvastatin. On their review of the SEARCH ( Study of the Effectiveness of Additional Reduction in Cholesterol and Homocysteine ) data, they found an obvious increase incidence of myopathy and muscle problems in those patients given high dose ( simvastatin 80mg ) of simvastatin ( Zocor ). There were 52 cases of myopathy in the 80mg group compared to 1 in the 20 mg group, and 22 cases of rhabdomyolysis in the 80 mg group compared to non in the 20 mg group. These numbers are frightening as rhabdomyolysis is a serious condition that can result in renal failure and death.
FDA also caution the use of more the 20 mg of simvastatin in patients already on Norvasc, amiodarone, diltiazem and verapramil, meaning that simvastatin may interact with these drugs, and increase the incidence of muscle problems.
Thank God, I do not believe in super-lowering of LDL-C, and have no patients on simvastatin 80mg. Simvastatin is a commonly prescribed statin and norvasc and diltiazem are commonly prescribed calcium channel blockers.
When I read this, I thought that all of you should know, as muscle problems with statins are getting more common and the use of calcium channel blockers are also quite common. I am sure the FDA will require MSD ( maker of Zocor ), to edit their box labelling to reflect this concern.

STANDARD OF CARE - HEART ATTACKS

As I alluded to in the last article, I thought I should post a series of standards of care, maybe every monday, so that the general public can know what to expect when they have to consult a doctor with the acute emergency. I have chosen emergency situations because that is when you must trust the doctor as there is often not much time to discuss many of the pressing issues. An emergency is when a life is at stake, and time is of the essence. If something is not done right, right away, the patient could die.
Heart attack is the number one killer in the country and it kills many of those in the 40-55 age group ( people at the peak of their career, with families to support ), and so their loss is very severely felt. One third of patients with a heart attack dies. The mortality rate is high. Fortunately, there is much that medical science and cardiology can offer, in terms of saving the life.A heart attack occurs when a plaque ( an accumulation of cholesterol material in the arterial wall, covered over by a thin lining ) cracks ( the thin lining ruptures ), exposing the cholesterol crystals below to the blood flowing on top of it. Cholesterol is thrombogenic and so a blood clots, almost instantly and blocks off the whole artery, thereby depriving the heart muscle of vital life - sustaining blood and so the heart muscle in the affected area dies, within minutes ( 20 minutes or so ), and circulation should be restored within 4 hours for maximal benefit.
Because of the death of heart muscle cells, TIME IS MUSCLE. The longer we wait around, the more muscle will die. To salvage the heart muscle, is to restore the artery circulation, to revascularise. We can revascularise in too ways.
1. With the use of chemical agents, drugs, called clot - busters, or thrombolytics. These agents will eat away the blood clot, and so re-establish a tiny channel for blood to flow. The success rates are in the 70-90%, depending on which agent you use and how long you wait before seeking treatment. The longer you wait, the harder the blood clot, the more damaged the muscle, and so the less the success. Any secondary or tertiary care hospital can have access to these drugs, and so this method is available to many in the community.
2. With the use of balloon catheters and stents. With the balloon, we can clear away the the blood clot, and also the cholesterol accumulation at the site, and so with can restore circulation very effectively. This is usually followed by the use of a stent, which reduces complications and also makes the passage more permanent by reinforcing the vessel wal. However, this method requires a technically skilled team, and may not be available at all hospital, except in selective tertiary care cardiac centers. Angioplasty does have its risk and so cannot be undertaken by untrained specialist. With a trained team, the success rate is 90-95%, again depending on when the patient presents ( how long after the onset of chest pains ), and also how long the center takes to assemble the angioplasty team. We like to re-establish blood flow, within 4 hours if possible, at worse before 8 hours. Any longer, the risk of procedure may outweigh the benefit ( meaning that you are not saving much muscle, but still taking the risk of the procedure ). we call this approach, primary angioplasty for AMI. It is also costly, but it is by far the best method to treat a heart attack patient if they present within 4-8 hours.
Upon effective re-vascularisation, the heart attack patient should get stable, and be able to get on his/her feet within a day or two, and be discharge within a week.

Just to reiterate, heart attacks kills. TIME IS MUSCLE. If you have significant chest pain, and you are in the heart attack risk group ( age 40 and above, smoke, hypertension, diabetes, high cholesterol, ), go see a doctor as soon as you can. An ECG would help to diagnose your condition. All other test can wait. If you have an ECG suggestive of a heart attack, go to the nearest medical center for treatment. TIME IS MUSCLE. The specialist there may offer you angioplasty, if you arrive within the time window ( 4-8 hours ), and they have the capability, or they may offer you IV thrombolytic therapy ( clot busters ). Rest is important. Of course, there will be the usual cardiac medications, aspirin, plavix, vaso-dilators, ACE-I, Also the advice of diet, not to smoke, lose weight, etc, etc. But these can all wait, till after blood flow is restored to the heart muscle.

That should be the standard of care nowadays.

ODDS AND ENDS

There are a few developments out there that merit some comments, just for public interest.

1. The present food scare in Germany and northern Europe is serious. I cannot understand, why after 1 week, they still have not got a handle to it. Either the healthcare system is bad, or it is not an infection. from what I know ( just reading from the lay press ), it would appear that some bacterial ( probably E Coli ), has contaminated some food ( looks like fresh vegetables ). Blaming Spain ( with little evidence ) just side track the issue, and wasted valuable time. This bacterial, when ingested, seem to cause red blood cells to break down ( The hemolytic part of the problem ). When red blood cells in the body breakdown in large numbers, the kidneys ( the bodies clearing house ), is suddenly flooded with a lot of large protein molecules ( the hemoglobin and its breakdown products). This severe protein load, damages the kidneys causing the kidneys to shutdown ( the uremic part of the problem ). It is rather unusual for E Coli to do this. The common food poisoning E Coli is present in food contaminated with excreta. It causes diarrhea, and is got rid off. It usually damages the intestines and the body handles it well. In the intestinal phase, they cause diarrhea. It can enter the blood stream, and poison the blood ( septicemia), this is already the severe form, and for it to damage red blood cells in large numbers, is very unusual. I hope that Germany has a good public health department to trace the source ( usually you can ). The infection must come from a certain locality, because it is usually food contamination. They must locate and isolate that community from where the infection seem to arise. as a public health measure, all diarrhea must be reported, and cases traced, while the individual cases are treated. There is a high likelihood, that it is contaminated water.
In the meantime, all visitors to Europe, and Germany, should only eat well washed, well prepared cooked food. Cooking kills E Coli. Hemolyic-Uremic syndrome, is a very serious condition. You do not wish to mess around with it. Prevention is much better then cure.

2. The New York state authorities, is banning the use of food coupons to buy fizzy drinks, in an attempt to prevent obesity, especially childhood obesity. This I believe is a step in the right direction. Of course there will be a hue and cry from the industry and also the teenagers, virtually addicted to coca cola, and all forms of carbonated drinks. But I believe, a right direction, as the epidermic of obesity, is causing to much money to healthcare. Maybe over here, the government should impose a higher GST on frizzy drinks ( when GST does come ), so that people will be less likely to take frizzy drinks.

3. Calling all local and overseas Malaysians. Please register to vote. Who you wish to vote for, it is your free choice. But please register and please vote.
Calling all overseas Malaysians who are eligible to vote, please register to vote. When GE 13 is announced, please take two days ( if you are in the Asia Pacific region ) leave, or 1 week ( if you are out of Asia Pacific region and across more then three time zones ) leave. Fly in, vote and return the next day or next week, to work. We need all your help to change this government which has become dysfunctional.

Thanks.

INTENSE FEAR AND THE HEART

There is a very simple, and yet important paper reported in the European Heart Journal, on the influence of fear following a heart attack and the outcomes. Otherwise seen as the influence of the emotions on the biological. This paper by the group of workers from Imperial college, studied 208 subjects ( I am sure that they can get more if they have more funds or time ) with a heart attack, assess their level of fear by questionaire ( this is the weak part of their study ), and measured their response, biochemically ( inflammatory markers ) and also physically, heart rate and BP variability. They found that intense fear was associated with increase levels of certain inflammatory markers and stress hormones, which usually correlates with more cardiac events and worse outcomes. That's simple.
What is important about this paper is the fact that we have now documented the association between an emotion ( fear ), and biological functions and responses. My interest in the area, started when we were trying to understand the effects of "vodoo" on sudden cardiac death? How did vodoo witches, make their subjects so afraid, that they died ( self fulfilling). In fact, one of the pioneer workers in this area in the 1980s was a certain doctor, called Regis de Silva. He is a graduate of the University of Malaya medical school ( first batch ), who migrated to USA, and landed with a job at Mass General, Boston. His interest was sudden cardiac death. He was trying to understand arrhythmic cardiac deaths from intense fear.
I remember seeing a patient in the 80's, when I was a lecturer in University Hospital, who was so afraid, when he was diagnosed with heart valve disease, that he passed away. Once diagnosed, he was so afraid, that he could not sleep, and literally panicked over every small feeling of unwell ( whether related to his heart or not ). One day, he just collapsed and died.
I suppose the lesson that we learn is, to remain calm and confident, when you suffer a cardiac event. Choose your cardiologist well. Trust him, if not get a second opinion. Rest assured that cardiology is very advanced, and most cardiac conditions have good modalities of treatment, albeit at a cost. In Malaysia, even the government hospitals have a good average standard of cardiac care. Angioplasty is widely available. Many young cardiologist are out there. Our role as seniors, is to help them shorten their learning curve, and their skill in decision making. They are doing a good job.
Should you or your love ones suffer an unplanned cardiac event, find a good practitioner. Discuss things with him / her calmly. Discuss all the pros and cons ( of course having learned from the internet - Google.com helps for the discussion to be more meaningful ), with him. Be satisfied with the explanations, and allow him to proceed as per discussed. If you are not happy, get a second opinion. Being fearful, always distressed and unhappy, does not help. It may worsen the situation.
In a few simple words, if you have suffered a heart attack, and should you reach a tertiary heart center within 4 hours ( some stretch to 8 hours ), it is an acute emergency, an immediate angioplasty is the treatment of choice. You have to trust your cardiologist there, and trust that he will do a good job. If you survive 8 hours and only see a practitioner after 8 hours, he will probably wait and stabilise you. Going for immediate angioplasty then carries more risk, and does not confer enough benefit to justify those risks. You have plenty of time for opinions and discussion, and pre-discharge angiogram or submaximal stress ECG, would be reasonable ( assuming that your heart attack is uncomplicated. A complicated heart attack, should always merit a pre-discharge angiogram. Some centers who cannot carry out immediate angioplasty in the first 4 hours, amy just treat you medically with thrombolytic agents ( clot busters ), and aspirin, in the immediate period, and then arrange for you to be transfered to a tertiary care center, when you are recovered and stabilised. That is also acceptable treatment.

Maybe, one day, we should write on treatment standard of care for various cardiac conditions.

In the meantime, should you have an acute cardiac problem. see a medical practitioner, stay calm, do some reading and trust him, or find another. Fear is damaging to your heart.