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CHOLESTEROL & STATINS – New Guidelines Drop Targets.

CHOLESTEROL & STATINS – New Guidelines Drop Targets.

HEART 01

New Guidelines on Statins Drop Cholesterol Targets

The nation’s leading heart organizations released new guidelines on Tuesday that will fundamentally reshape the use of cholesterol-lowering statin medicines that are now prescribed for a quarter of Americans over 40. Patients on statins will no longer need to lower their cholesterol levels to specific numerical targets monitored by regular blood tests, as has been recommended for decades. Simply taking the right dose of a statin will be sufficient, the guidelines say.

Have a question about heart health? Try Ask Well. Your question may be answered by a Times journalist or expert.

The new approach divides people needing treatment into two broad risk categories. Those at high risk because, for example, they have diabetes or have had a heart attack should take a statin except in rare cases. People with extremely high levels of the harmful cholesterol known as LDL — 190 or higher — should also be prescribed statins. In the past, people in these categories would also have been told to get their LDL down to 70, something no longer required.

Everyone else should be considered for a statin if their risk of a heart attack or stroke in the next 10 years is at least 7.5 percent. Doctors are advised to use a new risk calculator that factors in a person’s blood pressure, age and total cholesterol levels, among other things.

“Now one in four Americans over 40 will be saying, ‘Should I be taking this anymore?’” said Dr. Harlan M. Krumholz, a cardiologist and professor of medicine at Yale who was not on the guidelines committee.

The new guidelines, formulated by the American Heart Association and the American College of Cardiology and based on a four-year review of the evidence, simplify the current complex, five-step process for evaluating who needs to take statins. In a significant departure, the new method also counts strokes as well as heart attacks in its risk calculations, a step that will likely make some additional people candidates for the drugs.

It is not clear whether more or fewer people will end up taking the drugs under the new guidelines, experts said. Many women and African-Americans, who have a higher-than-average risk of stroke, might find themselves candidates for treatment, but others taking statins only to lower LDL cholesterol to target levels might no longer need them.

The previous guidelines put such a strong emphasis on lowering cholesterol levels by specific amounts that patients who did not hit their target levels just by taking statins often were prescribed additional drugs like Zetia, made by Merck. But the new guidelines say doctors should no longer prescribe those extra medicines because they have never been shown to prevent heart attacks or strokes.

Zetia has been viewed with increasing skepticism in recent years since studies showed it lowered LDL cholesterol but did not reduce the risk of cardiovascular disease or death. Still, it is among Merck’s top-selling drugs, earning $2.6 billion last year. Another drug, Vytorin, which combines Zetia with a statin, brought in $1.8 billion in 2012, according to company filings. And in May, Merck won approval for another drug, Liptrzeut, which also contains the active ingredient in Zetia and a statin, a development that surprised many cardiologists because of questions about its effectiveness.

The new guidelines are part of a package of recommendations to reduce the risk of heart attack and stroke that includes moderate exercise and a healthy diet. But its advice on cholesterol is the flash point, arousing the ire of critics who say the authors ignored evidence that did not come from gold-standard clinical trials and should also have counted less rigorous, but compelling, data.

For example, Dr. Daniel J. Rader, the director of the preventive cardiovascular medicine and lipid clinic at the University of Pennsylvania, points to studies of people with genes giving them low LDL levels over a lifetime. Their heart attack rate is greatly reduced, he said, suggesting the benefits of long-term cholesterol reduction.

Committee members counter his view, saying that cholesterol lowered by drugs may not have the same effect.

Critics also question the use of a 10-year risk of heart attack or stroke as the measure for determining who should be treated. Many people will have a lower risk simply because they are younger, yet could benefit from taking statins for decades to keep their cholesterol levels low, they say.

He and other experts also worry that without the goad of target numbers, patients and their doctors will lose motivation to control cholesterol levels.

Experts say it is still unclear how much the new guidelines will change clinical practice. Dr. Rader suspects many cardiologists will still strive for the old LDL targets, at least for patients with heart disease who are at high risk. “They are used to it and believe in it,” he said.

Dr. Steven E. Nissen, a cardiologist at the Cleveland Clinic, said he thought it would take several years for doctors to change their practices.

The process of developing the new guidelines was rocky, taking at least twice as long as previous efforts. The National Heart, Lung and Blood Institute dropped out, declaring that drafting the guidelines was no longer part of its mission. Several committee members, including Dr. Rader, also dropped out, unhappy with the direction the committee was going.

Have a question about heart health? Try Ask Well. Your question may be answered by a Times journalist or expert.

The architects of the guidelines say their recommendations are based on the best available evidence. Large clinical trials have consistently shown that statins reduce the risk of heart attacks and strokes, but the committee concluded that there is no evidence that hitting specific cholesterol targets makes a difference. No one has ever asked in a rigorous study if a person’s risk is lower with an LDL of 70 than 90 or 100, for example.

Dr. Stone said he was surprised by what the group discovered as it delved into the evidence. “We deliberated for several years,” he said, “and could not come up with solid evidence for targets.”

Dr. Nissen, who was not a member of the committee, agreed. “The science was never there” for the LDL targets, he said. Past committees “made them up out of thin air,” he added.

The Department of Veterans Affairs conducted its own independent review and came to the same conclusion. About a year ago, the department, the nation’s largest integrated health care system, dropped its LDL targets, said Dr. John Rumsfeld, the V.A.’s national director of cardiology.

“It is a shift,” he acknowledged, “but I would argue that it is not a radical change but is a course correction.”

The department had also used target LDL numbers as rewards for doctors and hospitals, but no longer does.

M. Ridker, the director of the center for cardiovascular disease prevention at Brigham and Women’s Hospital, in Boston, said he worried the new guidelines could easily lead to overtreatment. An older man with a low LDL level who smokes and has moderately elevated blood pressure would qualify for a statin under the new guidelines. But what he really needs is to stop smoking and get his blood pressure under control.

Dr. Stone said he hoped doctors would not reflexively prescribe a statin to such a patient. Doctors are supposed to talk to their patients and realize that, with a man like the one Dr. Ridker described, the real problem was not cholesterol.

“We are taking people out of their comfort zone,” Dr. Stone said. “Instead of being reassured that reaching this number means they will be fine, we are asking, ‘What is the best therapy to do the job?’”

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3 Things to Know About the New Cholesterol Guidelines

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The American College of Cardiology and the American Heart Association just released new cholesterol guidelines to reduce atherosclerotic cardiovascular risk –- and the change from the previous version, last updated in 2004, is profound. Here are three things you need to know about these new guidelines.

First, the guidelines have moved away from achieving target cholesterol levels.

Americans have long been urged to focus on their laboratory numbers. Many people are obsessive about checking their cholesterol levels and pursuing even better numbers. Doctors have been told to focus on these numbers and, in some cases, the quality of their care was assessed by the percentage of their patients with low cholesterol levels.

Those days are over. The new guidelines recognize that for patients who have exhausted lifestyle efforts and are considering drug therapy, the question is not whether a drug makes your lab tests better, but whether it lowers your risk of heart disease and stroke. Studies over the past several years have shown that improving your lab profile with drugs is not equivalent to lowering your heart risks. Drugs have thousands of effects on the body, and a drug’s effect on an individual lab test cannot necessarily predict its overall effect on you.

Importantly, the guidelines still state that cholesterol is important. But the point is that changing your cholesterol level with medications is now accompanied with the appreciation that other effects of the drugs may offset any benefit to reducing cholesterol.

There’s one exception to the numbers rule. People with very high cholesterol still need to worry about targets. The new guidelines set that level at 190 milligrams per deciliter – but the principle is that if people have very high cholesterol levels, then their cardiovascular risk is so high that it is likely that treatment to reduce the levels would offset any risks of the drug treatment.

So, the new guidelines are saying: we should not be chasing the cholesterol levels alone. The “know your number” campaign is no longer consistent with the guidelines, and the days of doctors adding additional medications to get you to some arbitrary cholesterol level should no longer occur.

Second, know your risk.

What is taking the place of cholesterol levels? What should you do now?

The guidelines are now focusing you on your overall risk of heart disease and stroke. They indicate that drug treatment is recommended for people with a high risk — and that more powerful treatments are best for those with the highest risk.

So what they are saying now is: know your risk of heart disease and stroke. They have published an online calculator to help you -– but more important is the general concept that drug treatment with effective medications (those proven to lower risk) should be used in people with the most to gain.

The guidelines do set thresholds for risk, but my view is that these recommendations should not be considered dictums to be followed without question. They say that if your 10-year risk of heart disease and stroke is 7.5 percent or higher, then you should be treated with drugs. However, I believe that only you can determine what constitutes a high enough risk that it is worth it to you to be treated with drugs. Such a decision depends on how you feel about your risk of heart disease and stroke and how you feel about taking drugs — and their risks and benefits.

Third, use medications proven to reduce risk.

The understanding that simply improving cholesterol lab tests may not reduce your risk for heart attack and stroke has focused attention on the choice of drug therapy. In the “treat to target” era, there was a sense that we could use any of the medications to lower LDL — and what was most important was the lab test.

However, there have been numerous studies showing that many popular drugs that may have improved lab tests for cholesterol failed to reduce risk. These studies led the authors of the guidelines to make a distinction between proven and unproven medications.

Thus, the focus of the guidelines is on statins, the drug class with clear evidence that it can lower risk in many groups of patients. In fact, statins seem to lower risk regardless of your cholesterol levels. This fact has led many of us to think about statins as risk-reduction medications rather than just medications that modify cholesterol levels. Regardless, the evidence that statins lower risk is very clear.

So the guidelines now make clear that if you use drug therapy for higher risk, you should use statins. If you cannot tolerate one statin, you might want to try another statin, after consultation with your doctor. If you use another type of drug, then you should know whether that drug has been shown to reduce risk in contemporary studies. Many popular drugs, like Zetia (ezetimibe), have yet been proven to save lives.

Bottom line: The new guidelines are a marked departure from the era of chasing targets and being agnostic to the drugs you used. The new message is don’t chase targets, know your risk, and — if you need drug therapy — use statins. These principles should guide your discussions with your doctor.


Harlan Krumholz is a cardiologist and the Harold H. Hines Jr. Professor of Medicine, director of the Yale-New Haven Hospital Center for Outcomes Research and Evaluation (CORE) and director of the Robert Wood Johnson Clinical Scholars Program at Yale University School of Medicine.

To view the original of this article CLICK HERE
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Regards,
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 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
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Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
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You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
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YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
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Healing the Heart

Healing the Heart
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Hi,

this article from National Geographic in 2007 makes an interesting read:

Healing the Heart

Human Heart

Mending Broken Hearts

Cheeseburgers, smoking, stress, the rise of the couch potato: These are the usual suspects on the list of risk factors for heart disease, a malady reaching global epidemic proportions. Now discoveries about genetic triggers may help us spot trouble before it starts.

By Jennifer Kahn
Photograph by Robert Clark

Gloria Stevens is lying on her back, sedated but alert, staring at an image of her own beating heart. Metaphorically, Gloria’s heart is the very core of her emotional self—not to be worn on the sleeve, much less displayed on an overhead monitor. More literally, it is a blood-filled pump about the size of a clenched fist whose rhythmic contractions have kept Gloria alive for 62 years, and with a little tinkering will keep her going for an indeterminate number more.

At this moment, her doctor is threading a thin catheter up through her femoral artery from an incision in her groin, on into the aorta, and from there into one of the arteries encircling Gloria’s heart. At the tip of the catheter is a small balloon. The doctor gently navigates the tip to a spot where plaque has narrowed the artery’s channel by 90 percent. With a quick, practiced movement he inflates the balloon to push back the artery wall, deflates the balloon, then inserts an expandable stent—it looks like a tiny tube of chicken wire—that will keep the passage open. As Gloria watches on the monitor, the crimp in her artery disappears, and a wide laminar flow gushes through the vessel, like a river in flood.

The procedure is over. It has lasted only half an hour. In all likelihood, Gloria will be able to go home the next day. So will a few thousand other patients in the United States undergoing such routine angioplasty—more than a million of them a year. Pipe fixed, patient cured, right?

Wrong.

Because of her treatment, Gloria’s quality of life will likely improve. She’ll breathe easier and maybe live longer. But she is hardly cured. Her coronary atherosclerosis—a hardening and narrowing of the arteries that supply the heart with oxygen-rich blood—still leaves her vulnerable to future blockages and coronary heart disease.

Although hearts suffer many maladies—valves leak, membranes become inflamed—coronary heart disease, which can lead to heart attack and ultimately to heart failure, is the number one killer of both men and women in the United States, where 500,000 die annually. Worldwide, it kills 7.2 million people every year. Exacerbated by the export of Western lifestyle—motorized transport, abundant meat and cheese, workdays conducted from the comfort of a well-padded chair—incidence of the disease is soaring.

To help stem this lethal tide, cardiologists can prescribe such cholesterol-lowering drugs as statins to help keep arteries clear. They can advise patients to change their habits, or they can operate to fix an immediate problem. Angioplasty is one procedure, and surgery to bypass the diseased arteries is another—each year more than 400,000 bypasses are performed in the U.S. Transplants can replace severely damaged hearts, and artificial ones can keep people alive while they wait for a donor heart. But in the face of an impending global epidemic, none of these stopgap measures addresses the essential question: Who gets heart attacks and why?

The human heart beats 100,000 times a day, propelling six quarts of blood through 60,000 miles (97,000 kilometers) of vessels—20 times the distance across the U.S. from coast to coast. The blood flows briskly, surging out of a ten-ounce (0.3 kilograms) heart so forcefully that large arteries, when severed, can send a jet of blood several feet into the air. Normally the relentless current helps keep blood vessels clean. But where an artery bends, tiny eddies form, as in a bend in a river. This is where bits of sticky, waxy cholesterol and fat can seep into the artery wall and oxidize, like butter going rancid. Other matter piles up too. Eventually, the whole mass calcifies into a kind of arterial stucco, or plaque.

Until recently, cardiologists approached heart disease as a plumbing problem. Just as mineral deposits restrict the flow of water through a pipe, an accretion of plaque impedes the flow of blood through an arterial channel. The more crud in the system, the greater likelihood that a dammed artery will trigger a heart attack. Doctors now dismiss this “clogged-pipes model” as an idea whose time has passed. It’s just not that simple.

Most heart attacks are caused by plaque embedded within the artery wall that ruptures, cracking the wall and triggering the formation of a blood clot. The clot blocks the flow of blood to the heart muscle, which can die from lack of oxygen and nutrients. Suddenly, the pump stops pumping.

Contrary to the clogged pipes model, heart attacks generally occur in arteries that have minimal or moderate blockage, and their occurrence depends more on the kindof plaque than on the quantity. Scientists have been struggling to figure out what type is most responsible. Paradoxically, findings suggest that immature, softer plaques rich in cholesterol are more unstable and likely to rupture than the hard, calcified, dense plaques that extensively narrow the artery channel. But understanding the root cause of the disease will require much more research. For one thing, human hearts, unlike plumbing fixtures, are not stamped from a mold. Like the rest of our body parts, they are products of our genes.

Don Steffensen was putting duck-hunting decoys out on a small lake one fall afternoon in southwestern Iowa when his heart attack hit. The infarction was massive and unexpected. It’s likely that Steffensen survived only because a buddy was carrying nitroglycerin tablets and quickly slipped one under his friend’s tongue. Nitroglycerin is used to make dynamite; in the body, a heavily diluted form releases nitric oxide, which signals the smooth muscle cells in veins and arteries to relax, dilating the vessels.

The Steffensen clan is enormous: more than 200 relatives spread over three generations, many of the youngest are now dispersed from Iowa to New York and beyond. Although heart trouble is common in the family, it had never struck anyone as unusual. “I attributed it to diet,” shrugs Tina, a slim 38-year-old and the family’s only vegetarian.

It was a reasonable conclusion. The Steffensens were raised on the kind of farm food that the state is famous for—ham balls, meatloaf, pie, macaroni and cheese—and still popular even as careers have moved indoors. Driving north through cornfields to meet some of the family in Buffalo Center, I dined at a restaurant offering deep-fried sandwiches. A single ham and cheese hoagie—dunked in hot fat and served sizzling—seemed capable of stopping a heart all on its own.

But could the high incidence of heart trouble among the Steffensens be related to something else besides high-fat diets? Eleven years after Don’s attack, his wife, Barbara, happened to overhear a doctor describing a study about the genetics of heart attacks.

Curious, Don and 20 of his relatives each sent a vial of blood to the Cleveland Clinic, where the research was being conducted. Eric Topol, a cardiologist and genetics researcher at the clinic, spent a year studying their DNA. Each person’s genome comes with millions of individual variations, but Topol was looking for something distinctive—and shared only by the members of the clan with heart trouble. The mutation he and his team finally spotted, in a gene called MEF2A, produced a faulty protein. “We knew we had something,” Topol says. “But the question was: How does this sick protein, present at birth, lead to heart attacks 50 years later in life?”

Topol himself is as lean as a greyhound and weathered in a cowboyish way. He talks slowly and eats minimally: salads for dinner and high-fiber cereal for breakfast. He doesn’t eat lunch at all. Like almost every cardiologist I’ve talked to, he takes statins preventively, and his cholesterol count is a low 135. His children, 22 and 25, also eat uncommonly well for their ages. “People have looked at the cadavers of men in their 20s who died in car accidents or as casualties of war, and nearly all had arterial cholesterol deposits,” Topol said as we walked to his lab. “This disease starts much earlier than people realize.”

Using endothelial cells (which line the inside of the artery wall) grown in culture, Topol set about figuring out what the MEF2A mutation does. He and his coworkers created some cells carrying the Steffensen variant, and others with the normal form of the protein. Both cell proteins were tagged fluorescent green so their locations could be visualized on a computer screen. The resulting images revealed a striking difference.

In a normal cell, all the MEF2A protein was inside the nucleus; on the screen, the cell resembled a fried egg with a fluorescent green yolk. But in the cells carrying the mutated version, the nucleus did not glow; instead the cell membrane was edged by a thin, luminous green line: a layer of MEF2A protein, trapped where it cannot serve its usual purpose. Topol believes that this defect affects the integrity of the coronary artery walls, rendering them more vulnerable to cracking when the plaque embedded in them ruptures. And each crack brings an increased chance of a heart attack.

Since this discovery, the Steffensens have become famous, appearing on shows like60 Minutes II. Their mutant gene turns up in a Robin Cook novel titled Marker, about a health insurance company in New York that secretly screens patients for theMEF2A mutation and then kills them to preempt future medical-care payouts. Lively reading, but the Steffensen gene is an unlikely target for an insurance company, in part because it is an uncommon genetic defect.

Topol’s study did find that although dysfunctional MEF2A is very rare, the chance of heart disease in those carrying it may approach 100 percent. Most other genetic variations identified thus far increase the risk by much less. As it turns out, Topol himself carries a bum gene: apoE4, which affects inflammation in the arteries. Unlike MEF2A, it is common; every fourth person has it.

“Heart disease is not a one- or two-gene problem,” says Steven Ellis, a Cleveland Clinic cardiologist who oversees a 10,000-person genetic study known as GeneBank that collects DNA samples from patients who enter hospitals with atherosclerosis. Ellis, like most cardiac researchers, suspects that dozens of genes end up contributing to a predisposition: Some affect arterial integrity, others inflammation (which both causes and exacerbates arterial cracks), and still others the processing of lipids (the fats and cholesterol that turn into plaques). Of the several dozen genes, each may contribute just one percent to a person’s total risk—an amount that may be compounded, or offset, by outside factors like diet. As one doctor told me, any person’s heart attack risk is “50 percent genetic and 50 percent cheeseburger.”

The point of tracking down all these small mutations, Ellis explains, is to create a comprehensive blood test—one that could calculate a person’s genetic susceptibility by adding up the number of risky (and, eventually, beneficial) variables. Combined with other important factors, such as smoking, weight, blood pressure, and cholesterol levels, doctors could decide which patients need aggressive treatment, such as high-dose statins, and which ones are likely to benefit from exercise or other lifestyle changes. Some genes already can predict whose cholesterol level will respond strongly to dietary changes and whose won’t. Assessing risk is crucial, Ellis says, because heart disease is often invisible. In fact, 50 percent of men and 64 percent of women who die of heart disease die suddenly, without experiencing any previous symptoms.

Although standard tests can detect atherosclerosis, they aren’t foolproof. They may reveal plaques, but give no indication whether or not they are life-threatening. Tests like angiography, for example, where doctors inject a dye into the bloodstream and track it with x-rays, can show how much blood is flowing through an artery, but not discern the plaques embedded inside the artery wall—often the culprit in a heart attack.

Researchers have been working to solve this problem with scanners that provide pictures of the arterial wall itself, but it’s a tricky task. Normal cardiac artery walls are about a millimeter thick. Coronary arteries move with every beat of the heart, 70 times a minute. It’s tough to get a clear image of something so small in constant motion.

Difficult, but not impossible. As I walk through the basement of the Cleveland Clinic, I pass a room containing a large, blue, plastic doughnut as tall as I am, with a woman’s legs sticking out of the middle. The doughnut is a computed tomography (CT) scanner, a kind of three-dimensional x-ray machine that’s also used for imaging tumors. The scanner, aided by medications that reduce a patient’s heart rate and an injectable dye that highlights the arteries, can produce startlingly clear pictures.

Scrolling through images on his computer monitor, Mario Garcia, the clinic’s director of cardiac imaging, retrieves one that looks like a black-and-white landscape photographed from a plane, with a single, large river running through it. As Garcia zooms in on the river, a series of white lumps appears on the bank—hard plaques bright with calcium. But there is also a tiny black smudge. “That’s the type we believe causes a heart attack,” he says with satisfaction, pointing to the smudge of soft plaque. “It’s a rare opportunity to see that.”

As compelling as the CT scan is, it’s still an imperfect tool for predicting heart disease. It’s expensive, for one, and the dose of radiation from the x-rays makes it ill suited for use in healthy-patient annual exams. And although it sees arterial plaques, even soft plaques inside arterial walls, it can’t reveal whether those plaques are likely to crack and cause a heart attack.

Until there are tests, genetic or otherwise, that give a clearer measure of risk, everyone would be advised to exercise, watch their diet, and take statins for elevated cholesterol—the same advice doctors gave when the clogged-pipes model of heart disease reigned unchallenged.

At the Cleveland Clinic, cardiologist Stephen Nissen has conducted several studies on statins such as Lipitor, which reduce the amount of LDL (“bad” low-density lipoprotein) cholesterol made by the liver. Nissen is an advocate of lowering cholesterol by any means necessary. Does he take a statin? “You bet!” he says. “I have no intention of dying of the disease I treat.” His LDL level is a paltry 51. Of eight cardiologists I spoke with, all but one were taking the medication. (Some studies now seem to show that lowering even normal cholesterol levels has a protective effect.) HDL (“good” high-density lipoprotein) cholesterol is another story. Nissen calls it the “arterial-wall garbage barge” because of its ability to remove cholesterol from clogged arteries. Not all HDL can do this; some is dysfunctional. But tests have shown that raising the HDL level in genetically engineered lab mice can shrink their arterial plaques.

A drug that could raise functional HDL levels in humans would likely become the next multibillion-dollar blockbuster, and a few are in various stages of testing. However, the trial of a Pfizer drug called torcetrapib ended in failure. Torcetrapib had been shown, in combination with Lipitor, to raise HDL levels 44 to 66 percent with a once-a-day pill. But the increase was not necessarily in functional HDL, and the drug was also associated with elevated blood pressure. In December, when data showed a 60 percent higher death rate in patients taking torcetrapib with Lipitor than in those taking Lipitor alone, Pfizer abruptly ended the trial.

It’s not clear whether the problem lay with one drug or an entire class of drugs. Until further research is completed, the several different statins on the market will remain the most prescribed class of drugs in the world, with 11.6 million prescriptions filled monthly in the U.S. alone. Pfizer’s Lipitor may be the best-selling drug ever made, with 12 billion dollars in annual worldwide sales.

But statins, like any drug, carry the risk of side effects: Muscle aches are a well-known effect, and periodic blood tests to check liver function are recommended. The fact is, many of us just like to eat cheeseburgers, watch television, and get around in cars. And it’s hard, says Leslie Cho, director of the Cleveland Clinic’s Women’s Cardiovascular Center, for a person to worry about a disease that hits ten years down the road—particularly since heart patients, unlike cancer patients, can’t easily observe the progress of their disease. “You’ve done damage over years, and it will take years to undo that damage,” she says. “That’s a very hard thing to sell to Americans. We do what we can, but then people go home.”

The good news is that genetic research continues to thrive. Should we want to, we will soon be able to know the state of our hearts—and our genes—in ever growing detail. That knowledge, and what we do with it, could make the difference between dying at 65 and living until 80. The choice, increasingly, will be ours.

To view the original article CLICK HERE.
.
Regards,
Greg_L-W.
.
 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
Accuracy & Copyright Statement: CLICK HERE
Summary, archive, facts & comments on UKIP: http://UKIP-vs-EUkip.com
DO MAKE USE of LINKS & >Right Side Bar< & The Top Bar >PAGES<
Also:
Details & Links: http://GregLanceWatkins.com
UKIP Its ASSOCIATES & DETAILS: CLICK HERE
Views I almost Totally Share: CLICK HERE
General Stuff archive: http://gl-w.blogspot.com
General Stuff ongoing: http://gl-w.com
Health Blog. Archive: http://GregLW.blogspot.com
Health Blog. Ongoing: http:GregLW.com

TWITTER: Greg_LW