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« on: July 31, 2006, 10:03:00 pm »

Stitch in Time Saves Lives: High Survival Seen for Patients With Aortic Dissection
Aortic dissection doesn't have to be deadly, international research shows

ANN ARBOR, M.I. -- July 10, 2006 -- Nearly three years ago, actor John Ritter collapsed on the set of his sitcom, the victim of a rare but often deadly condition called aortic dissection -- a tear in the largest blood vessel in the body. His death brought international attention to the catastrophic condition, which strikes 10,000 Americans a year and is often linked to high blood pressure and genetic disorders.

Now, researchers have published some rare good news about aortic dissection, showing that 90% of patients who survive emergency surgery and hospitalization for its most serious form will still be alive three years later. Those without pre-existing heart and blood vessel problems were even more likely to survive. The findings are published in a supplement to the journal Circulation.

The study, performed by an international team led by specialists at the University of Michigan Cardiovascular Center, involved data from 303 patients. All were treated in the late 1990s and early 2000s for the most serious form of aortic dissection, called Type A, which occurs in the upper part of the aorta near the heart.

It's a unique study looking at survival among Type A aortic dissection patients who live through their initial crisis. The authors say the results offer hope that with proper rapid diagnosis and successful surgery, more patients can survive.

However, because aortic dissection is rare and its symptoms can mimic those of a heart attack, it is often not diagnosed or treated quickly -- contributing to a 30% in-hospital death rate that includes a 25% risk of death during surgery. But less is known about the fate of those who survive long enough to leave the hospital.

"Clearly, this is one of those diseases where if you catch it early you can save lives in the hospital, and with successful surgery your outlook after discharge can look quite good," says lead author Thomas Tsai, MD, a cardiovascular research fellow at the U-M Medical School. "Of course, those who do survive will have a diagnosis for life of aortic disease, and will need medication and aggressive monitoring of their aorta."

Tsai and senior author Kim Eagle, MD, co-director of the U-M CVC, conducted the research with colleagues from the International Registry of Aortic Dissection, or IRAD, using data on patients treated at 21 medical centers in 11 countries. U-M is the coordinating center for IRAD.

"Aortic dissection is still very much a lethal health crisis, with mortality approaching 2% per hour. But these results show we're doing a pretty good job in helping patients after they weather the storm of diagnosis and surgery," says Eagle.

The new study drew its patients from a group of 885 Type A aortic dissection patients who came or were transferred to IRAD centers. Nearly 30% of the Type A patients died before leaving the hospital, and long-term follow-up data were available on many of the 617 who left the hospital after surgical or non-surgical treatment. The patients included in the final analysis were treated at eight IRAD centers that compiled long-term follow-up data on most of their patients.

Ninety percent of the 303 patients in the study had surgery; the rest received medical treatment because of advanced age, pre-existing conditions that made surgery too risky, or patients' refusal to have surgery. Death rates were much higher among the non-surgical patients.

The average age of all the patients was 59, but a quarter of the patients were over age 70 -- reflecting the fact that aortic dissection can strike relatively young patients with genetic diseases such as Marfan syndrome that prematurely weaken the walls of their aorta, or can arise from a lifetime of high blood pressure that stresses the aorta and creates weak spots.

Seventy-two percent of the patients in the study had hypertension before their dissection. Nearly 25% had atherosclerosis (clogged, stiffened blood vessels often linked to high cholesterol and blood pressure) and just under 13% had had some sort of cardiovascular surgery in the past.

These underlying problems -- and not any aspect of their in-hospital complications -- appear to have made a big impact on patients' risk of dying after leaving the hospital. In fact, patients who had atherosclerosis or previous cardiovascular surgery had twice the risk of dying in the three-year follow-up period as patients without these characteristics. "What predicts an aortic dissection patient's death after hospitalization are the risk factors they came in with," says Tsai.

Tsai and Eagle note that the good news of the new result may have a lot to do with recent advances in emergency diagnosis, surgical and anesthesiology techniques, and intensive-care practices, as well as better post-hospital care of patients using drugs and regular medical imaging. Because IRAD has collected data on so many patients treated within a seven-year period, the authors say, the study reflects the modern treatment of the condition, compared with other studies that have compiled data from patients treated over several decades at one or two medical centers.

Now, the researchers are hopeful that early diagnosis and rapid treatment will increase as more hospitals use advanced medical imaging to determine what is causing chest pain in patients who come to emergency rooms. Advanced CT scanners, for example, can make a "triple rule-out" scan that can quickly tell if a patient is experiencing a heart attack, an aortic dissection, or a blood clot in the lung. But, says Tsai, doctors need to order the right kind of scan or a dissection can be missed.

A "swat team" approach that combines the talents of emergency room doctors and nurses, cardiologists, radiologists, surgeons and anesthesiologists to make rapid diagnostic and treatment decisions may also help, says Eagle. Such an approach is now in place at the U-M Health System.

The IRAD team is also working to improve the screening tools that might be used to determine who is at high risk of an aortic dissection. Currently, people with Marfan syndrome, connective tissue disorders and some other conditions are known to have an elevated risk, as are people with long-term blood pressure problems. It can also occur during pregnancy or childbirth, or in cocaine users.

IRAD researchers are currently developing tests that would examine DNA or blood to screen high-risk people or the relatives of dissection patients, to make a rapid diagnosis in the emergency room, or to add to long-term monitoring of survivors. Better screening for aneurysms in the aorta, which are involved in a large percentage of dissections, could also help nip more dissections in the bud.

The study was funded by the U-M Faculty Group Practice, the U-M CVC Varbedian Fund for Aortic Research; and the National Institutes of Health.
« Last Edit: December 02, 2006, 09:28:46 am by Kathy » Logged


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« Reply #1 on: September 07, 2006, 06:29:27 am »

Virgin Olive Oil Better for Heart



 Sept. 5, 2006 -- All olive oils may not be created equal when it comes to protecting against heart disease.

A new study shows virgin olive oil, which contains more antioxidants than more refined olive oil, may offer better protection against heart disease.

Virgin olive oil is made from the first pressing of olives and contains higher levels of a class of antioxidants known as polyphenols than more refined olive oils that come from later pressings.

Researchers say these polyphenols may provide another way to reduce the risk of heart disease in addition to the heart-healthy benefits attributed to the monounsaturated fatty acids found in olive oil.

Recent studies have suggested that the bulk of olive oil's heart-healthy benefits comes from good fatty acids (monounsaturated fatty acids), but researchers say polyphenols may also contribute to those benefits and further reduce the risk of heart disease.

Virgin Olive Oil Best for Heart

In the study, published in the Annals of Internal Medicine, researchers compared the effects of consuming olive oils with varying levels of polyphenols on heart disease risk factors in 200 healthy European men.

The men were divided into three groups and ate about 1 tablespoon of either virgin olive oil, refined olive oil, or a mixture of the two, every day for three weeks. Then, after a two-week hiatus, they were retested with one of the other types of olive oil.

Researchers found that the virgin olive oil higher in polyphenols increased the level of good, high-density lipoprotein (HDL) cholesterol more than the other two types of olive oil.

Virgin olive oil also produced another healthy antioxidant effect. It increased the level of substances in the body that prevent the oxidation of bad, low-density lipoprotein (LDL) cholesterol. Oxidation of this type of cholesterol is linked to the formation of clots in blood vessels, which could lead to heart attack or stroke.

Researcher Maria-Isabel Covas, Msc, PhD, of the Municipal Institute for Medical Research in Barcelona, Spain, and colleagues say the results show "olive oil is more than a monounsaturated fat.

"The polyphenol content of an olive oil can account for further benefits on HDL cholesterol levels and oxidative damage, in addition to those from its monounsaturated fatty acid content," they write. "Our study provides evidence to recommend the use of polyphenol-rich olive oil, that is, virgin olive oil, as a source of fat to achieve additional benefits against cardiovascular risk factors."

More studies are needed to examine virgin olive oil versus more refined oil and the risk for developing heart disease.
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« Reply #2 on: September 23, 2006, 10:18:15 am »

Lupus Vasculitis and Blocked Blood Vessels

Vasculitis means inflammation of the blood vessels. (Vasc refers to blood vessels and itis means inflamation). Vasculitis is a problem that can arise independently of other illness, or it may co-exist with lupus or other autoimmune diseases. When it exists in lupus, it may simply confirm the diagnosis, causing no problems, or it may represent a change in the course of the lupus, with vasculitis as a serious complication. Thus, vasculitis may mean many things. If a doctor says you have vasculitis, ask what that really means - what disease process is going on and what it means for you.

Warning About Misuse of the Term "Vasculitis"

Vasculitis should not be confused with vasculopathy, which simply means something is wrong with the blood vessels, although it's usually not vasculitis. Some people use these words interchangeably, which is wrong. Some people, even physicians and especially on the Internet, use the term "vasculitis" very loosely. So you may see statistics about vasculitis on the Internet that are very frightening, but they don't provide any information on your situation. The term vasculitis is used ten times as often as it should be by people who are not really referring to this disease. Unfortunately, even some doctors often use the term vasculitis to mean "person with autoimmune disease and blood vessel abnormality that I don't understand." If your doctor says you have vasculitis, ask specifically what he/she means before you go to the Internet!

What is Vasculitis?

Vasculitis is blood vessel inflammation that causes fever, pain, local tenderness, and other evidence of blocked blood vessels. When a blood vessel becomes inflamed and narrowed, blood supply to that area can become partially or completely blocked. Complete blockage is called occlusion; it causes the vessel wall to swell and makes things stick to the wall -- so a clot forms. When vasculitis interferes with circulation in any part of the body, it causes local tenderness and pain. If the blood vessels are close to the skin, characteristic rashes occur. Depending on where the blockage occurs, almost any organ in the body can be affected. (Note: Vasculopathy can also block blood vessels, but it does not cause the fever, pain, and local tenderness associated with vasculitis.)

While vasculitis may involve arteries (the thick muscular vessel that carries blood away from the heart) and veins (the thinner, less muscled vessels that carry blood toward the heart), it is rare for both arteries and veins to be involved at the same time.

What Vasculitis is Not

Many problems that block blood vessels looks like vasculitis, and doctors often jump the gun and call them vasculitis, but greater care is needed to find out what's really going on. Among the diseases involving blocked blood vessels that are not vasculitis:

Atherosclerosis (hardening of the arteries);
Growths on the heart valves that break off, especially those due to infection;
Excessive blood clotting (antiphospholipid syndrome);
Vessel spasm, especially due to drugs (legal and illegal).
When Does Vasculitis Occur in Rheumatic Disease?

All of the rheumatic diseases involve some level of underlying vasculitis. That includes lupus, rheumatoid arthritis, scleroderma, and dermatomyositis. If you biopsy a swollen joint in RA, you routinely find vasculitis. That finding is used to confirm the diagnosis, but it doesn't mean anything important is happening. It just suggests that one of these autoimmune diseases is present. So vasculitis is a common finding in these diseases, important in diagnosis, but it doesn't necessarily mean anything more. It may never be a problem!

When is Vasculitis an Important Complication of an Autoimmune Disease?

There are times in lupus and RA when the disease takes a different course in the presence of vasculitis. You start getting sicker and develop fever - clues to the physician that there has been a change in the course of illness. Now we say "This is lupus complicated by vasculitis" or "This is rheumatoid arthritis complicated by vasculitis." The disease has changed its character and usually needs more vigorous treatment.

Diseases in Which Vasculitis is the Specific Illness

Polyarteritis nodosa, which affects middle aged older people;

Temporal arteritis or giant cell arteritis, which affects arteries in the head of older people;
Allergic vasculitis, which is an abrupt reaction that sometimes follows infection;
Takayasu's arteritis, which is a relatively rare disease of young women, largely in Asia, involving large blood vessels;
Wegener's granulomatosis, which affects the kidneys, lungs, and blood vessels;
These specific kinds of vasculitis are treated differently, depending on the underlying problem.
Vasculitis by the Size of the Vessel

Vasculitis is best discussed in terms of what blood vessels are involved: the small, medium, or large vessels.

- the large vessels are those that lead from your heart - the aorta and the arteries that go across the shoulders and down to the hips.

Small Vessel Vasculitis

This is the most common form of vasculitis seen in lupus and is fairly common in dermatomyositis and scleroderma, but less common in rheumatoid arthritis. The small vessels are at your finger tips and inside your organs, such as the kidney.

Some signs of it can be seen with a small lens that shows tiny broken vessels in the cuticle and hemorrhages along the edge or under the nail. Or on other parts of the skin, especially the legs, you see little red dots with black centers that sometimes burn a little bit. This small vessel vasculitis is not particularly threatening. It is a manageable but annoying category of the disease, with fairly mild symptoms that may not need treatment. Some people don't even know that they have the evidence of it. However, when the blood supply to the nerves in the feet are cut off by vasculitis, they may develop numbness.

Another type of small vessel vasculitis we see in people with lupus and rheumatoid arthritis causes kidney inflammation called glomerular nephritis.

Small vessel vasculitis can also be seen in children as palpable purpura, which causes a rash. It may come and go and be treated only when it's causing problems.

In addition, small vessel vasculitis can be seen in severe allergies and infections; when you treat the underlying cause, such as the infection, the vasculitis goes away.

Diagnosis of small vessel vasculitis can be made by an experienced clinician simply by observation. Here the question is not "Is it vasculitis?" but "What's causing this vasculitis?" Less experienced physicians want to do blood tests, skin biopsy, angiography, and X-rays, all of which are not useful for this type of small vessel vasculitis. Only a kidney biopsy may be needed in some circumstances.

What does it mean when small vessel vasculitis occurs in someone with long-term lupus or RA? You do not treat the vasculitis itself; you have to look at the whole patient and ask why has this complication has occurred. It could be an allergy or an infection, which should be found and treated. Small vessel vasculitis should not be ignored because it is important, but it's not life-threatening. If allergy or infection have been ruled out, treatment with corticosteroids (prednisone) or other immunosuppressants is more or less negotiable depending on what the patient wants to tolerate in terms of side effects.

Medium Vessel Vasculitis

These vessels lead down your arms and legs, that lead to your heart and brain, and that are in your intestines. Medium vessel vasculitis is what physicians mean when they call vasculitis a serious disease. (In polyarteritis nodosa, for example, it tends to be very dramatic. People say they have never felt worse in life.) Medium vessel disease can occur in lupus and RA, but it is very rare.

The symptoms of medium vessel vasculitis include: fever; severe muscle aches; sudden loss of power of specific muscles (perhaps a toe starts dragging) severe abdominal pain; sudden loss of circulation in a finger or toe that turns totally black; stroke; or heart attack. Again, the diagnosis can be made at bedside based on symptoms. Blood tests are useful for making the diagnosis. Sometimes a muscle biopsy or nerve conduction studies are done. These procedures provide information to confirm a diagnosis. The type also must be identified; it may be caused by infection, such as hepatitis B, or it may be polyarteritis nodosa alone, or it may be a complication of an autoimmune disease.

Medium vessel vasculitis can be life-threatening because the blocked vessels going to the heart can cause a heart attack or those going to the brain may cause a stroke. Survival depends on immediate recognition of the disease and immediate and vigorous treatment. When medium vessel vasculitis occurs, treatment is not negotiable. High dose steroids and cytoxan are needed to reverse it as soon as possible.

Large Vessel Vasculitis

We don't see large vessel vasculitis in lupus and rheumatoid arthritis. When the large blood vessels develop vasculitis, it's always an independent disease, such as Takayasu's or giant cell or cranial arteritis. This type of vasculitis has completely different symptoms, and it requires a bit of cleverness to figure out what's going on. It's not immediately threatening, but it can do a lot of damage if not treated for long periods. Treatment is aimed at preventing disability, such as the blindness that may be caused by giant cell arteritis.

Summary

Vasculitis is inflammation of the blood vessels; vasculopathy is everything else that may go wrong with blood vessels. Vasculitis occurs as a regular part of rheumatic disease, or vasculitis may occur as its own illness. Many other problems may mimic vasculitis.

Vasculitis may be serious but, in most cases in people with lupus and other rheumatic diseases, it is not serious. Trivial vasculitis in rheumatic disease, particularly of the small vessels, may not even require any change in treatment. However, when serious vasculitis occurs, very aggressive therapy is necessary, depending on the cause. In serious vasculitis related to autoimmune diseases such as lupus, aggressive therapy with prednisone and other immunosuppressants is essential.

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« Last Edit: September 23, 2006, 11:15:25 am by Kathy » Logged


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« Reply #3 on: September 23, 2006, 10:40:36 am »

“Unlocking the Mystery of Lupus: Lupus & the Heart” FAQs


What is lupus?


Systemic lupus erythematosus (SLE), commonly called lupus, is a chronic autoimmune disorder that can affect virtually any organ of the body. In lupus, the body's immune system, which normally functions to protect against foreign invaders, becomes hyperactive, forming antibodies that attack normal tissues and organs, including the skin, joints, kidneys, brain, heart, lungs, and blood. The disease is characterized by periods of illness, called flares, and periods of wellness, or remission.

Because its symptoms come and go and mimic those of other diseases, lupus can be difficult to diagnose. There is no single laboratory test that can definitively prove that a person has this complex illness. Thankfully, awareness of lupus is increasing and is therefore more readily identified.



Who gets lupus?


Lupus is estimated to affect nearly 1.5 million Americans. While it occurs in both sexes, 90 percent are women, and most are diagnosed during the childbearing years. African-American women are three times more likely to get the disease than Caucasian women, and they often suffer more severe disease. National Institutes of Health figures indicate that as many as one in every 250 African-American women has lupus. Lupus is also twice as prevalent in Asian-American and Hispanic women as it is among Caucasian women. Native American women are also disproportionately affected.


How is lupus treated?


While there is no cure for lupus, early diagnosis and appropriate treatment can help in managing the symptoms and lessening the chance of permanent damage to organs or tissues. Once a lupus diagnosis is established, an assessment is made of damage to major organs such as the brain, kidneys, heart, and lungs. Treatment strategies depend on the activity level and extent of the disease and can range from over-the-counter pain relievers and anti-inflammatory drugs to prescription medications, psychotherapy, healthy diet changes, and lifestyle revisions such as staying out of the sun and avoiding stress.


How serious a threat does lupus pose to heart health?


The cardiovascular system is a main target of lupus. It can directly weaken the heart by causing inflammation of the muscle itself (myocarditis) or its inner lining (endocarditis). But the most common heart involvement in people with lupus is inflammation in the sac around the heart (pericarditis), which causes shortness of breath and sharp chest pain. These complications are typically treated with powerful anti-inflammatory and immune system suppressants such as prednisone, a corticosteroid.


What about coronary artery disease?


More than a third of people with lupus are at risk for this complication, primarily because inflammation and various immune system abnormalities cause the coronary arteries to rapidly harden, narrow, and clog, a condition called atherosclerosis. In time, clots can form or bits of plaque can break off from artery linings, interfering with blood flow to the heart and brain. Less common causes of coronary artery problems in people with lupus include inflammation of the artery walls, actual spasms of the arteries, and blood clots. The potential for problems forms a chilling picture, with female lupus patients 50 times more likely than their peers to have chest pain or a heart attack. (Less is known about the increased risk among the 1 in 10 men with lupus.)

But I’m still young, and I take pretty good care of myself.


It appears that having lupus by itself means a person is more likely to develop coronary artery disease. Young women with lupus (under age 40) are nearly five times more likely to have this ailment than their same-age peers—regardless of whether they have other risk factors such as smoking, high blood pressure, diabetes, or excess weight. Over time, lessened blood and oxygen flow to the heart weaken the muscle. Bits of cholesterol can break off from artery linings, interfering with blood flow to the brain as well as the heart. Long-term use of corticosteroids can also cause harm.


What can I do to keep my heart healthy?


See your doctor regularly and always mention new or changing symptoms, including chest pain or shortness of breath. Ask about other warning signs of a heart attack or stroke and what to do if they develop. The goal is to detect and treat lupus flares as early as possible, limit corticosteroid use (in a smart way, with the doctor’s approval), take measures to stop other heart-damaging factors (smoking, high blood pressure, excess weight), get regular exercise (even a 30-minute daily walk helps), and follow a healthy diet. Also key: a close working relationship between you and the doctor, including heart specialists (cardiologists). Some doctors put lupus patients with coronary artery disease on cholesterol-lowering drugs called statins.


Are certain people with lupus at particularly high risk for heart problems?


Certain populations, such as black women, need to be particularly vigilant. Not only is heart disease the number one killer of  all black women, but the death rate from heart disease is nearly 70 percent higher in women of color than it is in white women. Black women are also three times more likely than white women to have lupus—which in itself raises the risk for heart damage.


What are the primary areas of research in lupus—and is the cardiovascular system one of them?


With no major new treatment approved in more than 40 years, lupus needs a breakthrough.  Researchers have made significant headway recently, however, reporting exciting findings in terms of how the disease works and what can be done to treat it. Among the discoveries are a deeper understanding of the genetic links to lupus and enhanced recognition of how lupus attacks the brain, kidneys, and skin. And several promising advances have also been made in figuring out lupus heart disease. Researchers have learned a lot more about immune system abnormalities that target this organ and have greater insight into biomarkers (predictors) of atherosclerosis. There are also improved techniques for early detection of heart disease, and more options for drug treatment.


Are companies developing new drugs to treat lupus?


Yes, finally. Several pharmaceutical companies are developing new medications. An online search will generate information on these companies and their drugs. You also can find websites that report new drug findings, such as www.lupusny.org and www.lupusresearchinstitute.org.


How can I help advance research and drug development?


As a person with lupus, you can directly help in advancing lupus science—and simultaneously help yourself—by participating in a clinical trial. A clinical trial is a research project that evaluates the safety and effectiveness of medical treatments, drugs, or devices in human beings. The Food and Drug Administration (FDA) requires that such trials be performed before a product can be prescribed to patients. For information on clinical trials in lupus, try visiting the following websites:
www.lupusresearchinstitute.com



What is the outlook for people with lupus?


There isn’t a cure yet, but every year now researchers are gaining promising new insights into this disease and uncovering promising treatments. Just twenty years ago, only 40 percent of people with lupus were expected to live more than three years following a lupus diagnosis. Now, with earlier diagnosis, refinements in treatments, and careful monitoring, most people with lupus can look forward to a normal lifespan.
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« Reply #4 on: September 23, 2006, 10:50:01 am »

Heart and Lung Involvement and Lupus: What You Need to Know

Systemic lupus erythematosus (SLE) as its name implies, (redness of the organs from the bite of a wolf) is a disease that affects all body parts. The heart and lungs are no exception. Patients with lupus may develop any combination of heart and lung disease in addition to involvement of other organ systems .

Systemic hypertension (high blood pressure) and hypertensive heart disease (thickening of the walls of the heart that occurs as a result of chronic high blood pressure) are common in patients with lupus, with or without associated kidney disease.

Another potential problem lupus patients face is pericarditis, an inflammation of the sac surrounding the heart. Patients may experience chest pain, and fluid may accumulate around the heart (pericardial effusion). If the fluid becomes constricting to the heart, symptoms such as shortness of breath and swelling of the legs and abdomen may occur.

Coronary artery disease is a blockage in the arteries of the heart. Coronary artery disease is dramatically increased in patients with SLE. Blockage of coronary arteries can result in chest pain (angina pectoris), heart attacks, damage to heart valves, electrical abnormalities of the heart beat (arrhythmias) and sudden cardiac death. For women 35 to 44 years of age with SLE, the rate ratio of heart attacks is over 50 times that for a comparative population without SLE.

SLE may cause inflammation of the heart valves and subsequent damage to the valvular mechanism with leakage, which can cause shortness of breath (congestive heart failure).

Disease of the small arteries of the lung in SLE may cause pulmonary arterial hypertension, a serious condition which is difficult to treat.

Lupus may affect the lungs in a variety of ways. Lupus can cause inflammation of the support mechanism of the lungs (parenchyma) or the lining of the lungs (pleura) making it difficult to breathe. It may also impair the movement of the diaphragm, leading to shortness of breath.

Because of the systemic nature of SLE, patients are more likely to get lung infections (bronchitis and pneumonia) than the general public, and patients with SLE have more difficulty recovering from these infections.

In addition to lupus causing cardiopulmonary disease, the side-effects of treatment may also be harmful. Specifically, the use of corticosteroids may elevate blood pressure by causing salt and water retention. Steroids are thought to be involved in the development of plaque in arteries by causing the "metabolic syndrome" with elevation of blood glucose, cholesterol and triglycerides.



Where Do I Begin?

Detection of cardiopulmonary problems begins with a thorough physical examination. During an office visit your health care provider (HCP) can check you for hypertension and signs of cardiovascular and cardiopulmonary disease.

Looking at the eyes with an ophthalmoscope, the provider can look at the blood vessels of the retina (a fundoscopic exam). Patients with SLE often have a specific type of arterial abnormality called "copper wiring." Evidence of increased cholesterol and hypertension can be graded by looking at the arteries of the retina.

Examination of the skin may provide clues about cardiovascular health as well. The presence of certain lesions of the skin, xanthoma and xanthelaema (the yellow accumulation of cholesterol) indicates that a patient’s lipid profile is extremely elevated.

The provider listens to the arteries in the neck and abdomen with a stethoscope. The presence of abnormal sounds, or bruits, can indicate arterial narrowing caused by plaque. The stethoscope can also detect heart murmurs and extra sounds called gallops which indicate stiffness and weakness of the heart muscle.

Examination of the neck veins is important in looking for cardiovascular disease. Swelling of the neck veins can indicate increased pressure in the right side of the heart. Listening to the heart in a patient with distended neck veins may reveal accentuated heart sounds associated with both systemic and pulmonary hypertension (elevation of pressure in the blood vessels of the lungs.)

Examination of the abdomen can reveal an enlarged liver. If the HCP presses on the abdomen and the veins in the neck distend, this is an indication of occult right sided congestive heart failure. If a patient coughs during this maneuver (called the hepatojugular reflux) it indicates the left side of the heart is also diseased.

Laboratory testing should include urinalysis and blood tests. Testing for urine microalbumin may indicate that hypertension has led to kidney damage or that there is a primary disorder of the kidney from lupus. A complete blood count would include checking for an elevated white blood cell count to rule out pulmonary or other infections and to rule out anemia, which can make the heart work harder and precipitate heart failure.

A cholesterol profile should include assessment of the LDL or low-density lipoprotein (the "bad" cholesterol) as well as the HDL (high-density lipoprotein or good cholesterol). In the general population, a patient should aim for LDL cholesterol less than 100 mg/dl. In rural populations who subside on vegetarian and fish diets, LDL cholesterols are as low as 70mg/dl. These populations have little coronary artery disease. Hence, cardiologists are now urging patients to try to reduce their LDL cholesterol to even less than 70 mg/dl.

Specialized cardiovascular blood tests include: the cardiac C - reactive protein: which measures cardiovascular inflammation; homocysteine, a protein which can cause vascular damage; lipoprotein-a, which is an LDL molecule with an attached protein which may also independently cause vascular damage.

If your lipids are abnormal, or if there is a family history of premature coronary heart disease (age at onset less than 55 years old) your provider may send your blood to a laboratory which can sub-fractionate your HDL and LDL. There are five different HDL molecules (Type II b being the most important for vascular health). There are seven different subsets of LDL with small Class III and IV being more damaging to the arteries than the large or "fluffy" Type I and Type II LDL molecules.

Fibrinogen is another important factor, which should be included in the evaluation of a patient with SLE. It is a protein produced by the liver, which is involved in the formation of blood clots. While fibrinogen is helpful in the presence of bleeding, a chronically elevated fibrinogen may lead to a predisposition for heart attacks and strokes by increasing the possibility of clots and plaques in arteries.

A chest x-ray should be performed in patients with SLE to assess for heart size and evidence of lung disease.

A routine electrocardiogram (ECG) may show subtle changes, which may lead your HCP to have an increased index of suspicion about heart disease. A Cornell cardiologist, Dr. Peter Okin, recently published a paper in Diabetes showing that ST-T wave changes seen on electrocardiograms may identify patients at increased risk for heart disease. Hence, an ECG may enable your healthcare provider to increase his or her suspicion that you have an unrecognized heart problem.

If by physical examination, chest x-ray, electrocardiogram or blood tests your HCP suspects that you may have a heart problem, then echocardiography and stress testing should be considered, or referral to a cardiologist.

An echocardiogram is an ultrasound examination of the heart. It evaluates the ability of the heart muscle to contract and of the valves to work. Moreover, the echocardiogram may show calcification of the valves and aorta, which is a sign of potential systemic vascular disease.

Patients with lupus who are thought to be at high risk for having blockages should undergo stress testing. Stress testing evaluates how the heart responds to exercise, usually by walking on a treadmill. The preferred methodology is myocardial perfusion scanning. The nuclear isotopes thallium and/or technetium are injected into a patient’s vein, and images of the heart are taken before and after exercise. If arthritic conditions prohibit exercise, a "pharmacologic" stress test can be performed. Medications administered intravenously can make the heart behave as though the patient were exercising are administered. The images of both kinds of stress tests can be used to assess changes in the coronary circulation indicative of a significant (>70%) blockage.

Another commonly used diagnostic test in assessing for coronary blockages is the electron beam computerized tomogram (ECBT). The EBCT is a specialized type of "CAT" scan. It takes approximately twenty minutes to perform and will identify calcium in the coronary arteries (a sign of plaque and potential blockage). The higher the calcium score, the more likely that the blockages will actually prevent blood flow and cause future heart attacks.

All these diagnostic tests should be coordinated with the cardiologist who is seeing you.

What is My Next Step?

Asymptomatic?
Fifty percent of patients with heart disease have no symptoms. Because of the high prevalence of cardiovascular and cardiopulmonary disease in SLE, visiting a cardiologist for an examination, blood tests, electrocardiogram and chest x-ray every 5 to 10 years is warranted. Even those SLE patients without cardiopulmonary heart symptoms should see a cardiologist and be assessed for possible hidden disease before it becomes symptomatic. In all disorders, there is a latent phase during which disease is present before it becomes symptomatic.

What are the Symptoms of Heart and Lung Disease?

Patients with shortness of breath, chest discomfort associated with activity, or fatigue with activity in the absence of any other explanation such as severe anemia or renal failure should suspect cardiopulmonary disease. For example, if you frequently walk up a hill near your home and one day experience tightness in your chest or shortness of breath, this may be a sign of coronary blockage. It behooves you to discuss this with your HCP immediately, and to be assessed for a potentially serious coronary condition.

Intervention

Medical and surgical intervention in patients with SLE and cardiopulmonary disease is varied. It may be as simple as taking a medication such as a statin (e.g. Pravachol, Lipitor, Zocor or Crestor) to reduce your LDL and raise your HDL cholesterol. In patients with abnormal LDL subtypes and elevated lipoprotein-a, the use of niacin may be advised. In addition, Zetia has been used in combination with statins as a dual mechanism of reducing cholesterol The statins reduce production of cholesterol in the liver and Zetia reduces cholesterol absorption in the intestine.

It is important for patients who are placed on these drugs to realize that both liver and muscle abnormalities may occur, and that your HCP needs to check certain blood tests on a regular basis to rule out occult irritation of the muscle and liver. In addition, you should report muscle aches to your HCP immediately, as this may be the first sign of muscular inflammation from these medications. Combination therapy of hyperlipidemia increases the chance of muscle and liver irritation.

In addition, use of some antibiotics such as erythromycin, Zithromax or Biaxin may exacerbate irritation from the statins. When an antibiotic is prescribed, ask your physician whether you should stop taking one or more of your medications temporarily to avoid a drug-drug interaction.

Percutaneous Intervention

If a serious plaque is found in your heart, you may require an invasive procedure called angioplasty with balloon dilatation and stenting to unblock the arteries. This procedure involves an overnight stay in the hospital.

In cases where blockages in the arteries are diffuse and severe, coronary artery bypass graft surgery (i.e., open-heart bypass) may be necessary. However, the frequency in performing this operation has plummeted in the last decade, with the increased use of balloons and stents.

As with any disease, prevention is the best medicine.
*Ask your Health Care Professional about whether you are at risk of having cardiopulmonary disease from SLE.
*Do not ignore symptoms such as unexplained fatigue, shortness of breath or chest pressure.
Healthcare begins and ends at home. It is your personal responsibility to make sure that you are getting the best medical attention possible.
*Get examined on a regular basis, ask questions, eat right, exercise and try to maximize your situation.
*While you may be despondent that lupus has affected your kidneys, skin or joints, don’t ignore the call from the wolf.
*Watch your heart and lungs!



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« Reply #5 on: October 27, 2006, 06:18:18 am »

WASHINGTON, Oct. 26 -- The use of Visipaque (iodixanol), an iso-osmolar, nonionic contrast agent, did not reduce the rate of nephropathy in angiography patients with renal failure compared with less-expensive agents, researchers reported here.

That finding emerged from a pair of trials that compared the low-osmolar contrast agents Isovue (iopamidol) and Hexabrix (ioxaglate) with Visipaque in high risk patients undergoing angiography.


On the basis of these data, it is reasonable to conclude that less expensive low-osmolar contrast agents such as Isovue "can be safely used in high risk patients when those patients receive some volume and possibly some antioxidant therapy," said Richard Solomon, M.D., of the University of Vermont in Burlington, who was principal investigator of the Cardiac Angiography in Renally Impaired Patients (CARE) trial.


The CARE trial and the Ionic Versus Nonionic Contrast to Obviate Worsening of Nephropathy in Chronic Renal Failure Patients (ICON), which was reported by Roxanna Mehran, M.D., of Columbia in New York, were both presented during a late-breaking clinical trials session at the Transcatheter Cardiovascular Therapeutics meeting here.


The CARE trial recruited 414 high-risk patients with an estimated glomerular filtration rate less than 60 mL/min and who were undergoing coronary angiography and randomized them to Visipaque or Isovue. In addition to renal insufficiency, 170 patients had diabetes. The endpoint was contrast-induced nephropathy as defined by three accepted definitions: increase in serum creatinine of 0.5 mg/dL or more, a 25% increase in serum creatinine, or a 25% reduction in estimated glomerular filtration rate.

"By every definition, there was no significant difference between the groups," Dr. Solomon said.

However, patients randomized to Isovue had "a significantly smaller mean increase in serum creatinine compared with the Visipaque group," Dr. Solomon said.

The mean increase in the Isovue arm was 0.07 +/- 0.22 mg/dL versus 0.12 +/-0.23 mg/dL in Visipaque (P=0.03).

Dr. Mehran said 145 patients were enrolled in the ICON study at seven participating clinical centers in the United States and Canada. Patients had renal insufficiency with serum creatinine of 1.5 to 3.0 mf/dL, and 45% were diabetics. All patients were initially hydrated with an average of 3.7 L of fluid and then randomized to Hexibrix (n= 74) or to Visipaque (n=71). Investigators had the option of using N-acetyl-cysteine and 72% of patients did receive it as well.

During catheterization about half of the patients in each arm received at least 200 cc of contrast.

The primary endpoint of ICON was peak increase in the serum creatinine concentration between day zero, when the contrast agent was administered, and day three.

As in the CARE trial, "a similar efficacy regarding the change of creatinine was consistently observed between the two groups, independent from the presence of diabetes mellitus or the volume of contrast media used," Dr. Mehran said.

At a press conference, Dr. Mehran said that contrast-induced nephropathy most often occurs 24 to 48 hours after angiography and is characterized by creatinine increases that peak five to seven days after exposure to a contrast agent. Typically creatinine returns to baseline levels within a week to 10 days.


But the condition remains a leading cause of iatrogenic renal failure, morbidity and mortality after coronary angiography, especially in patients with chronic renal disease, she said.


Cardiologist Cindy Grines, M.D., of William Beaumont Hospital in Royal Oak, Mich., who served as discussant for both studies, said the evidence now suggests "any low-osmolar contrast agent would be acceptable for patients undergoing catherization or PCI as long as the patient was adequately hydrated."

Primary source: Trancatheter Cardiovascular Therapeutics 2006
Source reference:
Solomon, R "Cardiac Angiography in Renally impaired patients"

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« Reply #6 on: November 02, 2006, 07:06:01 pm »


Coronary artery disease remains the number one killer of women and men in this country.   For individuals with Lupus there is even more reason to pay attention to risk factors such as high cholesterol and high blood pressure. Research performed at the University of Pittsburgh by Dr. Susan Manzi and others have clearly demonstrated an association between Lupus and the early development of plaque build-up in the arteries that supply blood to the heart muscle and other vital organs.   The accumulation of this plaque within the arteries, composed of cholesterol and cellular debris, is the cause of heart attack, angina, and even stroke.   The good news is that these events are preventable if proper attention is given to risk factor modification early in the disease process.

Daniel Edmundowicz, MD, FACC, is director of Preventive Cardiology within the UPMC Cardiovascular Institute and has collaborated with Dr. Manzi in studies detecting early heart disease in Lupus patients.   “It is clear that atherosclerosis, the process of plaque formation in the coronary arteries, develops early in women with Lupus.   The exact reason for this association is unknown, but it may be that the inflammation associated with Lupus makes the blood vessels more vulnerable to only modestly high cholesterol levels and blood pressure elevations.   It is therefore crucial to focus on early and aggressive risk factor control.”    Dr. Edmundowicz and his colleagues Suresh Mulukutla, MD, and Angel Lopez-Candales, MD see patients in consultation at the Lupus Center to assist with control of important modifiable risk factors.

“We take a very aggressive stance on the control of risk factors,” says Dr. Edmundowicz.   “This does not mean that we jump to using medications all the time.   We frequently will start by having our exercise physiologist and nutritionist work with the patients to assist them in building a foundation of healthy lifestyle habits.   This can be challenging for individuals with chronic joint and muscle aches limiting their exercise capacity or for those on steroid medications that may have other dietary limitations.”

Drug therapy for risk factor control is started early when necessary.   “We have very effective medications available to control cholesterol levels and blood pressure now,”Dr. Edmundowicz points out, “But it is crucial to know when to start these medications and how to use them safely, especially in combination with the multiple other medications we frequently find our Lupus patients needing to take.”

If concerning symptoms do occur and further heart testing is deemed necessary, patients at the Lupus Center can be conveniently evaluated at the new Heart Center at UPMC Magee-Womens Hospital. Oscar Marroquin, MD, of the UPMC Cardiovascular Institute directs the new Heart Center, which is located on the 5th floor of the hospital.   “We are extremely pleased to be able to offer cutting edge cardiovascular care to the patients of the Lupus Center and Magee- Womens Hospital,” says Dr. Marroquin.   “We perform echocardiography and nuclear cardiology procedures including exercise and pharmacologic stress testing, all with state of the art equipment.   Both inpatient and outpatient general cardiology consultation is available through the center as well.”

“This collaborative effort between the Lupus Center of Excellence, UPMC Magee-Womens Hospital, and the UPMC Cardiovascular Institute offers a unique opportunity for our patients to receive conveniently the finest preventive, diagnostic and therapeutic cardiovascular care available,” notes Dr. Manzi.   For more information, contact the Lupus Center at 412-641-7600
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« Reply #7 on: November 08, 2006, 07:51:43 am »

ST. LOUIS, Nov. 7 -- What a week for fat mice!

In mice, the drug Aralen (chloroquine) lowers blood pressure, improves glucose tolerance, suppresses the activity of an enzyme involved in insulin resistance, and decreases diet-induced atherosclerosis, according to Clay Semenkovich, M.D., of Washington University.


As well as a possible clinical application, the finding may have implications for understanding how metabolic syndrome - characterized by hypertriglyceridemia, low HDL cholesterol, hypertension, hyperglycemia, and excess visceral adiposity - is associated with vascular disease, Dr. Semenkovich and colleagues said in the November issue of Cell Metabolism.


As many as a quarter of American adults have metabolic syndrome, the researchers said, although the underlying mechanisms are not well understood, One view, they said, is that a common unifying mechanism underlies atherosclerosis, insulin resistance, and the clinical features of the metabolic syndrome.


Support for that view comes from the rare autosomal recessive disease ataxia telangiectasia, which is characterized by cerebellar ataxia, skin and eye telangiectasias, malignancies, and immune deficiency. However, affected children also have impaired growth and glucose intolerance suggestive of insulin resistance, the researchers said.


The disease is caused by a deficiency of a protein kinase -- Ataxia Telangiectasia Mutated, or ATM -- that is involved in responding to DNA damage and also in insulin signaling, Dr. Semenkovich and colleagues said.


In a series of experiments in genetically engineered mice, the researchers showed that mice deficient in ATM, when fed a high-fat diet, developed symptoms that resemble the metabolic syndrome, as well as insulin resistance and vascular disease. Also, cells lacking ATM also showed greater amounts of the enzyme known as Jun N-terminal kinase (JNK), which is linked to insulin resistance.


Knowing that Aralen activates ATM, Dr. Semenkovich and colleagues took mice prone to vascular disease, fed them a high-fat diet, and then treated them with 7.0 mg/kg weekly of the drug.


The dose is roughly equivalent to 40 mg a week for a 70-kg person, the researchers said, where the usual dose for malaria is 250 mg a day.


The drug had no effect on serum lipids, but decreased the area of atherosclerotic lesions (compared to control animals) by up to 37% in some locations. The decreases were statistically significant, at P-values ranging from 0.0030 to 0.0084, depending on location.


The drug also significantly lowered fasting and fed glucose levels and fasting insulin levels, at P<0.05, the researchers reported.


The research sheds new light on the underlying mechanism that links the metabolic syndrome to vascular disease, according to Steven Shoelson, M.D., of Harvard in an accompanying editorial, but the Aralen results are an "interesting twist" that may lead to better control of the metabolic syndrome.


It's unlikely that Aralen itself will be the drug of choice, Dr. Shoelson said, because "many adverse reactions have been attributed to chloroquine (of which) perhaps the most disturbing is visual impairment." Indeed, Dr. Shoelson said, retinopathy associated with the drug can be permanent and can progress even after the medication is stopped.


"Other drugs with less toxicity that also activate ATM, providing this is validated as chloroquine's mechanism in these disorders, might furnish an interesting new avenue for treatment," he suggested.


**Note that this study suggests a well-known anti-malaria drug can reverse the syndrome - at least in mice.
Only days after Harvard researchers squeaked with joy about the potential wonders of a compound in red wine, investigators here said a drug used to treat malaria can reverse the so-called metabolic syndrome in chubby rodents.

Advise patients who ask that the metabolic syndrome affects up to one in four Americans and has been linked to an increased risk of vascular disease.
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« Reply #8 on: November 16, 2006, 08:15:04 am »

CHICAGO, Nov. 14 -- A paclitaxel-coated balloon appears to be an effective treatment for in-stent restenosis, suggesting that an update of an old percutaneous coronary intervention may solve a condition that is the bane of stenting. Action Points

Explain to interested patients that this pilot study describes an experimental device that is not available for general clinical use.


Point out that these data are preliminary and do not yet confirm the clinical validity of this approach.
In a pilot study of 52 patients with in-stent restenosis, the investigational, proprietary paclitaxel-coated balloon reduced the six-month angiography-confirmed restenosis rate to 5%, versus 43% in patients treated with uncoated balloons, said Bruno Scheller, M.D., of Universitatsklinikum des Saarlandes, in Homburg, Germany.


Moreover, at 12 months the rate of major cardiac events was just 4% for patients treated with the drug-coated balloons versus 31% for those treated with standard balloons, he said.


Late lumen loss was 0.74 ±0.86 mm in for patients treated with standard balloons versus 0.03±0.48 mm for those who received the paclitaxel balloons (P=0.002).


Dr. Scheller reported the results at the American Heart Association meeting here. The findings were simultaneously published by the New England Journal of Medicine.


In his presentation at the meeting here, Dr. Scheller reported combined results from the 52 patients reported in the journal paper with findings from 56 patients who were enrolled in a second trial that followed the same PACCOCATH-ISR (Treatment of In-Stent Restenosis by Paclitaxel-Coated Balloon Catheters) protocol as the published study.


In this blended trail -- called PACCOCATH-ISR-2 study -- the results largely replicated the first trial except that late lumen loss at six months was more pronounced in both the drug coated and uncoated balloon treatment groups.


In PACCOCATH-ISR 2 the late lumen loss was 0.11 mm in the paclitaxel balloon arm and 0.84 in the uncoated balloon group (P<0.010).


Currently, in-stent restenosis is treated with a variety of options, all of which have had disappointing results, Dr. Scheller said.


The typical restenosis rate for balloon angioplasty of in-stent restenosis is 39% to 67%, brachytherapy has a restenosis rate of 16% to 23%, and when drug-eluting stents are used to treat in-stent restenosis of bare metal stents the restenosis rate ranges from 13% to more than 20%.


And when in-stent restenosis occurs in a vessel that has been opened with a drug-eluting stent like Cypher (sirolimus-eluting) or Taxus (paclitaxel-eluting) a 43% restenosis rate has been reported, he said.


In the PACCOCATH-ISR study, 80% of patients had multivessel disease and severe in-stent restenosis (>70%) in a single coronary artery. Lesions were shorter than 30 mm.


The patients were evenly randomized to treatment with balloons coated with paclitaxel (3 µg of drug per mm² of balloon surface).


Target lesions were assessed by quantitative coronary angiography.


All patients were treated with Plavix (clopidogrel) plus aspirin for one month after treatment, followed by aspirin indefinitely.


In an editorial that accompanied the journal report, Edoardo Camenzind, M.D., of the University of Geneva, wrote that the significant effect reported by Dr. Scheller and colleagues might be the result of their drug choice.


Paclitaxel, he wrote, "is a highly lipophilic cytostatic drug," as such it "allows for good penetration and persistence in tissue."


Another possible explanation, according Dr. Comenzind that the proprietary technique used to coat the balloon surface "provided good adhesion of the compound to the balloon without noticeably affecting its mechanical properties."


Finally, Dr. Scheller cautioned that his findings should be considered preliminary since the trial was not "aimed at justifying clinical application or regulatory approval of the drug-coated balloon; larger studies will be required to determine whether the effects observed in this trial can be replicated."


"A comparison of this treatment and optimal current therapy (such as brachytherapy) in randomized trials is required," he wrote.


The trial was supported by Bavaria Medizin Technologie. Dr. Scheller and Ulrich Speck, Ph.D., a co-author, report being coinventors on a patent application for various methods of inhibiting restenosis (including the technique used in this trial), which was submitted by Charité University Hospital in Berlin. Michael Böhm, M.D. another co-author, reports receiving lecture fees from Boehringer Ingelheim, Pfizer, Astra-Zeneca, and Sanofi Aventis. Dr. Speck reports receiving consulting fees from Schering and grant support from Bavaria Medizin Technologie

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« Reply #9 on: November 16, 2006, 09:44:03 am »

Patients With Systemic Lupus Erythematosus Display Signs of Premature Atherosclerosis


WASHINGTON, DC -- November 16, 2006 -- Patients with systemic lupus erythematosus (SLE) tend to suffer heart disease and acute myocardial infarctions more often than the general population.

Biji T. Kurien, PhD, senior research scientist, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, and colleagues set out to determine whether a subset of patients with SLE could be identified who are at higher risk of this complication. They presented results of this study here on November 12th at the American College of Rheumatology - Association of Rheumatology Health Professionals Annual Scientific Meeting (ACR-ARHP).

The researchers hypothesized that antibodies to oxidized low-density lipoprotein (anti-oxLDL) and antiphospholipid antibody (aPL) are present in serum among patients with SLE and how it would correlate with antibody subsets in SLE. They also hypothesized that these antibodies would be present in SLE sera prior to development of antibodies over time.

In their study, they tested 67 patients with SLE and 8 normal controls for antibodies to ox-LDL using a kit. To determine the timeline of origin of anti-oxLDL, the researchers also determined anti-immunoglobulin (Ig) G, IgM and IgA antibodies against phospholipids (cardiolipin) in 2 SLE patients.

Thirty-seven out of 67 patients were positive for anti-ox LDL antibodies and these antibodies correlated with elevated IgG APL antibodies. There was no corresponding increase in IgM and IgA APL antibodies. All 10 patients antibodies to 60 kD Ro, La and 52 kD Ro had significantly elevated anti-oxLDL vs normals. However, only four (4/11) of these patients were positive for anti-oxLDL.

Dr. Kurien concluded that Anti-oxLDL occurred more often and at higher levels in SLE patients with antibodies to 60 kD Ro, La and 52 kD Ro than in patients with other known autoantibodies. A majority of those with only ANA behaved like normal controls.

The emergence of anti-oxLDL and IgG aPL antibodies prior to the development of anti-60 kD Ro over time in a patient indicates that these antibodies could not be crossreactive in nature, at least in this particular patient.

Dr. Kurien said that the next step will be to determine in a prospective study whether the identified subgroups have higher incidence of cardiovascular events. If this subgroup does experience more events, he said, then preventive measures could be instituted in this group.

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« Reply #10 on: November 23, 2006, 10:36:23 am »

Diagnosis: Children’s Arteries Can Point to Heart Disease

Published: November 21, 2006

Thickening of the arteries, which can lead to a heart attack, is a condition most people associate with aging. But a new study finds that signs of the problem can be seen in some young children and urges doctors to take preventive action.
 

The study, presented at a recent conference of the American Heart Association, reviewed the findings of 26 earlier studies and found that some children had a subclinical form of atherosclerosis, as the condition is known.

“The arteries of those kids are thicker,” said the lead author of the study, Dr. Sanaz Piran, an internal medicine resident at McMaster University in Canada.
The children who exhibited the changes were already at higher risk for heart disease later in life. They were obese, had high blood pressure, diabetes or high cholesterol.

In all, the studies looked at more than 3,600 children, ages 5 to 18. The studies used a variety of noninvasive measures to assess thickening and stiffening of the arteries and blood flow.

The findings, the researchers said, reinforce the need for doctors to treat risk factors in children with the same attention they give to adults. Children in families with a history of high cholesterol, for example, should have their cholesterol checked, they said.

**NOTE~As a kid and throughout my adulthood, whenever I got a cut, my blood used to be so thick I never bled like a normal person . Mine was so thick it just stayed right at the wound.
Now being on blood thinners and having clogged arteries reading this, there is hope with this research they will all pin point it for the future of these kids .(I hope so)
~Kathy



**UPDATE~While merging topics in the "Lupus In The News", just this week I posted the latest info on ADULTS. Seems these two studies need to be in contact with each other. Do you see the pattern on what they are finding in these studies?




Patients With Systemic Lupus Erythematosus Display Signs of Premature Atherosclerosis
WASHINGTON, DC -- November 16, 2006 -- Patients with systemic lupus erythematosus (SLE) tend to suffer heart disease and acute myocardial infarctions more often than the general population.

Biji T. Kurien, PhD, senior research scientist, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, and colleagues set out to determine whether a subset of patients with SLE could be identified who are at higher risk of this complication. They presented results of this study here on November 12th at the American College of Rheumatology - Association of Rheumatology Health Professionals Annual Scientific Meeting (ACR-ARHP).

The researchers hypothesized that antibodies to oxidized low-density lipoprotein (anti-oxLDL) and antiphospholipid antibody (aPL) are present in serum among patients with SLE and how it would correlate with antibody subsets in SLE. They also hypothesized that these antibodies would be present in SLE sera prior to development of antibodies over time.

In their study, they tested 67 patients with SLE and 8 normal controls for antibodies to ox-LDL using a kit. To determine the timeline of origin of anti-oxLDL, the researchers also determined anti-immunoglobulin (Ig) G, IgM and IgA antibodies against phospholipids (cardiolipin) in 2 SLE patients.

Thirty-seven out of 67 patients were positive for anti-ox LDL antibodies and these antibodies correlated with elevated IgG APL antibodies. There was no corresponding increase in IgM and IgA APL antibodies. All 10 patients antibodies to 60 kD Ro, La and 52 kD Ro had significantly elevated anti-oxLDL vs normals. However, only four (4/11) of these patients were positive for anti-oxLDL.

Dr. Kurien concluded that Anti-oxLDL occurred more often and at higher levels in SLE patients with antibodies to 60 kD Ro, La and 52 kD Ro than in patients with other known autoantibodies. A majority of those with only ANA behaved like normal controls.

The emergence of anti-oxLDL and IgG aPL antibodies prior to the development of anti-60 kD Ro over time in a patient indicates that these antibodies could not be crossreactive in nature, at least in this particular patient.

Dr. Kurien said that the next step will be to determine in a prospective study whether the identified subgroups have higher incidence of cardiovascular events. If this subgroup does experience more events, he said, then preventive measures could be instituted in this group.
« Last Edit: November 23, 2006, 04:05:19 pm by Kathy » Logged


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« Reply #11 on: November 24, 2006, 03:53:23 pm »

New folder for all information related to Cardiology with Lupus, MCTD, Autoimmune disorders.
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« Reply #12 on: November 24, 2006, 06:52:33 pm »

Anticoagulant Reduces Major Bleeds in Acute Coronary Syndromes                         
     

 NEW YORK, Nov. 22 -- The thrombin-specific anticoagulant Angiomax (bivalirudin) as monotherapy in acute coronary syndromes reduced the risk of major bleeding by 47% compared with rates for heparin and glycoprotein IIb/IIIa inhibitors, researchers reported.
Action Points

Explain to interested patients that the findings from the ACUITY study reported here are still investigational and may not be applicable to broad clinical use.


Note that the editorialist suggested that patients who require urgent percutaneous coronary intervention but who have not been adequately pretreated with aspirin or Plavix, should receive a glycoprotein IIb/IIIa inhibitor.
When used alone in acute syndromes, Angiomax, approved to replace heparin in non-emergency percutaneous angioplasty procedures, was as effective as the standard anticoagulants, according to results from the Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial reported in the Nov. 23 issue of the New England Journal of Medicine.


In the ACUITY trial, supported by Medicines Company, maker of Angiomax, and Nycomed, the drug's European marketer, 59% of the patients had a myocardial infarction without ST-segment elevation, while 41% had unstable angina, said Gregg Stone, M.D., of Columbia University here, and co-authors in the U.S., Europe, and Australia.


In the 17-country study, 13,819 patients (median age 63, 70% men) with acute coronary syndromes were assigned to one of three antithrombotic regimens: traditional unfractionated heparin or the low-molecular-weight heparin enoxaparin combined with a glycoprotein IIb/IIIa inhibitor; Angiomax plus a glycoprotein IIb/IIIa inhibitor, or Angiomax alone.


The primary endpoints were a composite ischemia endpoint (death, myocardial infarction, or unplanned revascularization for ischemia), major bleeding, and the net clinical outcome (composite ischemia and major bleeding).


Angiomax plus a glycoprotein IIb/IIIa inhibitor, compared with a control group of heparin plus the glycoprotein inhibitor had equivalent (noninferior) 30-day rates for the composite ischemia end point (7.7% and 7.3%, respectively). Major bleeding rates were similar (5.3% and 5.7%), as was the net clinical outcome (11.8% and 11.7%), the researchers reported.


Angiomax alone, compared with heparin plus the glycoprotein inhibitor, produced a noninferior rate of the composite ischemia end point, the researchers said. They found that a 7% decrease in bleeding events offset a 7% increase in ischemic events (7.8% and 7.3%, respectively; P=0.32; relative risk, 1.08; 95% confidence interval 0.93 to 1.24).


On the plus side, the researchers reported that Angiomax had a significant 47% reduced rate of major bleeding (3.0% vs. 5.7%; P<0.001; relative risk, 0.53; CI, 0.43 to 0.65).


The net clinical outcome for Angiomax alone compared with the other anticoagulants was 10.1% vs. 11.7%; P=0.02; relative risk, 0.86; CI, 0.77 to 0.97), the researchers said.


In approximately 64% of the patients, a thienopyridine, in most cases Plavix (clopidogrel), was already in use or was given before angiography or percutaneous coronary intervention. The researchers noted that the point estimate for adverse ischemic events was slightly greater with Angiomax monotherapy than with heparin plus glycoprotein therapy in patients who were not pretreated with a thienopyridine.


Although information about the exact timing of this treatment was not available, Dr. Stone's team suggested that giving a thienopyridine prior to Angiomax monotherapy might be desirable.


Several limitations of the study deserved comment, the investigators said. First, the logistic complexities of the trial required an open-label design, which introduced a potential for bias. Second, 59% of the study cohort presented with myocardial infarction without ST-segment elevation, a percentage lower than that in certain other trials yet similar to still others.


Third, as in other trials, a significant proportion of the patients were pre-treated with some form of heparin before randomization. Nonetheless, the effects of Angiomax monotherapy were consistent, regardless of crossover, as shown in a subgroup analysis.


Finally, the researchers said, the 25% noninferiority margin used in the study may have been too wide. Because the observed rate of ischemic events in the control group was 7.3%, an estimated ischemic-event rate as high as 9.1% in the test groups would have been considered noninferior, even though it might be considered clinically important.


In summary, Dr. Stone said that testing several different combinations of anticoagulant therapies found that Angiomax used alone was as effective at the traditional drugs -- heparin plus glycoprotein IIb/IIIa inhibitors -- in preventing ischemic events, but with significantly lower rates of bleeding.


In an editorial in the same NEJM issue, John Bittl, M.D., of the Ocala Heart Institute, Munroe Regional Medical Center, in Florida, emphasized that patients assigned to Angiomax monotherapy who were not pretreated with Plavix had a significant 29% increase in ischemic events as compared with those treated with traditional drugs. Therefore, he said, patients who require urgent percutaneous coronary intervention but who have not been adequately pretreated with aspirin or Plavix, should receive a glycoprotein IIb/IIIa inhibitor.


"A noninferiority trial like the ACUITY trial, which was designed to test multiple composite outcomes, could be criticized as a shell game," Dr. Bittl wrote. However, he continued, "the significance of the study is its unique ability to evaluate the integrated antithrombotic and invasive therapies used in the contemporary treatment of patients with acute coronary syndromes."


Summing up, Dr. Bittl said, "the ACUITY trial provides strong support" for the use of Angiomax as a substitute for heparin plus glycoprotein IIb/IIIa inhibitors in patients with acute coronary syndromes who undergo early invasive treatment, in particular if they are pretreated with Plavix.


Dr. Stone reported receiving consulting fees from the Medicines Company, Boston Scientific, Guidant, Abbott, Volcano, St. Jude, and BMS Imaging and lecture fees from the Medicines Company, Boston Scientific, Nycomed, Guidant, Medtronic, and Abbott.

 
 


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« Reply #13 on: December 01, 2006, 11:56:38 am »




Drug May Fight Lupus and Atherosclerosis Simultaneously

 
     WINSTON-SALEM, N.C. – People with lupus are prone to premature accelerated atherosclerosis. Now scientists at Wake Forest University School of Medicine think they have a way to prevent or decrease this atherosclerosis and prevent heart attacks.

     “Premature accelerated atherosclerosis is one of the leading causes of death and disability in lupus,” said Nilamadhab Mishra, M.D., a  rheumatologist at Wake Forest University Baptist Medical Center.  Using a drug called Trichostatin A (TSA) “may prevent or decrease premature atherosclerosis in lupus.”

     Mishra presented his findings today (Nov. 16) at the American College of Rheumatology meeting in San Diego.

     The findings represent a merger of two lines of Mishra’s animal research using TSA – one showing that the drug reduced lupus symptoms, especially inflammation of the kidneys and enlarged spleens, and the other showing that TSA was effective against atherosclerosis.

     Mishra was joined in the atherosclerosis research by several leading scientists in the Medical School’s long-standing atherosclerosis research program. Their research uses a mouse that was created to be prone to atherosclerosis when fed a diet high in cholesterol and with 10 percent of calories from palm oil, one of the more dangerous dietary vegetable fats since it is high in saturated fat.

     Among the atherosclerosis researchers were John S. Parks, Ph.D., professor of comparative medicine, and Richard St. Clair, Ph.D., professor of pathology and head of the Section on Comparative Medicine.

     For 12 weeks, the researchers fed a high-fat, high-cholesterol diet to two groups of the atherosclerosis-prone mice. One group got injections of TSA from the time they went on the diet, while the other group got no TSA. The TSA-treated group had markedly less atherosclerosis in key arteries, such as the aorta – the body’s main blood vessel – and what plaque there was contained less cholesterol.

     Scientists increasingly are viewing the depositing of cholesterol in the walls of arteries as an inflammatory reaction that attracts the disease-fighting macrophages, a type of white blood cell, which then become incorporated with cholesterol deposits to become plaque. The mice that had the TSA injections had a reduction in the gathering of macrophages.

     Mishra said that TSA may be beneficial because it prevents certain genes from expressing proteins that are known to be involved in both lupus and atherosclerosis.

     Mishra had reported earlier that TSA showed promise in treating lupus in a different, lupus-prone mouse model. The research raises the hope, said Mishra, that “lupus and atherosclerosis can be treated simultaneously.”
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« Reply #14 on: December 01, 2006, 04:39:13 pm »


Heart Risk: Arthritis Drugs Compared


Nov. 29, 2006 - A new class of rheumatoid arthritis drugs is no different at cutting heart attack and stroke risk than an older treatment, a Harvard study shows.

In the study, patients taking biologics, which are designed to suppress a specific part of the immune system, were compared with patients taking only methotrexate, an older drug commonly used for rheumatoid arthritis.

Those taking biologics, such as Enbrel, Humira, Remicade, or Kineret, fared no better or worse than those on methotrexate alone, in terms of risk for heart attack or stroke, the study shows.

These drugs are called biologics because they are derived from living organisms.

However, the study did show that people taking oral steroids appeared to have slightly greater cardiovascular risk than patients who only took methotrexate.

Comparing Heart Risk

In rheumatoid arthritis, the immune system attacks the body instead of defending it. Doctors often prescribe drugs to suppress the immune system in order to control the disease.

Rheumatoid arthritis is also associated with a rise in heart risks.

This added risk is thought to be tied to the inflammation that is a key component of rheumatoid arthritis - and is increasingly thought to play a part in the development of heart disease as well.

This study, from Daniel Solomon, MD, MPH, and colleagues, looked at data from about 3,500 rheumatoid arthritis patients enrolled in Medicare.

The patients were 82 years old, on average. Most were elderly white women in frail health.

The patients had filled prescriptions for various drugs designed to suppress the immune system.

Over two years, 946 patients were hospitalized for a heart attack or stroke. Those taking biologic drugs weren't any more or less likely to have a heart attack or stroke than those only taking methotrexate.

While those taking oral steroids did appear to be more at risk than those on methotrexate, the researchers caution that this could be because methotrexate and biologic drugs may both protect the heart.

If that is the case, oral steroids may falsely look risky in comparison. The study doesn't settle that question.

The study has some limits.

The data didn't include information on some things that may affect cardiovascular risk, such as smoking, aspirin use, and BMI (body mass index) -- a gauge for appropriate weight.

With a mainly frail, elderly population, it was also hard to rule out other illnesses


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« Reply #15 on: December 03, 2006, 09:54:35 am »

Pfizer Ends Studies on Drug for Heart Disease
               
 
 December 3, 2006
Pfizer announced last night that it had discontinued research on its most important experimental drug, a treatment for heart disease. The decision is a stunning development that is likely to seriously damage the company’s prospects through the next decades.

Preliminary research found that the drug, torcetrapib, appeared to be linked with deaths and heart problems in the patients who were taking it.

For people with heart disease, Pfizer’s decision to stop the trial represents the failure of a drug that many cardiologists had viewed as a potentially major advance in efforts to reduce heart attacks and strokes.

Torcetrapib is designed to raise levels of so-called good cholesterol. It was to be used in combination with older drugs called statins, like Lipitor and Zocor, which reduce so-called bad cholesterol.

As recently as Thursday, Pfizer executives had hailed the drug at a meeting with investors and analysts at the company’s research center in Groton, Conn.

“This will be one of the most important compounds of our generation,” said Jeffrey B. Kindler, Pfizer’s chief executive.

Pfizer is the world’s biggest drug company, with 106,000 employees and $51 billion in sales in 2005.

In a news release issued yesterday, the company said that it would immediately halt clinical trials of the drug and end its development.

The decision was based on interim results from a 15,000-patient clinical trial. The trial, called Illuminate, was scheduled to be completed in 2009. Pfizer had hoped it would prove that the combination of the two drugs was significantly more likely to reduce heart attacks and strokes than Lipitor alone does.

Even before yesterday’s announcement, some cardiologists had raised concerns about torcetrapib, noting that the drug raised blood pressure in many patients, a serious side effect for a heart medicine. But Pfizer said those concerns would prove to be unfounded, arguing that torcetrapib’s effects on good cholesterol would overwhelm its negative impact on blood pressure.

At this point, it is unclear whether the drug’s failure was due to a specific problem with its chemistry or whether other drugs to raise good cholesterol will also face unexpected problems in clinical trials. Pfizer has other drugs similar to torcetrapib in its pipeline, but they are in much earlier stages of development.

For Pfizer, the end of the torcetrapib program is an enormous blow. Drugs for heart disease are among the most widely used prescription medicines. Lipitor, another Pfizer drug, is the best-selling drug in the world, with sales of $13 billion this year.

The company and investors had expected that torcetrapib would be another big seller, making up for sales that Pfizer will lose when Lipitor loses patent protection in the United States in 2010.

Despite a research budget of $7 billion annually, Pfizer has had difficulty bringing important new drugs to market this decade and its near-term pipeline of new drugs is also thin. On Tuesday, the company said it would cut 20 percent of its American sales force, almost 2,400 employees. Yesterday, it said it intended to accelerate its restructuring because of torcetrapib’s failure.

Pfizer had planned to sell the drug both as a stand-alone drug and in combination with Lipitor. The company had said it expected to file for federal approval in 2007 based on data from other clinical trials that will also be halted.

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