Judy Foreman

Nationally Sindicated Fitness, Health, and Medicine Columnist

A New Heart Disease Test That Could Save Your Life

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A new test called high sensitivity CRP, catapulted into the headlines last week by a study in the New England Journal of Medicine, appears to be better than cholesterol at predicting the risk of heart attack and stroke. The test measures levels of an inflammatory substance, C-reactive protein that plays a role in cardiovascular disease.

So, to cut to the chase, should you ask for the CRP test? Yes. It’s cheap (about $16).  It’s already on the market. It could save your life, especially if it a worrisome result gets you to exercise more and eat less. Besides, if it’s good enough for President George W. Bush, who has passed the test with flying colors, it’s good enough for the rest of us.

To be sure, an editorial last week in the New England Journal took a more cautious view, arguing that “it may be premature” to adopt widespread screening for C-reactive protein.

And there are legitimate caveats. No one -yet – is recommending that the test be done routinely for all adults. The experts – a committee of specialists from the Centers for Disease Control and Prevention and the American Heart Association – are still hashing out who should get it. Chances are their recommendations, due out soon, will initially recommend the test, if at all, only for people whose risk is unclear or moderate based on other tests. In any event, CRP will not replace cholesterol testing, but will be an add-on.

There’s also the concern, present with any screening test, that worrisome results could set you on a path of intervention that could do harm as well as good. For instance, if your CRP test is high, do you just exercise more and eat less? Or do you start taking statins, which can lower CRP as well as cholesterol? The evidence that statins lower CRP is growing, but it’s not conclusive, and statins do carry some risk.

Moreover, CRP testing might not pan out once it’s used widely, not just in research. After all, cholesterol hasn’t been such a great predictor – half of people who have heart attacks have normal cholesterol.

Finally, just for the record, much of the work on CRP, including the latest study, has been done by researchers at Brigham and Women’s Hospital, which owns the patents on inflammatory markers for cardiovascular disease. This does not taint the research. But CRP testing is a potentially lucrative business.

That said, the new study, which confirms a considerable body of previous work, is paradigm-shaking, poised to change the way doctors screen for heart disease.

Led by Dr. Paul Ridker, director of cardiovascular disease prevention at Brigham and Women’s, the new study followed 27,939 healthy middle-aged women for eight years to assess their risk of having a first heart attack, stroke, cardiac bypass surgery or death from cardiovascular causes.

The researchers found, as expected, that women with high levels of  both CRP and LDL cholesterol were at high risk of cardiovascular problems, and that women with low levels on both tests were at low risk. The surprise was the women in the middle.

In the study, women with high CRP but low cholesterol were actually at higher risk than those with high cholesterol and low CRP, even though the former group is usually deemed low risk by current screening.

“The study provides overwhelming evidence that inflammation is at least as important as LDL cholesterol in predicting vascular risk,” notes Ridker. In fact,25 percent of the US population has elevated CRP levels but normal to low levels of LDL, suggesting that millions of Americans may be at increased risk despite normal or low cholesterol.

 “The CRP story gets more interesting every day,” says Dr. Sidney Smith, chief scientific officer for the American Heart Association and professor of medicine at the University of North Carolina at Chapel Hill. “The evidence for its value is compelling, but not as a replacement for cholesterol. It will be useful for some patients in combination with other measures of risk.”

For years, doctors have known that cholesterol-filled plaques in artery walls pose a significant danger. If these plaques completely block an artery, the heart can be deprived – sometimes fatally – of adequate blood flow.

But doctors also know that even if plaques don’t completely block an artery, they can trigger heart attacks if they rupture, releasing blood clots that themselves can block an artery to the heart or brain.

Indeed, most heart attacks are actually caused by smaller, “vulnerable” plaques at risk of rupture, says Massachusetts General Hospital cardiologist Dr. James Muller, co-director of the vulnerable plaque program of CIMIT, the hospital’s center for integration of medicine and innovative technology.

So far, vulnerable plaques, which are filled with inflammatory cells from the immune system, cannot be detected with standard imaging techniques such as coronary angiograms or CT scans.

Enter C-reactive protein, a substance made in the liver and released during infections. Standard CRP tests are routinely used to gauge the degree of inflammatory response in everything from pneumonia to rheumatoid arthritis.

But the new, high sensitive cardiac CRP tests, sublicensed through Dade Behring in Deerfield, Ill., measure tiny fluctuations at the low end of the range. (A worrisome score on the new test could indicate nothing worse than a common cold; but if a repeat test several weeks later is still high, it may indicate a persistent inflammation in the body, including fragile, inflamed plaques.)

Moreover, CRP is not just a marker of inflammation, but a bad actor directly involved in the in process of inflammation in plaques, notes Dr. Richard  Pasternak, director of preventive cardiology at MGH.

That suggests that lowering CRP may directly lower the risk of cardiovascular disease. Indeed, with statin drugs (Lipitor, Pravachol, Lescol, Zocor and Mevacor), already used to lower cholesterol may be prescribed to lower CRP as well.

There’s already “an overwhelming abundance of data that statin drugs lower CRP levels,” says Dr. Karol Watson, co-director of the preventive cardiology program at the University of California, Los Angeles. In fact, one study, published in August in  the Circulation, the journal of the American  Heart Association, showed that such drug, simvastatin, lowers CRP levels very quickly – in just two weeks.

Still, not everyone believes CRP testing is ready for prime time, or that, even if it is,  doctors should begin prescribing statins for this reason, as Ridker is the first to note.

Compelling as the new data may be, it does not address whether treating people on the basis of high CRP test results is justified, notes Dr. Christopher O’Donnell, associate director of the Framingham Heart Study, a research effort sponsored by the National Heart Lung and Blood Institute..

Indeed, statins, though generally safe, can cause liver and muscle damage. One statin,  Baycol (cerivastatin), was voluntarily taken off the market last year because it was associated with 31 fatal cases of a kind of muscle damage called rhabdomyolysis.

In other words, key  questions remain, including whether the humble aspirin, an anti-inflammatory as well as anti-clotting drug, might also be used to lower CRP levels.

 Still, CRP is the most promising advance in a long time in detecting cardiovascular risk. At the very least, it makes sense to ask your doctor about it.

Coated Stents Show Huge Promise

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Vice President Dick Cheney made the problem famous, but thousands of  Americans each year need a new round of treatment to fix a heart problem they thought was already solved. 

The setback generally goes something like this: Having experienced a chest pain or heart attack, the patient undergoes a procedure to open up the clogged artery, and to install a tiny mesh-like device called a stent to keep the artery propped open. But in many cases, this foreign object causes the body to react with scar tissue and the artery narrows again.

To combat this re-clogging process – which is called restenosis and affects roughly 30 to 50 percent of patients, like Cheney, who have stents – scientists are aggressively testing a variety of drug-coated stents that would release inflammation-reducing medications. These drug-coated stents, which are available in Europe, are expected to radically alter the treatment of cardiovascular disease.

“The anticipation is extraordinary,” said Dr. Campbell Rogers, director of the cardiac catheterization laboratory at Brigham and Women’s Hospital. “The impact of having a new, less-invasive and more effective treament for coronary heart disease is vast.” Coated stents will probably be on the US market in the next year or so, with several major companies in various stages of clinical trials.

The leaders are Cordis (a Johnson & Johnson company), Boston Scientific and a joint effort by Guidant Corporation and Cook Inc. Some preliminary data show an almost unheard-of 100 percent success rate (meaning zero restenosis) for the drug-delivery stents after two years of follow up. These results are particularly impressive given that patients who receive regular stents often get a diagnosis of restenosis within a year.

Coated stents are expected to replace substantially coronary artery bypass surgery, an expensive, highly invasive operation now performed on more than 350,000 Americans a year. The bypass surgery will probably still be needed for some heart patients who also have diabetes and for those whose arteries are completely blocked.But the new stents will likely become the preferred option not just for the 1 million or so Americans a year who now get regular stents, but for hundreds of thousands of others currently deemed ineligible because they have too many bad arteries. They may also be used for hundreds of thousands of others with “vulnerable plaques,” that is, arteries with fatty deposits that have not yet ruptured (a process that can cause an instant heart attack).

Coated stents are nothing less than a “revolution,” says Dr. James  Muller, director of clinical research in cardiology at Massachusetts General Hospital and co-director of the CIMIT Vulnerable Plaque Program. “They are wonderful.”

Dr. Jesse Currier, associate director of the adult cardiac catheterization  lab at the UCLA Medical Center, puts it even more emphatically: “This is Neil Armstrong, one giant leap for interventional cardiology…this is a huge, huge quantum leap.”

Commonplace as they now are, regular stents have actually been on the US market for only a few years, after two major trials showed that simply placing an uncoated stent into an artery was better than angioplasty alone in reducing the risk of restenosis. (In angioplasty, doctors thread a tube called a catheter up through an artery in the groin to the coronary arteries, then push a button to inflate a balloon to compress the plaque against the artery wall.)Even though uncoated stents do just fine at keeping artery walls from collapsing, their sheer presence can create new problems, notes Dr. Elazer Edelman, director of the Harvard-MIT Biomedical Engineering Center, professor of Health Sciences and Technology at MIT and a cardiologist at Brigham and Women’s Hospital.

The worst possibility is that, immediately after insertion, the stent can trigger blood clots, a process that doctors guard against by giving patients anti-clotting drugs such as aspirin and Plavix. Some researchers have also tried coating stents with heparin, a blood thinner. But heparin-coated stents have not proved ideal, in part because heparin dissolves instantly in water – or blood – which means that it disappears rapidly from the area where it’s needed.

But there’s another danger, too, after insertion of a stent. “You’re leaving a foreign body behind. Now, as opposed to a single injury from inflating a balloon, you have a rigid, metal object that can trigger a slow, chronic inflammatory process, ” says Edelman.

Indeed, inflammation is now believed to be a root cause of both atherosclerosis, the initial formation of plaques, and of restenosis, the re-clogging of arteries during the healing process after angioplasty and stent insertion. Cholesterol, specifically LDL (the “bad” cholesterol) is still a major culprit in atherosclerosis. But its effects include stimulation of the body’s natural inflammatory response to injury – sending immune cells to clean up the area .To fight this inflammatory process in people with regular stents, doctors have tried local application of radiation, including radioactive stents and pellets placed temporarily within the stent. This approach has not been shown to prevent restenosis – and may actually impair normal healing of the artery – but can help combat restenosis that has already occurred.A potentially better solution, Edelman and other researchers reasoned, might be to coat stents with drugs that could stop proliferation of inflammatory cells. One idea was to coat a stent directly with a medication, the approach taken by Guidant/Cook. Another was to create polymers (chains of identical chemicals) that could act as a glue to hold drugs on and inside a stent in such a way as to release the drugs slowly, over a matter of days or even weeks.

Working with others at MIT, Edelman began years ago to search for ways to accomplish this slow release. Most drugs, he says, cannot move through sheets of polymer materials. But if the polymer sheet is melted and mixed with a drug, when it’s recast, it looks like a sponge with drug-filled channels supported by walls of the polymer materials.Once implanted in the body, fluid enters the channels and dissolves the drug so that it can then leave the polymer sponge. The more curvy (or “tortuous”) the channels, the longer it takes for the drug to be released. A number of teams have worked to adapt the polymer technology to stents.Yet another hurdle was figuring out which drugs to use. One early choice was an antibiotic called actinomycin-D. But to researchers’ surprise, it proved no better than a bare stent at reducing restenosis.Another was a coating with paclitaxel, the active form of Taxol, a drug used to treat cancers of the breast and other tissues. The drug works by slowing cell proliferation. At moderate doses, says Rogers at Brigham and Women’s Hospital, paclitaxel holds “tremendous promise, essentially wiping out restenosis.” But at the considerably higher doses used in one early trial, paclitaxel-coated stents triggered clots and heart attacks, Rogers notes.Still, researchers knew they were fundamentally on the right track and a compelling series of studies recently made public shows just how effective coated stents – using drugs, such as paclitaxel or sirolimus – can be.Two years ago, a pilot study involving 45 patients in the Netherlands and another 30 in Brazil suggested that the Cordis stent coated with a drug called sirolimus (also known as rapamycin) could help prevent restenosis.But it was the 2-year follow up on these patients, presented this spring at the meeting of the American College of Cardiology in Atlanta, that blew other scientists away: a restenosis rate of zero.

Another study called RAVEL was also presented at the Atlanta meeting. Like the pilot study, the stents in this research were coated with sirolimus, and the results on 238 patients in Europe and Latin America were “astonishing,” says Currier of UCLA. Several hundred patients were followed for up to one year “with no major adverse cardiac events, no restenosis.”

Currently, the sirolimus-coated stent is being tracked in an even bigger study of 1,100 patients (SIRIUS) at Lenox Hill Hospital in New York City and other centers. The 6-month follow up data are not yet public, but the initial data is being submitted to the US Food and Drug Administration for approval of this stent product. The sirolimus-coated stent, called Cypher, has already received regulatory approval for marketing in Europe.

The other main approach is coating stents with paclitaxel. Boston Scientific Corp., based in Natick, uses a polymer to stick paclitaxel onto its stent. In the pilot study of 61 patients, researchers found zero restenosis after six months of follow up.

A larger study of about 500 patients “provided further support for the safety of paclitaxel,” says company spokesman Paul Donovan. The paclitaxel stent also seems to prevent restenosis, a third study shows, as a stent placed inside a stent already in the artery – a kind of stent sandwich.

Boston Scientific’s most important study, TAXUS IV, which involves more than 1,000 patients at 80 medical centers, is still underway, but the company is optimistic: “We plan to launch a drug-coated stent in Europe this year and in the US next year,” says Donovan.

The third main contender for bringing a drug-coated stent to the US market is Guidant/Cook. Like Boston Scientific, Guidant/Cook uses paclitaxel to coat its stents. But therein lies a problem. Boston Scientific and Guidant/Cook are expected to square off in court in early June over distribution rights for stents coated with paclitaxel, which is made by a company called Angiotech Pharmaceuticals in Vancouver, Canada.

Guidant is currently conducting a trial of its paclitaxel stent in more than 1,000 patients in a study called DELIVER, which is now in its follow-up phase.There will certainly be bumps in the road to developing future generations of coated stents. But to a degree unusual in medical circles, cardiologists believe that even the first coated stents to reach the US market will bring vast improvements to America’s heart patients.

Granted, there is still a lot to learn about the use of stents, particularly in people who have already had bypass surgery. “Who knows? ” adds Edelman of MIT, “New delivery strategies may bring us to the day when we not only do not need coatings on stents, and we may not need the stents, either.”

Ties That Bind Help Stroke Patients

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Fred Kemp, 38, a former restaurant manager in Atlanta, Ga., has one simple goal: To open a refrigerator door with his left hand.

Five years ago, Kemp suffered a stroke as he dozed in front of his TV. When he woke up, he recalled, “I couldn’t get up. I tried again and again. I couldn’t move my left side,” forcing the former military hospital corpsman to dial 911 for an ambulance with his good right hand.

Ever since – until very recently – doctors gave him little hope that he would regain use of his left arm.

Every year, 600,000 Americans like Kemp have a stroke, a kind of heart attack in the brain caused by a blood clot or hemorrhage. Many stroke victims die, and many others don’t get effective treatment because they don’t get to the hospital soon enough. Indeed, stroke is still the third leading cause of death in America, after heart disease and cancer.

But, increasingly, people are surviving strokes. While that’s good news, it also means that there are more than 4.4 million stroke survivors living with varying degrees of disability.

Now, preliminary research shows that rehabilitation of long-paralyzed arms and legs may be far more possible than doctors once believed, at least for some types of stroke survivors. At the mecca for stroke rehabilitation, the University of Alabama at Birmingham, victims such as Kemp are achieving recovery levels once thought impossible.

There, psychologist Edward Taub has pioneered a simple but dramatic approach. It’s called CIM – constraint-induced movement therapy, or, as some put it, tough love.

The therapy involves putting the unaffected arm in a splint for most of a patient’s waking hours for two weeks and getting the patient to spend six hours every day using the bad arm in a series of increasingly precise exercises. For the therapy to work, the stroke survivor must have some control over the bad arm, such as the ability to open and close the hand.

To the astonishment of many in the stroke rehabilitation field, this approach seems to work, perhaps by rewiring parts of the brain or spinal cord.

“The idea that people can still experience improvement in the use of the affected side even years after their stroke, this is a revolutionary concept,” said Dr. Leonardo Cohen, chief of the human cortical physiology section at the National Institute of Neurological Disorders and Stroke. “The new approach, now being studied across the country, provides for the first time a treatment alternative for stroke patients, at a time when it was thought there was no treatment.”

One scientist who is not surprised at the way the new therapy is catching on is Taub. Back in the 1970s, Taub began working with monkeys who had had the sensory nerves surgically cut in one arm, but not the motor nerves. The monkeys could feel nothing in the bad arm, but the nerves that control movement were still intact.

Typically, Taub said, the monkeys learned that the bad arm was useless because they couldn’t feel anything. They’d try to move that arm, fail, and soon stop trying, a lesson that Taub calls “learned non-use.”

But, when he put a straightjacket on the monkey’s good arms, the results were remarkable. The animals started using their bad arms within two hours, Taub said, and, after just a week of training, used them fairly normally for the rest of their lives, even when their nerves had been injured as long as four years before treatment.

Recently, Taub and others have achieved similar results in people up to 21 years after they have survived strokes. So far, the method has been tried in about 200 patients.

In research published in June in the journal, Stroke, Taub, working with a German team led by Dr. Joachim Liepert, studied 13 people who had had strokes at least six months earlier and found that they were able to regain75 percent of their arm movement with constraint-induced movement therapy.

Moreover, a brain-mapping technique called Transcranial Magnetic Stimulation, or TMS, showed that, after constraint therapy, the part of the brain that controls the stroke-affected arm doubled in size, getting back nearly to normal.

That suggests that the damaged part of the brain might actually be coaxed to work again. In addition, the constraint therapy seems to boost activity in the side of the brain that does not control the paralyzed limbs. (Normally, the right side of the brain controls the left side of the body, so a stroke in the right brain may paralyze the left arm and leg.) That suggests that, for a person who had a stroke in the right brain, the left brain might be coaxed to take over the right’s work.

TMS does more than just show scientists what’s going on in the brain. It can also be used to change the pattern of electrical activity in parts of the brain, a technique that has already been used to treat severe depression.

In TMS, a coil of wire is placed on the head and an electrical current is passed through the wire in a rapid on-off pattern. That triggers a brief magnetic pulse that excites nerves in a specific region of the brain. Depending on how rapidly the current is turned on and off, the magnetic pulse can either increase or block nerve activity in the targeted brain area, explained Dr. Alvaro Pascual-Leone, director of the laboratory for magnetic brain stimulation at Beth Israel Deaconess Medical Center in Boston.

This suggests that, perhaps even without constraint therapy, TMS could be used to rewire the brain and restore movement to paralyzed limbs, though this has not yet been shown. And there’s one big caveat: Scientists must learn to control TMS sufficiently so that they don’t inadvertently block nerve activity where they’re trying to increase it. “That could actually make the outcome worse,” Pascual-Leone said.

For the immediate future, though, constraint therapy is grabbing the attention of patients and researchers, even though most insurers do not yet cover the technique.

At the National Institute of Neurological Disorders and Stroke, Cohen is analyzing the results of a controlled trial to see whether the constraint therapy is superior to conventional therapy, in which the patient is relatively passive and the therapist moves the patient’s paralyzed arm or leg.

At Emory University in Atlanta, neuroscientist and physical therapist Steven Wolf has begun enrolling 240 patients at seven medical centers around the country in a constraint therapy study called the EXCITE trial.

Like Taub’s monkeys, people learn not to use their weak arm or leg after a stroke, Wolf said, a problem made worse by the trend toward shorter hospital stays. Instead of being hospitalized for months as patients once were, most stroke victims are out in 14 days, which means “about the only thing a rehabilitation specialist can do is train people to get from the bed to the wheelchair,” he said. “That reinforces the notion of how not to use the impaired arm.”

In Boston, Judith Schaechter, who is both a neuroscientist and a physical therapist, has tried constraint therapy on four patients at Northeastern University. All four made clear gains, said Schaechter, who has moved her research to Massachusetts General Hospital.

One of her patients, Richard Mahoney, a 54-year-old Boston man who had a stroke last summer, barely used his right arm before constraint therapy. The treatment “helped me immensely,” he said. Now he uses his right hand all the time.

And Fred Kemp? After only three days of constraint therapy, he was able to open a refrigerator door with his bad left hand without having to think much about it. “I know I can open it. I couldn’t before.” The therapy is rigorous, he added. But it’s “going to be worth the effort to me to get something back.”

For more information on constraint-induced movement therapy, call:

  • The University of Alabama at Birmingham, Taub Training Clinic, at205-975-9799.
  • The EXCITE trial, headquartered at Emory University, at 404-712-2222 begin_of_the_skype_highlighting              404-712-2222      end_of_the_skype_highlighting.
  • Behavioral Neurorehabilitation Unit, Beth Israel Deaconess Medical Center, at 617-667-4074 begin_of_the_skype_highlighting              617-667-4074      end_of_the_skype_highlighting.

Plaque can gum up the works in legs

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Dr. Zdan Korduba, an anesthesiologist at St. Luke’s-Roosevelt Hospital Center in New York, wound up having one toe amputated, losing months of work and feeling like a total chump for missing symptoms he’d have spotted right away in a patient.

Beginning five years ago, he says ruefully, he began noticing that his legs hurt after tennis: “I got tremendous cramps, but I put it off as being out of shape.” Before long, he found he “couldn’t walk the same distance as before. I kept denying this to myself. My diabetes was not the best controlled, either.”

Seven months ago, he couldn’t even walk two blocks from the garage to the hospital without tremendous pain in his right leg. “It hit me I was in trouble. . .If a patient had come to me with these symptoms, I would have diagnosed it as peripheral vascular disease. But on yourself, you’re the worst patient there is. It was denial.”

Like Korduba, an estimated 10 million Americans, many of them over 50, have peripheral vascular disease, or PVD – clogged arteries in the legs (and occasionally, the arms) that trigger numbness or intense pain (a kind of “heart attack” in the legs) during even minimal activity. Many, like Korduba, are in denial, chalking up their pain to age or arthritis.

In fact, so many people go undiagnosed and untreated that, beginning today for a week, a coalition of medical organizations is taking the unusual step of offering free screening and referrals for peripheral vascular disease at 500 hospitals across the country, including three in the Boston area. (See sidebar for locations.)

Peripheral vascular disease is caused by the same phenomenon that clogs coronary arteries and triggers chest pain – atherosclerosis, the build-up of cholesterol-filled plaques. Just as angina, or chest pain, is a sign the heart isn’t getting enough oxygen-rich blood, especially upon exertion, leg pain after a minimal amount of walking means leg muscles are starving for oxygen, too.

And since atherosclerosis is a body-wide process, clogged arteries in the legs are often a sign that those that supply the heart and brain may be dangerously narrowed as well, notes Dr. Cameron Akbari , a vascular surgeon at Beth Israel Deaconess Medical Center in Boston.

In fact, if you have peripheral vascular disease and heart disease, you have six times the risk of dying of a heart attack as someone who has heart disease alone, says Dr. Rodney Raabe , director of radiology at the Sacred Heart Medical Center in Spokane, Wash., and co-director of the screening program “Legs for Life.”

But PVD can be a life-wrecker in its own right, too. It not only severely impairs mobility but can lead to skin ulcers and gangrene and ultimately, may require the amputation of toes, feet or legs, especially in diabetics, who are at high risk of circulatory problems to begin with, says Dr. Max Rosen , an interventional radiologist at Beth Israel.

Now, if you’re a reasonably active sort whose legs feel crampy after you overdo the weekend jock thing, don’t panic. There’s a world of difference between legs that feel sore the morning after a strenuous workout and legs that cramp up after a short walk across the kitchen or down the block. “People with PVD can’t do half an hour on the treadmill,” says Rosen.

PVD is also different from (though sometimes confused with) the leg pain that occurs during sleep, or sciatica, pressure on a major nerve to the leg caused by a ruptured spinal disk.

 The hallmark of PVD is the pain’s utter predictability. It comes on after a set amount of walking – often only a few minutes – and goes away when you stop, then starts up again when you walk the same distance again.

Screening for PVD is easy – and painless. The doctor or nurse simply takes your blood pressure on your arms and on your lower legs and calculates what’s called the ABI, or ankle-brachial index. The pressure should be roughly the same. If it’s lower in the legs, it means blood flow to the legs may be compromised.

If the screening shows you have or are at risk for peripheral vascular disease, you’ll be referred for further testing. This includes more sophisticated blood pressure monitoring all up and down on the legs and a “Doppler” ultrasound test as well.

This non-invasive test shows how fast blood is moving through blood vessels; if it speeds up in one spot, it means the blood is rushing to get through a narrowed area. If there’s no flow at all, that’s obviously even bigger trouble.

For some people, doctors may also recommend an angiogram, in which they thread a small catheter through an artery in the groin, inject dye, and watch on an X-ray screen to see where blood vessels narrow dangerously.

If you’re diagnosed with mild peripheral vascular disease, the remedy, believe it or not, may be to walk through the pain to force collateral blood vessels to take up the slack and, over time, supply leg muscles with oxygen. People with PVD are often given aspirin, too, notes Dr. Mitchell Rivitz , a radiologist at Newton-Wellesley Hospital. Aspirin makes blood less likely to clot as it travels through narrowed areas of blood vessels.

If those remedies don’t help, doctors can perform balloon angioplasty just as they would for a clogged coronary artery. They insert a small balloon-tipped catheter into the artery under X-ray guidance, inflate the balloon and push apart the artery walls to let more blood flow through.

They may also insert a stent, a metal device that stays in the narrowed area to keep the vessel open, or perform bypass surgery, stitching a small segment of vein taken from elsewhere in the patient’s body to carry blood around the bottleneck in the artery. If the narrowing of the artery is caused by a clot, they may inject clot-busting drugs like t-PA.

Some doctors are also experimenting with injections into the legs of a gene for vascular endothelial growth factor, a protein that causes new blood vessels to grow in the area. They’re also working on using radiation along with stents to stop vessel narrowing.

When Dr. Korduba finally consulted a surgeon, he recommended walking through the pain. It worked, for a while. He kept playing tennis, too, “not well, but I was playing.”

Then, he says, he got a blister on his little toe “which I did not pay attention to.” The pain soon spread to his foot. Before long, his wife noticed a black spot right under the blistered toe. He went back to his surgeon, who admitted him to the hospital immediately.

He had angioplasty, which increased blood flow in his leg overall. But he still had a gangrenous, black spot – dead tissue – in his toe, so the next day, he had surgery to have the toe amputated so that it didn’t cause a life-threatening infection. To make sure the wound drained as it healed, doctors did not close the incision.

That meant staying home from work – it’s been two months so far – and having a nurse come twice a day to clean and pack the wound. “I’m Dr. Mom now,” says Korduba, who spends a lot of time helping his kids with their homework.

And he’s learned two things. “I have now become a kinder and gentler doctor. I’ve been practicing for 29 years, and you get a little jaded. You forget the patient is not just a patient but a human being. When you start looking at the ceiling from a stretcher, you become restless and agitated with any little delay. . . .I’ve certainly learned a lot being a patient.”

He’s also got new respect for how serious peripheral vascular disease can be and for the dangers of denying it. “That denial is the worst thing. This is a sneaky disease. When you get the symptoms, you’re in trouble.” He’s “not looking for glory” by telling his story, he adds. “This is not my finest moment.”

Risks for vascular disease

You are at higher than normal risk for peripheral vascular disease if you are over 50, male or a smoker. Other risk factors include high blood pressure, diabetes, high cholesterol, a family or personal history of heart or vascular disease and being overweight.

Signs that you may already have PVD include leg cramps when you walk that go away when you rest, cold feet and ulcers or sores on your feet that are slow to heal.

To schedule an appointment at a hospital offering free “Legs for Life” screening this week for peripheral vascular disease, check the web under www.legsforlife.org. (Local libraries can help if you don’t have access to a computer.) For a brochure on the program, call 1-877-357-2847 begin_of_the_skype_highlighting              1-877-357-2847      end_of_the_skype_highlighting.

Eight medical centers in Massachusetts are participating in the screening, including three in the Boston area: Beth Israel Deaconess Medical Center (617-667-8194 begin_of_the_skype_highlighting              617-667-8194      end_of_the_skype_highlighting), Newton-Wellesley Hospital (617-243-6800 begin_of_the_skype_highlighting              617-243-6800      end_of_the_skype_highlighting), and North Shore Hospital in Salem (978-741-1215 begin_of_the_skype_highlighting              978-741-1215      end_of_the_skype_highlighting).

The screening is sponsored by the Society of Cardiovascular & Interventional Radiology and supported by the American College of Foot and Ankle Surgeons, the American Radiological Nurses Association and the Society for Vascular Nursing.

Picturing heart disease another way

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Richard Knorr’s heart is making medical history.

But there’s actually not much that’s unusual about it. Though two of his coronary arteries are partially blocked, the 64-year-old Framingham man has never had a heart attack and he can control his chest pain with medications.

Still, doctors are fascinated by his heart, and those of a handful of other coronary patients at Beth Israel Deaconess Medical Center in Boston, because they’ve found what seems to be a safe, painless, noninvasive way to detect heart blockages.

If the researchers, led by Dr. Warren J. Manning, co-director of the hospital’s Cardiac MRA Center, are right, the imaging technique – called 3-D coronary magnetic resonance angiography – could someday replace standard angiography. In this invasive procedure, doctors thread a catheter through an artery in the groin up to the heart, inject iodine dye through the catheter, and then view X-ray images of the arteries on a monitor, enabling them to see blockages.

Magnetic resonance imaging has actually been in use for about 10 years to scan blood vessels, but it’s mainly used in parts of the body, such as the brain, that don’t move. Imaging the heart and coronary vessels has proved tougher because of the blurring that’s caused by each heartbeat and respiration.

Indeed, imaging coronary vessels is “the holy grail of MR angiography,” says Dr. William Palmer, clinical director of magnetic resonance imaging at Massachusetts General Hospital.

If an international study now underway confirms Manning’s preliminary findings, which were published recently in the journal Circulation, the technique could be available in a couple of years, Manning says, though others think that’s too optimistic.

It’s also possible that the technique will not be able to match the 90 percent accuracy of standard angiography, warns Dr. Robert Herfkens, director of Magnetic Resonance Imaging at Stanford University.

Like 1.7 million other Americans who will have a coronary angiogram this year, Knorr can vouch for the fact that the current tests are no fun. The first time was “very, very intimidating,” says Knorr, who has had it done twice.

Most serious is the risk of heart attack, stroke or death, which occurs less than 1 percent of the time, says Dr. Peter Danias, a Beth Israel cardiologist and co-author on Manning’s paper. But there’s also risk of artery damage and bleeding from the incision where the catheter is inserted. To minimize bleeding, patients must lie still for four to six hours after an angiogram.

On top of that, some patients have allergic reactions to the dye (or “contrast agent”) injected to highlight the image of the arteries. And the radiation from the X-rays needed to “see” the arteries can damage tissue.

No wonder, then, that researchers have been scrambling for safer, noninvasive alternatives.

One hope is improved CT (computerized tomography) scans, though like regular angiograms, CT angiograms involve radiation (taking a series of X-ray slices that a computer stacks into 3-dimensional images) and injections of a contrast agent.

Newer, so-called fast CT scans that take four X-ray slices at once may be particularly useful for cardiac problems because they can be timed to get images of the heart between beats, says Dr. Andre Duerinckx , chief of cardiovascular magnetic resonance imaging at the Greater Los Angeles Health Care System.

Another alternative might be ultrasound, in which sound waves are bounced off the body and reflected back as an image. But sound waves don’t penetrate deeply enough to “see” coronary arteries, so this technique is mainly used to scan superficial vessels like the carotid arteries in the neck or veins in the leg.

In magnetic resonance, or MR, the patient is placed in a strong magnetic field and radio waves are sent into the body. This causes changes in the alignment of protons, or hydrogen atoms, the building blocks of molecules.

When the radio waves are stopped, the protons fall back into alignment with the magnetic field; in doing so, they send out their own radio waves, which are detected and used to create an image. With MR, doctors can track the flow of blood through vessels and the anatomy of the vessels as well, looking for spots where the flow is blocked by clots.

Several years ago, Manning’s team showed that coronary MR angiography could yield images if the patient held his breath repeatedly for 20 seconds or so at a time. Now, partly by tweaking the computer software, Manning’s new research shows it’s possible to get better images, at least in parts of arteries closest to the heart, without patients having to hold their breath.

In a tiny group of patients – Richard Knorr and four others – with known coronary disease, the MR scans corresponded “very well” with results from traditional angiograms, Manning says.

Still, MR imaging of the coronary arteries is “not ready for prime time” and may never be “comparable in quality” to standard angiograms, cautions Palmer of MGH, whose team is also working on the MR techique. In fact, because of the magnetic field, MR is not safe for people with pacemakers and some people with metal clips in their brains to treat aneurysms. MR may be safe for some of those who have metal stents implanted to keep arteries open.

But MR can only diagnose a clogged artery, not treat it. With standard angiography, doctors can not only image arteries but insert stents or use a balloon to compress artery-clogging clots as part of the procedure.

And while standard angiography can detect blockages anywhere in coronary arteries, so far MR works best at spotting problems only near the aorta, the heart’s largest artery.

Although one advantage of MR is that it can be done without a contrast agent, doctors sometimes inject a substance called gadolinium to make blood vessels show up better on scans. A new generation of contrast agents may further improve coronary MR, says Herfkens of Stanford.

But even in its current stage of development, the MR technique already has one enthusiastic fan: Richard Knorr. With each standard angiogram, he had to make two trips to the hospital – one for preliminary blood tests and one for the angiogram itself. With the standard angiogram, he says, “you’re confined all day in an OR,” compared to just an hour or so with magnetic resonance.

And with standard angiograms, he says, “you’re surrounded by three, four, five people getting you ready. . .I don’t want to put them out of a job, but. . ..”

Stress of surgery hard on the heart

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Dorothy Teixeira, a 76-year-old Peabody woman who had a history of chest pains, got even more bad news last summer: She had colon cancer and needed surgery.

In many hospitals, Teixeira would have been taken off her heart medications during and after surgery because of the fear that the drugs – called beta-blockers – might make her heart too sluggish.

But her doctor at Beverly Hospital, Dr. Lawrence Shinbaum, is one of a growing number of anesthesiologists who feel that not only should patients like Teixeira not be taken off beta-blockers, but that many others should be put on the drugs just before and for a week or so after surgery to reduce the risk of cardiac complications.

The issue can be a matter of life and death – but it’s hotly controversial as well.

Two years ago, Dr. Dennis T. Mangano, an anesthesiologist at the VA Medical Center in San Francisco, published a study of 200 patients who had heart disease or were at risk of it and were having noncardiac surgery. He found that atenolol, a beta-blocker, reduced the overall risk of death by 55 percent and the risk of death specifically from cardiac causes by 65 percent. The benefit was most pronounced in the six months after surgery, but persisted for two years.

“We were surprised,” says Mangano. It’s “very exciting.”

Given that 30 million Americans a year have noncardiac surgery and 3 million of them are at high risk for heart disease, wider use of atenolol – and presumably, other beta-blockers – could prevent thousands of deaths a year, he argues.

The problem is that, aside from some supporting research, Mangano’s study is the main evidence that would cause doctors to use beta-blockers more widely for this purpose, and many say that’s just not enough information to act on.

Mangano’s data “are suggestive because it’s such a well-done study, but it is still a relatively small study,” says Dr. Edward Lowenstein, a cardiac anesthesiologist at Massachusetts General Hospital.

Worse yet, it’s unlikely that much more data will be forthcoming, because many beta-blockers are now sold as generic drugs, and manufacturers have little incentive to fund the larger studies that could settle the issue.

That means doctors have to go with their guts on this one, and their guts are telling them vastly different things.

The nay-sayers stress that beta-blockers carry some risks – notably they can exacerbate asthma and suppress heart beat and blood pressure, especially in patients who have failing hearts.

Dr. Lee Fleisher, an anesthesiologist at Johns Hopkins Medical Institutes in Baltimore, for instance, agrees that heart function should be closely monitored and controlled during and after surgery. But he argues there’s too little data to recommend that beta-blockers be used more routinely in surgery.

Dr. Thomas Graboys, director of the Lown Cardiovascular Center at Boston’s Brigham and Women’s Hospital, puts it more bluntly. If a person is at risk for heart disease, he “should be on beta-blockers whether he’s having surgery or not,” he says. But giving beta-blockers routinely to surgical patients is risky because of the chance that the drugs might overly suppress heart rate and blood pressure.

On the other side, beta-blockers in general “are safe and have been administered . . .to hundreds of thousands of people,” argues Dr. Peter Rock, an anesthesiologist at Washington University in St. Louis, who advocates wider use of the drugs for surgical patients.

The American College of Physicians agrees. In 1997, it recommended that all surgical patients with heart disease or at risk for it take beta-blockers around the time of surgery, unless there is a strong reason not to.

Last year, the journal Anesthesiology threw its weight behind beta-blockers, too, in an editorial that concluded that “the majority of patients with risk factors for coronary artery disease should be treated with at least some type of [ beta] -blocker” at the time of surgery.

The reason is that surgery is a huge stress on the body.

 “Having an operation triggers a cascade of stress hormones,” including adrenalin, which makes the heart beat more strongly and rapidly, says Dr. Daniel Carr, vice chair for anesthesia research at the New England Medical Center. “Even if the person is unaware that his body is being operated upon because of general anesthesia, these primal reflexes are still present.”

And the stress from surgery, particularly on the heart, continues after a patient wakes up. “It’s like being on an exercise treadmill for five days,” says Mangano, “even when pain, a notorious stressor, is well-controlled.”

In fact, peak heart attack risk comes three days after surgery, says Dr. James B. Froehlich, co-director of vascular medicine at the University of Michigan Medical Center in Ann Arbor. That’s when fluids that have leaked from blood vessels into injured tissues seep back into circulation, increasing the workload of the heart.

The adrenalin surge that occurs during surgery also has a lingering effect on platelets, which become stickier and more likely to form clots that can clog coronary arteries. Surgical stress also causes the fatty plaque that lines artery walls to become unstable, which means that the pieces of the plaque can break off and block coronary arteries, even months later.

All of this has persuaded many doctors to lean toward wider use of beta-blockers for surgical patients with heart disease risk. “Even if the effect is half of what Mangano found, it’s still unbelievable,” says Shinbaum, the Beverly anesthesiologist.

Mangano puts it bluntly: “If we demand further studies, it will take three more years, during which time hundreds of thousands of patients will be deprived of an outstanding therapy and might die.”

Dorothy Teixeira isn’t about to argue with that. She had no heart problems during or after her colon surgery, she says. And despite having chemotherapy for her cancer, she says, “I went out New Year’s Eve. I’m doing pretty good, considering.”

What to ask the doctor

Things to talk to ask your doctor about if you have heart disease, or are at risk of it, and are facing noncardiac surgery:

  • Make sure everyone on your team – your internist, your surgeon and your anesthesiologist – know about your heart disease risk and all medications you are taking.

  • Ask how the stress of surgery may affect your heart and whether the risks of surgery outweigh this risk.

  • If you’re already on beta-blockers and any doctor on your team suggests stopping them around the time of surgery, ask why. – If you’re not on beta-blockers, ask if you should be and whether you should start before and continue after surgery.

  • Before you’re discharged, ask how well your heart tolerated the surgery and whether you should take beta-blockers at home.

For more information on the arguments for using beta blockers, you may call the Safe Surgery Hotline, 1-800-700-2617 begin_of_the_skype_highlighting              1-800-700-2617      end_of_the_skype_highlighting, organized by Dr. Dennis T. Mangano at the Ischemia Research and Education Foundation in San Francisco. There is believed to be no comparable site on the other side of the controversy.

Mining veins – Endoscopy emerging as safer, less painful way to gather grafts for coronary bypasses

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It’s early afternoon, a perfect spring day. Outside the UMass Medical Center, employees savor the last of their lunch break, faces tipped toward the sun, legs splayed on the grass.

Inside, in operating room 3, Evelyn Kolat, 74, lies inert, dwarfed by a vast array of surgical instruments, anesthesia paraphernalia, and a heart-lung machine.

2:10 p.m. The OR team proceeds gingerly. Kolat’s heart rhythm is unstable, so Dr. Ellie Duduch, the anesthesiologist, induces sleep slowly. As Dr. Robert Lancey, the surgeon, waits, he takes a last look at her angiogram, noting where blood flow to her coronary arteries is blocked.

2:42 p.m. Stable now, Kolat is deeply asleep. Duduch slips a breathing tube down her throat. Lancey gowns up. Nurses scrub Kolat’s chest and both legs.

Kolat is about to join the nearly 400,000 Americans who have coronary artery bypass surgery every year.

In most of these operations, a long incision – from knee to groin and often ankle to knee as well – is made to “harvest” a vein that will be cut into segments and stitched onto coronary arteries to bypass damaged areas. After surgery, patients often have more pain and infection from leg wounds than from incisions made in the chest through the breastbone to get to the heart. This is in part because fatty leg tissue does not have as good a blood supply as the chest.

But Kolat, like an estimated several thousand patients worldwide, has opted for a new technique – endoscopic vein harvesting, in which a member of the surgical team, usually a physician’s assistant, makes from one to three tiny incisions in the leg, slides a long viewing tube along the outside of the vein, snips off side branches that feed the vein, then slips the vein out.

2:56 p.m. Donna Iddings, a physician assistant, makes the first cut, a one-inch incision inside Kolat’s right knee. Moments later, Lancey, who has done 30 bypass operations in which the vein was harvested the new way, begins slicing open Kolat’s chest.

Endoscopic vein harvesting takes longer – an hour or more, if the physician’s assistant is new at it, versus 20 to 40 minutes for the traditional method. It costs more, too, in part because the disposable endoscopy kits – several are on the market – cost $ 300 to $ 500. Some proponents say that the costs of these kits may be offset by shorter hospital stays and fewer post-operative complications.

Granted the endoscopic technique doesn’t always work perfectly, but surgeons who try it are enthusiastic, as are patients.

Gaston Poudrette, a 64-year-old Leominster man who had the surgery in March, says his leg looks good and healed fast.

At the Lahey Clinic in Burlington, Dr. Richard D’Agostino, who has done seven operations with the technique, thinks “it will become the norm soon. It’s a significant advance.”

Dr. Willard Daggett says it’s clear from his 103 patients at Massachusetts General Hospital and St. Vincent’s Hospital in Worcester that the endoscopic procedure reduces infections, leaves minimal scars and that “patients love it.”

In fact, he says, while endoscopic surgery on the heart itself – using tiny incisions in the chest rather than opening the sternum – has captured more headlines, it is endoscopic vein harvesting that may prove more widely applicable. The minimal heart technique is chiefly for people who need only one coronary artery bypass and so far, the results have not been as good as the standard, open-chest surgery. By contrast, endoscopic vein surgery could help most bypass patients.

It’s so new – many hospitals have only offered it for a few months – that the data are mostly unpublished, but provocative: At the Indiana Heart Institute in Indianapolis, a published study of 112 patients – half were randomly chosen to have the new technique, half the old – showed that only 4 percent of those who had the new procedure got leg infections while 19 percent of the others did, says Dr. Keith Allen. Those who had the new procedure also left the hospital a day earlier.

At Chippenham Medical Center in Richmond, Va., physician assistant Nan Lambert has done more than 100 endoscopic vein surgeries and has compared them to the old technique. Nobody who had the new technique needed antibiotics or special care for leg wounds, but 5.8 percent of the others did.

At Hahnemann University Hospital in Philadelphia, Michael Butler, a physician assistant, has compared 25 patients who got the new technique and 25 who had the old one. Less than one percent of those who got the new procedure had leg infections, but 5 percent of the others did. The first group also had no leg swelling, while 42 percent of the second group did.

3:08 pm Iddings probes Kolat’s incision with her fingers, trying to find the vein. No luck. Lancey saws through Kolat’s sternum, then turns to help Iddings. He can’t find the vein either.

3:13 pm They find it. Lancey returns to Kolat’s chest, using a metal device to spread open the sternum. Iddings inserts a long tube with a camera attached into the leg incision.

3:17pm Trouble. The light doesn’t work. They fix it. Now there’s an image on the TV screen, but it’s bad. They call for new equipment. It comes, but the image is still blurry. Another call for help.

3:34pm Another nurse arrives, takes one look at the image, swears softly, and decides the problem is moisture on the lens of the camera in the endoscope. They clear it. Now the image is beautiful.

3:38 pm Iddings inserts the endoscope and squirts in carbon dioxide to expand the tissue around the vein. Her eyes glued to the TV screen, she begins snipping off the tiny branches that connect to the leg vein.

4:00 pm With the vein nearly free, Iddings makes an incision in Kolat’s leg at the groin, to tie off the end of the vein that will stay in the body.

4:15 pm They pull the vein out. It looks fragile and barely the diameter of spaghetti at one end, smaller than they’d hoped for.  Some veins, in fact, are simply too small to use, says Phillip Carpino, a physician assistant at New England Medical Center. But endoscopy can also “shred” veins, he says, especially in smaller, older women. “You have to be careful about the patients you select.”

4:16 pm Lancey mutters about the “poor quality” of this vein but places it on a drape over the patient’s chest and begins the painstaking process of fixing leaks, which he detects by repeatedly injecting a solution into the vein. For the next 41 minutes, he stitches up tears, many of which soon leak again. Finally, he cuts off and discards the worst part, saying “We can’t take a chance on using it if it’s too thin-walled.” He only nods to Iddings, but she understands.

4:56 pm Quickly, she begins slicing open Kolat’s other leg – this time from the groin to the knee. In barely 15 minutes, she’s removed a long stretch of vein. This one looks plump and healthy. The team relaxes palpably.

5:10 pm “Ready to go on bypass,” says surgeon Lancey. The heart-lung machine, already hooked up, will keep Kolat’s blood circulating for the next 93 minutes whirs.  Lancey stops the heart with a potassium injection. He works quickly, using two segments of leg vein to bypass two arteries. For the third bypass, he severs one end of the nearby internal mammary artery and connects it to the heart.

6:40 pm Kolat is off the heart-lung machine, her own heart back at work.

7:40 pm It’s over. She’s on her way to intensive care.

Four days later, she’s home, her left leg bearing a long incision, her right leg, two tiny ones. If endoscopy proponents are right, her right leg should be less painful than her left.

But surgery is art as well as science and Kolat refused to bow to mere statistics. The truth is that “neither one hurts!”

The other heart attack risks – Anger, grief, fear

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But just as you can protect against physical triggers, you can protect against the dangers of emotional stress

Fifteen years ago, at 10:53 on a February evening, the people of Athens were jolted by an earthquake that measured 6.7 on the Richter scale. Within an hour of the quake and for three days afterwards, terrified Athenians were dropping dead at more than twice the normal rate.

This suggested, at least to Harvard School of Public Health epidemiologist Dimitrios Trichopoulos, that mental stress had triggered the increased deaths, most of them from heart attacks.

Back in 1983, when Trichopoulos published his findings in a medical journal, the notion that strong emotions could trigger a nearly-instant heart attack was anathema to many doctors, though lay people were often inclined to believe it.

Although it had been popular since the mid-70s to think that people with hard-driving “Type A” personalities were more prone to heart attacks than others, these early attempts to link emotions to heart disease had looked mainly at lifelong traits, not at a person’s mood right before a heart attack.

But after years of focusing on longterm personality styles and chronic physical factors like high blood pressure and cholesterol, researchers are now finding considerable evidence that heart attacks can be “triggered” by immediate events as well, including powerful emotions like grief, fear and anger in the hours before an attack.

Lest merely reading about such triggers set hearts dangerously aflutter, a bit of perspective:

“We all have stressful experiences and most of us don’t have heart attacks” because of them, points out David S. Krantz, a medical psychologist at the Uniformed Services University in Bethesda.

Furthermore, most of the people who do have a heart attack after an identifiable triggering event have underlying heart disease that puts them at higher risk, says Dr. James Muller, chief of the cardiovascular division at Deaconess Hospital.

“And even people with underlying heart disease may not be vulnerable to a trigger, including emotional stress, at any given moment,” he adds.

Yet heart specialists are taking emotional triggers increasingly seriously because both mental stress and cardiovascular disease are so common. Cardiovascular disease is the No. 1 cause of death in America, killing one person every 34 seconds. About 1.5 million Americans have a heart attack every year, and a quarter of a million die before reaching a hospital.

Futhermore, evidence is mounting that emotions can trigger heart attacks, especially in people with heart disease. The primary villains:

— Anger. Last year, in a study of more than 1,600 heart attack survivors, Dr. Murray Mittleman and others at Deaconess found that in the two-hour period after someone feels intense anger, heart attack risk more than doubles, just as it does in the two hours after sex.

To be sure, says Mittleman, because the baseline risk of a heart attack is about one in a million for a healthy 50-year-old man in any given hour, this means anger — or sex — temporarily raises the risk to just 2 in a million, a seemingly small hazard. For people with known heart disease, the average baseline risk is 10 in a million in any given hour; anger or sex raises it to 20 in a million.

“But while this may seem trivial,” he says, “it’s not, because people get angry far more often than they have sex.”

In fact, people who are chronically angry — especially those with what researchers now call a “hostile” rather than a Type A personality — are at increased risk of dying not just from heart attacks but from all causes, says Dr. Redford Williams, a Duke University internist and author of the 1993 book, “Anger Kills.”

Hostility is defined as an unlovely combination of cynicism, anger and aggressiveness.

— Grief. In a study of 1,774 heart attack patients reported at an American Heart Association meeting, Mittleman found that the death of a loved one raises the risk of heart attack 14-fold for the next 24 hours — significantly more than anger or sex.

As with anger and sex, grief seems to pose the greatest risk for people with underlying heart disease. But unlike anger and sex, the heightened risk from grief declines very slowly, often persisting a month or more, albeit at ever-lower levels.

— Fear. Israeli researchers reported last year that on the January day in 1991 that the SCUD missile attack began during the Gulf War, there was a marked increase in deaths, even though nobody died of injuries caused by the missiles.

Most of the deaths were attributed to cardiovascular disease, including sudden cardiac death, which can be caused by blockages in arteriesor by abnormal heart rhythms. This year, other researchers also found the incidence of sudden cardiac death was higher in the first 10 days of the Gulf war, but not enough to be statistically significant.

Yet researchers say there is virtually no question that fear played a role in the nearly 5-fold increase in deaths from cardiac causes on the day of the 1994 Los Angeles quake.

— Stress. This month, Duke University researchers led by psychologist James A. Blumenthal found that stress — like public speaking anddoing arithmetic — significantly increased the risk of potentially fatal heart problems and ischemia, or decreased blood flow to the heart, at least in people who have heart disease and score poorly on exercise treadmill tests.

The more researchers study emotional triggers of heart attacks, the more they think mental stresses affect the heart in ways different from physical stresses like sudden exertion.

Both types of stress cause a surge of hormones, including adrenalin and noradrenalin, that make blood pressure and heart rate soar. The increase in the force and flow of blood through arteries can cause fatty plaques in artery walls to rupture, allowing clots to form and block blood flow to the heart.

Adrenalin can also trigger potentially fatal disturbances in heart rhythm, especially in people with heart disease. And it can make platelets in the blood more likely to clot and cause spasms in arteries, causing them to constrict too much.

In healthy people, a physical stress like running makes the arteries dilate, sending more blood to the heart to meet its increased demand, says medical psychologist Krantz.

But in someone with coronary artery disease, the arteries do not dilate properly, which means the heart gets too little blood. Angina, or chest pain, often results.

With emotional stresses, however, the heart does not “demand” as much blood as it does with physical stress, says Krantz. But because blood vessels often constrict in emotional stress, the heart may still get less blood than it needs.

Unlike ischemia caused by physical stress, ischemia from emotional stress is more often painless.

Fortunately, researchers are finding ways to reduce heart attack risk from both physical and emotional causes.

To combat longterm, chronic risk, Mittleman says, the old standbys still hold: Quit smoking, eat sensibly and exercise to keep blood pressure and cholesterol down.

In fact, if you’re sedentary and have heart disease, regular exercise can virtually abolish the risk of heart attack from sudden exertion.

And if it’s acute triggers like anger that worry you, there’s also lots you can do, including taking aspirin.

“It’s like the straw the broke the camel’s back,” says Mittleman. “The longterm, chronic things like high blood pressure are the straws that have accumulated over time.

“Anger or other strong emotions can be the final trigger. But it’s all the risk factors together that determine whether or when a heart attack occurs.”

SIDEBAR:

You can reduce your risk

 To reduce risk further, you might also consider taking aspirin — if your doctor agrees. Aspirin can reduce chronic heart disease risk, probably by making it harder for the blood to clot, and there is evidence it protects against damage from anger, too.

Other drugs, including beta-blockers that dampen the effect of adrenalin and calcium channel blockers that dilate blood vessels, may also combat heart problems triggered by emotional stress, researchers say, though this has not been proven.

Psychological approaches may also reduce risk.

Recent research has shown that socially isolated people fare more poorly after a heart attack than others. That has prompted a consortium of researchers from Harvard, Yale and other centers to begin a study called ENRICHD to see if cognitive or group therapy improve outcomes in such people after a heart attack.

Dr. Herbert Benson, president of the Mind/Body Institute at Deaconess Hospital, advocates “the relaxation response” to offset emotional stress. If you meditate for 10 to 20 minutes a day for several weeks, he says, the stress hormone adrenalin has less effect. People who meditate also get less angry, he says.

And if you do get angry, how you manage that anger counts, too, says Mara Julius, a psychosocial epidemiologist emeritus at the University of Michigan School of Public Health.

The evidence is mixed, but she says expressing anger may be more healthful keeping it in. The best approach, she says, may be to practice “reflective coping” — rationally trying to solve the problem that prompted the anger in the first place.

Dr. Redford Williams, a Duke University internist, says when you get angry, you should ask yourself three questions:

— Is this really important to me?

— Is my anger appropriate to the situation?

— Is there anything I can do to fix the situation?

If you answer no to any one of these, just chill out.

If you answer yes to all three, he says, “action is called for. If it’s a problem with another person, the solution is to be assertive, rather than blowing up or screaming.”

“If it’s a situational problem and there is no other person to be assertive with, like when an airline cancels your flight, go out and run to discharge adrenalin,” he says, and if you can’t do that, meditate or think about your next vacation.

“This is all damage control when you’re angry,” he says. But it’s better to reduce anger in the first place, which may be easier than you think.

Regular physical exercise — such as walking 20 minutes a day — has long been known to reduce longterm risk factors like high blood pressure and high cholesterol. More recent data suggests regular exercise also buffers the heart against acute “triggers” like sex or sudden exertion. 

SIDEBAR:

You can reduce your risk

 

To reduce risk further, you might also consider taking aspirin — if your doctor agrees. Aspirin can reduce chronic heart disease risk, probably by making it harder for the blood to clot, and there is evidence it protects against damage from anger, too.

Other drugs, including beta-blockers that dampen the effect of adrenalin and calcium channel blockers that dilate blood vessels, may also combat heart problems triggered by emotional stress, researchers say, though this has not been proven.

Psychological approaches may also reduce risk.

Recent research has shown that socially isolated people fare more poorly after a heart attack than others. That has prompted a consortium of researchers from Harvard, Yale and other centers to begin a study called ENRICHD to see if cognitive or group therapy improve outcomes in such people after a heart attack.

Dr. Herbert Benson, president of the Mind/Body Institute at Deaconess Hospital, advocates “the relaxation response” to offset emotional stress. If you meditate for 10 to 20 minutes a day for several weeks, he says, the stress hormone adrenalin has less effect. People who meditate also get less angry, he says.

And if you do get angry, how you manage that anger counts, too, says Mara Julius, a psychosocial epidemiologist emeritus at the University of Michigan School of Public Health.

The evidence is mixed, but she says expressing anger may be more healthful keeping it in. The best approach, she says, may be to practice “reflective coping” — rationally trying to solve the problem that prompted the anger in the first place.

Dr. Redford Williams, a Duke University internist, says when you get angry, you should ask yourself three questions:

— Is this really important to me?

— Is my anger appropriate to the situation?

— Is there anything I can do to fix the situation?

If you answer no to any one of these, just chill out.

If you answer yes to all three, he says, “action is called for. If it’s a problem with another person, the solution is to be assertive, rather than blowing up or screaming.”

“If it’s a situational problem and there is no other person to be assertive with, like when an airline cancels your flight, go out and run to discharge adrenalin,” he says, and if you can’t do that, meditate or think about your next vacation.

“This is all damage control when you’re angry,” he says. But it’s better to reduce anger in the first place, which may be easier than you think.

Regular physical exercise — such as walking 20 minutes a day — has long been known to reduce longterm risk factors like high blood pressure and high cholesterol. More recent data suggests regular exercise also buffers the heart against acute “triggers” like sex or sudden exertion.

Loneliness Can Be The Death Of Us

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A little over 100 years ago, a small band of Italians left Roseto Val Fortore, a village in the foothills of the Apennines, in hopes of a better life amid the slate quarries of eastern Pennsylvania.

Naming their new village Roseto, the group soon recreated the strong community ties they had nurtured in Italy. They lived in three-generation households, centered their lives on family and built their houses so close together that all it took to have in a neighborly chat was a walk to the front porch.

By the 1960s, Roseto stood out like a distinctly un-sore thumb, becoming a magnet for researchers. While Roseto shared the same water supply, doctors and hospital with nearby villages, the town had only 40 percent as many heart attack deaths.

At first, researchers thought the Rosetans might carry some special, protective genes. But this was not the case, for Rosetans who moved away — even to the nearby village of Bangor — lost whatever magic the town possessed against heart disease.

That magic, now known as “the Roseto effect,” is as simple as it is elusive in America today: Close ties to other people.

A growing body of data shows that closeness with other people has a strong protective effect against illness and death. And that the lack of such ties — social isolation — can kill just as surely as smoking, obesity or high blood pressure.

That is one of the conclusions of a new book, “Overcoming Loneliness in Everyday Life,” due out in June by a husband and wife team of McLean Hospital psychiatrists, Jacqueline Olds and Richard Schwartz, and journalist Harriet Webster.

Loneliness is no longer just a painful experience, but a “major public health problem,” says Schwartz, “and most psychiatrists haven’t registered the strength of the medical data on this.”

In 1950, only 10 percent of households consisted of just one person, according to census figures. By 1994, this number had soared to 24 percent. That means 12 percent of the adult population now lives alone.

And this trend is particularly strong among older people, who are more likely than ever before, and more likely than younger people, to live alone. While fewer than 10 percent of people aged 25 to 44 live alone, census data show, nearly a quarter of those 65 to 74 do, and 40 percent of people 75 and older.

While some people certainly maintain a high level of happiness — about three in 10, in fact, according to surveys by University of Chicago researchers cited in the May issue of Scientific American — others are clearly lonely. A 1990 Gallup poll found that more than 36 percent of Americans are lonely.

For many people, the worst part of loneliness is that it is often accompanied by shame. It is not okay in this culture to feel lonely, Olds and Schwartz write in their book, “because American culture prizes self-sufficiency above all else.”

“Our notion of success is being able to purchase what you need and not be obligated to anyone,” Schwartz explains in an interview.

“Yet in other cultures,” Olds adds, “people have always accepted leaning on each other as part of life.”

The mere fact of living alone, of course, does not mean a person is destined to be lonely, though it probably does increase the odds, notes Dr. Gene Cohen, director of the Center on Aging, Health and Humanities at George Washington University in Washington.

Nor should loneliness be confused with depression, he says, though both involve feelings of sadness. Loneliness is a state “you can pull out of,” says Cohen, “and you often maintain the motivation to get involved with other people.”

With depression, “you may lose the motivation to be involved,” he says, and while social support can help assuage depression, some people also need professional help, including “the talking therapies or the judicious use of medication.”

Certainly, the ability to spend time alone happily — creative solitude, if you will — is one of the great joys of life, and a hallmark of a mature personality.

But the evidence is now overwhelming in two directions: Social isolation — having few, meaningful interpersonal ties –can have severe medical consequences, and close ties with people can significantly increase health and longevity.

Consider:

– People who are isolated but healthy are twice as likely to die over a period of a decade or so as healthy people who are not isolated, according to a 1988 review of studies on 37,000 people in the United States, Finland and Sweden. Among adults of working age, the more-isolated men are one to four times more likely to die of all causes at any age than less-isolated men, and more-isolated women are one to three times more likely to die than less-isolated women, says sociologist James House, of the Survey Research Center at University of Michigan.

– Living alone after a heart attack significantly raises the risk of subsequent cardiac problems, according to a 1992 study of more than 1,000 people by Columbia University researchers published in the Journal of the American Medical Association.

– People with heart disease have a poorer chance of survival if they are unmarried and do not have a confidant than if they are married, have a confidant, or both, according to a study of 1,368 people by Duke University researchers in the same journal.

– Women with advanced breast cancer who join a support group live twice as long as those who do not, according to a study several years ago by Dr. David Spiegel, a Stanford University psychiatrist.

– Similarly, people with malignant melanoma who participate in group intervention live longer than those who do not, according to a 1993 study by Dr. Fawzy I. Fawzy, a UCLA psychiatrist.

– While chronic stress, such as taking care of a spouse with dementia, leads to marked declines in immune response, having a strong network of friends offsets this decline, according to studies by Ronald Glaser, an Ohio State University microbiologist, and his wife, Janice Kiecolt-Glaser, a psychiatrist.

“Primates, which we are, are a social species,” says Glaser. “We run in packs, in troops. Social interaction between individuals” is an important “buffer to the physiological changes that stress is inducing.”

And this may be particularly true for older people, whose immune systems decline with age.

“The research clearly shows that social isolation is a major health hazard for elderly people. Socially isolated elders have higher rates of physical and mental illness and even death. . .” said Karl Pillemer, director of the Applied Gerontology Research Institute at Cornell University, in an e-mail interview last week.

An older person who is isolated is also at increased risk of being abused, according to Pillemer’s studies, which show that older people who were abused had less contact with friends and family than those who were not, in some cases because the abuser forbad such contact.

Many Americans, young and old, turn to therapists, self-help groups and medications to combat isolation, but there may be a better way, and it’s not just seeking friends for friendship’s sake.

“The idea is that you need to be willing to enter into relationships of mutual obligation,” says Olds.

“The really naive notion of our time is that the way you make friends is just by being fascinated with someone, that you are drawn by pure attraction,” says Schwartz.

“But the fact is, people’s lives are so hectic that those purely fun relationships often don’t get sustained. It’s the relationships where people are really useful to each other that do get sustained, that deepen and that therefore fulfill people’s needs for longterm intimacy,” Olds adds.

If that has an old-fashioned ring to it, they say, so be it. After all, old wives’ tales often endure precisely because they do contain gems of hard-won wisdom.

Like this one: To have a friend is to be one