Stents, long famous for their success in propping open clogged arteries in the heart, are now being used in neck arteries in an effort to reduce strokes.

Technical advances have made the stents safer to insert in neck arteries, and some experts now fear that doctors may adopt the procedure — and patients may clamor for it — before there is sufficient research to support it.

With carotid stenting, doctors insert a mesh device into a clogged carotid artery in the neck to keep blood flowing to the brain. The stents can be placed in the carotid arteries without general anesthesia.

”The procedure is less invasive and recovery is faster than with endarterectomy,” the traditional surgical approach to fixing narrowed arteries, said Dr. Marc Mayberg, executive director of the Seattle Neuroscience Institute, a research center. But he said carotid stenting ”may be overapplied in patients who actually don’t need it, who don’t need any treatment at all, or who would do well on medications alone.”

So far, he said, ”there is little scientific data yet to show that stents are an effective way to prevent strokes, while there is such data for endarterectomy,” which involves cutting open the arteries and scraping out fatty debris. Every year, roughly 150,000 Americans undergo this procedure.

The new procedure does have a growing number of fans.

Carotid stenting is clearly ”the coming thing,” said Dr. Barry T. Katzen, medical director of the Baptist Cardiac and Vascular Institute in Miami. ”We are very excited about this technology.”

Although carotid stenting has been around since the early 1990s, it is taking off now because engineers have devised a way to catch debris that can be knocked off artery walls during insertion of the stent — and could otherwise travel to the brain and cause strokes.

”We now have equipment that is much smaller, much more elegant,” making the procedure easier and safer, said Dr. Piotr Sobieszczyk, a cardiologist at Brigham and Women’s Hospital. ”In the future this may well be the preferred way of treating carotid artery blockages.”

The addition of the debris filter has been ”crucial to the rapid development of this procedure,” said Sobieszczyk.

Carotid stenting got another boost last year when Medicare agreed to pay for the procedure in certain patients.

Despite its promise, though, stenting will probably not be the first choice for many people at risk of stroke.

In 2003, the latest year for which statistics are available, more than 700,000 Americans had strokes and nearly 158,000 were killed by them, according to the American Heart Association. High blood pressure, smoking, and clogged carotid arteries are all risk factors for strokes. Carotid stents are designed to address the small percentage of strokes that are caused by a buildup of plaque in the carotid arteries.

While there are not as much data on stenting as on surgery to prevent strokes, a major study called SAPPHIRE, published in 2004, did show that carotid stents were just as effective at reducing strokes in high-risk patients as endarterectomy and were linked to fewer heart attacks during the procedure. After three years, stroke risk in both groups about 5 percent, said Katzen, one of the study’s authors.

There are risks to both procedures. The major risks of endarterectomy include infection and injury to nerves in the neck, plus bleeding and heart rhythm disturbances; the major risks of stenting include bleeding from the artery in the groin through which the stent is threaded, and heart rhythm disturbances.

On the plus side, there is preliminary evidence that carotid stenting may improve cognitive function, said Dr. Rod Raabe, an interventional radiologist at the Sacred Heart Medical Center in Spokane, Wash. A study Raabe presented in March at the annual meeting of the Society of Interventional Radiology showed a statistically significant improvement in memory and other cognitive skills after stenting, even in patients who had not had strokes.

But the big outstanding question is this: Should stenting be used for people at moderate risk of stroke who have no overt symptoms, like transient ischemic attacks, also known as mini-strokes. That issue is now being addressed in a study called CREST funded by the National Institutes of Health, which is still open to new patients.

Until that study is finished, the prudent course, if you’re are at risk for stroke — because of high blood pressure, being a smoker, having clogged carotid arteries, or other risk factors — is to talk with your doctor and try medications first to reduce your risk. If these don’t work and you need something more invasive to keep your carotid arteries open, ask your doctor about endarterectomy and stents and how much training your doctor has had in these procedures. And don’t be afraid to get a second opinion.

The idea is as simple as it is radical: Chronic inflammation, spurred by an immune system run amok, appears to play a role in medical evils from arthritis to Alzheimer’s, diabetes to heart disease.

There’s no grand proof of this “theory of everything.” But doctors say it’s compelling enough that we should act as if it were true — which means eating an “anti-inflammatory diet,” getting lots of physical activity, and losing the dangerous, internal belly fat that pumps out the chemicals that drive inflammation (More on this nasty chemistry later).

Inflammation, of course, is not all bad. In fact, because it’s part of the typical immune response, it’s essential for battling germs and healing wounds. The familiar redness, heat, swelling and pain that come from, say, a hangnail or a splinter are signs of inflammation at work.

It’s when the inflammation process fails to shut off after an infection or injury is over that trouble sets in. Persistent, low-level inflammation may set the stage for the chronic diseases of later life, many doctors now believe.

Over the evolutionary eons, “we developed these important host defenses to let us get to reproductive age,” said Dr. Peter Libby, chief of cardiovascular medicine at Brigham and Women’s Hospital. “Now, the lifespan has almost doubled, and these same [immune responses] contribute to diseases in the end.”

Chronic inflammation is so similar in different diseases, Libby said, that when he lectures, he uses many of the same slides, whether he’s talking about diseases of the heart, kidneys, joints, lung or other tissues.

Only a few years ago, heart attacks were explained as a plumbing problem — blood vessels that became clogged with atherosclerotic plaque as “bad” (LDL) cholesterol was deposited on vessel walls.  Now, doctors know that this bad cholesterol gets embedded inside artery walls as well, where the immune system “sees” it as an invader to be attacked. The on-going inflammation in arteries, essentially a revved up immune response, can eventually damage arteries and cause “vulnerable” plaque to burst. It is because inflammation is now seen as such a hallmark of heart disease that many doctors use a test for inflammation called CRP to help assess a person’s cardiac risk.

It’s long been known that type 1 diabetes is linked to inflammation the body’s immune system attacks the cells that make insulin. Now, new research is suggesting that type 2 diabetes, the kind that generally sets in in adulthood, often begins with insulin resistance, in which cells stop responding properly to insulin. Doctors now know that during chronic inflammation, one of the chemicals released is TNF, or tumor necrosis factor, which makes cells more resistant to insulin.

“No one would have thought these things were related,” but they are, said Dr. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health. The TNF connection also helps explain why obesity, particularly abdominal obesity, leads to diabetes. “Fat cells used to be thought of as storage depots for energy, as metabolically inactive,” said Libby. “Now we know that fat cells are little hotbeds of inflammation — excess fat in the belly is a great source of inflammation.”

Auto-immune diseases like rheumatoid arthritis are also believed to be linked to inflammation. In arthritis, for instance, inflammatory cells called cytokines lead to the production of enzymes that break down cartilage in joints.

Inflammation also plays some role in Alzheimer’s disease, said Linda Van Eldik, a neurobiologist at the Northwestern University Feinberg School of Medicine.

Whenever the brain is injured or infected, cells in the brain called glia pump out cytokines. Normally, this response shuts down when the injury or infection is over.

“But in chronic neurodegenerative diseases like Alzheimer’s, these glial cells are activated too high or too long or both,” Van Eldik said. The plaques and tangles in patients’ brains attract the attention of glial cells, making them pump out even more cytokines to try to repair this damage and creating chronic inflammation.

Even cancer may have some inflammatory triggers, though the links are less well worked out, said Dr. David Heber, director of the UCLA Center for Human Nutrition. Among its other tricks, inflammation promotes the release of free radicals, dangerous forms of oxygen that can damage DNA. At chronic, low doses, Heber said, “free radicals can stimulate tumors to grow.”

There are other chemical overlaps between inflammation and cancer, too, said Dr. Robert Tepper , president of research and development for Millennium Pharmaceuticals in Cambridge. The same protein signaling molecules called chemokines that tell white blood cells when to flock to an injury or infection, also tell cancer cells when and where to spread, suggesting a link between cancer spread and the inflammatory response.

That’s the bad news. Now, the good: There’s a lot you can do to reduce the risks of chronic inflammation. First and foremost is to lose weight if you’re chubby, especially around the middle. It’s visceral fat that pumps out the lion’s share of pro-inflammatory cytokines. Exercise, of course, is the way to do it — anything that gets you moving and burns calories will help.

And diet is crucial. “Some types of food we eat can cause inflammation and others can decrease it,” said Lisa Davis, a nutritionist at the Center for Human Nutrition at the Johns Hopkins School of Public Health. On the good side, the Mediterranean diet, which is rich in fruits, vegetables, fish and olive oil, was shown in a randomized study in 2004 to be linked to reductions in weight, C-reactive protein and insulin resistance.

You can eat fats, but eat the right kind, like olive oil, and include those rich in omega-3 fatty acids, like that found in salmon, tuna, walnuts, soy and flax seed oil.

Finally, you can also consider statin drugs, which lowers cholesterol and may reduce the inflammation associated with heart disease. Also consider taking a baby aspirin a day, though you should check with your doctor first. Ditto for NSAIDS — over-the-counter non-steroidal anti-inflammatory drugs – which reduce inflammation but cause bleeding and other side effects.

Reducing the inflammation in your life won’t guarantee you’ll live forever, but it’s a step in the right direction.

More than 30 years ago, when Dr. David Heber was an intern at Beth Israel Deaconess Medical Center, he asked the senior doctors the same question over and over.

“How come all my patients have high blood pressure, high cholesterol and diabetes? Are these things linked?” His mentors would shrug and say, “Dave, common things occur commonly. Go back to work,” he said.

Today, doctors know Heber’s intuition was right. Type 2 diabetes and heart disease are physiologically linked. What’s more, according to new government figures, a whopping 64 million Americans now have what’s called Metabolic Syndrome [cq caps], also known as  insulin resistance, which doubles the risk of heart disease and raises diabetes risk by 30 percent.

“It’s a chain from obesity to diabetes to heart disease,” said Heber, now director of UCLA’s Center for Human Nutrition. “In the next 10 years, 80 percent of all heart disease will be due to Type 2 diabetes.”

Granted, you may never have heard of Metabolic Syndrome. But you probably have it if you have any three of the following five factors:

When Bill Clinton, 58, underwent quadruple coronary bypass surgery on Labor Day, the former president, like most Americans who have similar operations, spent time – in his case, 73 minutes – hooked up to a heart-lung machine while surgeons re-routed blood vessels to his heart.

With luck and his relative youth and health going for him, Clinton will hopefully rebound fit in both heart and mind from the bypass surgery, in which doctors replace clogged arteries to the heart with veins and arteries taken from elsewhere in the body.

But many people who go through the procedure — as 305,000 Americans did in 2001, the latest year for which figures are available — find that at least for a few days, often for weeks and sometimes for years afterwards, their brains don’t work as well as they did before.

Doctors who acknowledge the problem -and some still pooh-pooh it – call it post-surgical “neurocognitive deficits.” Everybody else calls it “pump head,” reflecting  the widespread, though unproven, belief that it’s the process of blood being pumped through a heart-lung machine while the heart is stopped for surgery that causes small blood clots, air bubbles or other debris to travel to the brain, disrupting memory.

Nobody really knows how common “pump head” is because, outside of research studies, most cardiac patients aren’t tested on intellectual function before and after surgery. Detecting all but the most subtle cognitive changes “depends on how hard you look,” said Dr. William Cohn [cq], director of minimally invasive surgical technology at the Texas Heart Institute in Houston.

Nonetheless, it has now been “convincingly demonstrated that measurable cognitive dysfunction is actually a common complication of CABG (coronary artery bypass graft) surgery, with an incidence of 80 to 90 percent at hospital discharge,” as Duke University researchers Dr. Daniel B. Mark [cq] and Dr. Mark F. Newman [cq]put it in an editorial in the Journal of the American Medical Association in 2002.

Even five years after discharge, 42 percent still show measurable cognitive decline, Mark and Newman found in their own study, published in 2001 in the New England Journal of Medicine, though some of this might have been due to normal aging.

In most patients with  “pump head,” the deficits are real, but small. “It’s not that you can’t solve a problem,” said Mark, “but that you can’t solve it as quickly.”

Many cardiologists, among them Dr. Christopher Cannon [cq] of Brigham and Women’s Hospital in Boston, also believe that deficits are most likely to occur in older patients who, in addition to having clogged arteries to the heart, may have blockages in blood vessels in the brain as well. In other words, what some see as a consequence of heart surgery may be a consequence of generalized atherosclerosis.

At the moment, there is no cure for “pump head.” Nor do doctors understand why some patients who get it get better over time and others do not.

Though it’s not clear today that the heart-lung machine is the real culprit in “pump head,” many doctors for years assumed it was and focused their prevention efforts  on the machine itself.

A common spice already enjoyed by many Americans appears to lower blood sugar and cholesterol, a potential boon to millions of people with diabetes and millions of others with high cholesterol.

The spice is cinnamon. In a paper published in December in Diabetes Care, researchers from the Beltsville Human Nutrition Research Center in Maryland, part of the US Department of Agriculture, reported on a  small, but encouraging study of 60 people with Type 2 diabetes in Pakistan.

It showed that as little as one gram a day of cinnamon -one-fourth of a teaspoon twice a day – can lower blood sugar by an average of 18 to 29 percent, triglycerides (fatty acids in the blood) by 23 to 30 percent, LDL (or “bad”) cholesterol by 7 to 27 percent and total cholesterol by 12 to 26 percent.

Although some scientists suspect that cinnamon may be toxic at very high doses, at the small doses used in this study, the spice appears to be safe, said Richard Anderson, (CQ)  the lead scientist in the Beltsville lab and senior author of the paper.

To be sure, one small study on 60 people and a handful of other studies on the biochemistry of cinnamon in cells in lab dishes provide far too little data to recommend that Americans immediately start wolfing down large quantities of the spice. On the other hand, the USDA study was “impressive,” said Melinda Maryniuk (CQ) , a senior dietician at the Joslin Diabetes Center in Boston.  Cinnamon “can’t harm in small doses, it may help, and it’s not adding calories,”  she said.

She warned, however, that people with Type 2 (or adult-onset) diabetes should monitor their blood sugar more frequently if they take cinnamon because it could intensify the effects of diabetes medications, including insulin.

Alice Lichtenstein (CQ), a professor of the Friedman School of Nutrition Science and Policy at Tufts University, added another caveat:  Don’t use the news on cinnamon to indulge regularly in calorie-laden cinnamon buns or muffins.

Scientists already have a pretty good, albeit incomplete, idea of how cinnamon may work, at least in diabetes, said Don Graves (CQ) , an adjunct professor of biochemistry at the University of California in Santa Barbara and a guest investigator at the Sansum Diabetes Research Institute, also in Santa Barbara.

An active, water-soluble ingredient in cinnamon, proanthocyanidin (cq) , part of a family of chemicals called polyphenols that are often found in plants,  somehow worms its way inside cells.

Once inside, it helps to phosphorylate, or activate, the part of the insulin receptor that sticks into the cell. (The other end of the receptor sticks out through the cell membrane into the bloodstream to catch molecules of insulin, which escort sugar to cells.)

Then, once the receptor is activated, whether by insulin or proanthocyanidin, a cascade of chemical reactions occurs so that the cell can use energy from sugar. Cinnamon, in other words, does much “the same thing as insulin,” said Graves.

“Cinnamon makes insulin more efficient,” added Anderson of the USDA.  In  diabetes, the problem is that insulin no longer does a good job of  escorting sugar into cells. Cinnamon “makes cells more sensitive to the insulin that is available. And if you improve insulin sensitivity, you improve blood lipids. Insulin is the driver.”

Dr. Frank Sacks (CQ), a physician at Brigham and Women’s Hospital and professor of nutrition at the Harvard School of Public Health, is cautious.  “There are certainly substances in plants that have very strong biological effects, so the concept is fine,” he said. And plant derivatives “are being intensively researched at many places – that’s a hot topic.”

But people should not rely on cinnamon to replace statin drugs, used by 20 million Americans to lower cholesterol.  “Cinnamon is a lot less effective than statins,” he said. Statins were tested in rigorous studies on 70,000 people for five years or more.” Compared to that, the research on cinnamon is weak. It’s also curious, he said, that the USDA study found that the beneficial effects of cinnamon lasted for at least 20 days after people stopped taking it. “I don’t know of any drug or product whose effects persist for 20 days.”

On the other hand, Dr. Andrew Greenberg, director of the obesity metabolism laboratory at Tufts, has reviewed the existing literature on cinnamon and is impressed enough to be starting a collaboration with Anderson, whose preliminary findings he described as “very exciting and promising.”

One note of caution is that coumarin, a substance found in cinnamon, may trigger cancer in animals. Cinnamon also contains cinnamaldehyde, which is toxic. But these toxic components are fat-soluble, while the beneficial ingredient, proanthocyanidin, is water-soluble. Water-soluble extracts of cinnamon are available in which “all the bad components are left behind,” said Anderson. (Ground cinnamon does allow both water- and fat-soluble components to be absorbed, but at the doses recommended, it does far more good than harm, he said; cinnamon sticks placed in hot water release only water-soluble components.)

It’s easy to add cinnamon to the diet, by sprinkling at bit of powder on cereal or coffee or soaking a cinnamon stick in a cup of tea. In fact, noted Anderson, one of his colleagues who did not have diabetes was able to lower his blood sugar just by using a cinnamon stick regularly in tea.

There may be an indirect health benefit to be had from cinnamon, too, according to Taiwanese scientists writing in the July 14 issue of Agriculture and Food Chemistry. Cinnamon oil, they found, kills mosquito larvae more effectively than DEET, a common pesticide and mosquito repellent. The next step is to test it against adult mosquitoes.

In December, a study of more than 42,000 white and black Americans found that old-fashioned, cheap diuretics – “water pills” – work at least as well and sometimes better than more expensive drugs to treat high blood pressure and certain heart problems.  The study, dubbed ALLHAT, was published in JAMA, the Journal of the American Medical Association.

In February, a study of more than 6,000 mostly white Australians came to a different conclusion – that drugs called ACE inhibitors were better than diuretics, although only for men (for unclear reasons). This study was published in the New England Journal of Medicine.

Between now and May, it falls to Dr. Aram Chobanian, dean of the Boston University School of Medicine, and his committee of experts picked by the National Heart Lung and Blood Institute to reconcile the studies and tell America’s 50 million hypertensives what to do.

Their conclusions are crucial. Hypertension doubles the risk of heart attack and is the leading risk factor for stroke and heart failure. One in four adult Americans has hypertension – defined as a reading of 140/90 millimeters of mercury or higher.

(The top number is the systolic pressure, taken as the heart muscle contracts. The lower number is the diastolic, as the heart relaxes. Normal blood pressure is 120/80, but even readings of 130/ 85 should be considered a red flag.) 

High blood pressure is so common, especially among older people,  that many patients don’t’ take it as seriously as they should. “High blood pressure doesn’t make you feel bad,” says Dr. Michele Hamilton, co-director of the heart failure program at the University of California, Los Angeles. This makes it harder for people to change their diets (and reduce salt), lose weight, reduce stress and take medications.

High blood pressure is also tricky for doctors because they usually don’t know what causes it. In 5 percent of cases, it’s caused by kidney and adrenal problems, or legal and illegal substances such as prednisone, cocaine, ephedrine, even licorice. But 95 percent of hypertension is deemed “essential” or “primary” because the cause is unknown.

Basically, blood pressure is a matter of hydraulics. If the pressure inside artery walls is too low, a person can go into shock and die. If the pressure is too high, because vessels are too narrow or rigid or the heart beats too hard, a person can develop heart and kidney failure and stroke. 

With age, the risks get worse because blood vessels become more rigid. Indeed, data from the Framingham Heart Study show that a person who has a normal blood pressure at 55 has a 90 percent chance of developing high blood pressure eventually.

Regulation of blood pressure is complex. Short term fluctuations are controlled by the nervous system, specifically hormones such as adrenalin and noradrenalin. Longer term, a key player is angiotensin II, a kidney hormone that makes vessels constrict.

If you have hypertension, the first remedy to try is behavioral: exercise and nutrition. This means losing weight if you’re heavy, adopting the DASH diet and restricting salt. Even losing just 10 pounds can lower blood pressure significantly.

It’s not fully clear whether consuming too much salt actually causes hypertension. But age-related increases in blood pressure can be minimized by reducing salt (sodium) intake to about  2.4 grams of sodium a day. (This equals 6 grams, about 1 teaspoon, of salt.)  In practice, this means not adding salt when cooking or eating and avoiding many canned and fried foods, including foods containing soy sauce.

The DASH diet, plus salt restriction, clearly lowers blood pressure. The DASH diet is rich in fruits, vegetables, lowfat diary foods, potassium, calcium, magnesium, fiber and protein. It’s low in total and saturated fat, red meat, sweet foods and sugary drinks.

Stress reduction helps, too. Dr. Thomas Graboys,  chairman of the Lown Cardiovascular Foundation, asks patients two questions: Do you look forward to going to work? And, do you look forward to going home at night? “If someone says no to either,” he says, stress may be contributing to that person’s problems.

To combat stress, Dr. Herbert Benson, president of the Mind/Body Medical Institute and associate professor of medicine at Harvard Medical School, recommends the “relaxation response.” That means taking 10 to 20 minutes a day to meditate, pray or quiet the mind and body through focused concentration. Stress reduction, he says, can minimize the “vicious cycle” in which people panic about their hypertension, making it worse.

If you’ve done all this and still have high blood pressure, you probably need medication. And that’s where doctors disagree – not on whether medication is needed, but on which drugs to try first. If hypertension is stubborn, you’ll probably need several drugs, and there are many to choose from.

Diuretics such as hydrochlorothiazide (Hydrodiuril) or chlorthalidone (Hygroton) flush excess water and salt from the body, allowing the heart to work less hard. One reason diuretics fared well in the ALLHAT study is that 32 percent of participants were black. Blacks, perhaps for genetic reasons, tend to be sensitive to salt and hence, highly responsive to diuretics.

Beta-blockers such as propanolol (Inderal) are another staple. They reduce nerve impulses to the heart and blood vessels, making the heart beat more slowly and with less force.

A similar class of drugs is the alpha blockers such as doxazosin (Cardura), which also reduce nerve impulses to blood vessels. But the Doxazosin arm of the ALLHAT study was stopped early because those patients had higher rates of cardiac problems.

ACE-inhibitors such as lisinopril (Zestril) relax blood vessels by blocking the formation of angiotensin II. (A newer class of drugs called angiotensin antagonists such as losartan (Lotrel Cozaar) act differently, by blocking receptors for angiotensin II in vessels.)

And then there are the calcium channel blockers (CCBs), drugs such as amlodipine  a combination of amlodipine and benazepril (Lotrel). They lower pressure by blocking calcium, which causes vessels to constrict.

Granted, it’s a bit confusing. But it’s “very reassuring” that the ALLHAT study found diuretics to be so effective, says Dr. Sid Smith, past president of the American Heart Association and professor of medicine at the University of North Carolina at Chapel Hill.

And because diuretics are cheap – about 13 cents a pill versus 10 times that for other medications – “there is no cost-quality tradeoff,” as Dr. Lawrence J. Appel, a hypertension specialist at Johns Hopkins Medical Institutions noted in a JAMA editorial.

As to which drug to start with, stay tuned for the findings from Chobanian’s committee. In the meantime, work with your doctor until you find a drug, or combination of drugs, that get your blood pressure out of the danger zone.

I was very scared, shivering as much from fear as from the chilly room temperature. I was waiting on a gurney at Brigham and Women’s Hospital to be wheeled in for a catheter ablation, an invasive cardiac “procedure.” (Ah, the euphemisms.)

In a totally bizarre twist of fate, I had several weeks earlier interviewed Dr. Laurence Epstein, chief of the cardiac arrhythmia service, in preparation for a column I was working on about new treatments for arrhythmias.

He had shown me his very cool, animated PowerPoint presentations and explained the details of the procedure. As a medical writer, I was fascinated. The process involves inserting catheters through veins in the patient’s groin, snaking them up into the heart, then using the wires to record the heart’s electrical activity – from the inside. Once this activity is “mapped,” the catheters deliver radio frequency waves to ablate (i.e., kill) the clusters of cardiac cells that trigger the abnormal rhythms.

As Epstein showed me his pictures and scholarly articles, I casually mentioned that, once a year or so, I got tachycardia – very rapid heart beat. He instantly drew me pictures of what he guessed was wrong – SVT, or supra-ventricular tachycardia, which affects an estimated 500,000 to 1 million people with varying severity.

Like many of these people, I had probably been born with two electrical pathways through a key switching station in the heart, the atrial-ventricular (AV) node, instead of the normal one. In people like me, electrical signals from the right atrium (one of the upper chambers of the heart) that tell the heart when to beat sometimes go down the wrong pathway and then back up the normal pathway, creating an electrical circuit that causes the heart to beat very rapidly.

“We can cure that with catheter ablation, you know,” he said. “Great,” I said nervously. “If it ever gets worse, I’ll be back.”

Several weeks later, totally out of the blue, it did get worse, much worse. I’m pretty fit – I either swim a mile or do 10 miles on my exercise bike nearly every day. But suddenly, I couldn’t walk a block without sending my heart rate up to 190 beats a minute. Even just washing my hair in the shower triggered it. I was fast becoming a cardiac cripple, afraid of climbing even one set of stairs lest I become short of breath or pass out.

The whole thing was frightening, even though, rationally at least, I knew that SVT was not life-threatening.

But fear and discomfort weren’t the only things I had to cope with. Suddenly, I had a brand new, tricky role: Patient. On the plus side, telling people about my unexpected medical problem meant that I got a huge amount of support from friends.

But becoming a Patient also meant that I instantly became the target of masses of unsolicited advice from people. I was a Rorschach ink blot upon people could now feel free to foist their pet theories.

Interestingly, the doctors I talked to – both friends who are doctors and doctors I consulted for this- were uniformly terrific listeners, contrary to the bad rap they often get. They listened calmly, respectfully, and took me seriously.  When I asked, they offered advice, including one doctor-friend’s very useful mantra, “Stay cool.”

My close friends did all the right things, too. They called during the interminable weekend while I waited to have the procedure. They emailed. They hugged.  They brought flowers, and excellent squash soup. But most important, they neither pooh-poohed my problem nor rushed in to solve it. They had a natural way of simply listening, with attention and kindness, taking in to their own hearts what I was going through, without trying to take over or tell me what to do.

On the other hand, I rapidly came to the conclusion that my friends are pretty special because a number of other people were truly awful at listening and giving support. Their insensitivity ended up putting the burden of patience and diplomacy on me, as a tried to fend off unsolicited advice diplomatically – at a time when I had little patience to spare.

For instance, some people couldn’t stand to let me finish before interrupting with their own horror stories.

Others insisted, quite adamantly, that my problem must be “stress.” This was especially annoying, first, because it seemed to imply that my arrhythmia was my own fault and, second, because it seemed to invalidate the reality of my symptoms, which had been confirmed by cardiac testing. As one friend put it, “Telling someone they sound stressed blames them. Saying, ‘What a stressful situation you’re in’ doesn’t.”

Sure, stress can sometimes boost the chances of getting some diseases, mostly notably, the common cold. But it shouldn’t be the explanation of first resort, partly because it blames people and partly because lots of people get very stressed and never get sick.

Indeed, military studies show that soldiers discharged during World War II for neuroses had no high cancer rates 24 years later than their mentally healthier comrades. And a report in the November 15 issue of Cancer shows that even extreme stress (such as losing a child) is not a risk factor for cancer.

If some people were too eager to blame the victim, others were almost too kind – so eager to DO SOMETHING that they trampled a bit on my autonomy, not giving me the open space to decide what concrete help, if any, I really wanted.

Some people, I discovered, also seem programmed to pounce on someone else’s illness as an opportunity to promulgate their religious views. Several years ago, when a dear friend of mine got a bad diagnosis, one woman actually said to me, “It’s up to God, not the doctors.” Whether this is true or not, it was her worldview, not mine. Which meant I had the burden of fending it off, as tactfully as I could.

Why are some people such naturally good listeners and others find listening so hard?  I wondered aloud about this with my across-the-street neighbor, a psychiatrist, in the count-down days before my procedure. His conclusion makes sense: “When you tell people how helpless you feel,” he said, “they feel helpless. They can’t stand feeling helpless, so they jump in with advice.”

Mercifully, the big day came and, scared though I was, the procedure was substantially less awful than I expected. The nice guys with the great drugs konked me out briefly while they inserted the catheters and when I woke up (the type of anesthesia I had is called “conscious sedation”)  the procedure was already underway. I could feel the arrhythmias as Epstein and his team intentionally triggered them. But none of these was anywhere near as disconcerting as the ones I’d been having spontaneously. I also knew that they could stop any arrhythmia at any time, a huge comfort.

The actual ablation felt a bit hot from my left hip bone to my left collar bone, but not uncomfortable. In fact, I found I was able to chat with the nurse through much of the procedure. I was also lucky. Sometimes, catheter ablations take three to four hours or longer, but mine was quick – an hour and a half.

Then it was OVER! I was ecstatic. I had to lie still for four hours so the puncture wounds in my leg veins could begin to heal, but that was easy.

I went home that same night, feeling terrific. No more tachycardia. No more worries about walking, or climbing stairs. Not even a hangover from the drugs.

I had trusted Epstein and his team and they were magnificent. Thanks to them, I could trust my own heart again.

As for the creepiness of researching a medical problem, then actually getting it. That’s solved, too. I’m writing about hangnails and pimples from now on.

Until last winter, Joseph Moniz, 50, a Fall River man with congestive heart failure was waiting, like 4,000 other Americans, for a heart transplant to save his life.

He never got it. But he got something better: a small device called an implantable cardioverter defibrillator (ICD) like the one Dick Cheney got, a familiar gadget but with a new twist.

Like older defibrillators, Moniz’ device can shock his heart back to normal if the lower chambers, or ventricles, start beating in a rapid, life-threatening rhythm. This kind of arrhythmia, called ventricular fibrillation, causes 350,000 sudden deaths every year.

But the new device in Moniz’ chest can also do something else – re-synchronize the beating of the ventricles so that they work efficiently. This is a potentially a huge boon for many of the 5 million Americans with congestive heart failure, a condition in which the heart beats inefficiently and fluid accumulates in tissues.

Other heart patients, at a handful of medical centers around the country, are getting a variety of other novel treatments for the electrical problems in their hearts, including a promising technique called catheter ablation for atrial fibrillation and other arrhythmias.

For decades, cardiology was ruled by medical plumbers, doctors whose main concern was fixing crucial coronary arteries that become clogged with cholesterol. But now, a number of (literally) electrifying advances has put a new batch of cardiac gurus in the limelight as well: the cardiac electricians, or more precisely, the electrophysiologists.

In the heart, the electrical signals that control rhythms originate in a built-in pacemaker, the SA, or sinoatrial node, a small bit of tissue at the top of the right atrium. Normally, the SA node produces about 60 heartbeats a minute. The electrical signal spreads through the right and left atrium, then activates the AV, or atrioventricular node, a relay point between the upper and lower chambers.

From there, the electrical signal spreads through the ventricles. After the ventricles contract, the signal dies out and the heart waits for a new signal from the SA node.

When these electrical signals become deranged, cardiac hell can break loose, including atrial and ventricular fibrillations, in both of which the heart beats wildly and very rapidly. Such arrhythmias “are becoming an epidemic” because the risk goes up with age and the population is aging, notes Dr. Valentin Fuster, director of the Cardiovascular Institute and Health Center at Mt. Sinai Medical Center in New York.

But treatments often help. Last March, the New England Journal of Medicine published a major study called MADIT II that was stopped early because the results were so clear. It involved more than 1,200 patients and showed that those randomly assigned to get standard ICDs to shock their hearts back into normal rhythm when ventricular arrhythmias occurred had a 31 percent decreased risk of death compared to those receiving standard drug (non-ICD) therapy. Roughly one million Americans have heart attacks every year, and more than a third wind up with poor ventricular function as a result.)

The new generation of ICDs not only can shock the heart back to normal rhythm but can synchronize the coordination of the ventricles by way of an extra wire, or lead, that runs from a pacemaker in the chest to the left ventricle, the main pumping chamber of the heart.

Several new ICDs – Contak CD by Guidant and InSync ICD by Medtronic – were approved for marketing this summer. (A third such device, Epic HF made by St. Jude Medical, is in US testing now and is on the market in a limited way in Europe.)

Some congestive heart failure patients now getting resynchrozining ICDs are “turning their beepers in and feeling so well with ventricular resynchronization that they no longer need a heart transplant,” says Dr. Lynne Warner Stevenson, co-director of the cardiomyopathy and heart failure program at Brigham and Women’s Hospital.

Just as ever-improving ICDs are transforming care for patients with ventricular arrhythmias, so, too, is catheter ablation improving care for people with atrial fibrillation, a problem that strikes more than 2 million Americans.

In “A Fib,” electrical signals in the heart’s upper chambers, or atria cause the heart muscle to flutter wildly, which in turn reduces the efficiency of the ventricles. This allows blood to pool and form clots that can lead to strokes.

Some people with A Fib don’t mind the symptoms and mainly need to worry about the risk of stroke from blood clots. Others find the erratic heartbeats drive them crazy.

In a recent study published in the New England Journal of Medicine, researchers found that for older patients who were at risk of stroke from atrial fibrillation, treatments to control heart rhythm were no better at preventing death than treatments to control heart rate.

But other data suggest that for people whose main concern is disruption of quality of life because of A Fib, catheter ablation may provide substantial relief.

In this treatment, electrophysiologists place catheters, or tubes, into the heart and use them to send use radio waves to burn away specific, tiny areas, particularly those on veins going from the lungs to the heart, that trigger arrhythmias.

“Until a year or two ago, no one ever thought you could use catheters to approach this problem,” says Dr. Kalyanam Shivkumar, director of interventional cardiac electrophysiology at the David Geffen School of Medicine at UCLA.

Now, says Dr. Davendra Mehta, director of the cardiac electrophysiological lab at Mt. Sinai Medical Center in New York, the technique could become for some patients “the treatment of choice.”

Indeed, catheter ablation is a potential “cure” for atrial fibrillation, says Dr. Laurence M. Epstein, chief of the arrhythmia service at Brigham and Women’s Hospital in Boston, although Dr. Jeremy Ruskin, director of Cardiac Arrhythmia Service at Massachusetts General Hospital, is more cautious. The technique is “results in dramatic outcomes in some patients,” Ruskin agrees,  but “the long-term cure rate is only about 50 percent in the best hands.”

Initially, electrophysiologists thought they had to carefully map out the regions of the heart that were triggering the arrhythmias, says Epstein of Brigham and Women’s Hospital.

To do this, doctors threaded a tube (the catheter) through a blood vessel in the groin up to the heart. Under X-ray guidance, doctors then watched on TV screens as they passed the catheter over different regions of heart muscle, recording electrical activity. Areas of the heart that produced bursts of rapid beats were deemed to be arrhythmia trigger centers. To stop the arrhythmias, doctors then delivered radio waves to the troublesome regions.

But recently, electrophysiologists have found that the mapping step is not always necessary because in many cases of atrial fibrillation, the trigger is the region where the pulmonary veins attach to the heart.  Destroying this region can get rid of arrhythmias.

Researchers are also experimenting with destroying electrically-dangerous tissue with ultrasound, microwaves and cryogenic techniques that burn by freezing tissue.

There is still, as Ruskin of MGH and others warn, a long way to go before all arrhythmias can be controlled. But it’s “a very exciting area – there’s a tremendous amount happening.”

Nobody needs to tell that to Joseph Moniz, whose electrophysiologist, Epstein of Brigham and Women’s Hospital, says, “He’s like a new man.” Now off the heart transplant list, Moniz is climbing stairs, playing drums and doing other things he thought he’d never do again.

“I washed my truck for the first time in a couple of years,” Moniz says jubilantly. He still can’t work, but says, “I feel excellent.”