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For this month's special package on the heart, contributing editor TED ALLEN reports on a condition called hypertrophic cardiomyopathy (HCM), in which the heart's septum is dangerously enlarged, blocking the flow of blood and, in many cases, causing death. The disease, which affects one in five hundred people, tends to be an inherited condition and is a leading cause of sudden death among young athletes. Allen traveled to Prague, where he interviewed an American expatriate with HCM who recently underwent a cutting-edge procedure called alcohol septal ablation, in which German cardiologist Hubert Seggewiss inflicted a small heart attack in order to kill the excess tissue. "You've taken an oath to first do no harm, and here you are about to very delicately cause a heart attack on a patient who is wide-awake and watching you," says Allen. "It's incredibly dramatic and just so alien to people. It made me really consider my own mortality."


The Coronary Event
The ultimate guide to whether your heart's going to blow, what the doctors can do about that now, and the weirdest, most promising story of heart surgery that you'll ever read.

by Ted Allen
Esquire, Nov 2002 v138 i5 p118(11)


Seven years ago, an amazing, noninvasive form of heart surgery was first performed in London. It uses a shot of pure alcohol to kill the portion of your heart that threatens to ruin you. The problem is, you have to be awake while that part of your heart dies. Which means you are awake for your own heart attack. If you want to know what that feels like, you'll have to ask Pete Baumgartner.

THE PATIENT IS AWAKE. He is flat on his back in the heart-catheter lab in Leopoldina Krankenhaus, a community hospital in the Bavarian town of Schweinfurt, Germany, about an hour east of Frankfurt. He is wearing nothing but underwear, and the room is cold. His arms are stretched above his head, and his hands cling to a metal bar positioned there to clear the way for the echocardiogram equipment that's above him and aimed at his chest. To his right, seated on a stool and draped in a heavy apron to protect him from X rays, is a forty-six-year-old German cardiologist named Hubert Seggewiss. To his left are two TV monitors big enough for a sports bar, one displaying readouts of his vital signs--heart rate, blood pressure, temperature--the other a black-and-white echocardiogram picture of his quivering, thirty-four-year-old heart.

It's August 10, 2001, a Friday. The room is quiet, save for the rhythmic beep that announces the pumping of blood through his veins.

The patient is an American, Peter Baumgartner, who drove the four hours to Schweinfurt on the previous day with his fiancée, Eva, from their home in Prague. Pete works as an editor for Radio Free Europe. He has short brown hair, crinkly blue eyes, broad shoulders, and the hint of a belly. He is here today because he has hypertrophic cardiomyopathy (HCM), a heart condition that has reduced his ability to pump blood, to the point where he cannot climb two flights of stairs without stopping to rest. If left untreated, it will probably kill him.

When Pete arrived at Leopoldina yesterday, he was checked in, looked over, and handed a disposable razor, which he used to remove a patch of hair from each of his thighs. Now, in each of those shaved regions, Seggewiss administers a local anesthetic and makes a quarter-inch incision; he then locates the femoral arteries that run up either side of the body. Pete feels his own blood running between and under his thighs; it feels surprisingly, unpleasantly warm.

From his seat below Pete's waist, Seggewiss punctures the femoral vessel on Pete's left side with a needle and inserts a flexible guide wire. Then, using the X-ray fluoroscopy pictures to guide him, he begins pushing the wire upstream into the artery, slowly moving north, through the intestines, behind the stomach, between the kidneys, past the liver--about twenty-four inches from groin to chest.

When the guide wire reaches Pete's heart, Seggewiss slips a hollow plastic catheter about two millimeters in diameter over the wire and slides the catheter all the way up to the heart; then he removes the guide wire. Seggewiss will use the catheter as a sleeve through which he'll slide cables carrying other tiny pieces of equipment into position.

On the tip of the first cable are two electrodes attached to an external pacemaker, a machine that Seggewiss will employ only if things go seriously wrong. He parks the electrodes at the bottom of Pete's right ventricle and shifts his attention to the opposite leg. From there, he installs another catheter, through which he snakes a smaller tube tipped with a one-and-a-half-millimeter balloon. He begins inching this tiny craft, too, up toward the aorta.

It occurs to Pete that Seggewiss looks a little like he's fishing, sliding the cable in a bit, tugging, reeling back slightly, twisting, pushing in another inch. He swears he can feel all these catheters creeping up through his plumbing like a Roto-Rooter, like tiny snakes. And it's this that scares him, almost as much as the idea of the procedure itself, a new technique still considered experimental in many medical circles--notably those in the United States. Pete's read on the Internet of a place just above the heart where the vessels take a sharp turn and where, in a few patients, the catheter has "dissected" the arterial wall (meaning that it pierced it), causing massive internal bleeding in the chest cavity and death.

Seggewiss makes it around the bend without incident.

From there, he steers through Pete's aorta, takes a turn into the left coronary artery, then guides the balloon into the smaller branches that envelop and feed the heart. As the balloon nears its target, Pete can see it on the monitor, a little speck creeping along the organ's surface, winding into vessels that branch off smaller and smaller, like limbs on trees, and then disappearing into the meat of the muscle.

The balloon arrives at the artery in question. Seggewiss is now ready for the procedure, called alcohol septal ablation, in which he will inject about half a teaspoon of pure ethanol into the blood vessel, saturating it and the portion of the heart that it feeds, killing every tissue cell it touches. When a part of a person's heart dies, that is called a heart attack. In this case, it is a small one, a controlled one, affecting only a few centimeters of tissue, but a heart attack nonetheless.

Meanwhile, the patient is awake. The patient has to be awake so the cardiologist can instruct him to cough, to hold his breath, or to exhale, motions that shift the innards and the circulatory labyrinth the doctor is trying to navigate. Seggewiss tells Pete to take deep, even breaths. Pete is keeping it together, an endeavor made slightly less difficult when Seggewiss injects ten milligrams of morphine into his IV. It will prove inadequate when the burning begins; still, it will be the highlight of his day.

And then, Seggewiss informs him, it's time.

YOU GROW UP IN THE FOOTHILLS of the Colorado Rockies and this is what you do: You climb, you ride, you run. Pete has always been an athlete, and for most of his life his heart condition seemed a harmless footnote in his files; doctors placed no limits on his activity. He played competitive soccer. He ran the Bolder Boulder 10K, the Garden of the Gods 10-Mile Run, the occasional half marathon, and, for a time, he logged sixty to seventy miles a week cross-country. Basketball, tennis, softball, too.

He was sixteen when he was diagnosed with HCM, an inherited condition that affects about one in five hundred people in the U. S., men and women equally. (Pete's mother, Chris, also has HCM and suffered a minor heart attack in her thirties but is otherwise in good health. Her father died of a heart attack at forty-eight. None of Pete's three siblings are affected.) HCM essentially means the heart has an enlarged septum, the vertical wall that separates the left and right sides of the heart's chambers. About 80 percent of people with HCM--including Pete, for most of his life--suffer only minor effects, if any, which are treatable with medication. In the other 20 percent, that overgrown septum can seriously obstruct the blood flow, causing blood to back up in the heart: hypertrophic obstructive cardiomyopathy. When young athletes are affected by HCM, they're often not diagnosed until they pass out on the field--or until it kills them there. Cardiomyopathies were responsible for the deaths of Boston Celtic Reggie Lewis and the college basketball star Hank Gathers, among others.

It was in the late nineties that Pete's breathing problems came. In particular, he was having increasing difficulty managing the six flights of steps to his apartment. By 2000, attempting the climb would usually bring him to his knees before the second flight, gasping and dizzy, chest burning, head swimming until he bent over to flood his brain with blood and oxygen. He often had to rest twice more before staggering through his door.

As serious as those symptoms were, Pete didn't really think they had anything to do with his heart. It just didn't occur to him. He had no idea that shortness of breath is among the most common symptoms of HCM. He'd been told his whole life that his heart was robust enough for the most taxing sports. Rather, he wondered if Prague's poor air quality may have given him some kind of respiratory ailment. (When he arrived there in 1995, most of the city was still heated with brown coal that left the sky dingy and pungent.) He also allows now that he might have been in a certain state of denial. A few years ago, when Eva took up jogging with some friends, he thought he would take it up again, too. But after just a few hundred yards, he was huffing like a fat man in a fire drill. Repeated efforts brought no improvement.

And then, in the spring of 2001, at his regular Thursday basketball game with a crowd of Serbs, Czechs, and fellow American expats at his gym, he was running upcourt when he passed out cold. It lasted just a few seconds, but it was a shock. He could feel it coming on--as if his batteries were running out. He suffered similar incidents in ensuing weeks, once while playing center field in a softball tournament, a few more times on his stairs, another time while running to catch the Metro.

He finally went to a Czech cardiologist. The doctor looked at his heart with an echocardiogram.

Oh, I see it, he said. You've had a big change from the last time you were here, he said. You have to do something.

The doctor noticed that Pete's enlarged septum was jutting out into his left ventricle and preventing the mitral valve from functioning properly, causing blood to back up into the atrium. This explained the shortness of breath; his lungs and heart were working much harder than they should have to supply his tissues with oxygen. This put him at grave risk of a heart attack, especially during exertion.

The severity of the problem in an HCM patient is gauged by measuring the difference between the blood pressure inside the left ventricle and just outside it, in the aorta. With a clear, unobstructed flow of blood, this gradient should be as low as possible, even approaching zero in a normal ticker at rest, because the pressure inside and outside the heart should be about the same. Pete registered seventy-eight. During exercise, he logged an outrageously bad gradient of one hundred.

He was told to stop playing sports, to stop working out. He was told to be careful walking to work. He was told that something needed to be done. Immediately.

Until very recently, there has been only one way to treat Pete's condition: a myectomy. That's open-heart surgery. Going in and trimming the septum with a scalpel. In the best-case scenario--that is, one in which complications don't present themselves--this is how open-heart surgery goes: Cut through the skin and the chest muscles, saw through the sternum, crack open the rib cage and pry it wide with a vise, connect the patient to a heart-lung machine to oxygenate and pump his blood, stop the heart, enter the heart through the aortic valve, shave a little tissue off the septal wall, and then stitch it all back up, wire the sternum shut, stretch the skin into place, and staple it together. For a healthy man in his thirties, it could be six to eight weeks before he can return to work.

When Pete was in college, the mere act of attempting to participate in a blood drive caused him to faint and go into convulsions. He did not like the sound of this open-heart-surgery business at all. So he began researching his condition, scouring the Internet, digging up articles, grilling surgeons and cardiologists across Europe and in the States.
When Pete's cardiologist in Prague presented another option--alcohol septal ablation, a relatively new but promising nonsurgical technique that can have a patient back in fighting form within a week, one that's been performed more often than anywhere else in the world just four hours away in Germany--he was listening.

THE DOCTOR IS NERVOUS. It's August 10, Pete's on the table, and he doesn't see the sweat on Seggewiss's brow, but later the doctor will confess it. This despite the fact that Seggewiss has performed more alcohol ablations than anyone in the world--at least five hundred by the time Pete shows up (and another hundred since). He's a charismatic man who came to Schweinfurt from one of Germany's most prestigious heart centers so that he could run his own show as the director of cardiology. People travel from all over the world for his services.

But even the most experienced cardiologist will tell you that shooting alcohol into a living person's heart--where it will fry the precious tissue as surely as if you'd cooked it with a blowtorch--is a nerve-racking, emotionally draining procedure under any circumstances. Not only are you giving someone a heart attack, the patient is awake and watching you do it. Seggewiss will also admit that he's taken a particular liking to the young American with a passion for European soccer, that he's not as detached as he might be.

The idea here is for Seggewiss to inject a tiny amount of ethanol into Pete's heart in order to kill the offending excess tissue, causing it to wither and shrink and cease to obstruct blood flow.

This is not easy. First, the alcohol must be confined to the target area; if it leaks elsewhere, it will kill every bit of tissue it touches. Second, you cannot be absolutely certain that ablating the artery you target will kill enough tissue, or the right tissue, to reduce the blockage. Third, the septum is quite close to the atrioventricular (AV) node, a crucial pathway in the heart's electrical system that helps conduct the current that makes the organ beat; if the alcohol is injected too close to the node, thus killing part or all of the AV-node tissue, the patient may require a pacemaker for the rest of his life. (For this reason alone, some doctors are reluctant to perform ablation on younger patients like Pete--including doctors such as Harry Lever, an authority on HCM at the prestigious Cleveland Clinic Heart Center who, under the right circumstances, approves of the technique.) Seggewiss's statistics are very good in this department; fewer than 2 percent of his patients have required pacemakers, whereas other institutions' rates reach upwards of 22 percent. To prepare for that chance, the pacemaker electrodes must be positioned on the heart via the first catheter before anything else happens.

Seggewiss then identifies the septal branch he thinks is feeding the enlarged tissue and selects the correct-size balloon with which to block it. He has several sizes of them, special-ordered at a cost of about $600 each. He threads the catheter up the artery toward the target and inflates the balloon. This serves a few functions. Inflating the balloon will deprive the growth and the tissue of blood. This deprivation alone should produce a measurable improvement in the pressure gradient--the difference in pressure created by the growth's interference with the blood flow--which helps confirm that the doctor has targeted the correct artery. (This effect, first noted in London in the mid-nineties by Swiss cardiologist Ulrich Sigwart, was the inspiration for ablation in the first place.) No less important, before any alcohol is introduced, the balloon must completely block the vessel; any unchecked leakage of alcohol back into the coronary artery could cause fatal damage to the heart.

Satisfied with the position of the balloon, Seggewiss takes a syringe and shoots about a milliliter of contrast medium into the tube, which floods the artery and turns it black on the X-ray screen, and--so long as the balloon is seated properly--verifies that no liquid will leak back out of it. If all looks good, he's ready for the alcohol ablation. He injects the dye; no leaks.

Seggewiss has had concerns about Pete from the beginning. For one thing, based on the earlier echos and the severity of his blockage, Pete is going to need a big, painful attack. Furthermore, his anatomy is difficult; that is, he has many branches in the arteries that feed his septum, complicating the question of where to target and forcing a crucial decision. There are two branches feeding the growth that threatens Pete's life: branch one, which goes straight into the meat of the heart; and branch two, which splits again into smaller vessels before it goes in. There's no sure way to determine which vessel is the best candidate, and Seggewiss is unwilling to target them both. He prefers to attack branch number one because it would mean killing a smaller portion of the heart, and less killing is, obviously, better. Based on the echo, Seggewiss believes the vessel he has chosen feeds about half the overgrown septal tissue. The hope is that killing this area of tissue will do the job.

Seggewiss shoots the morphine into Pete's IV, picks up another syringe containing the pure ethanol, gives his patient the nod, and begins slowly injecting it, one cc at a time.

The clear liquid sluices its way up the femoral vessel, around the intestines, behind the stomach, between the kidneys, past the liver, and begins soaking into the tissue of Pete's heart.

Here's how it feels:

"You're lying down and you're holding on to this trapeze thing that dangles, this metal bar. And you're just gritting your teeth and biting your lip the whole time, and you're holding on to that thing and squeezing your fists. The two things I'm thinking about are how nasty is this heart attack going to be, and how long is it going to last? Dr. Seggewiss is making jokes and asking soccer trivia questions and stuff like that to take my mind off it. And before they give you the heart attack, you get a really good shot of morphine. That was really incredible, and I'm sure that made it much more bearable than it would have been. The morphine is definitely something you notice right away, and you feel great, even though you know what's happening and you still feel this incredible burning in your chest.

"It builds up, but slowly. It starts off slow, I guess as the blood kind of goes away and gets replaced by the alcohol, and it's a light burning in the beginning, and then it just gets more intense and more intense and... wow. It builds up, and, ugghh.

"It's like you have a fire in your chest. This terrible, awful burning. You want to scream out, but because of all the people there, you kind of... you break out in a full-body sweat. It was all concentrated there in the center of my chest. You have to keep your arms up the whole time, there's the bar hanging down that you're kind of gripping the whole time, and you're just squeezing the hell out of that and biting your lip and... wow. I can't imagine ever having anything that would be similar to that. Maybe someone who's been burned would feel a similar kind of pain. Or a gunshot or something. It's intense.

"And then it kind of dissipates over a period of fifteen seconds until you have no pain there. You're breathing normally and just glad it's over. Of course, you also have the effect of the morphine and you're kind of groggy. It's not like you're out or even close to being unconscious, but you feel really good. It's like you're really high.

"The first time, the amount of heart tissue that was being affected was much smaller than it was the second time, so it was only, I would say, maybe a minute and a half, this bad sensation of burning."

After a few minutes, Seggewiss flushes the vessel with saline. Pete's heart attack is over.

THE DOCTOR IS WATCHING the echo monitor and reading his instruments as the alcohol is absorbed and Pete's pain subsides. Upon a successful ablation, there is almost always a noticeable, instant improvement; some patients liken it to feeling as if they've just been given a third lung. This improvement should be evident in the blood-pressure measurements; the killing of the obstruction should immediately cause the gradient in pressure on either side of the shriveling obstruction in the heart to reduce substantially.

Pete feels no improvement.

He can see that Seggewiss is displeased, although the doctor tries to put a brave face on it. The alcohol can spread through the desired area for up to three months, he tells Pete, gradually killing and shrinking the tissue. There is still cause for hope.

Twenty minutes after the procedure, Eva goes in to see Pete. He's exhausted and nauseated from the drugs and the stress. He'll stay in the hospital for four more days, the first two in intensive care, where doctors will watch for aftershock heart attacks or arrhythmias. For those two days, the pacemaker leads stay in. He will have his thighs wrapped tightly in pressure bandages to heal the catheter-entry wounds. After he checks out, his thighs will be covered with bruises for three weeks.

It will not be officially confirmed until his postablation checkup three months later, but the failure of the procedure is plain. Pete is still short of breath. He still can't climb stairs, let alone play ball.

Eva says that when Pete loses in sports, he gets a flush of anger, but the anger goes away quickly. Then he starts analyzing, What happened? What didn't happen? Why didn't it happen? And then, always, he says, Well, next time.

THE PATIENT IS AWAKE. He is flat on his back again in the cath lab in Leopoldina Krankenhaus. It's February 15, 2002. This time, he's a little less nervous.

Which is not to say he is happy to be back. Pete is an even-keeled guy, but he'll admit to being pretty angry about this one. Having a heart attack is nerve-racking and painful, no less so if you know when it's coming. Pete also dislikes what this return visit means statistically: Only thirteen people out of Seggewiss's then five hundred ablation patients required a second procedure, he points out, reasoning that he is pushing his luck, oddswise. He also knows this heart attack needs to be bigger than the first one, that it's going to involve killing a larger percentage of tissue and will last longer than the first one.

Pete goes into the procedure knowing that it is his last chance with the procedure in which he's invested so much hope. Seggewiss will not do it a third time, because two failures suggests ablation is simply the wrong approach for the patient in question. That is to say, the first ablation having failed, Pete goes into his second ablation knowing that if it, too, fails to work, he will still have to undergo open-heart surgery.

He's angry, yes, but not with Seggewiss. He realized when the doctor performed the first ablation that he had a weird configuration of arteries. Seggewiss told him on the table that he was not sure which one to target. It's hard to fault a doctor for attempting to damage as little of someone's heart as possible. And to Pete's way of thinking, the second time will go more smoothly than the first. He has, at least, shaken his fears about the catheters slicing through his arteries, figuring that if they survived one fantastic voyage, they can withstand another.

This time, Seggewiss, too, is more sanguine. He can detect the small scar from the first ablation; which tells him that Pete's heart tissue responds to the technique. He also knows which vessel to ablate: the one he opted against last time. He again taps into Pete's femoral arteries, installs the pacemaker leads, sends up the balloon catheter, tests the seal with dye. This time, he tells Pete, he is going to inject the alcohol more slowly than before, which he hopes will lessen the pain. And he does so, one cc at a time, checking the pressure monitors after each tiny injection, the liquid coursing through the catheter and into the septal branch.

This time, the attack lasts about two and a half minutes.

This time, Pete understands what the other patients meant about feeling as if they'd gotten a third lung.

His fiancée is waiting outside the door to the cath lab when Seggewiss emerges in surgical gloves, bloodied up to the elbows; he is so elated, he has forgotten to remove them before he shares the news. This time it worked, he says. Pete's gradient plunged in response to the alcohol.

Six days later, Pete leaves the hospital at the wheel of Eva's Jetta. A few weeks later, his at-rest gradient measures twenty-four, and it goes up to just thirty-two under stress from exercise--well within an acceptable range. It's looking like he's got his life back.

THE PATIENT IS MUCH BETTER NOW. It's the Fourth of July, 2002, and he's standing in Wenceslas Square on a warm day in Prague, a stone's throw from his desk at Radio Free Europe. In the past couple of weeks, he's played softball and tennis, and he's back to sprinting up the stairs of his Metro stop two at a time. Each morning he takes one tablet of Concor, a beta blocker that slows his heartbeat and lessens the intensity of his heart's contractions. He's cleared to exercise, to walk to work, to play any sport he likes.

Of course, when you have a heart attack--the natural kind, that is--and it fails to kill you, your future becomes less certain. When part of your heart has died, it becomes less reliable; untimely heart failure becomes much more likely, as do additional attacks. The scar tissue left behind when tissue dies can change the electrical conductivity of the heart. You're more prone to developing arrhythmias, among them ventricular tachycardia, a superfast heartbeat of up to three hundred beats per minute that can result in sudden death. In the absence of adequate research on the long-term effects of alcohol ablation, some cardiologists fear that it could bring about similar complications. But most of those risks are proportional to the amount of heart tissue that is lost; thus, the key is to lose as little tissue as possible. In most ablations, certainly Pete's, the quantity of tissue affected is minuscule. Seggewiss believes that the prognosis for one of his ablation patients should be identical to that of a patient who chose open-heart surgery.

Furthermore, the future promise of the ablation technique extends to other heart conditions. Rick Nishimura, of the Mayo Clinic, for one, is already using ablation to treat tachycardias (fast heart rhythm) and other problems with the electrical system of the heart. He's also looking into ways to use it to treat atrial fibrillation, a common condition.

As for Pete, Seggewiss does ask that he take it a little easy, which Pete interprets to mean that if you're playing a game of tennis and you have a rally going, and it's a great rally, and you know the other guy is good at the net, you don't race after a lob and hit it back, because if he's good at the net he's probably going to win the point anyway. This gives Pete pause. The doctor is telling him, at a certain point in the game, to stop trying, to give up.

Which may be the reason why, as of September 2002, Pete hasn't yet ventured back to the basketball court. Pete says he's not interested in showing up, for real, until he's got his game back.

There's a 50 percent chance that any children born to Pete and Eva will inherit the gene for HCM from him, a mathematical fact of which they are all too aware. But Pete's not one to settle for lousy odds; he's been at it again with the research. There are gene therapies on the horizon with enormous potential, he says. And next summer, in St. Nicholas Church on Prague's Old Town Square, they are scheduled to be married.


SIDEBAR: ALCOHOL ABLATION: THE PROS AND CONS

YOU MAKE THE CALL: Have a surgeon saw open your rib cage and whittle down your septum with a scalpel, or pop in for a one-hour, noninvasive catheterization that costs considerably less and will have you back on the golf course in a week. At first glance, alcohol ablation is the obvious choice. But many cardiologists, particularly in the U. S., aren't ready to endorse it yet. Why? Because it's still too new. It was just seven years ago that Ulrich Sigwart performed the first one in London; there have been only a couple thousand since. American hospitals, that perform ablations--like the Mayo Clinic, the Cleveland Clinic, the Baylor Heart Clinic, and the NIH--require voluminous release forms and still consider the technique experimental. Open-heart surgery clearly creates more immediate misery for the patient, but it's a surer thing.

There are other issues, says Rick Nishimura, a cardiologist at Mayo. First, HCM is a complex disease that few cardiologists know well. Second, ablation is an option for only a very small pool of HCM patients. Then there is the pacemaker problem. As many as 22 percent of ablation patients suffer enough heart damage to necessitate a pacemaker. The figure is less than 10 percent with traditional surgery. Hubert Seggewiss attributes those lousy odds to doctors using ablations on patients who shouldn't get them and on the injection of too much alcohol; slightly fewer than 2 percent of his patients have needed pacemakers. American doctors have another crucial disadvantage in comparison with the Germans, says Harry Lever of the Cleveland Clinic. In Germany, a patient who develops arrhythmias can be monitored in intensive care for days, even weeks, during which his heart will often recover its rhythm. To the cost-crippled American health-care system, such a stay is an impossible extravagance. "If in the U.S. we cause an atrioventricular block, we have to put in a pacemaker in three or four days," Lever says.

It's not that Lever or Nishimura disapproves of the new technique. The issue is the current lack of data. "I think the procedure itself is a very good procedure and works very well and may be the procedure of choice in four or five years," Nishimura says. "My reticence is because of the unknowns." For more information, visit hcma-heart.com.
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