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Stents : Do they save lives?

MagazineApril 2009 (Vol. 20 Issue 1)Stents : Do they save lives?

The treatment requires dangerous drugs to be effective, and there is no evidence proving that it actually saves lives

The treatment requires dangerous drugs to be effective, and there is no evidence proving that it actually saves lives. In fact, studies link stents to a whole host of problems, including blood clots, cancer and premature death. Even the procedure itself is hazardous-one in three operations causes side-effects and one in a hundred is fatal.

It was an invention that was predicted to revolutionize the treatment of heart disease when, in 1986, the very first stent was inserted into the artery of a heart-attack patient. The world of medicine rejoiced as here, at last, there appeared to be a permanent high-tech solution to atherosclerosis (furred-up and blocked arteries). To doctors trained to see the body as nothing more than a machine, the stent was perfect, being an artificial bit of artery made of metal.

Today, stents have become the most widespread high-tech bionic device in the whole of medicine. They are used on millions of people across the globe.

And, yet, in the 20 years since their invention, they have almost totally failed to deliver. There is no evidence that they save lives-in fact, the evidence shows quite the reverse. New studies link them to thousands of premature deaths. In addition, they require a potentially hazardous cock-tail of drugs to work; they cause a new kind of blood clot, and they may be a factor in seemingly unrelated fatal illnesses such as cancer. In fact, even the stent-implant procedure itself is hazardous: one in three operations causes major adverse events, and one in 100 is fatal (see box, right).

The problems with stents may stem from the limitations of the rationale on which they are based: the so-called 'plumbing' concept of heart disease.

Unblocking pipes

Doctors tell us that heart attacks are caused by the heart being temporarily starved of blood, primarily due to a constriction in the nearby arteries. They also claim that these narrowings are caused by a buildup of plaque in the blood vessels, a problem mainly caused by eating fatty foods. WDDTY readers will know, however, that the last two elements of the theory are probably wrong on two counts: first, a high-fat diet isn't the main cause of atherosclerosis; and second, so-called arterial plaque is simply the body's inbuilt way of strengthening arteries to compensate for a lack of vitamin C, which some doctors in the vanguard believe is the primary cause of weak arterial walls (see WDDTY vol 17 no 11, February 2007).

However, the conventional view is that our arteries are rather like pipes, which are constantly in danger of becoming blocked up by plaque deposition. The solution has been to treat our blood vessels like drains and clean them out, using the medical equivalent of Dyno-Rod. The tech-nique, called 'angioplasty', involves threading a tiny balloon-catheter tube into the artery and inflating it at the site of the constriction, thus widening the artery. More advanced techniques involve shaving off the plaque, using a mini-tunnel borer attached to the end of the catheter.

Angioplasty was first developed in the 1970s and, at first, they appeared to work wonders, unblocking arteries and preventing the pain of angina, the precursor of a heart attack. However, it soon became apparent that, for up to alf of all heart patients, the procedure was useless. Within as little as three months, the artery became obstructed again. Part of the problem, it was realized, is that angioplasty is not a genteel process, as it can often damage the arterial walls and cause blood clots. So, medicine developed a solution to solve the problem caused by the first solution: it gave the patient drugs to prevent blood-clotting. Special anti-platelet drugs, called 'IIb/IIIa inhib-itors' and including the agents abciximab and eptifabatide, are commonly used. However, these drugs make the patient vulnerable to potentially fatal haemorrhages, particularly in the lungs (Heart Lung, 2006; 35: 423-6).

But the blunt-force trauma of angioplasty also triggers another natural response: the body's attempts to heal the wounded artery. Perhaps because an internal injury to a deep-lying artery is otherwise so unlikely and unnatural, the body's reaction may be overexuberant, resulting in a considerable amount of scar tissue, thus blocking the artery again. This process is called 'restenosis'.

So, it's the body's natural response to an assault that is the major reason why angioplasty is so often a failure. Nevertheless, rather than rethinking the entire approach, medicine's answer has been to throw more technology at the problem-hereby enters the stent.

Flat-pack tubing

Here is high-tech medicine at its most impressive. Stents are tiny metal-mesh tubes that can be threaded as a kind of flat-pack into the artery, and then cleverly made to unfold out into a rounded scaffolding to prop up the arterial walls involved in the angio-plasty. Because blockages in the artery tend to be localized, the stent needs only to be about a centimetre or two in length.

After the invention of stents in the 1980s, heart doctors were soon routinely using them after virtually every angioplasty, specifically to prevent the problem of restenosis. But, once again, while Man proposed, Nature disposed. Although stents appeared to solve the short-term blood-clotting issue, the restenosis problem often recurred. In fact, within six months, up to 40 per cent of stents were found to have become blocked again, requiring a repeat operation (Medicina [Kaunas], 2007; 43: 183-9).

Initially, the explanation for this unhappy outcome was that it was the result of a recurrence of coronary artery disease (and, by implication, the patient's fault), but doctors gradually came to realize that this theory just didn't wash. Eventually, they had to acknowledge that the culprit was the medical intervention itself. Even the inventor of angioplasty, Dr Andreas Gruentzig, was forced to admit that what he called the "controlled injury" of the angioplasty-stent procedure was the root of the problem.

By now, it might have been expected that physicians would have got the message that Nature doesn't accept that arteries should be treated like drainpipes. Yet, apparently, this was not so. Medicine's response to the stent-restenosis problem has been not to admit defeat but, in a sense, to punish the body for its intransigence.

It was decided that the best course of action was to block the body's natural-healing processes, thereby preventing the occurrence of restenosis-rather like straightjacketing the fireman to stop him from putting out the fire.

By the 1990s, the race was on to find drugs that could prevent re-stenosis. First onto the market was American pharma giant Johnson & Johnson, with its drug sirolimus. This powerful immunosuppressive drug is often used to prevent organ rejection in transplant patients. However, the idea of giving such a powerful system-wide compound to a patient with just a few narrowed heart arteries would seem to be a case of overkill (possibly even literally), so the industry came up with an ingenious solution: to target the drug directly to the artery. This is achieved by coating the stent with a thin polymer containing the immuno-suppressant, allowing low doses of the drug to slowly leach out onto the artery walls. The process is called 'elution', so these new stents are known as 'drug-eluting stents' (DES).

Drip-fed drugs

The DES are now the fastest-growing sector in the field of medical appli-ances. Cypher, Johnson & Johnson's version, hit the market in April 2003, and cardiologists couldn't get hold of them fast enough. Within less than a year, 350,000 Americans had been implanted with them. But other drug companies have been close at J&J's heels. Today, at least three major companies are vying for a share of what is turning out to be an extraordinarily lucrative market-these high-priced devices have made it worth $5 billion

a year from worldwide sales. Already, the latest estimate is that some four million people are wandering around with DES inside them.

Manufacturers claim that the new devices have dramatically reduced restenosis rates to less than 15 per cent-and the crude statistics show that it's true. Be that as it may, behind the glowing headlines is what the manufacturers may not readily tell you-that these devices also come with a lot of baggage.

First, DES require that patients take yet more drugs. Why?

Almost as soon as the first DES were implanted, doctors were alarmed to find the patients dying in relatively large numbers. The problem was quickly traced to subacute arterial thromboses-blood clots around the stent. As a result, barely six months after they had given DES the go-ahead, the US' regulatory Food and Drug Administration (FDA) had to issue an official Public Health Notification, warning of the excess mortality associated with these devices. Indeed, the FDA required J&J to send a flurry of 'Dear Colleague' cautionary letters to doctors-so often the first toll of the bell for doomed drugs in the past.

How has Medicine dealt with the DES clotting problem? The solution has been, yet again, to attempt to thwart the body's natural healing, this time by employing more powerful anticlotting agents. Today, this means that virtually every patient fitted with a DES is routinely required to take a minimum of two so-called antiplatelet drugs, such as clopidogrel and aspirin. Of course, none of these drugs comes without side-effects-not least of which are the hazards of excessive bleeding after injury, both outside of and within the body.

So, doctors now have a difficult high-wire act to perform, as they must strike a fine balance between giving enough antiplatelet drugs to prevent clotting, but not so much as to endanger the patient's life. The added problem is that these drugs may need to be taken 'indefinitely', says leading DES researcher Dr Robert Harrington, of the Duke Clinical Research Institute, "or at least until we have definitive clinical trials to prove otherwise".

The headlong rush into stenting has also obscured another major problem with DES. For some patients, these new devices have turned out to be killers.

Matters of life and death

The most recent bombshell was dropped in March of this year. Swedish doctors had spent three years tracking the health of over 20,000 patients fitted with either DES or the earlier versions, so-called 'bare-metal' stents. What they found sent a shiver through the industry. The Swedish medical records showed that more people had heart attacks or died with the DES inside them than with the old-fashioned plain metal stents. Nor was this just a statistical blip. Month after month, the death and heart attack rates consistently diverged so that, by the third year of tracking, there was an average of 30 per cent more deaths among the DES patients (N Engl J Med, 2007; 356: 1009-19).

Why have people been dying from DES? Many experts now believe the major reason is that these stents seem to cause a new kind of blood clot, one that gradually increases over time-in blood clots with the old bare-metal stents. According to the most recent study by a Swiss and Dutch team of experts, the incidence of this so-called 'late stent thrombosis' is now about 3 per cent, but increasing annually by 0.6 per cent a year (Lancet, 2007; 369: 667-78). These figures may not sound like much, but American cardiologists have calculated that they translate into more than 2000 unnecessary, pre-mature deaths a year in the US alone (Ann Intern Med, 2006; 144: 913-9).

Even cardiologists who have ties with the stent industry now acknow-ledge that DES have a problem. "We were seduced by the early clinical data into believing DES conferred coronary artery immortality," admits Professor Martin Leon, of Columbia University and an advisor to three major stent manufacturers. "Unfortunately, there are aberrant pathobiological res-ponses, with local inflammation and delayed healing."

It's the very drugs within the stents that are thought to be the issue. In preventing restenosis, the eluting drugs inevitably also interfere with the artery's own natural-healing processes. It's now dawning on cardiologists that the early bare-metal stents may have been superior after all because, in some cases, the body was able to incor-porate the stent into the arterial wall by growing a protective skin over it.

One of the fiercest critics of DES is top pathologist Dr Renu Virmani, of the Armed Forces Institute of Pathology in Washington, DC. Her attacks on the DES industry are fuelled by the evidence she has found on the mortuary slab. Repeatedly, she has discovered what she calls "substantial impairments in arterial healing" in the corpses of DES patients (Circulation, 2007; 115: 2435-41). "It takes much longer for a vessel with a DES to heal; late stent thrombosis is a serious problem," she says.

Other problems have been popping up, too. In a worldwide survey of stent patients, Swiss doctors have shown that, compared with bare-metal stents, J&J's Cypher (the market-leading DES) has caused a significant number of excess deaths-and not from cardiac problems, but cancer (Eur Heart J, 2006; 27: 2784-814). So far, this appears to be the only evidence showing a cancer connection, but the discovery remains a serious straw in the wind.

"It's eerily reminiscent of Vioxx," says US cardiologist Dr Sanjay Kaul, referring to the infamous antiarthritis painkilling drug that was taken off the market in 2004 after being linked to heart attack and stroke. "Initially, we didn't see the signal because the incidence is so rare."

Quo vadis?

The world of cardiology is currently in ferment over stents, with doctors arguing fiercely over the data for blood clots, side-effects and the value of DES. But all of this turmoil obscures the true bottom-line issue at stake here: what is the evidence that stents-of any ilk-save lives?

Eight years ago, before the advent of DES, a full scientific review of the clinical data on stents was conducted by experts at the University of Birmingham. "Stents are expensive; are they effective?" was their simple question. Their answer-no. There is "no evidence" that stents reduce the rates of death or even prevent heart attacks, they reported. The only value they appear to have is for the pain of angina but, even then, it's only "a small advantage" (Health Technol Assess, 2000;

4: 1-153).

What about after DES? When these first came onto the market, they were confidently predicted to reduce death rates by at least 20 per cent. However, a major meta-analysis by a team at the University of Liverpool found that these devices have had not the slightest effect on patient mortality: death rates after DES implants are exactly the same as with the older stents. For the long term, the researchers say that even an arterial graft (a heart bypass) would be a better bet, despite its expense and initial dangers (Health Technol Assess, 2004; 8: iii-iv, 1-242).

This bleak assessment becomes even blacker in light of the above-mentioned data from the 20,000 Swedish patients, showing increased death rates with the DES.

The history of medicine is already littered with treatment disasters. They have often been well-intentioned, but have failed because of an error in the underlying medical model-specifically, that the body is a machine. The stent was clearly born out of this mechanistic paradigm-yet another good reason that stents should now be added to the long list of modern medical failures.

Tony Edwards

Stent side-effects

The basic angioplasty-stent procedure is not at all risk-free:

- In nearly one in two cases, it can cause "impairment of cardiac function"

(Ital Heart J Suppl, 2005; 6: 553-60)

- In one in 25 cases, it can, ironically, bring on a heart attack

- In one in 100 cases, it can even cause death (Coron Artery Dis, 2006; 17: 71-5).

Once in place, stents can cause pain, rash, respiratory problems, hives, itching, fever and blood-pressure changes.

The antiplatelet drugs that have to be prescribed with stents may cause:

- increased bleeding in the brain and other internal organs

- bleeding in the stomach and intestines

- increased bruising

- stomach irritation

- allergic reactions

- low white-blood-cell counts (neutropenia) and low red-cell counts (anaemia).

Fact: 30 per cent of stent patients subsequently have a "major adverse coronary and cerebral event", which is nearly three times the rate following coronary artery bypass surgery (BMJ, 2007; 334: 617-21).

Stents we've been spared

CoStar

This futuristic DES uses a new 'bioresorbable' polymer. Unlike conventional DES, it is not coated with drugs, but bears hundreds of tiny holes, each acting as a drug reservoir. After the drug is released, the polymers are absorbed into the body, "leaving no permanent residual polymers or drug at the target site", according to the manufacturers. First launched in Europe in February 2006 after clinical trials showed that it offered "significant patient benefits", it has now been withdrawn-barely a year later. A few months ago, a clinical trial in the US was prematurely discontinued after revealing "significantly higher major adverse cardiac events" with CoStar than with conventional DES. Made by Conor Medsystems, which is a subsidiary of Johnson & Johnson (who make the Cypher stent), J&J say they'll dump CoStar and just concentrate on selling more Cyphers instead.

Magnesium stent

So new that it hasn't even got a name, this is another bioabsorbable stent meant to dissolve away "within a few months", having temporarily bolstered the artery. However, a muticentre European trial reported last month that, in nearly half of the patients, the artery became obstructed again, requiring a repeat operation (Lancet, 2007; 369: 1869-75). Although its manufacturer Biotroniks has made no formal announcement yet, our prediction is that this stent will be quietly binned.

Ancure

A stent designed for aneurysms in the abdominal aorta, the main artery from the heart, this was approved in 1999 by the US Food and Drug Administration after clinical trials had shown it to be effective. Yet, by 2003-after being voluntarily recalled by its manufacturer Guidant, then reapproved by the FDA in 2001-it was finally discontinued because of serious malfunctions that resulted in patient deaths. Guidant was fined $92.4 million for various criminal and civil charges, including covering up the problems they knew came with the device. The company was bought by Boston Scientific in 2006.

Saying no to stents

Stents do work for reducing angina, the pain that comes from having narrowed arteries. However, if you have angina, try:

- Lifestyle changes. One clinical trial involving 2297 heart patients with at least one blocked coronary artery found that simple improvements in lifestyle can be just as effective as stents. In the study, some patients were given stents, while others were told to stop smoking, exercise more and improve their diet. The researchers found that the latter patients fared significantly better than the stented patients: they lived as long, if not longer, and their quality of life was far higher (JAMA, 2007; 297: 1967-8).

Dr Steven Nissen, the immediate past-president of the American College of Cardiology, hopes that this bombshell discovery may put an end to the "irrational exuberance that surrounds stenting".

- Chelation therapy. This unconventional treatment is offered by some alternative cardiologists. It involves transfusing the synthetic amino-acid EDTA (ethylenediaminetetraacetic acid) through the patient's veins in order to unblock the arteries. The technique is already well accepted as a treatment for heavy-metal poisoning, but there have been no convincing clinical trials of its value in heart disease. Thus, it remains an unproven technique at present. In spite of this, US government advisors believe that the many thousands of successful case histories justify putting $30 million towards a major clinical trial involving more than 2000 patients. The study began in 2003, and the results are expected to be announced next year.

Preventing blocked arteries

Avoid

- processed foods containing trans or hydrogenated fats

- low-fat/low-cholesterol foods

- a high dairy intake.

Choose

- foods high in omega-3 fatty acids (such as trout, salmon, mackerel and walnuts)

- a Mediterranean diet (olive oil, wholegrains, fruits and vegetables, and red wine in moderation)

- green tea-seven cups a day (Arch Latinoam Nutr, 2004; 54: 380-94).

Take

- vitamin C (at least 500 mg/day)

- folic acid (1 mg/day)

- vitamin B12 (0.5 mg/day)

- regular exercise in the form of "intermediate to vigorous physical activity" (Scand J Public Health, 2007; 35: 4-10).

- Make lots of friends-sad and lonely people are three times more likely to have a heart attack (Am J Epidemiol, 1988; 128: 370-80).


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