Millions of Americans have had stents, small wire cages, inserted in their coronary arteries to prop them open. And many are convinced the devices are protecting them from heart attacks. After all, a partly blocked artery is now cleared, and the pain in a heart muscle starved of blood often vanishes once the artery is open again.
But while stents unquestionably save the lives of patients in the throes of a heart attack or a threatened heart attack, there is no convincing evidence that stents reduce heart attack risk for people suffering from the chest pains known as stable angina.
These are people who feel tightness or discomfort walking up a hill, for example, because a partly blocked coronary artery is depriving their heart of blood. But the pain or tightness goes away if they stop and rest or just stay still. And there is a reasonable argument that drugs, cholesterol-lowering statins in particular, might be just as good at reducing such pain.
“It is kind of amazing that we don’t have the evidence,” said Dr. David J. Maron, the director of preventive cardiology at Stanford.
Now, the National Heart, Lung and Blood Institute is trying to find out whether stents do in fact prevent heart attacks. The answer could change the standard of care for the more than half a million Americans annually who receive a new diagnosis of heart disease after they see a doctor for angina.
Heart disease remains the biggest killer of Americans despite significant treatment advances in the past decade.
The typical treatment for angina is to thread a narrow catheter up from a blood vessel in the groin to the heart, squirt in a dye that allows a cardiologist to see blockages in arteries on X-rays, and then insert a stent in the blocked areas. Stents are safe but expensive. Medicare payments vary depending on what kind of stent is used and how many, but are generally above $10,000 and can be more than $17,000.
And stents are not always a permanent solution to chest pain, as Albert Nassar of New York discovered. When he had angina four years ago, the reason seemed clear and the solution straightforward. An angiogram, the test in which dye is injected into the coronary arteries, showed one was 90 percent blocked. When a doctor inserted a stent to open that artery, the pain vanished.
But three years later, Nassar, 59, again felt tightness in his chest as he rode a recumbent bike at the gym. He said he expected another stent, but his cardiologist surprised him. He told Nassar that the medical profession does not actually know if stents help people like him with moderate to severely blocked coronary arteries.
Then he asked Nassar if he would be part of the National Heart, Lung and Blood Institute clinical trial, known as Ischemia, and have his treatment decided randomly between two options. If he was assigned to one group, his doctors would look at his blocked artery with X-rays and open it mechanically with a stent or, if the X-rays showed he was among the minority whose blockage could not be opened with a stent, with bypass surgery. He would also be asked to take drugs and change his lifestyle to protect his heart. In the other, his treatment would consist solely of drugs and the lifestyle changes. There would be no peeking at his blockage.
Nassar leapt at the chance and when he was assigned to take the drugs — a statin, blood pressure drugs and an aspirin — he was delighted.
“I didn’t feel the urge to have another surgical procedure,” he said. “I’ve had enough of those.”
Underlying the debate about the utility of stents is an uncertainty about how and why heart attacks occur.
For years, the common notion was they were caused by a plumbing problem. In this view, plaque — pimplelike lumps — partly blocked a coronary artery and grew until no blood could get through, and a stent was needed to open an artery before it closed completely.
But a leading hypothesis says there is no predicting where a heart attack will originate. It could start anywhere there is plaque, even if the plaque is not obstructing the flow of blood in an artery. Unpredictably, a piece of plaque can burst open. Blood starts to clot on the injured area. Soon, the blood clot clogs blocks the artery. The result is a heart attack.
It is known that certain plaques, with thin walls and bursting with fat-filled white blood cells, are prone to rupture. A study published in 2011 found that only a third of heart attacks originated in plaques that were blocking at least half of an artery, as seen on an angiogram. The rest began with the rupture of plaques that appeared to be causing no problems.
According to this view of how and why heart attacks happen, stenting would not be protective because people with atherosclerosis have arteries studded with plaque. The partly blocked area visible in an angiogram is no more likely to be the site of a heart attack than any other with plaque. But statins could work because they change the nature of plaques, making them less likely to rupture.
Although stents relieve chest pain, today’s medical therapy can, too, though it may take weeks or months.
The issue potentially affects many heart patients. “Half the people over 65 have blockages,” Dr. Gregg W. Stone, an interventional cardiologist at Columbia, said. “If you have some degree of atherosclerosis, you have blockages.”
And once a stress test or an angiogram reveals a blockage, it can be hard to ignore a partly blocked artery, hard to avoid thinking a stent has to help.
“People believe that if they have a blockage, they have to fix it mechanically,” said Dr. Judith S. Hochman, the study chairwoman for the Ischemia trial and a cardiologist at NYU Langone. “It seems logical, but in medicine, many things that seem logical are not true.”