The Future of Your Heart Attack
SO CARDIOLOGY HAS JUST GIVEN UP ON TAKING THE KNIFE OUT OF TREATING HEART DISEASE?
Certainly it's gone more slowly than my doctor buddies predicted, and perhaps with good reason. Though open-heart surgery is among the bloodiest of operations, It is also quite effective: It can give heart-disease patients another fifteen years of life or more, and the mortality risk of the operation itself is less than 2 percent. This has made a lot of surgeons reluctant to look beyond it too seriously, even though patient--and potential patients--continue to clamor for less-traumatic approaches.
But cheer up. Some reel advances may be just beyond the horizon. At the Texas Heart Institute in Houston, scientists have been pursuing a new schema of heart disease, one that eschews the idea that heart attacks are caused simply by an accumulation of cholesterol-based plaque in the coronary arteries--like a clogged drain--and asserts that they're caused more by an inflammation of some of that plaque, which causes it to rupture and then form a blood clot, which is the true evil-doer in the heart-attack process. Moreover, they've discovered that often the most "vulnerable" plaque is that which is contained in the thinnest blockages, leading to one of the enduring mysteries of heart disease: the fact that about half of all heart attacks occur in arteries where the plaque is blocking no more than 50 percent of the vessel. Given this scenario, they have reasoned, the key to preventing heart attacks is identifying which portions of artery walls are most prone to this sort of rupture and medically or surgically reducing or eliminating the threat.
Working with other scientists, Texas doctors James T. Willerson and Ward Casscells have figured out the most vulnerable plaques are those that are most inflamed, and the most inflamed tend to be hotter than normal tissue by about 3 to 5 degrees. So they've devised a special catheter rigged with microscopic thermometers that can be eased into the coronary arteries to identify the hot spots.
The catheter is now in clinical trials and is probably several years from being in your cardiologist's bag of tricks. And, of course, even when he does have it at his disposal, he won't necessarily know what to do about those hot spots that he discovers. It's tempting to think that if we could just take care of wherever it is that's causing the inflammation, we'd have the magic bullet for heart disease. The problem is, the more science learns about the inflammation process in coronary arteries, the more complicated things get The interior walls of arteries can be inflamed by cigarette smoke, the oxidation of LDL (bad) cholesterol, hypertension, high levels of homocysteine or C-reactive protein, and certain viruses and bacteria that may be living in your system asymptomatically. It's doubtful that even the most obsessive-compulsive dieter, exerciser, and cholesterol and blood-pressure checker could keep all those variables stabilized, particularly since in many cases they are mediated by genes, not behavior.
Some doctors see the answer in earlier and better-targeted use of stents and statins (cholesterol-lowering drugs, which also seem to have an effect on inflammation), but that sounds a bit timid. Willerson and other scientists think they may have struck upon a new approach that has to do with exposing the inflamed tissue to... lasers. Willerson's idea is that if vulnerable plaque can be pinpointed by a heat-sensing catheter, it can be melted away by simply heating it just a bit with a laser attached to the same catheter. And a California biotech concern, Pharmacyclics, is testing the combination of a drug treatment with the intense light of a laser to effect apoptosis, or cell suicide, of plaque cells.