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| Archive : Fall 2005 |
Reasons for Hope:
Vampire bats, cell-suicide preventers, free-radical scavengers, neuron revivers, improved logistics for better care faster.
Why Strokes Still Kill
 By Cathryn M. Delude
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C onsidering the plight of most people in her situation, Becky Hemingway was faring well. Her
right side had gone numb, and she couldn't speak. But her family had immediately suspected a stroke, and emergency room physicians at a hospital in South-bridge, Mass., not only made the diagnosis but also rushed the 31-year-old new mother to a regional stroke center in Boston, two hours to the east, where she could receive specialized care.
In contrast, the average stroke victim doesn't get treated for almost a day, though the only approved current drug therapy must begin within three hours. Nine out of 10 strokes are ischemic, resulting from blood clots that cut off the oxygen supply to brain tissue, and the drug—tissue plasminogen activator, or TPA—dissolves clots. Given too late, however, TPA can further weaken blood vessels in the brain, increasing the risk of a potentially fatal hemorrhage. What's worse, medical researchers have recently concluded that TPA itself might be toxic to some brain cells. Because of such risks, most physicians are reluctant to administer TPA even within the three-hour window. And the 3% of patients who receive the drug on time have a less than even chance of a positive outcome.
So stroke remains a prodigious killer, taking 165,000 lives annually in the U.S. (Only heart attacks and cancer are deadlier.) Another 535,000 stroke victims survive each year, but many have lifelong disabilities—ranging from complete paralysis and cognitive dysfunction to impaired speech. That makes stroke one of the nation's most expensive diseases, costing an estimated $57 billion a year.
With a large clot obstructing her middle cerebral artery, Hemingway risked landing on the wrong side of the statistical divide. Yet after her ambulance arrived at the Massachusetts General Hospital and she was rushed to the neurology unit for a CAT scan, the images of her brain gave neurologist Lee Schwamm hope. Though the tissue adjacent to the clot was already dead, the surrounding area might still be saved if blood flow could be quickly restored, a process known as reperfusion.
Normally, stroke patients receive high doses of TPA intravenously. But in Hemingway's case, a chest X-ray suggested that her heart was enlarged and possibly surrounded by fluid, and TPA, coursing through her bloodstream, could cause fatal bleeding. Moreover, her blood clot was so large that it might not respond to conventional intravenous TPA treatment. "Intravenous TPA is good at dissolving small clots in smaller arteries but not so good with clots in major arteries, which can be centimeters long," says Schwamm, the head of the hospital's Acute Stroke Service.
Schwamm recommended an experimental procedure intended to deliver TPA directly into the blocked artery, thereby reducing the amount of the drug needed as well as the risk of hemorrhage. The hospital's interventional neuroradiology team inched a catheter through an artery in Hemingway's groin, using real-time X-ray images to guide the threadlike wire into the middle cerebral artery. When the catheter tip reached the clot, the endovascular team squirted the TPA. The massive blockage melted away under the direct hit.
Such alternative treatments are few and experimental; they're used in pilot studies and clinical trials or as a last resort. And they're available only at large research hospitals and specialized stroke centers. Very few victims benefit, and statistically, improvement has been slow. Between 1991 and 2001, the death rate from stroke fell by 11%—less than half the 25% improvement for deaths from coronary heart disease. Still, progress may finally be picking up, in part through a better understanding of what happens during a stroke and the development of better drugs and combinations of therapies. But another part of the solution involves logistics—quickly getting patients to stroke centers where they can receive state-of-the-art treatment.
The first big clinical breakthrough came in 1996, when the FDA approved TPA for stroke treatment, eight years after the drug was cleared as a heart attack therapy. It's a genetically modified form of a naturally occurring enzyme whose normal role is to activate plasmin, another enzyme, which degrades the fibrin fibers that form a mesh netting for platelets and other blood cells when a clot forms. By snipping apart the fibrin, plasmin dissolves the clot.
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Photo: Creatas
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