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Drug fails to arrest cardiac aftereffects.

Imagine the unthinkable: Your heart suddenly stops beating. Within minutes, paramedics jump-start it with an electrical jolt and rush you to a nearby hospital emergency room. But even with such rapid treatment, you face more than a 50-50 chance of dying from the cardiac arrest. And if you survive it, you may suffer lingering brain damage.

That's because scientists have yet to discover a way to block the damaging aftershocks of cardiac arrest. When the fist-sized heart muscle stops pumping blood, calcium rushes into cells throughout the body. This microscopic event interferes with the cells' energy-producing machinery, often destroying particularly vulnerable cells such as those in the heart and brain.

Animal studies have suggested that drugs called calcium-channel blockers can protect fragile brain and heart cells after heart stoppage. But bad news about calcium-channel blockers surfaced late last year, when a Finnish team reported that one such drug, called nimodipine, failed to guard against calcium-inflicted damage in most men and women who had suffered cardiac arrest.

A large, international research team now reports discouraging results with another calcium-channel blocker, called lidoflazine.

"The bottom line is this particular drug doesn't work," concludes cardiac-care specialist Normal S. Abramson, who codirected the study with Peter Safar, a colleague of his at the University of Pittsburgh. Nonetheless, the study may point the way to an effective weapon against the brain-damaging aftermath of cardiac arrest, they say.

The international team studied 516 people whose hearts had stopped beating, including victims of heart attack, severe asthma and other respiratory difficulties that can trigger cardiac arrest. All 516 men and women remained in a coma for at least 10 minutes after emergency treatment to restart the heart. Within 30 minutes of restarting the heart, the investigators randomly assigned each patient to one of two groups to receive intravenous infusions of either lidoflazine or placebo solution. Because the solution vials were coded, the researchers remained unaware of who got the placebo and who got the experimental drug.

After six months, the team found that lidoflazine had provided no survival benefit: 82 percent of the lidoflazine group and 83 percent of the placebo group had died at some point after the cardiac arrest, in most cases succumbing to serious brain injury or a second heart attack.

And among the survivors, the experimental drug proved no more likely to stave off brain damage than did the placebo. In the May 2 NEW ENGLAND JOURNAL OF MEDICINE the investigators report that 15 percent of the lidoflazine group, compared with 13 percent of the controls, showed good recovery of brain function at the end of the six months.

Even so, Safar remains hopeful about lidoflazine's ability to minimize brain damage. For instance, he told SCIENCE NEWS, unpublished data from the same study hint that lidoflazine may provide some brain protection to a subgroup of cardiac arrest patients -- those who show stable blood pressure soon after the arrest. He declined to elaborate on this preliminary finding.

It remains unclear why the drug failed in its mission to protect brain and heart cells from the toxic effects of calcium, notes Fred Plum of the Cornell Medical Center, who wrote an editorial accompanying the lidoflazine report. In future studies, he says, scientists may find that the drug didn't reach damaged areas of the heart and brain quickly enough and/or in sufficient concentrations.

On the other hand, adds Abramson, it may take several drugs to safeguard the heart and brain against the destructive cascade triggered by reduced blood flow. "We have a long way to go," he says.
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Title Annotation:lidoflazine, a calcium-channel blocker
Author:Fackelmann, Kathy A.
Publication:Science News
Date:May 4, 1991
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