Vulnerability of the brain and heart after cardiac arrest

Article Abstract:

In the May 2, 1991 issue of The New England Journal of Medicine a team of physicians report the results of a trial of the calcium-channel blocking drug lidoflazine for the prevention of death or brain damage after a heart attack. The treatment did not work, and the Journal is to be commended for publishing a negative result. Although negative results are often less exciting, they may be exceedingly important for the actual practice of medicine. However, the question must be asked, "Why didn't lidoflazine work?" In the laboratory, lidoflazine and other calcium channel blockers prevent the flow of calcium into cells, which harms cells and ultimately contributes to their death. In the real hospital setting, however, heart attacks do not occur according to a carefully planned laboratory protocol. The most likely explanation for the failure of the treatment is that, in the real world, the damage proceeds too quickly for intervention to be practical. In laboratory research, 15 to 20 minutes of interrupted blood supply is sufficient to cause extensive brain damage. And this, of course, is under controlled conditions in which the circulation is turned back to good-as-new when the 20 minutes are up, a condition which is not met when heart attacks occur on the ward. Curiously, though, in the enthusiasm to protect the brain against damage when the heart stops beating, some people seem to have forgotten that the heart itself is more sensitive to oxygen deprivation than the brain. While the search for drugs that might prevent brain damage is admirable, greater benefit might accrue from learning to prevent the heart attack in the beginning, or quickly reestablishing circulation to the heart muscle. Even at present, patients with good recovery of neurological function after a heart attack die a month or two later because of damage sustained by their hearts. (Consumer Summary produced by Reliance Medical Information, Inc.)

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A randomized clinical study of a calcium-entry blocker (lidoflazine) in the treatment of comatose survivors of cardiac arrest

Article Abstract:

Resuscitation is necessary, but not sufficient, to save a heart attack victim. More than half of resuscitated patients die during hospitalization. In many cases, the cause of death is injury sustained by the brain because of lack of adequate blood flow, a condition called ischemia. There is some reason to believe that the flow of calcium ions into brain cells might play a role in the cell death which follows ischemia in the brain. Calcium flow clearly precedes cell death in the brain, and experiments in laboratory animals have shown that drugs which decrease the influx of calcium also reduce the extent of the resulting brain damage. However, as convincing as some of the laboratory data might be, it has not yet been shown that similar calcium-blocking treatments might be of value to human heart attack victims at risk for ischemic brain damage. Lidoflazine, an experimental drug which blocks calcium channels in the cell membrane, was used in the treatment of patients who remained comatose after resuscitation for cardiac arrest. A total of 520 patients were included in the study; they were randomly assigned to receive either lidoflazine or placebo. No statistically significant differences were found between the lidoflazine group and the control group. Eighty-two and 83 percent of the lidoflazine and placebo group, respectively, died during six months of follow-up. Fifteen and 13 percent of the lidoflazine and placebo group, respectively, recovered good cerebral function, and 1.2 and 1.9 percent, respectively, suffered severe neurological damage. Other calcium-channel blocking drugs may yet be shown to provide benefit. However, the present data indicate that lidoflazine is of no benefit in the treatment of comatose survivors of cardiac arrest. (Consumer Summary produced by Reliance Medical Information, Inc.)

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Amaurosis fugax

Article Abstract:

Amaurosis fugax, a temporary loss of vision in one eye, can be caused by several disorders. These include atherosclerosis of the carotid artery, increased blood viscosity or blockage of a blood vessel by a blood clot or other material. Amaurosis fugax caused by spasm of a blood vessel is not common. One research study examined the treatment of nine patients with spastic amaurosis fugax. Three patients had an episode of amaurosis fugax while their eye was being examined. Spasm of a blood vessel is often difficult to diagnose. Some patients diagnosed with these spasms may have other underlying diseases that cause blood vessel obstruction. Obstruction of a blood vessel may be the actual cause of amaurosis fugax in these patients.

Editorial, Causes of, Amaurosis fugax, Angiospasm

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