Using a “clot buster” drug normally reserved for treating patients during a heart attack, emergency room doctors were able to double the number of patients who could be revived from cardiac arrest. This sudden loss of heart function occurs in more than 260,000 people a year nationwide – and at least 93 percent of them die.
“Clot-busting agents show promise as a new therapy for this abrupt and catastrophic loss of heart function,” said William P. Bozeman, M.D., an emergency medicine specialist at Wake Forest University Baptist Medical Center and lead author on the study, reported in the June issue of the journal Resuscitation and available now on-line.
The pilot study involved patients with cardiac arrest who didn’t respond to standard therapy. Of 50 patients who received clot-busting therapy, 26 percent were revived, compared to 12 percent of patients who got standard therapy alone. However, not all patients who were revived lived long enough to be discharged from the hospital.
The study was conducted while Bozeman was at the University of Florida’s Shands Medical Center and included three affiliated hospitals. It involved patients with cardiac arrest, which often occurs when the electrical signals that regulate the heart become erratic or irregular because of a heart attack, coronary heart disease, a blood clot in the lungs, or other causes. The heart stops beating and the brain starts to suffer permanent damage within four to six minutes. Death quickly follows.
The standard treatment for cardiac arrest is Advanced Cardiac Life Support (ACLS) measures, which include cardiopulmonary resuscitation (CPR), drugs such as adrenaline, and defibrillation, an electric shock to the heart.
“We are in dire need of additional treatment options for sudden cardiac arrest because there is only a 5 percent to 7 percent survival rate using interventions we now have,” said Bozeman, associate professor of emergency medicine. “We hope this small study will lead the way for additional research on this promising new approach.”
Fifty patients who did not respond to treatment with ACLS interventions were given the clot-buster tenecteplase, known medically as a fibrinolytic agent. Spontaneous circulation returned in 26 percent of these patients. Four percent survived and were discharged from the hospital and had normal brain function. In the group of 113 patients who received ACLS alone, 12 percent were revived, but none lived long enough to leave the hospital.
The patients who were treated with tenecteplase had been receiving ACLS measures for a mean of 30 minutes and received a mean of eight doses of standard medications.
“The study supports the use of fibrinolytic drugs in select cases of cardiac arrest where patients don’t respond to standard therapy, and it reinforces the need for additional studies of this therapy,” said Bozeman.
Tenecteplase is approved by the Food and Drug Administration for treating patients suffering from acute heart attacks or pulmonary embolism (blockage of an artery in the lungs that can cause heart rhythm problems). Clot-busting drugs aren’t typically used in patients with cardiac arrest because of concerns that the chest compressions used during CPR could cause bleeding complications.
Several small studies, however, have suggested that clot-busting medications, in combination with CPR, may improve overall survival. Bozeman’s study is the first in the United States to observe the effects of treatment with tenecteplase and with standard therapy.
Tenecteplase was developed and is marketed by Genentech Inc. of South San Francisco as TNKaseTM. Genentech also provided support for the study.
