Cardiologist: potential benefits outweigh small time delay in enrolling patients with chest pain in clinical trial

November 14, 2000

NEW ORLEANS - Enrolling patients with chest pain in a cardiology clinical trial takes time, but not enough to offset the benefits of clinical research, researchers at Duke University Medical Center say.

In the first study that examines such time issues, researchers found it takes an average of 8+ minutes longer to enroll a patient in a trial of clot-busting drugs than to treat patients directly (50+ minutes compared to 42 minutes).

While that time difference is "statistically significant," it isn't nearly as important as many doctors assume it is, said the study's lead researcher, Duke Clinical Research Institute cardiologist Dr. John Alexander, who prepared his study for presentation Wednesday at the 73rd annual scientific session of the American Heart Association.

"Many doctors have the impression there is a great delay in enrolling patients in trials, and for that reason, they often are hesitant to have their sickest patients participate, believing that every minute to therapy counts," he said.

"This is a mistake. Participation in clinical trials is good for patients and critical for advancing the treatment of heart attacks," Alexander said. "While time is of the essence, especially in the use of thrombolytic therapy, we've found that the delay in enrolling patients in clinical trials is small enough, and the potential benefits large enough, that we believe physicians should change their practice and enroll more of their patients in these trials."

Physicians should, however, work in general to reduce the time it takes to use thrombolytic therapy - whether or not a patient is enrolled in a clinical trial. Guidelines for use of these clot-busting drugs suggest they should be administered to a patient with a suspected heart attack within 30 minutes of arrival at a hospital. "For each hour delay, 1.6 lives are lost per 1,000 patients treated," Alexander said.

The eight additional minutes needed to enroll a patient in a clinical trial is used to determine if the patient qualifies for the trial, to explain the trial to the patient or family member and have a consent form signed, to telephone a study center to "randomize" the patient to a treatment arm, and to retrieve a specified drug kit and administer it. While that seems like a lot to do in a small amount of time, Alexander said researchers have to continue to work to reduce the time even further, such as by making trials less complex. "There is no amount of time when shorter is not better," he said.

Alexander led the "Emergency Department Registry" sub-study, an offshoot of the ASSENT-2 clinical trial that compared two different thrombolytic therapies in patients experiencing a heart attack. He and a team of researchers examined the records of all patients at 63 hospitals in the United States and Canada who had been given clot-busting drugs in the emergency department of these medical centers within a two-month period in 1999. Of these patients, 176 were enrolled in ASSENT-2 and 307 were not. All the patients had chest pain that had lasted less than 12 hours.

The researchers simply examined how long, on average, it took for ASSENT-2 patients to receive their clot-busters (50.5 minutes), compared to the other patients (42 minutes) - a difference of 8.5 minutes. They then "adjusted" those times to reflect differences in the medical condition between patients enrolled in ASSENT-2 and those not enrolled. When the groups were made similar, the difference in time-to-treatment between the two groups was reduced to 38 minutes for patients not enrolled in ASSENT-2 and 43 minutes for ASSENT-2 patients - a difference of only five minutes.

Alexander called this adjusted five-minute delay "modest."

The researchers did not examine differences in the medical outcome of treatment due to the delay in enrolling patients into the trial. "That's not calculable from this study, although I doubt there were significant clinical consequences due to the eight-minute delay," Alexander says. "But we also know, based on other large studies, that the benefit of thrombolytic therapy does decrease as more time passes."
-end-


Duke University Medical Center

Related Heart Attack Articles from Brightsurf:

Top Science Tip Sheet on heart failure, heart muscle cells, heart attack and atrial fibrillation results
Newly discovered pathway may have potential for treating heart failure - New research model helps predict heart muscle cells' impact on heart function after injury - New mass spectrometry approach generates libraries of glycans in human heart tissue - Understanding heart damage after heart attack and treatment may provide clues for prevention - Understanding atrial fibrillation's effects on heart cells may help find treatments - New research may lead to therapy for heart failure caused by ICI cancer medication

Molecular imaging identifies link between heart and kidney inflammation after heart attack
Whole body positron emission tomography (PET) has, for the first time, illustrated the existence of inter-organ communication between the heart and kidneys via the immune system following acute myocardial infarction.

Muscle protein abundant in the heart plays key role in blood clotting during heart attack
A prevalent heart protein known as cardiac myosin, which is released into the body when a person suffers a heart attack, can cause blood to thicken or clot--worsening damage to heart tissue, a new study shows.

New target identified for repairing the heart after heart attack
An immune cell is shown for the first time to be involved in creating the scar that repairs the heart after damage.

Heart cells respond to heart attack and increase the chance of survival
The heart of humans and mice does not completely recover after a heart attack.

A simple method to improve heart-attack repair using stem cell-derived heart muscle cells
The heart cannot regenerate muscle after a heart attack, and this can lead to lethal heart failure.

Mount Sinai discovers placental stem cells that can regenerate heart after heart attack
Study identifies new stem cell type that can significantly improve cardiac function.

Fixing a broken heart: Exploring new ways to heal damage after a heart attack
The days immediately following a heart attack are critical for survivors' longevity and long-term healing of tissue.

Heart patch could limit muscle damage in heart attack aftermath
Guided by computer simulations, an international team of researchers has developed an adhesive patch that can provide support for damaged heart tissue, potentially reducing the stretching of heart muscle that's common after a heart attack.

How the heart sends an SOS signal to bone marrow cells after a heart attack
Exosomes are key to the SOS signal that the heart muscle sends out after a heart attack.

Read More: Heart Attack News and Heart Attack Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.