|
Stroke-associated damage to brain structure
may lead to heart attack
Image analysis clarifies role of
brain area involved with physiologic stress response
BOSTON - April 24, 2006 - Researchers using a new method
of analyzing brain images have identified an area of the brain that,
when affected by a stroke, may also cause damage to the heart muscle.
The study, from the Martinos
Center for Biomedical Imaging at Massachusetts General Hospital
(MGH), finds that stroke patients with damage to the right insula,
an area deep within the brain, were much more likely also to have
biochemical evidence of myocardial damage occurring in the days
following their stroke. Their report will appear in the May 9 issue
of the journal Neurology and has received early online release.
"The link between the brain and the heart in stroke patients
is fascinating. For instance, most patients with acute stroke have
elevated blood pressure that returns to baseline over three to seven
days. The connection is believed to be through the autonomic nervous
system, but what the mechanism is has been unclear," says A.
Gregory Sorensen, MD, of the Martinos Center, the paper's senior
author. "By finding a specific brain area associated with a
dramatically increased risk of heart damage, we can identify at-risk
patients when they arrive at the hospital and put them on protective
therapy, which should have a direct impact on their care."
About 5 percent of stroke patients will also have a heart attack
- damage to their heart muscle - soon after the initial stroke.
While many of these patients have generalized cardiovascular disease
that can cause blockage to arteries supplying either the brain or
the heart, some have no known previous vascular disease. One theory
has been that the damaged brain sends signals through the autonomic
nervous system - which controls heart rate, blood pressure, digestion
and other involuntary activities - that stress the heart.
"Some patients can develop what looks like terrible heart failure
during the weeks after their stroke," says Walter Koroshetz,
MD, director of the MGH
Stroke and Neurointensive Care Service, a co-author of the paper.
"Animal studies have suggested this could be caused by damage
in the insula, which is known to be a controller of the autonomic
nervous system. But evidence regarding what part of the insula is
involved with that effect has been contradictory."
The current study led by first author Hakan Ay, MD, analyzed data
from 50 MGH patients with ischemic (caused by arterial blockage)
strokes who also had myocardial damage as measured by elevated levels
of troponins, enzymes released by damaged heart muscle that are
considered definitive indicators of such damage. Information from
50 other stroke patients, randomly selected from those who did not
have increased troponins, was used for control comparison.
To determine exactly what area of the brain might cause myocardial
damage when injured by a stroke, the researchers used a sophisticated
way of analyzing brain images from the patients' original evaluation.
MR imaging data from all the patients was combined to create brain
maps highlighting areas where brain tissue was more likely to be
injured in patients with elevated troponins than in those with no
evidence of cardiac damage. The results showed that patients whose
stroke affected the right insular area had a 15 times greater risk
for subsequent heart muscle injury than did patients with damage
in other areas. The right insula is known to be involved with the
sympathetic nervous system, the portion of the autonomic system
that sets off stress-related responses.
"This image analysis technique is a more sophisticated way
of understanding how the brain is organized and what are the effects
of damage to specific structures," says Sorensen, an associate
professor of Radiology at Harvard Medical School. "Future studies
may help us determine which stroke patients are more likely to have
complications like pneumonia or disruptions in heart rhythm."
Koroshetz adds, "In treating stroke patients, we often raise
their blood pressures to try and increase bloodflow into the affected
areas, but we don't know why that works well for some patients and
not for others. This technique may help us identify which patients
will do well with that approach, and it has great potential for
helping us get unbiased answers to many other questions regarding
localized effects in the brain."
Additional authors of the study are Thomas Benner, PhD, Mark Vangel,
PhD, Ethem Arsava, MD, Christopher Melinosky and Mingwang Zhu, MD,
PhD, of the Martinos Center at MGH; and Cenk Ayata, MD, and Lee
Schwamm, MD, of the MGH Stroke Service. The study was supported
by grants from the Agency for Health Research and Quality and the
National Institutes of Health.
Massachusetts General Hospital, established in 1811, is the original
and largest teaching hospital of Harvard Medical School. The MGH
conducts the largest hospital-based research program in the United
States, with an annual research budget of nearly $500 million and
major research centers in AIDS, cardiovascular research, cancer,
cutaneous biology, medical imaging, neurodegenerative disorders,
transplantation biology and photomedicine. In 1994, MGH and Brigham
and Women's Hospital joined to form Partners HealthCare System,
an integrated health care delivery system comprising the two academic
medical centers, specialty and community hospitals, a network of
physician groups, and nonacute and home health services.
Media Contact: Sue
McGreevey, MGH Public Affairs
Physician Referral Service: 1-800-388-4644
Information about Clinical Trials
|
|
 |
