Public Release: 

Stroke-associated damage to brain structure may lead to heart attack

Image analysis clarifies role of brain area involved with physiologic stress response

Massachusetts General Hospital

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.

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