"Broken heart" syndrome: real, potentially deadly but recovery quick

February 9, 2005

-- Hopkins scientists discover that emotional shock can trigger sudden, reversible heart failure that is not a classic heart attack
 
Shocking news, such as learning of the unexpected death of a loved one, has been known to cause catastrophic events, such as a heart attack. 

Now, researchers at Johns Hopkins have discovered that sudden emotional stress can also result in severe but reversible heart muscle weakness that mimics a classic heart attack.  Patients with this condition, called stress cardiomyopathy but known colloquially as “broken heart” syndrome, are often misdiagnosed with a massive heart attack when, indeed, they have suffered from a days-long surge in adrenalin (epinephrine) and other stress hormones that temporarily “stun” the heart. 

“Our study should help physicians distinguish between stress cardiomyopathy and heart attacks,” says study lead author and cardiologist Ilan Wittstein, M.D., an assistant professor at The Johns Hopkins University School of Medicine and its Heart Institute.  “And it should also reassure patients that they have not had permanent heart damage.”

In the Hopkins study, to be published in The New England Journal of Medicine online Feb. 10, the research team found that some people may respond to sudden, overwhelming emotional stress by releasing large amounts of catecholamines (notably adrenalin and noradrenalin, also called epinephrine and norepinephrine) into the blood stream, along with their breakdown products and small proteins produced by an excited nervous system.  These chemicals can be temporarily toxic to the heart, effectively stunning the muscle and producing symptoms similar to a typical heart attack, including chest pain, fluid in the lungs, shortness of breath and heart failure. 

Upon closer examination, though, the researchers determined that cases of stress cardiomyopathy were clinically very different from a typical heart attack. 

“After observing several cases of ‘broken heart’ syndrome at Hopkins hospitals - most of them in middle-aged or elderly women - we realized that these patients had clinical features quite different from typical cases of heart attack, and that something very different was happening,” says Wittstein.  “These cases were, initially, difficult to explain because most of the patients were previously healthy and had few risk factors for heart disease.”

For example, examination by angiogram showed no blockages in the arteries supplying the heart.  Blood tests also failed to reveal some typical signs of a heart attack, such as highly elevated levels of cardiac enzymes that are released into the blood stream from damaged heart muscle.  Magnetic resonance imaging (MRI) scans confirmed that none of the stressed patients had suffered irreversible muscle damage.  Of greatest surprise, the team says, was that recovery rates were much faster than typically seen after a heart attack.  Stressed patients showed dramatic improvement in their hearts’ ability to pump within a few days and had complete recovery within two weeks.  In contrast, partial recovery after a heart attack can take weeks or months and, frequently, the heart muscle damage is permanent.  

The researchers collected detailed histories and conducted several tests, including blood work, echocardiograms, electrocardiograms, coronary angiograms, MRI scans and heart biopsies, on a total of 19 patients who came to Hopkins between November 1999 and September 2003.  All had signs of an apparent heart attack immediately after some kind of sudden emotional stress, including news of a death, shock from a surprise party, fear of public speaking, armed robbery, a court appearance and a car accident.  Eighteen of the stressed patients were female, between the age of 27 and 87, with a median age of 63.  The results were then compared to seven other patients, all of whom had suffered classic, severe cases of heart attack, called a Killip class III myocardial infarction.

When results from both groups were compared, the researchers found that initial levels of catecholamines in the stress cardiomyopathy patients were two to three times the levels among patients with classic heart attack, and seven to 34 times normal levels. 

Catecholamine metabolites, such as metanephrine and normetanephrine, were also massively elevated, as were other stress-related proteins, such as neuropeptide Y, brain natriuretic peptide and serotonin.  These results provided added confirmation that the syndrome was stress induced.  Heart biopsies also showed an injury pattern consistent with a high catecholamine state and not heart attack.

A hallmark feature of the syndrome was the heart’s unique contraction pattern as viewed by echocardiogram, or ultrasound.  While the base of the heart’s main pumping chamber, the left ventricle, contracted normally, there was weakened contraction in the middle and upper portions of the muscle.  Other characteristics included a distinctive pattern on electrocardiogram, or EKG.

“How stress hormones act to stun the heart remains unknown, but there are several possible explanations that will be the subject of additional studies,” says study co-investigator and cardiologist Hunter Champion, M.D., Ph.D., an assistant professor at Hopkins and its Heart Institute.  “The chemicals may cause spasm in the coronary arteries, or have a direct toxic effect on the heart muscle, or cause calcium overload that results in temporary dysfunction.”

The researchers also plan to study whether certain patients have a specific genetic vulnerability for developing stress cardiomyopathy, and why it predominantly strikes older women.

While the folklore of “broken heart” syndrome has been around for decades, the prevalence of the condition remains unknown.  According to Wittstein, some reports exist, mainly from Japan, and describe similar syndromes, but no biochemical analyses have previously been performed that link the condition to elevated catecholamine levels.  The researchers contend that while stress cardiomyopathy is not as common as a typical heart attack, it likely occurs more frequently than doctors realize.  They expect its numbers to increase as more physicians learn to recognize the syndrome’s unique clinical features.

Funding for this study, conducted solely at Johns Hopkins, was provided by the Bernard A. and Rebecca S. Bernard Foundation.  Other researchers who took part in this study were Trinity Bivalacqua, M.D., Ph.D.; Jeffrey Rade, M.D.; Katherine Wu, M.D.; Gary Gerstenblith, M.D.; Steven Schulman, M.D.; Kenneth Baughman, M.D.; João Lima, M.D.; and David Thiemann, M.D. 

- JHMI -

Johns Hopkins Medicine
Office of Corporate Communications
Media contact: David March
410-955-1534; dmarch1@jhmi.edu

Sometimes a Heart Attack Is Really a 'Broken Heart'

Stress can temporarily stun main pumping chamber, study finds

WEDNESDAY, Feb. 9 (HealthDay News) -- It seems the heart can really break, although it can also recover rapidly from the damage wrought by a sudden emotional shock.

The phenomenon is known as "broken heart syndrome," and it can trigger severe, temporary heart muscle weakness that mimics a classic heart attack, Johns Hopkins scientists claim in a new report.

Their study describes 20 patients, almost all of them women, who were hospitalized with all the symptoms of a heart attack, including chest pain, shortness of breath, fluid in the lungs and drastically reduced ability of the heart to pump blood.

But careful study found the problems were just temporary, caused by a massive release of stress hormones called catecholamines that can "stun" the heart. They include adrenaline, and flood the body following emotional shocks ranging from news of a loved one's death, to an armed robbery, to an auto accident, the report said. Rather than requiring the drastic treatment necessary for a heart attack, the patients needed only supportive therapy for a few days to allow the heart to recover, the researchers said.

"This kind of thing has been described by others," said study author Dr. Hunter C. Champion, an assistant professor of medicine at Johns Hopkins School of Medicine. But, he added, it's still important to remind physicians that the cardiac problem might be due to stress cardiomyopathy, rather than a heart attack.

"You can save patients from having treatments such as an implanted defibrillator or even a heart transplant," Champion said.

The study appears in the Feb. 10 issue of the New England Journal of Medicine.

The report described 19 patients, 18 of them women, whose median age was 63 when they came to Hopkins for emergency treatment. "Everyone thought they were having heart attacks," Champion said.

But physical exams and blood tests did not show the symptoms of a heart attack -- no blockage of the coronary arteries, no increased levels of the enzymes released when the heart muscle is damaged, no physical signs of heart damage. However, a striking feature of the syndrome was the heart's unique contraction pattern when viewed by echocardiogram. Although the base of the heart's main pumping chamber, the left ventricle, contracted normally, there was weakened contraction in the middle and upper portions of the muscle.

The patients' condition improved considerably in a few days, and they recovered completely within two weeks, while even partial recovery from a heart attack can take weeks or months, the researchers said.

The Hopkins physicians are doing studies to determine how stress hormones can stun the heart, why the condition strikes predominantly older women and whether there might be a genetic vulnerability to the condition, Champion said.

They also are trying to determine how often it occurs. There have been several reports on stress cardiomyopathy, most from Japan but a few from the United States, Champion said. "But my guess is that it happens much more frequently than has been thought," he added.

"We do see this quite regularly," said Dr. Marc S. Penn, medical director of the coronary intensive care unit at the Cleveland Clinic. "It is not uncommon to see it in patients who have been referred to us."

The Hopkins report "will lead to more questioning of patients before the physician comes up with a diagnosis," Penn said. It also should prompt more measurements to detect elevated levels of the stress hormones described in the new report, he said.

The condition appears to be associated only with "significant life events," Penn said. "We don't think that everyone who has an argument with a spouse goes into heart failure."

More information

Johns Hopkins has more on stress cardiomyopathy.


SOURCES: Hunter C. Champion, M.D., Ph.D, assistant professor, medicine, Johns Hopkins School of Medicine, Baltimore; Marc S. Penn, M.D., medical director, Cleveland Clinic coronary intensive care unit; Feb. 10, 2005, New England Journal of Medicine

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