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Heart Attack from Broken Heart May Just Be Temporary
Stress Hormones
 Feb.
10, 2005 – People may think they are having a heart attack after
receiving extremely shocking news but new research says it may be just a
temporary stun to the heart caused by a rush of adrenalin and other
stress hormones. Often called the “broken heart” syndrome, it is usually
temporary.
Extreme stress such as learning of the unexpected
death of a loved one, has been known to cause catastrophic events, such
as a heart attack. Researchers at Johns Hopkins have now 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.
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