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 and other stress hormones that
temporarily "stun" the heart.
"Our study should help physicians distinguish between
stress cardiomyopathy and heart attacks," said study lead
cardiologist Ilan Wittstein, an assistant professor at
the School of Medicine and its Heart Institute. "And it
should also reassure patients that they have not had
permanent heart damage."
In the Johns Hopkins study, 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
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," Wittstein said. "These cases were, initially,
difficult to explain because most of the patients were
previously healthy and had few risk factors for heart
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 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 Johns 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
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.
"How stress hormones act to stun the heart remains
unknown, but there are several possible explanations that
will be the subject of additional studies," said study
co-investigator and cardiologist Hunter Champion, an
assistant professor at Johns 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
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, Jeffrey Rade, Katherine Wu,
Gary Gerstenblith, Steven Schulman, Kenneth Baughman, Joao
Lima and David Thiemann.