Shocking news 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.
From Johns Hopkins