As poets and philosophers through the ages have written, the sudden death or departure of a loved one can cause a broken heart. And now research has proven that a broken heart isn't just a clever play on words.
In a study published the week before Valentine's Day in the New England Journal of Medicine, doctors at Johns Hopkins University gave a name to the condition and demonstrated through sophisticated heart tests how the condition differs from a heart attack.
The study reports how a tragic or shocking event can stun the heart and produce classic heart-attack-like symptoms, including chest pain, shortness of breath, and fluid in the lungs. Because the symptoms are so similar, the condition is often misdiagnosed as a heart attack.
But unlike a heart attack, the condition is fully reversible. Patients often are hospitalized but typically recover within days after little more than bed rest and fluids, and suffer no permanent damage to their hearts.
For centuries, doctors have known that emotional shocks can trigger heart attacks and sudden deaths. But broken heart syndrome, technically known as stress cardiomyopathy, is a different phenomenon. The just-published study offers an explanation for what causes the problem.
The Johns Hopkins doctors documented how a surge of adrenaline and other stress hormones that lasts for days at a time can cause a decline in the heart's pumping capacity. The researchers theorized that the hormones probably cause tiny heart blood vessels to contract, but other explanations are possible.
Until now, doctors "were trying to explain it away, but the pieces never quite fit," said Dr. Hunter Champion, an assistant professor. "By our ability to recognize it and document it, we've saved people from getting unnecessary (heart) procedures."Champion and his colleagues treated 19 emergency room patients with the syndrome between 1999 and 2003.
The patients all underwent coronary angiography and echocardiography, and five underwent endomyocardial biopsy, but only one of the patients had any evidence of clinically significant coronary disease.
For reasons that are not entirely clear, 95% of the patients were postmenopausal women. Many were grieving over the death of a husband, parent, or child. Other triggers included a surprise party, car accident, armed robbery, fierce argument, court appearance, and fear of public speaking.
MRIs and other tests showed that they had not suffered heart attacks, though they exhibited classic symptoms. Other doctors have told Champion that they have seen the same thing and researchers in Japan and Minnesota have reported similar cases. "This is probably something that happens all the time," but most people do not seek treatment, Champion said.
Dr. Sidney Smith, former American Heart Association president and the director of University of North Carolina's Center for Cardiovascular Science and Medicine, said the influential study will lead more emergency room and heart doctors to consider the syndrome when examining patients with chest pain, rather than assuming a heart attack is taking place.
Dr. Daniel Shindler, director of the echocardiography lab at Robert Wood Johnson Medical School in New Brunswick, N.J., said it apparently happened to his wife recently, when she was upset over her sister's death. The wife, who is also a doctor, sensed abnormalities in her heart.
Testing showed abnormal rhythms, but she is fine now. After learning of the Johns Hopkins study, Shindler said the researchers' conclusions make sense, given the well-known link between the brain and the heart, and the study offers the first explanation he has heard for the phenomenon.
The primary conclusion of the study was that emotional stress can precipitate severe, reversible left ventricular dysfunction in patients without coronary disease. "We'll definitely be paying more attention now than before" to patients who are grieving, Shindler said.