Further Evidence Explains 'Broken Heart Syndrome'

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Further Evidence Explains 'Broken Heart Syndrome'
More evidence emerged that stress cardiomyopathy, popularly known as "broken heart syndrome," is not a classic heart attack.


    * Inform patients that stress cardiomyopathy goes by several different names and can be triggered by a variety of sudden emotional or physiological stressors.


    * Note that stress cardiomyopathy appears to be largely reversible if patients are adequately supported for the first 48 hours after symptom onset.

The long-term effects of the syndrome's heart attack-like symptoms, brought on by sudden emotional or physical trauma, appeared almost fully reversible, Richard A. Regnante, M.D., of the Miriam Hospital and Brown University here, and colleagues found.

Their registry of Takotsubo cardiomyopathy, as it is also known, revealed incidence spikes in summer, compared with the typical upswing in MI during winter.

An overwhelming majority of cases involved women, most of whom suffered from hypertension.

These findings suggested that the pathophysiologic mechanism truly differs from acute MI, they wrote in the April 1 issue of the American Journal of Cardiology.

This agreed with the conclusions of another, smaller case series reported recently in the Journal of the American College of Cardiology that uncovered evidence for causal mediation by excessive sympathetic stimulation.

Some researchers believe the syndrome is merely an aborted heart attack that doesn't leave permanent heart muscle damage, while others say it reflects a problem with the heart muscle rather than coronary arteries, Dr. Regnante said.

The syndrome was first described in the early '90s by Japanese researchers, who named it Takotsubo cardiomyopathy for the resemblance of the characteristic apical ballooning to the takotsubo pot used to catch octopus.

Its characteristic clinical features include mild cardiac enzyme elevation in the absence of obstructive coronary disease, a prolonged QTc interval and diffuse T-wave abnormalities on ECG, ventricular ballooning, and rapid recovery of LV systolic function.

Because many other aspects of the relatively rare syndrome were still poorly understood, Dr. Regnante's group created a registry at the two major hospitals in Rhode Island from July 2004 through April 2008.

The 70 cases they found represented a frequency of 0.4% among all patients who underwent diagnostic cardiac catheterization.

Occurrence, divided into three-month seasons, showed a distinct and significant increase during summer in each of the three years (P<0.001).

Since the hospitals performed fewer catheterizations during the summer months, the spike in stress cardiomyopathy could not be explained away as ascertainment bias, the researchers said.

Notably, 95% of stress cardiomyopathy patients were women, typically with pre-existing hypertension (66%). Only 37% had a preadmission diagnosis of depression or generalized anxiety disorder.

The trigger was emotional for 45% of those with a clearly identified preceding stressor, most frequently bad news about a family member or a domestic argument.

Physical triggers included severe illness, chronic obstructive pulmonary disease exacerbation, and falls, but the condition could also precipitated by routine procedures such as colonoscopy preparation and tooth extraction.

The researchers noted a wide range of symptom severity. About 20% were critically ill in the acute period, including three patients who sustained ventricular tachycardia or fibrillation.

However, the syndrome was rarely fatal. One patient died within 24 hours of acute heart failure after the family decided against reattempting a failed extubation. Two others died of noncardiac causes.

The investigators noted that patients treated beforehand with angiotensin-converting enzyme inhibitors (usually for hypertension) seemed to be protected from the most severe manifestations of the syndrome.

Two patients had a recurrence of stress cardiomyopathy, but there were no thromboembolic events, regardless of treatment regimen.

Treatment typically followed the pattern for acute coronary syndromes, with 43% of patients discharged on warfarin because of severe apical wall motion abnormalities.

Patients adequately supported during the first 48 hours after onset all had an excellent prognosis and recovered left ventricular function to an average of 59%, the researchers said.

They cautioned that the observational findings were limited by the relatively small cohort who were treated empirically, which may reflect biases that were not accounted for in the study.

The researchers provided no information on conflicts of interest.
Source: American Journal of Cardiology