Broken heart syndrome is a recently recognized, fairly common, distinct cardiovascular condition that if left untreated could be fatal. By far the most common sufferers are postmenopausal women who have suffered the loss of a loved one and as many as 40,000 women could experience this condition every year. The steps that can be taken to try and prevent TTC have not been discussed in the literature because professional recognition of this condition is so recent, but programs and educational material which discuss how to cope with bereavement are probably most relevant.
Broken Heart Syndrome
Cardiovascular Case Study
Broken heart syndrome, otherwise called stress or Takotsubo cardiomyopathy (TTC), represents an adverse physiological response to an acute psychological or physical stressor (Derrick, 2009). The death of a loved one or experiencing a physically traumatic event, represent two examples of life stressors that can cause this reversible form of cardiomyopathy. Although effective treatment is available, the seriousness of the condition is such that it explains how a person can literally die of a broken heart.
TTC Demographics
An estimated 1.2 million people suffered from an myocardial infarction (MI) in 2007 and approximately 1% (Derrick, 2009, p. 50) to 2% (Wittstein, 2012, p. 2) of MI events was probably due to TTC. Women are far more susceptible to TTC than men and represent approximately 89% of all cases (Derrick, 2009, p. 50). This gender bias shifts the estimated prevalence of TTC among female MI patients to between 4.7 and 7.5% (Wittstein, 2012, p. 2). Based on 2008 estimates of MI for women in the U.S. (American Heart Association, 2011), an estimated 24,000 to 40,000 women suffer from TTC each year.
TTC Signs and Symptoms
Patients often present with signs and symptoms indistinguishable from MI, including chest pain, dyspnea, ECG abnormalities, and elevated levels of cardiac biomarkers (Derrick, 2009, p. 49), but a knowledgeable clinician can discriminate between the two by an absence of plaque rupture and coronary thrombosis, and complete reversibility (Wittstein, 2012, p. 1).
Formal diagnostic guidelines for TTC do not exist, but enough is known that several respected medical institutions have published their own (reviewed by Wittstein, 2012, p. 3). The Mayo Clinic bases a TTC diagnosis on the following: (1) transient hypokinesis, akinesis, or dyskinesis of left ventricle midsegments, with or without apical involvement, and regional wall motion abnormalities that extend beyond a single epicardial vascular distribution, (2) identifiable stressor, (3) absence of coronary artery disease (CAD) or acute plaque rupture, (4) new ECG abnormalities, and (5) absence of myocarditis or pheochromocytoma. Johns Hopkins, which houses leaders in the TTC field, would add to the above the following: (1) mild elevation of cardiac troponin, (2) ST-segment elevation when admitted, (3) diffuse deep T-wave diffusion, (4) QT interval prolongation, and (5) complete recovery of regional wall motion abnormalities within a few days or weeks.
TTC Etiology and Pathophysiology
The cause is known to be psychological stress, but the underlying mechanism is unknown. Probably the most prevalent hypothesis is that 'psychic pain' induces a sustained, abnormally high sympathetic activation (Derrick, 2009, p. 51). Accordingly, catecholamine levels were found to be 2 to 3 times higher in TTC patients when compared to MI patients. Heart biopsies of TTC patients have revealed contraction band necrosis on the left ventricle, which is consistent with prolonged excess catecholamine exposure.
TTC Case Study
A 65-year-old Caucasian woman (DR) sought medical help after experiencing chest pains that radiated to the left arm (Soares-Filho, Felix, Mesquita, Valenca, and Nardi, 2010). Several weeks ago her husband of 45 years passed away suddenly from a MI, after spending a week in the intensive care unit. DR presented with rapid pulse and 100/60 mmHg. She was negative for cardiovascular risk factors and a remarkable cardiac medical history, and angiography did not show signs of CAD. Left ventriculography revealed basal hypokinesis and hyperkinesis of the mid and apical segments, and apical ballooning during systole. Cardiac troponin levels were above normal and estimated left ventricle ejection fraction was 25% (Derrick, 2009, p. 52-53).
Intervention involved left ventricle support by an intra-aortic balloon pump in the intensive care unit for two days (Derrick, 2009, p. 52-53). Intravenous furosemide was administered. DR was moved out of intensive care on the fourth day and prescribed oral furosemide and a ? -- blocker. By the fifth day normal systolic function had returned and left ventricle ejection fraction was over 55%, which was consistent with a complete left ventricle recovery. All medications except the ? -- blocker were stopped and six months later the patient reported having returned to a normal life.
The Role of Caregivers
Science and medicine can only do so much for a person suffering from TTC, as was so eloquently captured in a poem by a Baylor College of Medicine cardiologist (Liao, 2011). Our society tends to emphasize the virtue of independence and therefore the amount of attention paid to the grief and bereavement process is relatively minor. Since most TTC sufferers are postmenopausal women who have recently experienced the loss of a loved one, family members are likely to be grieving the same loss (Fitzgerald, 2009). The possibility of confronting another loss can significantly increase the amount of stress that family members and close friends experience, so it is imperative that once TTC is confirmed a good prognosis is communicated (Derrick, 2009, p. 56). Education concerning the nature of TTC then becomes key in aiding the recovery process for everyone concerned and grief counseling can be suggested (Fitzgerald, 2009).
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