Broken Heart Syndrome Cardiovascular Case Study Broken Case Study

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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.

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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….....

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