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Takotsubo Cardiomyopathy: Diagnosis, Treatment, and Prevalence of the “Broken-Heart Syndrome”

Erich M. Weldon, MICP, AAS.PEM

Kaplan College, San Diego



2 Abstract

Found typically in postmenopausal women, Takotsubo Cardiomyopathy has been otherwise termed transient apical ballooning syndrome, stress cardiomyopathy, or simply broken-heart syndrome. Presentation of takotsubo cardiomyopathy is often secondary to increased stressors and an irrational increase in norepinephrine which presents a potentially life-threatening “stunning� effect on the left ventricle, creating a congestive heart failure situation. Clinical electrocardiography will often show abnormalities seen in the patient with acute coronary syndrome or ST-Elevation myocardial infarct; however, unlike a true MI, laboratory cardiac enzyme biomarkers (CPK, CKMB, and Troponin) remain relatively unaffected. After exclusion of other cardiac disorders, patients with Takotsubo cardiomyopathy have a prognostic advantage over cardiac malfunctions of an ischemic or traumatic nature, with a 95% recovery rate after removing the causative stressor and little to no medical treatment.

TAKUTSUBO CARDIOMYOPATHY Takotsubo Cardiomyopathy: Diagnosis, Treatment, and Prevalence of the “Broken-Heart Syndrome” The vigilant practitioner will, without exception, aggressively treat a patient’s chief complaint of chest pain, shortness of breath, weakness, dizziness, or any combination thereof with oxygen, aspirin, nitroglycerin, morphine, thrombolytics, and other medications as needed. A battery of diagnostic tests will be requested and will include standard vital signs and pulse oximetry, 12-lead electrocardiography, cardiac laboratory markers, x-rays, and possible computed tomography angiography. The urgency for the rapid sequencing in both the diagnosis and treatment of cardiac or cardiac-suspect complaints is secondary to the swift potential for progression of negative effects in the acute coronary syndrome (ACS). With true ACS, the patient suffers an occlusion of one or more of the arteries feeding the heart, precluding blood and oxygen from reaching its target tissue – the heart muscle; if the heart is ischemic, its tissue will die and cause systemic perfusion deficits, ultimately resulting in organ system failure and body system cessation (death). Like ACS, takotsubo cardiomyopathy (TS) can present with chest pain, shortness of breath, weakness, dizziness, and syncope. Unlike ACS, however, TS does not have an ischemic etiology secondary to coronary occlusion. Rather, the disease known as transient apical ballooning syndrome, stress cardiomyopathy, or broken-heart syndrome is rooted in emotions. Japanese investigators Sato, et al (Akashi, Goldstein, Barbaro, & Ueyama, 2008) first described TS in 1990 as resembling a Japanese octopus trap after observing regional hypokinesis of the left ventricle during the angiography of patients after traumatic or emotional events. The occurrence of left ventricular insufficiency and a subsequently lower ejection fraction and peripheral perfusion level was reported clearly again in Japan after the October 23, 2004 Niigata Prefecture


TAKUTSUBO CARDIOMYOPATHY earthquake that registered 6.8 on the Richter scale. It was here that 16 patients were diagnosed with TC within one month of the earthquake. The composition of these individuals was 1 man and 15 women, with a mean age of 71.5 years; 11 of these patients developed symptoms on the day of the earthquake. (Sato, et al., 2006). Postmenopausal women make up 90% of diagnosed patients with symptoms and 12-lead electrocardiographic signs of ST-elevation myocardial infarctions (STEMI) while maintaining relatively normal cardiac laboratory markers and no residual cardiac deficit after the stressor has been removed and the patient has clinically recuperated (Zeb, Sambu, Scott, & Curzen, 2010), so the population diagnosed with TC after the Niigata Prefecture earthquake is not surprising. Stress in patients diagnosed with TC produces an acute, unnatural increase in catecholamines, specifically norepinephrine. This increase in the sympathetic nervous system taxes the heart so dramatically that it becomes “stunned” and considerably decreases its efficacy. In one case study, it was shown that patient’s norepinephrine concentration was elevated in 74.3% of the cohort and the stunned heart’s mean ejection fraction ranged from 20 to 49%. (Gianni, et al., 2006). During this period of cardiac stunning, the myocardium decreases its normal mechanical functionality, but we do not find, a residual oxygen debt nor subsequent myocardial tissue damage, even if the initial diagnosis of TC was accompanied with some ischemia. As the myocardium is essentially undamaged, it follows that cardiac markers for STEMIs remain unaffected and present relatively normal against patients experiencing true ACS. The theories behind the make-up of the population of those diagnosed with TC are two: 1) when men experience stressful events that would otherwise present as TC, it is more likely that they will sustain a true cardiac event, leading to a definitive STEMI and classic ACS. This theory is used as an exclusionary basis for men in the diagnosed cohort. 2) Postmenopausal


TAKUTSUBO CARDIOMYOPATHY women have a naturally lower level of estrogen which is instrumental in the regulation of norepinephrine. It is secondary to this decrease in estrogen that allows for the unregulated uptake of norepinephrine, causing unnatural sympathomimetic strain on the myocardium. In essence, the postmenopausal woman is more susceptible to cholinergic toxicity than the general population. These theories are solid, as theory one leaves the patient with a diagnosis other than TC, and most likely ischemic injury, and theory two physiologically explains the prevalence of diagnosis of TC in the population of postmenopausal women. Initial treatment is similar to that of any suspected STEMI or cardiac-related concern. If, however, after chest x-rays, echocardiogram, and ultimately, angiography, TC is confirmed, the patient’s prognosis becomes quite optimistic. As noted, takotsubo cardiomyopathy rarely causes long-term ischemic damage and has no lasting congestive heart failure effects. Removal of causative stressors is the best medicine for those with broken-heart syndrome; however, failure to remove these stressors can lead to long-term apical ballooning which, secondary to a severe decrease in cardiac ejection fractions, can produce thrombi leading to strokes, pulmonary emboli, or deep vein thrombosis. Further, a continued decrease in peripheral perfusion can lead to peripheral tissue death, lethargy, acidosis, and peripheral ulcerative lesions. While takotsubo cardiomyopathy may present like an acute ST-elevation myocardial infarction, and initial treatment should represent this presentation, CT should be considered in patients whose cardiac markers remain relatively unchanged, have undergone recent stress, and are women who are postmenopausal. Correct diagnosis of CT will ensure patients do not leave definitive care with unnecessary medications or therapeutic measures. As CT does not lead to myocardial injury, diagnosed patients have a positive prognosis, so long as they adhere to the guidelines given during their patient education sessions.



6 Works Cited

Akashi, Y. J., Goldstein, D. S., Barbaro, G., & Ueyama, T. (2008). Takotsubo Cardiomyopathy: A New Form of Acute, Reversible Heart Failure. Circulation(118:2754-2762), 10. Retrieved from Gianni, M., Dentali, F., Grandi, A. M., Sumner, G., Hiralal, R., & Lonn, E. (2006). Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. European Heart Journal, 7. Retrieved from Sato, M., Fujita, S., Saito, A., Ikeda, Y., Kitazawa, H., Takahashi, M., . . . Aizawa, Y. (2006). Increased incidence of transient left ventricular apical ballooning (so-called 'Takotsubo' cardiomyopathy) after the mid-Niigata Prefecture earthquake. Cardiovascular Center, Tachikawa General Hospital, and Niigata University Graduate School of Medical and Dental Science, Japan. Niigata, Japan: The Japanese Circulation Society. Retrieved from Zeb, M., Sambu, N., Scott, P., & Curzen, N. (2010, November 07). Takotsubo cardiomyopathy: a diagnostic challenge. Postgraduate Medical Journal(87), 10. Retrieved from

Takotsubo Cardiomyopathy: Diagnosis, Treatment, and Prevalence of the “Broken-Heart Syndrome”