Zumba-induced Takotsubo cardiomyopathy: a case report.

Takotsubo cardiomyopathy or stress cardiomyopathy is characterized by transient left ventricular apical ballooning in the absence of coronary occlusion. The underlying pathophysiological mechanism is still unclear but possible causes have been proposed mainly catecholamine cardiotoxicity, followed by metabolic disturbance, coronary microvascular impairment, and multivessel epicardial coronary artery vasospasm. Takotsubo cardiomyopathy accounts for 1–2% of patients presenting with acute coronary syndrome with the majority of patients diagnosed with Takotsubo cardiomyopathy being women > 55 years of age. Here, we discuss the case of a 38-year-old woman presenting with typical chest pain, electrocardiography changes and cardiac markers consistent with acute coronary syndrome, who was subsequently diagnosed with Takotsubo cardiomyopathy. A 38-year-old healthy American woman with negative past medical history presented to our Emergency Department with chest pain developing while participating in intense outdoor physical activities (Zumba) at a fundraising event. Our patient had typical substernal chest pain induced with exercise and was relieved by sublingual nitroglycerin in the Emergency Department. The pain started after 2 h of intensive Zumba workout. On review of her history, our patient was noted to be taking spironolactone 125 mg once daily for hirsutism for the past year. Our patient denied any family history of cardiac disease or heart failure. She admitted to being a former occasional smoker and to drinking alcohol socially. She denied any illicit drug use. She works as a social worker, and reported that she does not experience much stress in her life and denied any “one big life-changing event” or any major stressful news. While in the Emergency Department, our patient was hemodynamically stable and an electrocardiography was performed and showed sinus rhythm with no ST elevation/depression but noted T-wave inversion in leads I and aVL, and T wave flattening in leads V1 and V2. Her troponin levels were 0.294 and 0.231 consecutively. An echocardiogram was done and showed hypokinetic apical and mid-distal walls and hyperdynamic basal walls of the left ventricle with an ejection fraction of 35–40%, consistent with apical ballooning syndrome. Cardiac catheterization was subsequently done and showed depressed left ventricle systolic function, ejection fraction of 30–35% with anteroapical dyskinesia and no evidence of coronary artery disease. Our patient was diagnosed with Takotsubo cardiomyopathy after fulfilling all four of the Mayo Clinic’s diagnostic criteria and was subsequently treated with a beta blocker, and angiotensin-converting enzyme inhibitor. Our patient did not have one clear trigger for her overt Takotsubo cardiomyopathy other than the Zumba activity. Zumba is considered an activity with excessive sympathetic stimulation leading to catecholamine-induced microvascular spasm or through to direct myocardial toxicity, which is postulated to be behind the pathophysiology of Takotsubo cardiomyopathy. Another interesting finding in our patient was her use of spironolactone, as treatment for hirsutism, which is an aldosterone antagonist. Aldosterone actually potentiates the effects of catecholamine and thus activates the sympathetic system. Spironolactone can thus be considered as cardioprotective against the effects of catecholamine on the heart and that is why it is considered to be beneficial and subsequently improves mortality in chronic heart failure as described in several studies.