Takotsubo cardiomyopathy is a relatively rare disease entity with a rapid reversible ventricular dysfunction, which usually occurs in post–menopausal women, and is frequently associated with a stressful event. Diagnosing Takotsubo cardiomyopathy can sometimes be challenging. The absence of coronary artery obstructive disease, and the dramatic presentation of the patient mimicking acute coronary syndrome, make this disease unique. We discuss here a case of Takotsubo cardiomyopathy with extremely rapid resolution in just two days, which we believe is being reported for the first time and touch briefly on the salient features, pathogenesis, diagnosis, treatment, prognosis, and clinical significance of this unique entity.
Takotsubo cardiomyopathy (TTC) is a unique disease entity, with a characteristic reversible ventricular dysfunction, making its timely diagnosis quite often a daunting proposition. The ventricular dysfunction associated with this usual entity is often but not always characterized by apical akinesis, and basal hyperkinesis, in a distribution which does not correlate, with a specific, unique, epicardial coronary artery blood supply [
A 62 year old lady, with past medical history of hypertension, and chronic obstructive pulmonary disease was admitted with sudden shortness of breath, and chest pain. A few days before this episode, her youngest daughter had died in a traffic accident. Just prior to admission, she experienced sudden and severe shortness of breath at night, along with unrelenting chest pain located in central lower chest area, with no radiation. The chest pain resolved within half an hour, but the shortness of breath persisted, and rapidly worsened.
Upon presentation to the emergency room (ER), her physical exam revealed a blood pressure of 119/87, pulse rate of 84/min, oxygen saturation of 86% on room air, and body temperature of 97.1˚F. There were no murmurs, rubs or gallops, no crackles on chest auscultation, no jugular venous distension, and no pedal edema. She had a mild elevation in her cardiac enzymes (Troponin = 0.05, CK-MB = 1.7, CK = 97), and her Brain-Natriuretic Peptide (BNP) level was 1400. Her laboratory work-up was otherwise within normal limits. Her EKG showed nonspecific ST-T changes, and QT prolongation, with a corrected QT interval (QTc) of 505 ms, and her chest X-Ray showed hyperexpanded lung fields, with flattened diaphragms.
Given her low oxygen saturations, and her shortness of breath, she was initially started on BIPAP (Bi-level positive airway pressure) and was given furosemide, aspirin, heparin infusion, and statin, with the most likely diagnosis being: heart failure secondary to Non-ST Elevation Myocardial Infarction (NSTEMI).
A Transthoracic Echocardiogram (TTE), was performed the next day, and showed marked left ventricular systolic dysfunction (ejection fraction of 15% - 20%), severe apical hypokinesis, basal hyperkinesis, moderately reduced right ventricular function, and mild mitral regurgitation (
A repeat TTE was obtained, after two days, following a dramatic resolution of patient’s symptoms. The latter revealed a normal systolic function with an ejection fraction of 55% - 65% with absence of apical hypokinesis (
Interestingly, the nonspecific ST-T changes, and prolonged QTc on admission resolved as well, over a time period of two days.
Stress-induced cardiomyopathy, also called apical ballooning syndrome, is generally characterized by transient systolic dysfunction of the apical, and/or mid segments of the left ventricle (LV), that mimics myocardial infarction, in the absence of significant coronary artery disease [
Typically, the contractile function of the mid, and apical segments, of the LV is depressed with compensatory
hyperkinesis of the basal walls, producing “ballooning of the apex, during systole. A different type of transient cardiomyopathy, with mid-ventricular akinesis, has also been described (mid-ventricular ballooning syndrome). In a description, of six cases of mid-ventricular ballooning, there was mild ventricular dysfunction (ejection fraction 40%), and shorter recovery times (1 - 7 days) [
Stress-induced cardiomyopathy, is much more common in women than men. In a review of ten prospective series, women accounted for 80% - 100% of cases, with a mean age of onset, of 61 - 76 years [
The clinical presentation, of stress-induced cardiomyopathy, is similar to that of an acute myocardial infarction (MI) [
The EKG often reveals ST elevation (mostly precordial) during the acute phase, followed by T wave inversion, QT prolongation, and sometimes deep Q waves during the subacute phase [9,10]. In a comparison study of takotsubo cardiomyopathy and acute myocardial infarction (MI) 34% to 56% of takotsubo patients showed ST elevation in anterior leads [9,10], with absence of reciprocal changes, prolongation of QTc interval, and deep T wave inversion [9,10]. Cardiac biomarkers are usually mildly elevated [
Despite the severity of the acute illness, stress-induced cardiomyopathy is a transient disorder, managed with supportive therapy. Conservative medical treatment with beta-blockers when possible has been thought to be associated with lower mortality during the acute phase [
In-hospital mortality rates have been reported by Gianni et al., as 1.1%, along with a recurrence rate of 3.5% [
The recovery times, for typical cases with apical ballooning, are highly variable. Patients who survive the acute episode, typically recover normal ventricular function within 1 - 4 weeks, as shown in a study of 30 patients, with takotsubo cardiomyopathy [
In a study of 22 patients, over a 32 month period the mean LVEF increased from 29% at initial presentation to 63% at a mean of 6 days [
This case is to our knowledge, the first case that highlights the dramatic resolution of takotsubo cardiomyopathy, which occurred within two days of presentation. We believe this to be the most rapid EF normalization, ever published to date, for a case of takotsubo cardiomyopathy with typical apical ballooning pattern [