a 72-year old woman presented with a two hour history of chest pain and mild respiratory distress . she reported a dull ache across the anterior chest unrelated to exertion , with some radiation to the left shoulder . she had no significant past medical history and no prior history of similar chest pain . physical examination revealed a heart rate of 76 , blood pressure 130/65 mmhg , and a respiratory rate of 20/minute . cardiovascular examination revealed normal jugular venous pressure , soft heart sounds , no gallop rhythm , and no murmur . the 12-lead electrocardiogram showed minor st - segment elevation and inverted t - waves in leads v3-v6 . serum creatinine phosphokinase was elevated at 330 u / l ( normal range : 45 - 130 u / l ) and serum troponin i at 3.6 ( normal < 0.01 ) . chest - x - ray was unremarkable . coronary angiogram on admission showed no significant coronary artery disease . left ventriculogram revealed apical dyskinesis and basal hyperkinesis , a picture consistent with ttc ( figure 1 ) . she was discharged on metoprolol 25 mg twice a day , ramipril 5 mg daily , and warfarin . a repeated cardiac catheterization three months later revealed normal left ventricle function with complete resolution of apical dyskinesis ( figure 2 ) . ( b ) left ventriculogram in systole showing apical dyskinesis ( ballooning ) and basal hyperkinesis . ( b ) left ventriculogram in systole showing normal systolic function and complete resolution of apical dyskinesis ( ballooning ) . tako - tsubo cardiomyopathy is a potentially lifethreatening cardiac syndrome characterized bytransient left ventricular dysfunction , without angiographically significant coronary artery stenosis . the disease takes its name from the typical left apical ballooning observed on end systolic left ventriculogram , which has the appearance of a tako - tsubo , a term for an ancient device used in japan to trap octopuses in the sea . other names , stress cardiomyopathy , tako - tsubo cardiomyopathy , left ventricular apical ballooning syndrome , and broken heart syndrome are used interchangeably . it is estimated that about 2% of patients presenting with suspected acute coronary syndromes may actually have ttc . although initially reported only in japan , it has been reported in patients with diverse ethnic background from all over the world [ 26 ] . the most frequent presentation is chest pain ( 66% ) , followed by dyspnea ( 16% ) . these include an acute and excessive rise of catecholamine levels , calcium overload with direct myocyte damage , estrogen depletion , multiple vessel epicardial coronary spasm or diffuse microvascular spasm [ 810 ] . increased sympathetic tone with elevated levels of plasma catecholamines and stress neuropeptides may play an important role in the pathogenesis of myocardial stunning following emotional and physical stress . electrocardiography ( ecg ) can be normal , or can have nonspecific st- and t - wave abnormalities . the most common ecg abnormality ( in 70% of cases ) is st - segment elevation in the anterior precordial leads [ 4 , 11 ] . there is less inferior reciprocal st - depression than is typically seen with an anterior st - segment elevation myocardial infarction . ten percent of patients develop q - waves ( most frequently in leads v2-v4 ) . within 24 to 48 hours of the acute presentation , the ecg frequently shows deeply inverted t - waves and a markedly prolonged qtinterval in both precordial and limb leads . the qtinterval prolongation often normalizes within two days , but the t - wave abnormalities can take weeks or even months to normalize [ 6 , 11 ] . most patients with ttc have mildly elevated cardiac enzymes ( including creatine phosphokinase , troponin i , and t levels ) at the time of presentation . these enzyme elevations , however , are much lower than those typically observed with acute myocardial infarction [ 4 , 6 ] . perhaps the most specific diagnostic feature of this syndrome is the unusual left ventricular contractile pattern in the absence of significant coronary artery disease . the left ventriculogram frequently shows akinesis or dyskinesis of the apical and midventricular segments with hyperkinesis of the basal segments ( figure 1 ) . the standard supportive care for congestive heart failure with diuretics and vasodilators remains largely empirical . for hemodynamically stable patients , diuretics are used to treat pulmonary congestion , and angiotensin - converting enzyme ( ace ) inhibitors and beta - blockers are frequently used during the period of lv recovery . there is no consensus on how long to continue these medications ; it is probably safe to stop them once lv function has completely recovered . unless there is a contraindication , systemic anticoagulation hemodynamically unstable patients , the treatment includes inotropic therapy , vasopressor support , and intra - aortic balloon counterpulsation . recent data implicate massive catecholamine release as the pathogenesis of stress - induced myocardial stunning . therefore , it has been recommended to avoid the administration of exogenous catecholamines and beta - agonists whenever possible and to rely on mechanical circulatory support , e.g. , intra - aortic balloon counterpulsation . whichever form of hemodynamic support is chosen , most patients only require it for a short time and typically demonstrate rapid clinical recovery . in most patients , the left ventricular function returns to normal within two weeks . the ecg abnormalities usually disappear completely within six months . complications like shock , followed by heart failure , lv thrombus formation , dynamic lv outflow tract obstruction , acute mitral valve regurgitation , and ventricular arrhythmias are seen in 18% of cases ( 13 , 14 ) . interestingly , physical stress has higher mortality rates when compared to patients presenting with emotional stress . its clinical presentation mimics the presentation of acute stelevation myocardial infarction without concomitant epicardial coronary artery disease . despite the initial dramatic presentation of this disease