since its first description in 1990 , transient apical cardiomyopathy ( also known as takot - subo - like left ventricular dysfunction ) has been recognized more frequently with the widespread use of echocardiography . it represents a unique model of stress - related , acute reversible ventricular dysfunction that mimics an acute coronary syndrome in the very early stages . despite multiple mechanisms suggested to explain its pathophysiology , there is increasing evidence that supports direct neuroadrenergic myocardial stimulation with concomitant transient , reversible , coronary vasospasm as the inciting event , either at the epicardial or arteriolar level recurrence is rare , and estimated to be less than 3.5% of all documented cases . intense , reciprocal input between the esophagus and coronary arteries has been well documented in both animal and human models . hence , we present the challenging case of a postmenopausal female with severe esophageal spasms , who presented with recurrent transient apical cardiomyopathy ( tac ) in the setting of emotional distress and probable coronary vasospasm . a 66-year - old woman with a history of av nodal ablation for atrial fibrillation and severe , diffuse esophageal spasms which required multiple dilations and surgical myectomy had been hospitalized multiple times at a nearby institution with shortness of breath and chest pain . most of her symptoms had been attributed to esophageal spasms confirmed by manometry . during her first admission , an echocardiogram demonstrated an ejection fraction of 25 - 30% with apical anterior , inferior and lateral wall akinesis , compatible with tako - tsubo - like cardiomyopathy . she underwent a coronary angiogram 48 h later with no evidence of obstructive disease and normalization of left ventricular function . she presented six months later to our hospital complaining of severe chest pressure that started abruptly after she became furious at her driver for being late . her ecg on admission [ figure 1a ] displayed a ventricular paced rhythm , with hyperacute t waves and new st segment elevation in anterior precordial leads ; she was given aspirin and started on heparin infusion . once intravenous infusion of nitroglycerin was initiated , she had resolution of her index symptoms , as well as most of her ecg changes [ figure 1b ] . echocardiogram performed the next morning [ figure 2 ] revealed an ejection fraction of 15% with apical ballooning , consistent with tako - tsubo - like cardiomyopathy . she received supportive management and was started on long acting nitrates and calcium channel blockers with no recurrence of symptoms . on admission day # 5 , her left ventricular function was reassessed by echocardiogram and noted to be within normal limits . ( a ) 12-lead ecg on presentation while the patient was experiencing angina , reveals a ventricular - paced rhythm with hyperacute t - waves in anterior precordial leads ( arrows ) , along with st segment elevation of more than 1 mm in those leads . ( b ) 12- lead ecg after initiation of nitroglycerin infusion ; the patient had resolution of angina symptoms . notice the reversal of acute changes in precordial leads as compared to fig 1a transthoracic echocardiogram with contrast that shows apical akinesis with a hyperkinetic base , consistent with transient apical ( tako - tsubo - like ) cardiomyopathy . in clinical practice , the diagnosis of transient apical cardiomyopathy with chest pain is usually achieved after exclusion of a typical obstructive acute coronary syndrome , since both entities share common elements , particularly during the early stages of presentation . defining features of tac include the sudden onset of new st and t wave abnormalities ( usually st elevation , t wave inversion or both ) in the setting of a stressor , mild elevation in cardiac enzymes , transient , disproportionate left ventricular dysfunction that does not follow a typical coronary distribution , and finally , absence of angiographic obstructive coronary disease that can explain the ventricular dysfunction . data from the caspar trial showed that as many as 25 % of patients who present with chest pain at rest suspicious for a coronary event have no evident culprit lesion ; furthermore , in this select group of patients , intracoronary challenge with acetylcholine ( ach ) is able to induce spasm in almost half of them . it has been noted that individuals with a persistently positive ach response have higher tendency for recurrent left ventricular dysfunction , and therefore use of ach becomes both a diagnostic and prognostic tool . unfortunately , our patient was not challenged during her first presentation when an angiogram was performed , which might have yielded a definitive , specific diagnosis early on . the combination of angiography with provocative testing , along with perfusion echocardiography has been proposed as a comprehensive strategy to characterize this subset of patients with non - obstructed coronaries [ figure 3 ] . the lack of consistent results in the literature regarding ach testing after tac could be due to variable timing of testing or dosing ; furthermore , the difference in angiographic response might be related to the location of susceptible coronary arteries ( epicardial arteries versus arterioles ) . the combination of provocative testing with simultaneous echocardiography could detect a subset of patients with vasospastic features and  normal  coronaries the pathophysiology of tac is likely multifactorial , and there is growing evidence to suggest that complex neuro - hormonal stimulation and endothelial dysfunction is responsible ; the initial mechanism appears to be neuroadrenergic stimulation of the myocytes under physical or emotional stress , resulting in myocardial stunning . vascular sympathetic stimulation at the epicardial and/or arteriolar levels can lead to severe , diffuse , and transient coronary vasospasm , which in turn aggravates left ventricular dysfunction and associated metabolic abnormalities [ figure 4 ] . diagram that summarizes the pathophysiology of left ventricular dysfunction seen in transient apical cardiomyopathy as a consequence of neuro - hormonal mediated myocardial stimulation galiuto and colleagues conducted an insightful protocol to assess the role of vasospasm in tac . they assessed a group of patients with evidence of tac by commonly accepted criteria ( n = 15 ) , including absence of epicardial obstructive disease , with a similar control group of patients ( n = 15 ) with an anterior stemi . both groups were studied using myocardial contrast echocardiography within 3  2 days of the onset of symptoms , at the time that an intravenous infusion of adenosine ( 140 ug / kg / min ) was administered . all myocardial functional variables ( wall motion score index , contrast score index , myocardial perfusion defect length ) significantly improved in the tac group , promptly returning to resting conditions after discontinuation of adenosine infusion . at one month follow - up , myocardial perfusion significantly improved when compared to baseline in tac subjects , but not in patients who sustained an anterior stemi . furthermore , the investigators were able to find a match between the extent of perfusion defects by echocardiography and the size of regional dysfunctional areas , both improved with vasodilation of probably non - obstructed or minimally - obstructive coronary arteries , responsive to adenosine . it is important to emphasize that during adenosine infusion , myocardial functional parameters did not completely normalize , suggesting that restoration of blood flow can partially improve contractile reserve of a metabolically stunned but viable myocardium . fatty acid metabolism also appears significantly impaired in tac , particularly during the early phase . timi frame count , an index of coronary flow velocity , has been noted to be significantly higher ( representing slower blood flow ) in all coronary arteries in patients with tac compared with controls , even after resolution of ventricular dysfunction . these clinical experiments strongly support the concept that irrespective of the original insult , early reversible vascular dysfunction is a common element in patients with tac . a notorious feedback loop has been documented between the coronary arteries and the esophageal system . coronary vasospasm can be elicited by stimulation of alpha - adrenergic , histaminic , serotoninergic and muscarinic receptors ; similarly alpha - adrenergic , histaminic and muscarinic receptors mediate esophageal contraction . patients with variant angina have been compared to symptomatic patients with obstructive cad and nocturnal angina , with the concurrent use of esophageal manometry and continuous ecg monitoring . in individuals with variant angina , episodes of esophageal spasms are clearly time related to periods of ecg - recorded ischemia ; bidirectional analysis of causal effects demonstrates that the influences are mutual and reciprocal . abnormal sympathetic stimulation could be a common trigger , which would be consistent with the neuroadrenergic hypothesis of myocardial stunning in tac . in clinical practice , this poses significant diagnostic challenges , as demonstrated in our case , since these patients with  linked angina  can present with atypical chest pain , at times attributable to the esophageal system , and others to transient coronary ischemia . it would be interesting to speculate if such reciprocal stimulation pathways exist between the coronaries and the bronchial tree in humans , since copd and asthma have been reported in a high percentage of patients with tac . there are no specific guidelines for the management of tac presenting with chest pain ; initial approach usually overlaps with that of an obstructive acute coronary syndrome , due to the inability to distinguish these entities on clinical or electrocardiographic grounds alone ; urgent angiogram is key to make such distinction in the acute setting . given current insight into the pathophysiology of tac , it appears reasonable that drugs that can alleviate vasospasm or blunt adrenergic response such as alpha - beta blockers , nitrates and calcium - channel blockers could prove beneficial in the process of supporting patients with this condition ; prospective comparative trials are needed to address this hypothesis . it is important to emphasize that despite its reversible nature , tac is not always a benign condition , particularly in the acute phase , when pulmonary edema , ventricular dysrhythmias and cardiogenic shock can significantly compromise patients . transient apical cardiomyopathy that presents with chest pain continues to be a challenging entity , given its similarities to an acute atherosclerotic coronary syndrome in its early phase . regardless of the initial insult , intense , neuroadrenergic myocardial stimulation with vasogenic and metabolic changes appears as the unifying mechanism that explains transient ventricular dysfunction . due to the reciprocal feedback between coronary and esophageal spasms , some patients might be predisposed to a form of  linked angina  , manifesting as a smooth muscle hyper - contractility syndrome .
transient apical cardiomyopathy , also known as takot - tsubo - like left ventricular dysfunction , is a clinical syndrome characterized by reversible left ventricular dysfunction at the apex with preserved basal contractility , in the setting of new st and t wave changes suggestive of ischemia but no evidence of obstructive coronary artery disease on angiography . 
 the main mechanism appears to be intense neuroadrenergic myocardial stimulation with endothelial dysfunction of the coronary vasculature . 
 it has been noted that patients with esophageal spasms also have a tendency for coronary spasms . 
 we present the case of a postmenopausal female with documented severe esophageal spasms who presented with atypical angina and recurrent tako - tsubo cardiomyopathy .