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P1332 Breaking the dichotomy of myocardial infarction and stress cardiomyopathy


 
 
 An 83-year-old woman with a past medical history of hypertension, dyslipidaemia and recent diagnosis of disseminated breast cancer was admitted at Emergency department for acute heart failure. She complained about short chest pain episodes on previous days, the ECG showed new T negative waves on precordial leads and high sensitive troponin serum levels were modestly increased (TropT 1200ng/l). Echocardiographic assessment documented moderate left ventricular dysfunction (LVEF 40%) with apical and midventricular dyskinesia associated with hypercontractility off basal segments.
 The following day the patient underwent a coronary angiography that showed an occlusion in the distal segment of a large obtuse marginal branch (Panel A) with no other significant stenosis in the remaining vessels. Ventriculography showed a typical apical ballooning pattern (Panel B). Despite the occluded coronary artery was reaching the apex, the myocardial wall motion abnormalities extended beyond the ischemic territory. Therefore, a cardiac magnetic resonance (CMR) was performed a few days later in order to clarify the diagnosis.
 CMR confirmed the mid LVEF dysfunction with apical dyskinesia and the T2 weighted spin echo images showed myocardial oedema in all the apical segments (Panel C). Remarkably, a subedocardial late gadolinium enhancement (LGE) restricted to the apical segment of the inferolateral wall was detected, being consistent with the ischaemic territory of the occluded obtuse marginal branch (Panel D). These findings supported the concomitant diagnosis of an apical stress cardiomyopathy and an acute inferolateral myocardial infarction. The patient was successfully discharged one week later with a normal LVEF and no signs of congestion.
 
 
 
 Apical ballooning in the scenario of an acute coronary syndrome may be secondary to both an acute coronary artery occlusion or to stress cardiomyopathy. Cardiac MR has a key role to resolve the differential diagnosis of these two aetiologies, since ischemia typically produces a subendocardial late gadolinium enhancement pattern and stress cardiomyopathy shows an apical oedema without coronary stenosis or extending beyond a localized ischemic territory. Our case is astonishing because in the clinical practice these two diagnoses frequently excludes each other, but as demonstrated in our case, the differential diagnosis between myocardial infarction and stress cardiomyopathy is not a proper dichotomy.
 Abstract P1332 Figure
