There are two phenotypes of stress-induced cardiomyopathy. The first is more typical of this case, in which a patient experiences some sort of stressor, develops chest pain, and is found to have a cardiac process upon medical evaluation. The second is common of patients who have an underlying critical illness – such as sepsis, intracranial hemorrhage, or respiratory failure – and the cardiac process develops in response to that stress of critical illness.  

There is a suggestion that 1-2% of patients who present with STEMI/NSTEMI may actually have takotsubo cardiomyopathy, and that this is a more common disease process than originally thought  

Pathophysiology is poorly understood, but it is thought that a catecholamine surge disproportionately affects the apex of the heart due to a higher concentration of adrenergic receptors on that part of the myocardium, leading to apical stunning and reduced EF.  

Several different presentations possible:  

Chest pain, which may/may not have typical features such as dyspnea, nausea, radiation, and diaphoresis 

Lightheadedness/syncope due to arrhythmia  

Embolization due to mural thrombus formed 

Heart failure due to reduced EF  

Labs will show elevated troponins and BNP/pro-BNP. Troponin elevation out of proportion to regional wall motion abnormalities seen on echo may suggest takotsubo cardiomyopathy rather than ischemia  

EKGs follow a pattern:  

Day 1: anterior STEMI mimic. However, lack of q waves and reciprocal ST depressions may suggest takotsubo rather than LAD occlusion  

Days 1-2: ST elevations lower and are replaced by TWIs that are not localized to a single arterial distribution  

Days 2-3: TWIs become deeper, broader, and out of proportion to what is usually seen in cardiac ischemia  

Echo has a typical pattern: apical hypokinesis (ballooning) while the base of the heart is hyperdynamic. The apical hypokinesis is circumferential and less regional than would be expected in an LAD occlusion. Can also get basal hypokinesis with apical hyperkinesis (reverse takotsubo), left ventricular outflow obstruction, and global hypokinesis. Global hypokinesis is a poor prognostic indicator.  

An emergency physician can suspect but should never diagnosis takotsubo. This is a catheterization-negative diagnosis, and this patient should be treated as a STEMI/NSTEMI until proven otherwise. This is especially true given the similarities in cardiac biomarkers, EKG, and regional wall motion abnormalities seen on echo.  

In-hospital mortality is 2-5%, but most patient will do well and recover LV function in about 12 weeks  

Cardiology echo showed LVEF 25-29% with hyperkinetic basal function and hypokinesis of all other segments 

Cardiac catheterization showed a normal left main, RCA, and LCx with 20% stenosis of the LAD  

The patient was started on goal-directed medical therapy with a statin, ACEi, β-blocker, and ASA due to a presumed diagnosis of takotsubo cardiomyopathy  

The patient was stabilized and discharged from the hospital with outpatient follow-up