A 77-year-old female diabetes and hypertension presents to the emergency department for generalized weakness, shortness of breath, and abdominal pain. A brief initial exam demonstrates that she is in respiratory distress, diaphoretic, tachypneic. The patient is immediately brought to the resuscitation bay and she is found to have an oxygen saturation of 77% on room air and a point-of-care glucose of 500. An EKG (Figure 1) was obtained.
Interpretation: Rate: 78 bpm; Rhythm: sinus rhythm with first degree AV block; Axis: normal axis (I: pos., II: pos., aVF: pos.) Intervals: PR: 225, long; QRS: 86, normal; QT: 497, long; P-Waves: present; QRS Complex: normal, low voltage in limb leads; ST Segment/T-waves: 1.5-2mm ST elevations in leads V1-V3, aVF and III, Inverted T waves in V2-6
A troponin was obtained given the anterior ST elevations and a code STEMI was called. A chest xray showed diffuse pulmonary edema so the patient was placed on BiPAP. The VBG resulted with significant acidosis with a pH of 6.89, bicarbonate of 14, glucose of 775, and potassium of 7.8 consistent with for DKA with hyperkalemia. The patient was given calcium, furosemide, and sodium bicarbonate and was started on insulin. At this time, the patient became hypotensive and was started on a norepinephrine drip. Due to her severe acidosis, altered mental status, acute hypercapnic, hypoxic respiratory failure the patient was intubated prior to being taken to the cath lab.
The cath lab report demonstrated no obstructive coronary lesions, but did note left ventricular dysfunction, and postcapillary pulmonary hypertension with normal cardiac output. Subsequently a transthoracic echocardiogram was performed which demonstrated a left ventricle of normal size with moderate focal basal hypertrophy and ejection fraction of 35-40% with akinesis of the apical anterior, apical inferior, apical septal, and apical myocardium and severe hypokinesis of the mid anteroseptal, mid inferoseptal, and mid inferolateral myocardium. The patient was admitted to the CCU for continued management and had a prolonged stay.
Discussion
From a cardiac perspective, the patient initially was diagnosed with an anterior occlusive myocardial infarction (OMI) which prompted both the ED to activate the cath lab and Cardiology to take the patient urgently once stabilized. However, the left heart cath showed no occlusive coronary lesions. Based on the cath and echo findings (Figure 2), what is the suggested diagnosis?
Figure 2.
Figure 2. Transthoracic echocardiogram demonstrating apical dyskinesia of the left ventricle resembling an octopus pot of “takotsubo”
Cardiology ultimately diagnosed the patient with left ventricular dysfunction due to stress cardiomyopathy, also known as Takotsubo syndrome. The pathophysiology of this condition is thought to be caused by a response to acute stress that causes a catecholamine surge. This surge causes a systemic sympathetic response that leads to vascular and microvascular spasm. Specifically, the heart has the highest density of sympathetic fibers in the apical distribution of the left ventricle. The sympathetic activation of these fibers causes microvascular spasm, regional ischemia, and the subsequent clinically observable regional wall motion abnormalities on POCUS, as well as ST segment elevations in the anterior and apical distributions, and troponin elevation [1-2].
In this case, there was no “emotional stressor” as occurs in the classicality taught version of Takotsubo cardiomyopathy known as Broken Heart Syndrome. Rather, it appears this patient’s stress cardiomyopathy likely resulted from severe DKA.
The patient’s acute hypercapnic, hypoxic respiratory failure was likely resultant from the Takotsubo syndrome itself. Around one third of cases result in a partial or transient left ventricular outflow tract obstruction. This obstruction increases preload, exaggerates sympathetic activation, and, in a vicious cycle, worsens apical vasospasm, ischemia, and dyskinesis [1].
Most patients do well with complete recovery observed in around 90% of patients in the acute setting. Relapse is rare. Pertinent to this case, diabetes mellitus was identified in some studies as an independent predictor of mortality [3]. However, some studies have demonstrated, in the long term, mortality was significantly higher when compared with matched STEMI patients [3]. As such, it is important to not only identify this condition in the ED, but ensure these patients are connected to Cardiology and follow-up care.
Take Away Points
Takutsubo syndrome is a OMI mimic and is impossible to differentiate without cardiac catheterization, when detected in the ED, activate STEMI protocol
While stress cardiomyopathy has a better acute outcomes compared to OMI, newer data indicated chronic outcomes may be worse, so identifying this condition is critical
References
Burns E, Buttner R, Buttner EB and R. Takotsubo cardiomyopathy. Life in the Fast Lane. October 8, 2024. Accessible at: https://litfl.com/takotsubo-cardiomyopathy-ecg-library/.
Komamura K, Fukui M, Iwasaku T, Hirotani S, Masuyama T. Takotsubo cardiomyopathy: Pathophysiology, diagnosis and treatment. World J Cardiol. 2014;6(7):602-609. doi:10.4330/wjc.v6.i7.602
Bairashevskaia AV, Belogubova SY, Kondratiuk MR, et al. Update of Takotsubo cardiomyopathy: Present experience and outlook for the future. Int J Cardiol Heart Vasc. 2022;39:100990. Published 2022 Mar 7. doi:10.1016/j.ijcha.2022.100990
Authored by Michael Hohl MD and Ari Edelheit MD