Echo Case: Comatose 62-Year-Old Woman Following Cardiopulmonary Resuscitation

Authors: Kan Liu MD, PhD, Megha Dogra MD

Affiliations of Authors:

University of Iowa, Iowa city, and State University of New York, Upstate Medical University Hospital, Syracuse,

Corresponding Author: Kan Liu MD, PhD

Associate Professor of Cardiovascular Medicine

Director of Echocardiography, Heart and Vascular center

University of Iowa,

Iowa city, IA (319-356-7481; Kan-Liu@uiowa.edu)

WHAT WOULD YOU DO NEXT?

1. Cardiac catheterization
2. Computed tomography of the head
3. Pulmonary computed tomography angiography
4. Transesophageal echocardiography

DIAGNOSIS

Neurogenic stress cardiomyopathy

WHAT TO DO NEXT

1. Computed tomography of the head

DISCUSSION.

Elevated cardiac enzyme, ST segment depression in the precordial leads on the ECG (Figure 1A), and regional wall motion abnormalities on TTE (Figure 1B, and Supplemental Video 1) were all concerning for an acute myocardial infarction (AMI) and cardiac arrest. Cardiac catheterization with coronary angiography (option A) could be considered after return of spontaneous circulation.  Nevertheless, there were also important discriminating imaging features in the TTE to entertain another diagnosis: the wall motion abnormality only involved the mid-ventricular wall, without involvement of the basal or apical segments of the left ventricle. The mid-ventricular (hypokinetic) and apical/basal (hyperkinetic) segments exhibited a discrepant contractile pattern. This “spindle-shaped” ventricular contractile dysfunction was not consistent with the myocardial territory of a single coronary artery. Taking her manifestation and unique imaging findings into account, we gave priority to computed tomography of the head (option B), which showed a diffuse subarachnoid hemorrhage (SAH) with intraventricular extension (Figure 2). Therefore, neurogenic stress cardiomyopathy (NSC) was diagnosed. Given her history of DVT, pulmonary embolism could possibly cause PEA and new onset atrial fibrillation. However, the characteristic TTE findings prompted us to seek a different diagnosis, and performing pulmonary computed tomography angiography (optional C) was not the first choice. A transesophageal echocardiography (option D) might improve the visualization of intra-cardiac anatomic structures, but unlikely offered further diagnostic help.

Intracranial hemorrhage, particularly SAH, is the leading cause of NSC.  Left ventricular (LV) dysfunction can occur acutely and improve spontaneously over days to weeks. NSC is thought to be caused by hemorrhage, ischemia or edema of the hypothalamus, which stimulates the release of endogenous catecholamine and results in extensive spasm of systemic arteries including the coronary arteries (1). In contrast to classical stress-induced cardiomyopathy, or Takotsubo syndrome, which is often associated with a LV “apical ballooning” pattern, NSC more commonly causes an “inverse” contractile dysfunction, which involves basal and middle, but not apical LV segments (2).  The cause of this difference is unclear, but neither ventricular contractile pattern is consistent with the myocardial territory of a single coronary artery, helping distinguish NSC and Takotsubo cardiomyopathy from AMI.

Clinical manifestation and ECG changes of NSC can resemble those of AMI, including ST segment elevation myocardial infarction.  Current guidelines advocate using coronary angiography to direct the diagnosis and therapy (3). However, if SAH induced NSC is misdiagnosed as AMI, anticoagulation and antiplatelet treatment can exacerbate the bleed.  Even more catastrophic would be the use of fibrinolytic therapy in those hospitals lacking a catheterization laboratory. Characteristic noninvasive cardiac imaging findings can  help appropriately triage patients with NSC, avoiding harmful procedures/treatments and adverse events. Surveillance echocardiography can help assess the recovery of LV function during follow up.

Timely diagnosis of NSC also has important implications in management. In patients with hemodynamic instability, catecholamine inotropic and pressor agents should be avoided.  Alpha-adrenergic agonists are useful in maintaining peripheral vascular pressure and supporting cerebral perfusion.  While the actual effect of intra-aortic balloon pumps is uncertain in patients with LV outflow tract obstruction, hemodynamic support from baroreflex activation therapy (3) and percutaneously inserted ventricular assist devices (4) are targets of current and future research.

Due to limited donor organ availability, only about 10% of patients in the United States who may benefit from heart transplantation undergo this procedures annually.  Meanwhile, many of the patients who experience brain death from neurological insults are deemed unsuitable donors for cardiac transplantation because of NSC.The LV dysfunction during stress-induced cardiomyopathy are usually  reversible .  In the largest analysis of donor hearts with transient LV dysfunction, such hearts have been successfully transplanted without increasing recipient mortality (5). Further investigation is warranted to better understand the underlying pathophysiology and reversibility of NSC, which may increase the number of donor hearts that would otherwise be rejected primarily because of poor LV function.

PATIENT OUTCOME

Because of anoxic brain injury and irreversible neurological dysfunction, the goals of care were transitioned to comfort measures. As a candidate for organ donation, she underwent serial echocardiography that documented complete resolution of LV systolic dysfunction within 48 hours. Cardiac catheterization confirmed normal coronary anatomy.  However, she did not become a heart donor eventually due to controversies on acceptance of donor hearts with transient LV dysfunction.

Reference

1. Hravnak M, Frangiskakis JM, Crago EA, et al. Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage. 2009;40(11):3478-3484.
2. Ancona F, Bertoldi LF, Ruggieri F, et al. Takotsubo cardiomyopathy and neurogenic stunned myocardium: similar albeit different. Eur Heart J. 2016;37(37):2830-2832.
3. Abraham WT, Zile MR, Weaver FA, et al. Baroreflex activation therapy for the treatment of heart failure with a reduced ejection fraction. JACC Heart Fail. 2015;3(6):487-496.
4. Kato K, Lyon AR, Ghadri JR, Templin Takotsubo syndrome: aetiology, presentation and treatment. Heart.2017;103(18):1461-1469.
5. Madan S, Saeed O, Vlismas P, et al. Outcomes after transplantation of donor hearts with improving left ventricular systolic dysfunction. J Am Coll Cardiol. 2017;70(10):1248-1258.

 Figure Legends

Figure 1.  Electrocardiogram (panel A) and transthoracic echocardiogram (panel B, and Supplemental Video 1)

Figure 2. Computed tomography of the head showing diffuse subarachnoid hemorrhage (arrow)with intraventricular extension