Reverse Takotsubo Cardiomyopathy After Treatment of Asymptomatic Bradycardia Prior to Anesthesia Induction in a Young Woman Undergoing Elective Rhinoplasty: A Case Report

Introduction

Takotsubo cardiomyopathy (TC), more commonly known as “broken heart syndrome,” is typically characterized by transient regional wall motion abnormalities of the ventricle and is usually unrelated to coronary artery disease [1]. TC may mimic a myocardial infarction, presenting with transient systolic dysfunction of the apical segments of the left ventricle. This pattern can be described as apical ballooning [2]. TC represents approximately 1.2% of all troponin-positive acute coronary syndrome events. Reverse takotsubo cardiomyopathy (rTC) is a rare variant in which the basal and midventricular segments of the left ventricle are akinetic [3]. The overall incidence of TC is estimated at 2% among troponin-positive patients, and rTC comprises only 6% to 8% of TC cases. rTC is most common among young women [4]. This condition is generally associated with catastrophic life events that provoke a catecholamine surge; however, anticholinergic drugs have also been reported to adversely affect myocardial contractility [5]. Here, we describe the case of a young woman undergoing elective surgery who developed rTC after the administration of an anticholinergic drug for asymptomatic bradycardia.

Case Report

A 27-year-old woman presented for elective rhinoplasty. She had no history of tobacco smoking, alcohol use, or substance abuse. Her medical history comprised Marfan syndrome, sinus bradycardia with intermittent junctional escape rhythm, and mitral valve prolapse of the A2 segment resulting in mitral regurgitation but preserved biventricular systolic function. Prior to anesthesia induction, she displayed sinus bradycardia with a ventricular rate of 45 beats per minute (bpm). She received 0.2 mg of glycopyrrolate, which precipitated recurrent episodes of wide-complex tachycardia. Administration of 40 mg of esmolol did not result in clinically significant improvement; the rhythm progressed to cardiac arrest requiring advanced cardiac life support (ACLS). After 2 rounds of ACLS, return of spontaneous circulation (ROSC) was achieved. Following ROSC, the patient was neurologically intact but developed cardiogenic shock. A transthoracic echocardiogram (TTE) revealed a newly reduced ejection fraction (EF) of approximately 42%, as well as apical and basal hypokinesis consistent with rTC, along with mild mitral regurgitation.

The patient was transferred to the Heart and Vascular Intensive Care Unit and placed on the following infusions: milrinone 0.25 μg/kg/min, norepinephrine 0.02 μg/kg/min, and vasopressin 0.06 units/min. She also received stress-dose steroids. Pertinent laboratory results demonstrated leukocytosis with a white blood cell count of 21 K/μL, an elevated creatinine level of 1.96 mg/dL, and a lactic acid concentration that peaked at 6.3 mmol/L. Empiric antimicrobial therapy was initiated with azithromycin 500 mg once daily and piperacillin-tazobactam 4.5 g every 8 h.

A repeat TTE performed 2 days after the cardiac arrest revealed a further reduction in EF to 25% while on vasopressors and inotropes (Figure 1); wall motion abnormalities were consistent with rTC. Due to reduced cardiac function and mitral regurgitation, the patient experienced multiple episodes of acute flash pulmonary edema requiring aggressive diuresis with a bumetanide infusion at 2 mg/h. Left and right heart catheterization demonstrated clean coronary arteries and normal filling pressures. An advanced therapy work-up was initiated, including evaluation for surgical Impella® 5.5 placement, left ventricular assist device implantation, and possible heart transplantation.

One week after the initial cardiac arrest, a follow-up TTE showed a substantially improved EF of 60%, without evidence of valvular abnormalities or dysfunction (Figure 2). Care was transitioned to the Cardiology service, and goal-directed medical therapy was initiated. The patient was discharged on hospital day 13 without an implantable cardioverter-defibrillator, given the reversible etiology of her ventricular tachycardia. She continues to be followed by the heart failure cardiology team and remains stable at follow-up.

Discussion

This case highlights the potential for severe adverse cardiac events in stress-induced cardiomyopathy precipitated by a catecholamine surge related to psychological or physical stress. In this instance, preoperative stress combined with anticholinergic treatment of asymptomatic bradycardia precipitated wide-complex tachycardia, cardiac arrest, and subsequent rTC. The underlying physiology involves an excess of catecholamines leading to multivessel and arterial vasospasm, increased ventricular afterload, and elevated mean arterial pressure, ultimately resulting in myocardial stunning. Severe ventricular dysfunction, compounded by valvular pathology in the form of mitral regurgitation, contributed to pulmonary backflow and pulmonary edema, requiring aggressive diuretic treatment [6].

The primary mechanism of action of glycopyrrolate comprises inhibition of acetylcholine and its effects on the parasympathetic nervous system at multiple sites throughout the body, including the central nervous system, smooth muscle, and secretory glands [7]. Glycopyrrolate has a rapid anticholinergic onset of action. This suppression of parasympathetic activity may exaggerate the sympathetic response and trigger the development of rTC. Several reported cases have linked rTC with the administration of antimuscarinic agents [8]. In the present case, the patient had asymptomatic bradycardia, which was treated with a standard dose of glycopyrrolate. Although such instances are rare, this case provides clinical evidence that inhibition of the parasympathetic nervous system with an anticholinergic, specifically an antimuscarinic agent, may precipitate rTC. We recommend that treatment of asymptomatic bradycardia with anticholinergics be undertaken cautiously, considering the potential for this complication.

Our patient, similar to others with rTC pathology, was relatively young and exposed to an identifiable physical or emotional trigger that resulted in basal and midventricular hypokinesis with preserved apical contractility. Prior studies have shown that rTC can be complicated by pulmonary edema and cardiogenic shock. The present case reinforces these concerns, given the patient’s severe left ventricular dysfunction, need for inotropic support, and evaluation for advanced therapies including heart transplantation. Despite this severity, she achieved complete resolution of left ventricular dysfunction within 10 days of the cardiac arrest. However, limited information has been published concerning the clinical characteristics and inpatient course of rTC [7,9], and further investigation is warranted.

In summary, this case illustrates a potential complication related to anesthesia induction after administration of an anticholinergic. By emphasizing the rarity of this variant of TC, we aim to raise awareness of potential complications that may mimic nonischemic cardiomyopathy. Avoidance of anticholinergics should be considered in patients with known or suspected TC or its variants. In the present case, although advanced therapies and heart transplantation were considered, the patient’s symptoms resolved within 10 days of the initial event.

Conclusions

The use of anticholinergics in patients with asymptomatic bradycardia should be approached with caution, given the potential to precipitate rTC and prolong hospitalization.