1 Introduction

Takotsubo syndrome is characterized by transient, acute severe left ventricular systolic dysfunction and motion abnormalities like akinesia or dyskinesia of apical ventricular wall.¹ It was originally described in Japanese literature by Satoh et al. in 1990, eponym of apical ballooning of heart resembling round-bottomed pot for trapping octopus.^2,3 It is a reversible cardiomyopathy and usually triggered by acute psychological or physical stress. It is more common in the post-menopausal women and frequently presents at 7th to 8th decade of life.¹ The hallmarks of the syndrome are electrocardiographic abnormalities in precordial leads, ventricular apical ballooning in the echocardiogram, elevated biomarkers mimicking acute myocardial infarction but with normal coronal angiography.¹ It is also called as stress induced cardiomyopathy, non-ischemic cardiomyopathy, ampulla-shaped cardiomyopathy or “broken-heart syndrome”.^1,4

Cardiac complications represents a major cause of morbidity and mortality especially after bilateral simultaneous total knee arthroplasty (TKA). The incidence of perioperative acute myocardial infarction rate was 0.18% for TKA in a nationwide analysis.⁵ The incidence of cardiac complications has been reduced after strict selection criteria for performing simultaneous bilateral TKA.^6,7 One recent study has shown that about 15% of patients had Takotsubo syndrome with hip fracture and preoperative myocardial damage.¹ To the best of our knowledge, Takotsubo syndrome after bilateral simultaneous TKA has not been described in the literature. Informed written consent has been obtained from the patient for publication of this case report.

2 Case report

A 60 years-old women presented with bilateral progressive knee pain not responding to conservative therapy for osteoarthritis for about two years. Her body mass index was 31.2. Her Type 2 DM was well controlled (HbA1C 7.8 g m%) with oral hypoglycemic agents. She is a known systemic hypertensive patient on beta blockers and angiotensin receptor blockers. Her preoperative renal and liver function tests were within normal limits. On personal history, she lives with her aged and ailing husband and has no children. She has an anxiety temperament but not on any treatment.

Her clinical examination of knee revealed 0–100 degrees of range of motion, bilateral varus deformity and grade 2 medio-lateral instability. Her long leg alignment radiographs, lateral and skyline views showed severe tricompartmental osteoarthritis of both knees. On admission, she had stable vitals parameters and her electrocardiography and echocardiography was normal (no regional wall abnormalities, normal LV function (left ventricular ejection fraction (LVEF)- 60%), and mild mitral regurgitation).

After anaesthetic fitness, under combined spinal-epidural anaesthesia, she underwent bilateral simultaneous robotic-assisted TKA under tourniquet control (Fig. 1). Intraoperatively, her vital parameters were stable and the blood loss was about 450 ml and the total duration of the surgery was 210 min. After the second knee wound closure, suddenly she became apneic, unresponsive and developed bradycardia with hypotension.

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Fig. 1 (a) Preoperative long-leg alignment radiographs showing osteoarthritis of both knees with varus alignment (b) postoperative radiographs showing total knee arthroplasty prosthesis in situ with neutral alignment.

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Mask ventilation with 100% oxygen was started, then endotracheal intubation was done and mechanical ventilation started. Patient was resuscitated with adrenaline, atropine, with ionotropic support. Her initial arterial blood gas analysis revealed a mixed respiratory and metabolic acidosis with a pH of 7.15. A 12-lead electrocardiography showed ST elevation (2 mm) in V1–V4 with reciprocal ST depression in the inferior leads, suggestive of an anterior wall myocardial infraction (Fig. 2). 2D echocardiography showed hypokinesia and ballooning of the left ventricular apex and apical segments with an LVEF of 30% (Fig. 3). Her serum troponin I was 115.2 ng/L (Normal range <19 ng/L). She was initially treated with dual antiplatelets, statins, and low molecular weight heparin. Urgent coronary angiography revealed normal epicardial coronaries (Fig. 4), and an initial diagnosis of Takotsubo syndrome was made.

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Fig. 2 A 12-lead electrocardiography showed ST elevation (2 mm) in V1–V4 with reciprocal ST depression in the inferior leads, suggestive of an anterior wall myocardial infraction.

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Fig. 3 2D echocardiography showed hypokinesia and ballooning of the left ventricular apex.

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Fig. 4 Coronary angiography revealed normal epicardial coronaries with no flow limiting disease.

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There was a serial reduction in NT-proBNP, troponin with an improvement in LV function over the next 4 days. By the 5th postoperative day, she was weaned of the ventilator, with a normal LV function and no regional wall abnormalities. A single antiplatelet, low-dose statin, and beta blockers were continued. She gradually improved and started mobilizing with walker support and able to do knee range of motion exercises and quadriceps strengthening exercises. Patient recovered well completely and got discharged on 12th postoperative day. On one-year follow up, she was able to do all her normal activities, and 12-lead electrocardiography were back to normal (Fig. 5).

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Fig. 5 12-lead electrocardiography had become normalized at one-year follow up.

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3 Discussion

Takotsubo syndrome has been described during orthopaedic procedures like knee arthroscopy, spinal fusion surgery and hemiarthroplasty.^2,4,8 This case report highlights the reporting of first occurrence of Takotsubo cardiomyopathy after bilateral simultaneous TKA. The pathophysiology described for its occurrence are sympathetic activation, sudden catecholamine surge, estrogen deficiency and endothelial dysfunction leading to microvascular spasms and resultant myocardial dysfunction.^3,4,8,9 Higher densities of beta-adrenergic receptors are noted in the apical myocardium, that may be responsible for pathological findings in the heart during the period of stress and subsequent catecholamine surge.

Takotsubo syndrome is characterized clinically by chest pain, dyspnea, tachy-or bradyarrhythmia, heart failure and shock.⁴ Mayo criteria and InterTAK diagnostic score developed by international Takotsubo registry has been proposed for clinical diagnosis of this syndrome.^3,10 In electrocardiography, acute ST segment elevation in the precordial leads, T-wave inversion and QT prolongation is seen mimicking myocardial infarction.⁹ Cardiac enzymes like troponin I might be elevated and echocardiography typically shows an apical or mid-ventricular ballooning with transient akinesia or dyskinesia. But, significant coronary artery stenosis more than 50% is not detectable during the coronary angiography.^1,4 Our patient also had sudden hypotension and bradycardia, ST elevation in the precordial leads, troponin I elevation, apical ballooning of heart with normal vessels during the coronary angiography consistent with the typical Takotsubo syndrome. She had physical stress factors like chronic bilateral knee pain and functional disability in the background of psychological stress like anxiety and dependence on other family members.

Earlier, Takotsubo syndrome was considered a transient syndrome with favourable long-term prognosis if the patient survives the acute episode.^1,4 However, recent studies have shown that functional abnormalities may persist beyond 12 months post diagnosis.¹¹ The complications can range from mitral regurgitation, left ventricular outflow tract obstruction, arrhythmia, congestive heart failure, pulmonary edema to cardiogenic shock.^3,10 Also, short-term and long-term mortality are higher than previously recognized.⁹ Supportive therapy with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers are associated with lower prevalence of recurrence, while beta-blockers have no evidence of any survival benefit and does not appear to prevent recurrence.^3,4,10

4 Conclusion

In elderly postmenopausal patients, Takotsubo syndrome should be considered as a differential diagnosis with features of acute coronary syndrome. Recognition of the problem and prompt supportive therapy is essential for favourable prognosis. Surgeons must be vigilant in the postoperative period for any likely precipitating factors of stress induced cardiomyopathy especially after bilateral simultaneous total knee arthroplasty.

Ethics approval

This case report was performed in line with the principles of the Declaration of Helsinki. Informed written consent has been obtained from the patient for publication of this case report.

Funding

The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

Consent to participate

Informed written consent has been obtained from the patient for publication of this case report.

Consent to publish

The authors affirm that the patient provided informed consent for publication of the images in Figs. 1–5.

CRediT authorship contribution statement

Dhanasekaran Soundarrajan: Conceptualization, Methodology, Writing – original draft. Rithika Singh: Data curation, Visualization. Muthiah Subramaniam: Data curation, Visualization, Investigation. Palanisami Dhanasekararaja: Supervision. Natesan Rajkumar: Supervision. Shanmuganathan Rajasekaran: Conceptualization, Supervision, Writing – review & editing.