A 22-year-old woman presented to the OR for a rectal examination and rectal fistula repair. She had a body mass index of 35 kg/m2 and a history of hypothyroidism, depression and migraines. Upon presentation, her hypothyroidism had resolved and levels of thyroid-stimulating hormone and free thyroxine were normal. Her medications consisted of ibuprofen, oxycodone, sumatriptan and venlafaxine. She received 2 mg of IV midazolam on the way to the OR. In the OR, standard monitors were placed and vital signs were normal. General anesthesia was induced with lidocaine 60 mg, fentanyl 50 mcg, propofol 120 mg and succinylcholine 60 mg, and a 7.0-mm endotracheal tube was placed on the first attempt. Anesthesia was maintained with sevoflurane.

Immediately after the patient was placed in the high lithotomy position, bradycardia ensued with a heart rate in the 30s beats per minute, which was treated with glycopyrrolate 0.2 mg IV. The patient developed supraventricular tachycardia and hypertension, with values reaching 220 mm Hg systolic over 110 mm Hg diastolic. Esmolol IV in 10-mg increments was administered with a total of 50 mg IV, with no response. Blood pressure decreased after administration of labetalol 20 mg IV and the short surgical procedure was completed. The patient resumed spontaneous breathing, but immediately after discontinuation of sevoflurane she developed acute pulmonary edema, severe hypotension and ST segment depression.

Resolution of the Case

A norepinephrine infusion was started and the patient was transferred intubated to the ICU. The ECG showed findings consistent with acute coronary ischemia (inferior Q waves, flattened T waves in lateral leads and prolonged QT interval). A chest CT scan showed opacification of the pulmonary arterial vascular system, consolidation and ground glass opacities affecting all lung lobes. An echocardiogram showed moderate to severe mid-left ventricular hypokinesis, mild tricuspid regurgitation, severely reduced left ventricular systolic ejection fraction of 38%, restrictive grade III diastolic dysfunction, and elevated left ventricular filling pressure. The N-terminal pro-brain natriuretic peptide (NT proBNP) was elevated at 456 pg/mL. Based on these findings, the patient was diagnosed with Takotsubo stress cardiomyopathy. On the first postoperative day (POD), the patient was weaned off the norepinephrine infusion and was extubated later that day. A repeat ECG and echocardiogram the next day, POD 2, showed normal findings, and the patient was discharged without sequelae.

Cardiovascular Implications and Treatment

Stress cardiomyopathy, also known as “broken heart syndrome,” left ventricular apical ballooning syndrome and Takotsubo cardiomyopathy (TCM), was first described in Japan in 1991.1 The condition is characterized by transient acute heart failure with systolic and/or diastolic left ventricular dysfunction mimicking acute coronary syndrome, in the absence of obstructive coronary disease.2-4 In Japanese, takotsubo means “fishing pot for trapping octopus,” and refers to the shape of the left ventricle caused by apical ballooning (Figure).5

image

Figure. The Japanese octopus traps after which this disease is named.

The pathophysiology of TCM is still not fully understood; however, it seems that a catecholamine surge caused by severe emotional or physical stress is the common denominator in the majority of cases.6,7 The term “broken heart syndrome” reflects the association of the syndrome with profound emotional stress. Women of postmenopausal age are most commonly affected, but TCM is also reported in younger patients, including pregnant women.6,8

Templin et al analyzed data from the International Takotsubo Registry, including 1,750 patients; 89% were female with a mean age of 66.8 years. The authors reported a significantly higher incidence of TCM in patients with neurologic or psychiatric disorders.3 A possible genetic predisposition was suggested based on case reports of familial involvement.9,10 Serotonin–norepinephrine reuptake inhibitors (SNRIs) have been involved in triggering TCM.11 The symptoms of TCM mimic acute coronary syndrome (chest pain, shortness of breath, sweating, dizziness, nausea/vomiting, weakness and palpitations) and may not be identified under general anesthesia. An ECG may show ST segment elevation and depression, T-wave inversion, QT interval prolongation, abnormal Q waves and other changes.2,3 Apical or left mid-ventricular ballooning, akinesia or hypokinesia with compensatory hypercontractility of the basal wall are the characteristic echocardiographic findings along with a significant decrease in the ejection fraction (observed in approximately 90% of patients with TCM).3,12

Cardiac biomarkers are elevated in the vast majority of patients with TCM. Troponin levels are typically increased but to a lesser extent than in patients presenting with acute myocardial infarction. Level of NT proBNP was identified as a reliable predictor of short- and long-term complications.13

Treatment is mainly supportive, with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta blockers and diuretics.14 Ueyama showed in an animal model that beta blockade may be particularly beneficial in treating TCM.15

Usually, TCM is reversible with a favorable short- and long-term prognosis. However, severe complications, such as acute heart failure, arrhythmias, mitral regurgitation, left ventricular outflow obstruction, ventricular thrombus, left ventricular wall rupture and death have been reported.16

The incidence of TCM developing in the perioperative period is one in 6,700 cases. Multiple types of surgical procedures have been reported in patients developing perioperative TCM, including gastrointestinal, cardiothoracic, orthopedic and transplant surgeries as well as cesarean delivery.17,18 Although TCM is most frequently associated with general anesthesia, it has also been reported with regional anesthesia and sedation. Agarwal et al reviewed 93 articles describing 102 patients with perioperative TCM. The majority of cases (58%) developed in the postoperative period. Preoperative occurrence of TCM has also been reported, most likely triggered by the patient’s anxiety.19 Intraoperative triggers reported to cause TCM are mainly related to intensive catecholamine discharge, such as laryngoscopy, intubation, extubation and light levels of anesthesia. Isoflurane has been shown to lessen the apical akinesia in animals with TCM induced by intraperitoneal injection of isoprenaline.20

In the patient described here, the ECG and echocardiographic pathognomonic signs, along with elevated NT proBNP levels, allowed for a quick diagnosis without the need to perform an unnecessary cardiac catheterization.

Conclusion

The following points about TCM are most noteworthy:

  • TCM can occur anytime during the perioperative period with any type of surgery.
  • TCM is a stress-induced cardiomyopathy with apical and mid-ventricular wall motion abnormalities in the absence of coronary artery disease.
  • TCM is mostly transient, resulting in complete recovery of the ventricular function and wall motion abnormalities; however, severe complications can occur.
  • Therapy is supportive and aimed to prevent complications.

References

  1. Dote K, Sato H, Tateishi H, et al. [Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases]. J Cardiol. 1991;21(2):203-214.
  2. Summers MR, Prasad A. Takotsubo cardiomyopathy: definition and clinical profile. Heart Fail Clin. 2013;9(2):111-122.
  3. Templin C, Ghadri JR, Diekmann J, et al. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy. N Engl J Med.2015;373(10):929-938.
  4. Sharkey SW, Windenburg DC, Lesser JR, et al. Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol. 2010;55(4):333-341.
  5. Virani ss, Khan AN, Mendoza CE, et al. Takotsubo cardiomyopathy, or broken-heart syndrome. Tex Heart Inst J.2007;34(1):76-79.
  6. Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med. 2005;352(6):539-548.
  7. Park JH, Kang SJ, Song JK, et al. Left ventricular apical ballooning due to severe physical stress in patients admitted to the medical ICU. Chest. 2005;128(1):296-302.
  8. Minatoguchi M, Itakura A, Takagi E, et al. Takotsubo cardiomyopathy after cesarean: a case report and published work review of pregnancy-related cases. J Obstet Gynaecol Res. 2014;40(6):1534-1539.
  9. Ikutomi M, Yamasaki M, Matsusita M, et al. Takotsubo cardiomyopathy in siblings. Heart Vessels. 2014;29(1):119-122.
  10. Kumar G, Holmes DR Jr, Prasad A. “Familial” apical ballooning syndrome (Takotsubo cardiomyopathy). Int J Cardiol.2010;144(3):444-445.
  11. Woronow D, Suggs C, Levin RL, et al. Takotsubo common pathways and SNRI medications. JACC Heart Fail. 2018;6(4):347-348.
  12. Gianni M, Dentali F, Grandi AM, et al. Apical ballooning syndrome or takutsubo cardiomyopathy: a systematic review. Eur Heart J. 2006;27(13):1523-1529.
  13. Stiermaier T, Santoro F, Graf T, et al. Prognostic value of N-Terminal Pro-B-Type natriuretic peptide in Takotsubo syndrome. Clin Res Cardiol. 2018;107(7):597-606.
  14. Kono T, Sabbah HN. Takotsubo cardiomyopathy. Heart Fail Rev. 2014;19(5):585-593.
  15. Ueyama T. Emotional stress-induced Tako-tsubo cardiomyopathy: animal model and molecular mechanism. Ann N Y Acad Sci. 2004;1018:437-444.
  16. Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141(11):858-865.
  17. Hessel EA 2nd. Takotsubo cardiomyopathy and its relevance to anesthesiology: a narrative review. Can J Anaesth.2016;63(9):1059-1074.
  18. Agarwal S, Bean MG, Hata SJ, et al. Perioperative takotsubo cardiomyopathy: a systemic review of published cases. Sem Cardiothorac Vasc Anesth. 2017;21(4):277-290.
  19. Wong AK, Vernick WJ, Wiegers SE, et al. Preoperative Takotsubo cardiomyopathy identified in the operating room before induction of anesthesia. Anesth Analg. 2010;110(3):712-715.
  20. Redfors B, Oras J, Shao Y, et al. Cardioprotective effects of isoflurane in a rat model of stress-induced cardiomyopathy (Takotsubo). Int J Cardiol. 2014;176(3):815-821.