Case Report of High-Grade Atrioventricular Block and Takotsubo Cardiomyopathy



 

Rohan Prasad DO1; Mohammad Fahad Salam MD1; Shaurya Srivastava DO1; FNU Samreen MD2; Zulfiqar Qutrio Baloch MD3

Perm J 2021;25:21.006

https://doi.org/10.7812/TPP/21.006
E-pub: 05/12/2021

Introduction: Takotsubo cardiomyopathy (TTC) is a condition with a good long-term prognosis. However, when the TTC is due to a life-threatening arrhythmia, such as atrioventricular block (AVB), several considerations must be made regarding treatment.

Case Presentation: A 71-year-old woman with a history of ischemic stroke presented after a syncopal episode. Before passing out, the patient was walking, nauseous, lightheaded, dizzy, and short of breath. In the emergency department, the blood pressure was 230/120 mmHg, and the heart rate was 38 beats per minute, but the patient was asymptomatic. An electrocardiogram showed a new-onset 2:1 AVB, bifascicular block, and prolonged PR and corrected QT intervals. An echocardiogram revealed a new-onset ejection fraction of 30% to 35%; hypokinesis of the apex, mid-inferoseptum, mid-anterolateral, apical to mid-inferior, and apical to mid-anterior walls; and hyperkinesis of the basal segments. The cardiac catheterization illustrated normal coronary arteries without significant stenosis. Therefore, the patient was diagnosed with TTC and 2:1 AVB. She was treated with lisinopril and metoprolol succinate and received a dual-chamber pacemaker. At the follow-up visit, the patient’s ejection fraction and hypokinetic segments improved. She denied any recurrence of syncope, and her pacemaker was functioning appropriately.

Conclusion: When AVB or other arrhythmias initiate a TTC, the patient can experience sudden cardiac death and decompensate quickly. Therefore, clinicians should understand this rare but fatal complication because these patients require pacemakers and beta blockers.

INTRODUCTION

Takotsubo cardiomyopathy (TTC) is a disease in which a patient develops transient hypokinesis, akinesis, or dyskinesis with compensatory excessive contraction in the other areas. Usually, this is preceded by a stressor. Despite the possibility of acute life-threatening symptoms and hemodynamic compromise at its onset, the long-term prognosis is generally favorable, and the wall motion abnormality improves within 2 weeks.1,2

In this case presentation, we report a 71-year-old woman who developed new-onset TTC, 2:1 atrioventricular block (AVB), bifascicular block, and prolonged PR and corrected QT (QTc) intervals after a syncopal episode. The prevalence of AVB in TTC has been reported at 2.2%3 and 2.9%.4 Although TTC resolves, the comorbid bradyarrhythmias are typically persistent and require the placement of a pacemaker.4,5 This case report was prepared following the CARE guidelines.6

CASE PRESENTATION

A 71-year-old woman with a history of ischemic stroke and chronic lymphocytic leukemia in remission presented after a syncopal episode. The patient stated before passing out that she had walked about 10 feet and was nauseous, lightheaded, dizzy, and short of breath. The patient denied preceding chest pain and palpitations. At first, the patient denied any recent emotional stress or possible triggers, but on further questioning, she admitted to a tense verbal conversation with her son earlier that morning. She was not taking any antiplatelet, anticoagulant, anti-arrhythmic, or beta-blocker medication. In the emergency department, the patient’s vital signs included a blood pressure of 230/120 mmHg and a heart rate of 38 beats per minute, but she was otherwise stable and asymptomatic. Moreover, the physical examination, laboratory investigations, and pan imaging were unremarkable (Table 1). However, an electrocardiogram showed a new-onset 2:1 AVB, bifascicular block and prolonged PR and QTc intervals (Figure 1). An echocardiogram revealed an ejection fraction of 30% to 35%; hypokinesis of the apex, mid-inferoseptum, mid-anterolateral, apical to mid-inferior, and apical to mid-anterior walls; and hyperkinesis of basal segments. The cardiac catheterization illustrated normal coronary arteries without significant stenosis. Finally, the left ventriculography confirmed the 30% to 35% ejection fraction, apical hypokinesis, and basal hyperkinesis. Therefore, the patient was diagnosed with TTC and 2:1 AVB. Subsequently, she was started on lisinopril and metoprolol succinate. The patient underwent an emergent implantation of a dual-chamber pacemaker. The patient was discharged home on daily lisinopril and instructed to follow up in the office after obtaining an echocardiogram in 6 weeks. This echocardiogram showed an improved ejection fraction of 50% and improvement in the mid-to-apical hypokinetic segments and device lead in the right heart chambers. Moreover, the patient had not had a recurrence of syncope or AVB, and her pacemaker was functioning appropriately.

Table 1. Timeline: relevant medical history and interventions for a 71-year-old woman presenting with a history of ischemic stroke and chronic lymphocytic leukemia in remission

Date Summaries from initial and follow-up visits Diagnostic testing Treatment  
12/23/2019 The patient presented to the emergency department with acute syncope with prodromal symptoms. Blood pressure, 230/120 mmHg; heart rate, 38 beats per minute; temperature, 98.2°F Started lisinopril and metoprolol succinate  
Electrocardiogram: 2:1 atrioventricular block; bifascicular block; PR interval, 293 ms; QTc interval, 514 ms    
A dual-chamber pacemaker was placed emergently  
Echocardiogram: ejection fraction, 30%-35%; hypokinesis of the apex, mid-inferoseptum, mid-anterolateral, apical to mid-inferior, and apical to mid-anterior walls; and hyperkinesis of basal segments  
Cardiac catheterization: normal coronary arteries without significant stenosis  
Left ventriculography: ejection fraction, 30%-35%, apical hypokinesis, and basal hyperkinesis  
White blood cells, 12.5 10^3/μL  
Troponin I, 7 and 10 pg/mL  
Serum potassium, 3.9 meq/L  
Serum magnesium, 2.0 mg/dL  
Thyroid-stimulating hormone, 7.01 u[IU]/mL  
Free T4, 0.90 ng/dL  
12/24/20   Deemed to be medically stable Instructed to follow up in 6 weeks  
Discharged home  
2/7/2020 The patient presented to the office for a follow-up echocardiogram and denied any recurrence of syncope or atrioventricular block. Follow-up echocardiogram: ejection fraction of 50%, improvement in the mid-to-apical hypokinetic segments, and device lead in the right heart chambers    

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Figure 1. Admission electrocardiogram showing new-onset 2:1 atrioventricular block, bifascicular block, PR interval of 293 ms, and QTc interval of 514 ms.

DISCUSSION

The differential diagnosis for acute myocardial infarction includes TTC, named after the resemblance of the left ventricular apical ballooning in systole to a Japanese octopus trap. The left ventricular mid-segments, with or without the apex, had transient hypokinesis, akinesis, or dyskinesis, with compensatory excessive contraction in the other areas. Other diagnostic criteria are regional wall motion abnormalities extending beyond a single coronary vascular bed, absence of obstructive coronary disease or angiographic evidence of acute plaque rupture, and presence of new-onset electrocardiographic abnormalities or modest elevations in cardiac troponin. Typically, the trigger of these symptoms is a physical or emotional stressor; thus, it is also known as broken-heart syndrome or stress-induced cardiomyopathy.1,7 At its onset, TTC can develop life-threatening symptoms and hemodynamic compromise. However, the long-term prognosis is generally favorable, and the wall motion disorder improves within 2 weeks.1,2

Two studies evaluating AVB among patients with TTC reported a rare prevalence of 2.2% (4/178)3 and 2.9% (24/816).4 The difficult task in these patients is determining its pathophysiology. One hypothesis is based on the fact that although TTC resolves rather quickly, the bradyarrhythmias are usually present long term.2,4,5 Therefore, TTC is unlikely to be the precipitating factor, but rather the effect of the AVB. This is proposed to be through an increased catecholamine secretion that produces a vagal response and eventually AVB and TTC. Possible etiologies of this are blood flow disruption by alpha-receptors and multiple branch coronary artery spasm.2,8 With this in mind, beta blockers are potentially indicated to stunt the catecholamine surge, but are limited by the patient’ s hemodynamics.9 Beta blockers have even been reported to prevent the development of arrhythmias.10 Our patient was not on beta blockers before admission, but based on the above recommendations, we discharged her on metoprolol succinate.

The bradyarrhythmias seen with TTC are: AVB (2.2% [4/178] and 2.9% [24/816]), sinus node dysfunction (1% [3/178] and 1.3% [11/816]), asystole (1.7% [5/178] and 0.5% [4/816]), and pulseless electrical activity (0.3% [1/178]). 3,4 Although these bradyarrhythmias have been reported to resolve, the fatal bradyarrhythmia can reoccur and cause sudden cardiac death. Thus, lifelong pacemakers should be considered in these patients, even if the patient becomes asymptomatic.2,4,8 Furthermore, life-threatening arrhythmias have been illustrated to have a lower ejection fraction (39.7% ± 11.0%), longer QTc interval (476.5 ± 74.4 ms and 491 ± 81 ms), longer PR interval (207 ± 96 ms), and longer maximal R-R interval (30.6 ± 14.5 ms). Our patient had an ejection fraction of 30% to 35%, QTc interval of 516 ms, PR interval of 293 ms, and R-R interval of 1452 ms. We placed a dual-chamber pacemaker in our patient. At her follow-up appointment, she had not had a recurrence of syncope, AVB, or TTC, but the decision was made to keep the pacemaker. Because this is a case report, it has the limitation that it can only indicate associations, not causations. Moreover, the association inferred from our patient may not be generalizable to a larger population.

Although bradyarrhythmias should be actively monitored for and expectantly treated, patients with TTC can also develop other dire complications that require urgent intervention. It should be noted that these recommendations are only suggestions based on retrospective and literature reviews, because prospective and clinical trials have yet to be completed. In those who develop heart failure, one should initiate a typical heart failure regimen of beta blockers, angiotensin-converting enzymes or angiotensin receptor blockers, and diuretics.11 Beta blockers are also indicated to prevent the TTC sequelae of developing a cardiac rupture.12 Additionally, patients with a history of left ventricular thrombus or embolic complications who develop extensive mid-apical ballooning should receive anticoagulation treatment for a minimum of 2 to 3 months.13,14 Finally, cardiogenic shock can be seen in patients with TTC. When due to left ventricular outflow tract obstruction, one should start parenteral beta blockers and intravenous fluids, with phenylephrine being a second-line medication. Due to the obstruction, diuretics, nitroglycerin, and intra-aortic balloon pumps are contraindicated.15 However, venoarterial extracorporeal membrane oxygenation, left ventricular assist device, or noncatecholamine inotropes such as levosimendan may be indicated in patients with primary pump failure.13,16

CONCLUSION

Increased catecholamine secretion is likely to cause AVB and subsequently TTC. TTC is a rare but life-threatening condition that should be managed expectantly, even if the patient’s symptoms resolve. Furthermore, beta blockers may help decrease the catecholamine surge and prevent the onset or recurrence of an arrhythmia.

Disclosure Statement

The author(s) have no conflicts of interest to disclose.

Funding

The authors received no funding for the writing this case report.

Acknowledgments

Kathleen Louden, ELS, of Louden Health Communications performed a primary copy edit.

Author Affiliations

1Department of Internal Medicine, Michigan State University - Sparrow Hospital, Lansing, MI

2Department of Internal Medicine, Michigan State University - Sparrow Hospital, Lansing, MI

3Sparrow Thoracic and Cardiovascular Institute, Lansing, MI

Corresponding Author

Rohan Prasad, DO (prasadr1@msu.edu)

Author Contributions

Rohan Prasad, DO, wrote the Case Narrative and Discussion, conducted the literature review, obtained consent, and edited final draft. Mohammad Fahad Salam, XX, wrote the Abstract and Introduction, assisted in writing the Discussion, conducted the literature review, and edited final draft. Shaurya Srivastava, XX, wrote the Conclusion and References, formatted the table, and edited the final draft. FNU Samreen, XX, obtained the figure, formatted the table, and edited final draft. Zulfiqar Qutrio Baloch, XX, assisted in writing the Discussion and literature review, and edited the final draft.

Abbreviations

AVB, atrioventricular block; QTc, corrected QT interval; TTC, takotsubo cardiomyopathy

References

1. Hurst RT, Prasad A, Askew JW, Sengupta PP, Tajik AJ. Takotsubo cardiomyopathy: A unique cardiomyopathy with variable ventricular morphology. J Am Coll Cardiol 2010 Jun;3(6):641-9. DOI: https://doi.org/10.1016/j.jcmg.2010.01.009

2. Kodama S, Miyoshi K, Shiga Y, et al Takotsubo cardiomyopathy complicated by high-grade atrioventricular block: A report of two cases. Exp Clin Cardiol Nov 2009 Summer;14(2):e35-8, PMID:19675818.

3. Syed FF, Asirvatham SJ, Francis J. Arrhythmia occurrence with takotsubo cardiomyopathy: A literature review. Europace 2011 Jun;13(6):780-8. DOI: https://doi.org/10.1093/europace/euq435, PMID:21131373.

4. Stiermaier T, Rommel KP, Eitel C, et al Management of arrhythmias in patients with takotsubo cardiomyopathy: Is the implantation of permanent devices necessary?. Heart Rhythm 2016 Oct;13(10):1979-86. DOI: https://doi.org/10.1016/j.hrthm.2016.06.013, PMID:27298201.

5. Jesel L, Berthon C, Messas N, et al Ventricular arrhythmias and sudden cardiac arrest in takotsubo cardiomyopathy: Incidence, predictive factors, and clinical implications. Heart Rhythm 2018 Aug;15(8):1171-8. DOI: https://doi.org/10.1016/j.hrthm.2018.04.002, PMID:29627435

6. Riley DS, Barber MS, Kienle GS, et al CARE guidelines for case reports: Explanation and elaboration document. J Clin Epidemiol 2017 Sep;89:218-35. DOI: https://doi.org/10.1016/jclinepi.2017.04.026.

7. Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: A new form of acute, reversible heart failure. Circulation 2008 Dec;118(25):2754-62. DOI: https://doi.org/10.1161/CIRCULATIONAHA.108.767012, PMID:19106400.

8. Korantzopoulos P, Nikas DN, Letsas K, et al High-grade atrioventricular block and takotsubo cardiomyopathy: Case report and review of the literature. Int Cardiovasc Res J 2015;9(2):119-24.

9. Bonello L, Com O, Ait-Moktar O, et al Ventricular arrhythmias during tako-tsubo syndrome. Int J Cardiol 2008 Aug;128(2):e50-3. DOI: https://doi.org/10.1016/j.ijcard.2007.04.166, PMID:17706815

10. Dib C, Prasad A, Friedman PA, et al Malignant arrhythmia in apical ballooning syndrome: Risk factors and outcomes. Indian Pacing Electrophysiol J 2008 Aug;8(3):182-92, PMID:18679529.

11. Brunetti ND, Santoro F, De Gennaro L, et al Combined therapy with beta-blockers and ACE-inhibitors/angiotensin receptor blockers and recurrence of takotsubo (stress) cardiomyopathy: A meta-regression study. Int J Cardiol 2017 Mar;230:281-3. DOI: https://doi.org/10.1016/j.ijcard.2016.12.124, PMID:28040283

12. Kumar S, Kaushik S, Nautiyal A, et al Cardiac rupture in takotsubo cardiomyopathy: A systematic review. Clin Cardiol 2011 Nov;34(11):672–6. DOI: https://doi.org/10.1002/clc.20957, PMID:21919012

13. Lyon AR, Bossone E, Schneider B, et al Current state of knowledge on takotsubo syndrome: A Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail 2016 Jan;18(1):8-27. DOI: https://doi.org/10.1002/ejhf.424, PMID:26548803

14. El-Battrawy I, Borggrefe M, Akin I. Takotsubo syndrome and embolic events. Heart Fail Clin 2016 Oct;12(4):543-50. DOI: https://doi.org/10.1016/j.hfc.2016.06.011, PMID:27638024

15. Migliore F, Bilato C, Isabella G, Iliceto S, Tarantini G. Haemodynamic effects of acute intravenous metoprolol in apical ballooning syndrome with dynamic left ventricular outflow tract obstruction. Eur J Heart Fail 2010 Mar;12(3):305-8. DOI: https://doi.org/10.1093/eurjhf/hfp205, PMID:20097684

16. Santoro F, Ieva R, Ferraretti A, et al Safety and feasibility of levosimendan administration in takotsubo cardiomyopathy: A case series. Cardiovasc Ther 2013 Dec;31(6):e133-7. DOI: https://doi.org/10.1111/1755-5922.12047, PMID:24119220

Keywords: atrioventricular block, takotsubo cardiomyopathy

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