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Case Report
Open Access Peer-reviewed

Subarachnoid Hemorrhage Presenting with Second-Degree Type I Sinoatrial Exit Block: A Case Report

Pramod Theetha Kariyanna, Ruchi Yadav, Vivek Yadav, Samuel Apple, Naseem A. Hossain, Neema Jayachamarajapura Onkaramurthy, Apoorva Jayarangaiah, Ayesha Saad, Isabel M. McFarlane
American Journal of Medical Case Reports. 2020, 8(10), 341-347. DOI: 10.12691/ajmcr-8-10-6
Received May 14, 2020; Revised June 16, 2020; Accepted June 22, 2020

Abstract

The understanding of neural regulation of the cardiovascular function and the implications of a “Heart-Brain Axis “has been a topic of interest for clinicians for many years. Electrocardiographic (ECG) and structural cardiac changes, ranging from mild, asymptomatic, transient alteration in cardiovascular function to severe, irreversible, and potentially life-threatening injury, can actually be a manifestation of several neurological disorders. When managing cardiac disorders, a high index of clinical suspicion, detailed history-taking and physical examination skills, and an extensive workup that covers both cardiac and non-cardiac causes should be utilized. It is important to consider that cardiovascular dysfunction of an underlying neurological etiology may lead to difficulty in diagnosing and optimizing treatment of the latter. We report the case of a middle-aged female with the chief complaint of syncope preceded by a headache with no focal neurological deficits, originally diagnosed with- and whose syncope was attributed to sinus bradycardia and type I sinoatrial (SA) exit block on ECG. Subsequently, when the patient became altered, however, computer tomography (CT) angiography revealed subarachnoid hemorrhage (SAH) with middle cerebral artery aneurysm. This presentation emphasizes the importance of tabulating neurological injury as one of the differential diagnoses while managing ECG changes in cardiovascular disease (CVD), as missing and delaying the former can result in disastrous consequences.

1. Introduction

Syncope, defined as an abrupt and transient loss of consciousness due to cerebral hypoperfusion, accounts for 1-1.5% of emergency department (ED) visits 1. It is categorized into neurally-mediated, cardiac, and orthostatic syncope according to the underlying cause. Neurally-mediated syncope is the most common cause of syncope in the general population and has a benign course, while cardiac syncope tends to correlate with an increased mortality and morbidity 1. One trigger that can lead to electrocardiography (ECG) changes in patients is aneurysmal subarachnoid hemorrhage (SAH), a type of hemorrhagic stroke affecting approximately 30,000 persons per year in the United States 2, 3. ECG changes are the most studied and widely recognized abnormalities following SAH, seen in 25-90% of SAH patients 4, 5, 6, 7, 8. In addition, rhythm and conduction abnormalities either can occur alone or in combination with other ECG changes. Several prospective and retrospective clinical studies on SAH have reported arrhythmias such as sinus bradycardia (15%), sinus tachycardia (13%), premature ventricular beats (13%), atrial fibrillation and ventricular tachycardia (2%), AV block (1.5%), and asystole (1%) 9, 10, 11, 12, 13, 14. Neurogenic heart disease is defined as the brain’s effects on the heart, with underlying mechanisms including excessive catecholamine activity, acute stressors, autonomic disturbances, and reperfusion injury 15. To the best of our knowledge, to date, there is no published literature revealing second degree type I sinoatrial (SA) exit block as a manifestation of aneurysmal SAH. Higher risk of rebleeding and related mortality is associated with a delay in the diagnosis and treatment of SAH 16. Therefore, to avoid any catastrophic consequences, neurological injury must be considered a part of the list of potential etiological conditions causing cardiac conduction disorders.

2. Case Report

A 63-year-old African American female with a past medical history of hypertension, asthma and hyperlipidemia presented to the emergency department with a chief complaint of syncope preceded by headache. In the ED, the patient was noted to have regained consciousness shortly after her syncopal episode, but she complained of persistent headache and dizziness. On physical examination, no focal neurologic deficits were found. Her vitals at that time showed a blood pressure of 141/82 mmHg, heart rate of 48 beats per minute, temperature of 34.5°C (94.1°F), and respiratory rate of 19 cycles per minute. Her ECG showed sinus rhythm and pauses with junctional escape beats and atrial premature contractions with a ventricular rate of 46 beats per minute (Figure 1 and Figure 2). Laboratory investigations were within normal limits (Table 1). Cardiology was consulted for management of sinus bradycardia, sinoatrial block, and junctional escape. A transvenous pacemaker was placed with good capture (Figure 3).

The patient was initially admitted to the critical care unit for management of the bradyarrhythmia. Soon after admission to the critical care unit, she became altered, agitated, and unable to follow commands. Neurology recommended a head CT to rule out intracranial pathology. The imaging study revealed a diffuse SAH with hydrocephalus. An emergent extra-ventricular drain was placed by Neurosurgery. The bradyarrhythmia and the altered mental status then resolved. A follow up CT angiography of the brain showed a right middle cerebral artery (MCA) aneurysm (Figure 4). She was transferred to the surgical intensive care unit for further management of her SAH and right MCA aneurysm. The patient was started on intravenous tranexamic acid, levetiracetam, and nimodipine. She underwent cerebral angiography with Neuro-interventional Radiology. Cerebral angiography showed a ruptured posterior communicating artery aneurysm (Figure 5, left image) which was subsequently embolized with coil placement (Figure 5, middle image), resulting in near-complete aneurysm occlusion and preservation of the adjacent arteries (Figure 5, right image). The patient was transferred back to the surgical intensive care unit neurologically intact with mild functional limitations.

3. Discussion

Cardiac manifestations of SAH 17 are a well-known entity, ranging from mild ECG variability, reversible left ventricular dysfunction (Takotsubo), non-ST-elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI), to cardiac arrest 18, 19, 20, 21, 22, 23. As per a systematic review analysis, the crude global incidence of SAH declined from 10.2 per 100 000 person-years in 1980 to 6.1 in 2010, with large variation according to region, age, and sex 24. In the United States, the annual incidence of aneurysmal SAH is 6-16 cases per 100,000 population, with approximately 30,000 episodes occurring each year 25. Out of all strokes, 20% are hemorrhagic, with SAH and intracerebral hemorrhage each accounting for 10% 26. 75-85% of non-traumatic SAH is caused by ruptured cerebral aneurysms 27. The major cardiac manifestations resulting from SAH are arrhythmias 13 (35%), myocardial injury seen as troponin elevations in the first 24 hours 28 (28%), wall motion abnormalities 29 (28%), and classic deep septal T-wave inversion or QTc prolongation on ECG 30, 31. Most of the rhythm alterations are benign, including sinus bradycardia or tachycardia; atrial fibrillation, ventricular ectopics, and junctional rhythm have also been described in SAH patients 31. To the best of our knowledge, there has been no prior report describing SAH as the underlying cause of a second-degree type 1 SA nodal exit block; such a scenario is being reported for the first time in this case report. The possible risk factors for arrhythmia occurrence include female gender, QTc prolongation, excessive sympathetic discharge, coronary vasospasm, electrolyte disturbances, and pre-existing hypertension 32. Life-threatening arrhythmias occur in about 5% of cases 13. Extensive myocardial injury following SAH can result in severely depressed global cardiac function, as well as reduction particularly in the left ventricular function. This condition is known as neurogenic stunned myocardium (NMS), recently restyled as stress-related cardiomyopathy syndrome 33.

New progress in neuroanatomic studies, pathological assessments, and imaging modalities have have helped illuminate the neural regulation of cardiovascular functions 34, a design that involves a complex network of cortical and subcortical brain regions 35 along with the intrinsic cardiac system. Figure 6 elucidates the role of the central nervous system (CNS) in regulating the cardiovascular system (CVS) functions.

The orbitofrontal cortex and dorsal cingulate cortex process afferent information and control efferent autonomic outflow to the CVS. The insular cortex is the main center regulating the ‘Heart-Brain Axis’ 36. Some studies hypothesize that the right insula controls sympathetic actions, and when damaged, can effect ECG changes and lead to increased mortality 37, 38. Others postulate the same for the left insula 39. The amygdala receives inhibitory inputs from the prefrontal and orbitofrontal cortices and processes them with the hypothalamus and the brain stem nuclei 40, 41. In this way, it modulates the effect of emotional stimuli on the heart 42. The nucleus tractus solitarius (NTS), located in the posterior medulla, receives hemodynamic inputs and sends efferents to the rostral ventrolateral medulla (RVLM) and dorsal motor nucleus (DMN) of the vagus, which control the sympathetic and parasympathetic outflow, respectively, to the heart 34. The CNS regulates the CV function through cardiomotor sympathetic and parasympathetic outflow of the autonomic nervous system (ANS) to the myocardium and cardiac conduction system 43. In addition, there is an intrinsic cardiac nervous system, composed of interconnected ganglionated plexi in epicardial fat tissue, innervating the SA node, AV node, and pulmonary veins 44. Oxidative stress, nitric oxide levels, and abnormal baroreceptor and chemoreceptor signals are conveyed to NTS, paraventricular nucleus, and RVLM through cardiac afferent fibers, which results in fatal arrhythmias and ischemia 45, 46.

The neuronal control of the CVS undergoes major alterations in different circumstances and may contribute to progression of the underlying heart disease. Immediately after SAH, there is intense activity in the hypothalamus, insula, and brain stem, causing significant activation of sympathetic nerve endings, with release of norepinephrine 32. In patients with SAH, repolarization abnormalities, caused by an increase in sympathetic activity in SAH, are the most common ECG finding 47. The SA node acts as the normal pacemaker of the heart, generating action potentials that travel through the conduction system to cause myocardial contraction 48. SA nodal exit block is a condition in which the impulse fired by the SA node is unable to reach the neighboring atrial tissue 49. It is divided into three degrees of block, similar to AV blocks. On ECG, SA nodal exit block can be inferred from the P wave activity, but only a second degree SA block can be detected in the ED using a 12-lead ECG 50. Second degree SA nodal exit block is of two types: type I Wenckebach and type II. Type I has a P-P interval that progressively shortens in duration until there is a dropped P wave 49.

At times, it can be difficult to establish neurological injury as the cause or the consequence of cardiovascular dysfunction due to the high prevalence of coexistent cardiac disorders and shared risk factors in these patients. Electrocardiographic alterations and conduction defects, both benign and fatal, are commonly seen after brain injury even without a preexisting heart disease. However, when the cardiovascular presentation of the symptoms are not correlated with their neurological cause, it can result in delayed or missed diagnosis of neurological diseases.

4. Conclusion

Between 50 to 100% of patients experience cardiac rhythm disturbances during the acute phase of SAH, but only 1-4% of patients experience a clinically significant arrhythmia. SAH is a serious condition that frequently leads to neurological impairment and death; therefore, its timely diagnosis and management is of utmost significance. The current article is an effort at consolidating the information available in an attempt to avoid errors in the diagnosis of neurological disease presenting in an atypical manner. Recently, the ‘Heart-Brain Axis’ concept, which acknowledges a complex network of neural regulation of cardiovascular functions, has gained much popularity. More collaborative studies and research are likely to further advance our understanding of the neural control of the cardiac tissue.

Acknowledgments

This work is supported, in part, by the efforts of Dr. Moro O. Salifu M.D., M.P.H., M.B.A., M.A.C.P., Professor and Chairman of Medicine through NIH Grant No. S21MD012474.

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Published with license by Science and Education Publishing, Copyright © 2020 Pramod Theetha Kariyanna, Ruchi Yadav, Vivek Yadav, Samuel Apple, Naseem A. Hossain, Neema Jayachamarajapura Onkaramurthy, Apoorva Jayarangaiah, Ayesha Saad and Isabel M. McFarlane

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Cite this article:

Normal Style
Pramod Theetha Kariyanna, Ruchi Yadav, Vivek Yadav, Samuel Apple, Naseem A. Hossain, Neema Jayachamarajapura Onkaramurthy, Apoorva Jayarangaiah, Ayesha Saad, Isabel M. McFarlane. Subarachnoid Hemorrhage Presenting with Second-Degree Type I Sinoatrial Exit Block: A Case Report. American Journal of Medical Case Reports. Vol. 8, No. 10, 2020, pp 341-347. http://pubs.sciepub.com/ajmcr/8/10/6
MLA Style
Kariyanna, Pramod Theetha, et al. "Subarachnoid Hemorrhage Presenting with Second-Degree Type I Sinoatrial Exit Block: A Case Report." American Journal of Medical Case Reports 8.10 (2020): 341-347.
APA Style
Kariyanna, P. T. , Yadav, R. , Yadav, V. , Apple, S. , Hossain, N. A. , Onkaramurthy, N. J. , Jayarangaiah, A. , Saad, A. , & McFarlane, I. M. (2020). Subarachnoid Hemorrhage Presenting with Second-Degree Type I Sinoatrial Exit Block: A Case Report. American Journal of Medical Case Reports, 8(10), 341-347.
Chicago Style
Kariyanna, Pramod Theetha, Ruchi Yadav, Vivek Yadav, Samuel Apple, Naseem A. Hossain, Neema Jayachamarajapura Onkaramurthy, Apoorva Jayarangaiah, Ayesha Saad, and Isabel M. McFarlane. "Subarachnoid Hemorrhage Presenting with Second-Degree Type I Sinoatrial Exit Block: A Case Report." American Journal of Medical Case Reports 8, no. 10 (2020): 341-347.
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  • Figure 5. Cerebral angiogram showing an aneurysm in the right posterior communicating artery (left), during endovascular coil placement (middle), and complete regression of aneurysm following endovascular coil placement (right)
  • Figure 6. This flow diagram outlines the Heart-Brain Axis (Legend: RVLM- rostral ventrolateral medulla, DMN- dorsal motor nucleus, ANS- autonomic nervous system, CNS- central nervous system, SA- sinus atrial, AV- atrioventricular)
[1]  Syncope: Evaluation and Differential Diagnosis - American Family Physician. Accessed May 3, 2020. https://www.aafp.org/afp/2017/0301/p303.html.
In article      
 
[2]  Zacharia BE, Hickman ZL, Grobelny BT, et al. Epidemiology of aneurysmal subarachnoid hemorrhage. Neurosurg Clin N Am. 2010; 21(2): 221-233.
In article      View Article  PubMed
 
[3]  Lantigua H, Ortega-Gutierrez S, Schmidt JM, et al. Subarachnoid hemorrhage: who dies, and why? Crit Care. 2015; 19(1).
In article      View Article  PubMed
 
[4]  Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999; 44(1): 34-39; discussion 39-40.
In article      View Article  PubMed
 
[5]  Sommargren CE, Zaroff JG, Banki N, Drew BJ. Electrocardiographic repolarization abnormalities in subarachnoid hemorrhage. J Electrocardiol. 2002; 35 Suppl: 257-262.
In article      View Article  PubMed
 
[6]  Di Pasquale G, Andreoli A, Lusa AM, et al. Cardiologic complications of subarachnoid hemorrhage. J Neurosurg Sci. 1998; 42(1 Suppl 1): 33-36.
In article      
 
[7]  Kawasaki T, Azuma A, Sawada T, et al. Electrocardiographic score as a predictor of mortality after subarachnoid hemorrhage. Circ J Off J Jpn Circ Soc. 2002; 66(6): 567-570.
In article      View Article  PubMed
 
[8]  Rose JJ, Vanhecke TE, McCullough PA. Subarachnoid hemorrhage with neurocardiogenic stunning. Rev Cardiovasc Med. 2010; 11(4): 254-263.
In article      
 
[9]  High-degree atrioventricular block with superimposed sinoatrial node exit block secondary to increased intracranial pressure. Shm Abstracts. Accessed May 3, 2020. https://www.shmabstracts.com/abstract/high-degree- atrioventricular-block-with-superimposed-sinoatrial-node-exit- block-secondary-to-increased-intracranial-pressure/.
In article      
 
[10]  Di Pasquale G, Pinelli G, Andreoli A, Manini G, Grazi P, Tognetti F. Holter detection of cardiac arrhythmias in intracranial subarachnoid hemorrhage. Am J Cardiol. 1987; 59(6): 596-600.
In article      View Article
 
[11]  Andreoli A, di Pasquale G, Pinelli G, Grazi P, Tognetti F, Testa C. Subarachnoid hemorrhage: frequency and severity of cardiac arrhythmias. A survey of 70 cases studied in the acute phase. Stroke. 1987; 18(3): 558-564.
In article      View Article  PubMed
 
[12]  Estañol Vidal B, Badui Dergal E, Cesarman E, et al. Cardiac arrhythmias associated with subarachnoid hemorrhage: prospective study. Neurosurgery. 1979; 5(6): 675-680.
In article      View Article  PubMed
 
[13]  Solenski NJ, Haley EC, Kassell NF, et al. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med. 1995; 23(6): 1007-1017.
In article      View Article  PubMed
 
[14]  Estanol BV, Loyo MV, Mateos JH, Foyo E, Cornejo A, Guevara J. Cardiac arrhythmias in experimental subarachnoid hemorrhage. Stroke. 1977; 8(4): 440-449.
In article      View Article  PubMed
 
[15]  Samuels Martin A. The Brain-Heart Connection. Circulation. 2007; 116(1): 77-84.
In article      View Article  PubMed
 
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