International Journal of Cardiology 181 (2015) 3–4
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Nonsustained monomorphic ventricular tachycardia following arousal from sleep after face trauma☆ Simon W. Rabkin ⁎ Department of Medicine (Cardiology), University of British Columbia, Vancouver, BC, Canada
a r t i c l e
i n f o
Article history: Received 25 November 2014 Accepted 26 November 2014 Available online 27 November 2014 Keywords: Nonsustained ventricular tachycardia Head and neck trauma CNS mediated arrhythmias
A role for the brain in mediating cardiac arrhythmias has been based mainly on experimental data with comparatively little clinical evidence supporting the concept [1–3]. The nature of the stimulus that has the potential to induce ventricular arrhythmias is of considerable importance to understand the mechanism of arrhythmia induction as well as to prevent its occurrence. A 39-year-old man, 5 months after successful repair of a flail leaflet mitral valve with severe mitral regurgitation, had a 24 h ECG prior to anticipated discontinuation of beta blockers and warfarin initiated after surgery because of mitral valve repair and post-operative atrial fibrillation. His medications were bisoprolol 10 mg a day, warfarin and valproic acid 500 mg bid. Vaproic acid had effectively suppressed epilepsy without seizures for almost 10 years. There was no family history of sudden death. Preoperatively, his coronary CT angiogram showed normal coronary arteries. An echocardiogram done two months after surgery showed a left ventricular ejection fraction of 55%, no regional wall motion abnormalities, trivial mitral regurgitation and a 5 mm gradient intercross the mitral valve. The 24 h ECG showed an episode of paroxysmal ventricular tachycardia (Fig 1). There was no QTc prolongation and no bradycardia prior to the onset of the tachyarrhythmia which started long after the preceding T wave and increased slightly in rate thereafter. The ventricular rate of 143 bpm was maintained until, the sudden termination of the arrhythmia. A 12 lead ECG was normal. Subsequent to the 24-hour monitor, an exercise stress test showed that he was able to exercise 6 min and 54 s with no ST-segment changes and no exercise-induced arrhythmias. ☆ Financial support: None. ⁎ University of British Columbia, Level 9, 2775 Laurel St, Vancouver, BC, Canada V5Z 1M9. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.11.213 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The QT intervals were: resting ECG (recumbent) QTcF of 350 ms, standing 350 ms, maximum exercise 321 ms and recovery 344 ms. The episode of VT occurred at 03:06 h. The patient's wife related that in the middle of the night, she was awoken by their daughter coming into bed. She saw her husband turning over onto the child. As her husband was a large man she was concerned that he might smothered the child, so she immediately flailed out striking him ‘hard’ on the left side of the neck and jaw area. The patient recalls waking with a startle. He did not appreciate palpitations and neither was he aware of a sense of pre-syncope and he did not lose consciousness. He noted the time was around 03:00 h and he eventually went back to sleep. This case demonstrates monomorphic ventricular tachycardia in a unique setting of arousal from sleep after face and neck trauma. The patient had none of the usual substrates for ventricular tachycardia in that he had normal coronary arteries, almost normal LV ejection fraction and no QT prolongation. There were no arrhythmias on exercise stress testing. There were no arrhythmias on repeat 24 h ECG monitoring in the absence of face and neck injury. The patient was taking valproic acid which is not known to be associated with production of ventricular tachycardia, he did not take an overdose of the medication and neither was the arrhythmia Torsade de Pointe which is associated with some drug-induced ventricular tachycardia. One can speculate that he had an area of the ventricle vulnerable to arrhythmia induction. However in the absence of significant cardiac conditions, central nervous system factors most likely played a role in the genesis of this arrhythmia. Stimulation of nerves that innervate the head and neck are well described to induce bradyarrhythmias [4] that can be profound [5] and are attributed to increases in parasympathetic nervous system activity [4, 5]. In contrast in this case, ventricular tachycardia occurred. The combination of both sudden arousal from sleep plus stimulation of nerves innervating the head and neck likely were a requirement for arrhythmia induction. In this case, the occurrence of ventricular tachyarrhythmia suggest a sympathetic nervous system mediated arrhythmia that is operative in part though the CNS [6]. Arousal from sleep has been implicated in generation of ventricular arrhythmias but it is usually attributed to the increase in catecholamines that occurs in the morning upon normal waking at usual waking hours [7]. This case suggests that it is the arousal from sleep rather than the time of day that is important in arrhythmogenesis. CNS endogenous opioids and neurotransmitters modulate catecholamine mediated arrhythmias. In the brain, some kappa-opioid receptor stimulation accentuates fatal ventricular arrhythmias induced by epinephrine [8] while other kinds of kappa opioid receptor stimulation do not [9]. Mu opioid receptor stimulation suppresses epinephrine-
4
S.W. Rabkin / International Journal of Cardiology 181 (2015) 3–4
Fig. 1. Continuous ECG recording from a 24 H ECG.
induced fatal ventricular arrhythmias [10]. It is interesting to speculate that a CNS kappa receptor subtype might have been involved in accentuating the occurrence of ventricular tachycardia in this case. In conclusion, this case demonstrates a first report of a specific stimulus and circumstance that can induce ventricular tachycardia. It contributes to our understanding of the brain–heart interconnections in the genesis of potentially fatal ventricular arrhythmias. Conflicts of interest None. References [1] W.P. Harvey, S.A. Levine, Paroxysmal ventricular tachycardia due to emotion: possible mechanism of death from fright, J. Am. Med. Assoc. 150 (1952) 479–480.
[2] S. Wolf, Forebrain involvement in fatal cardiac arrhythmia, Integr. Physiol. Behav. Sci. 30 (1995) 215–225. [3] J.A. Armour, J. Ardell, Neurocardiology, Oxford University Press, New York, 1995. [4] N.A. Barnard, R. Bainton, Bradycardia and the trigeminal nerve, J. Craniomaxillofac. Surg. 18 (1990) 359–360. [5] S. O'Donoghue, H. Abdallah, Asystole due to head scratching: a newly confirmed situational syncope, Heart Rhythm 10 (2013) 1728–1729. [6] M.J. Shen, D.P. Zipes, Role of the autonomic nervous system in modulating cardiac arrhythmias, Circ. Res. 114 (2014) 1004–1021. [7] R. Lampert, L. Rosenfeld, W. Batsford, F. Lee, C. McPherson, Circadian variation of sustained ventricular tachycardia in patients with coronary artery disease and implantable cardioverter-defibrillators, Circulation 90 (1994) 241–247. [8] S.W. Rabkin, The opioid agonist ethylketocyclazocine accentuates epinephrineinduced cardiac arrhythmias in the rat through an action in the brain, Brain Res. Bull. 31 (1993) 427–432. [9] S.W. Rabkin, Morphine and the endogenous opioid dynorphin in the brain attenuate digoxin-induced arrhythmias in guinea pigs, Pharmacol. Toxicol. 71 (1992) 353–360. [10] S.W. Rabkin, Morphine and morphiceptin increase the threshold for epinephrineinduced cardiac arrhythmias in the rat through brain mu opioid receptors, Clin. Exp. Pharmacol. Physiol. 20 (1993) 95–102.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Nonsustained monomorphic ventricular tachycardia following arousal from sleep after face trauma☆ Simon W. Rabkin ⁎ Department of Medicine (Cardiology), University of British Columbia, Vancouver, BC, Canada
a r t i c l e
i n f o
Article history: Received 25 November 2014 Accepted 26 November 2014 Available online 27 November 2014 Keywords: Nonsustained ventricular tachycardia Head and neck trauma CNS mediated arrhythmias
A role for the brain in mediating cardiac arrhythmias has been based mainly on experimental data with comparatively little clinical evidence supporting the concept [1–3]. The nature of the stimulus that has the potential to induce ventricular arrhythmias is of considerable importance to understand the mechanism of arrhythmia induction as well as to prevent its occurrence. A 39-year-old man, 5 months after successful repair of a flail leaflet mitral valve with severe mitral regurgitation, had a 24 h ECG prior to anticipated discontinuation of beta blockers and warfarin initiated after surgery because of mitral valve repair and post-operative atrial fibrillation. His medications were bisoprolol 10 mg a day, warfarin and valproic acid 500 mg bid. Vaproic acid had effectively suppressed epilepsy without seizures for almost 10 years. There was no family history of sudden death. Preoperatively, his coronary CT angiogram showed normal coronary arteries. An echocardiogram done two months after surgery showed a left ventricular ejection fraction of 55%, no regional wall motion abnormalities, trivial mitral regurgitation and a 5 mm gradient intercross the mitral valve. The 24 h ECG showed an episode of paroxysmal ventricular tachycardia (Fig 1). There was no QTc prolongation and no bradycardia prior to the onset of the tachyarrhythmia which started long after the preceding T wave and increased slightly in rate thereafter. The ventricular rate of 143 bpm was maintained until, the sudden termination of the arrhythmia. A 12 lead ECG was normal. Subsequent to the 24-hour monitor, an exercise stress test showed that he was able to exercise 6 min and 54 s with no ST-segment changes and no exercise-induced arrhythmias. ☆ Financial support: None. ⁎ University of British Columbia, Level 9, 2775 Laurel St, Vancouver, BC, Canada V5Z 1M9. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.11.213 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The QT intervals were: resting ECG (recumbent) QTcF of 350 ms, standing 350 ms, maximum exercise 321 ms and recovery 344 ms. The episode of VT occurred at 03:06 h. The patient's wife related that in the middle of the night, she was awoken by their daughter coming into bed. She saw her husband turning over onto the child. As her husband was a large man she was concerned that he might smothered the child, so she immediately flailed out striking him ‘hard’ on the left side of the neck and jaw area. The patient recalls waking with a startle. He did not appreciate palpitations and neither was he aware of a sense of pre-syncope and he did not lose consciousness. He noted the time was around 03:00 h and he eventually went back to sleep. This case demonstrates monomorphic ventricular tachycardia in a unique setting of arousal from sleep after face and neck trauma. The patient had none of the usual substrates for ventricular tachycardia in that he had normal coronary arteries, almost normal LV ejection fraction and no QT prolongation. There were no arrhythmias on exercise stress testing. There were no arrhythmias on repeat 24 h ECG monitoring in the absence of face and neck injury. The patient was taking valproic acid which is not known to be associated with production of ventricular tachycardia, he did not take an overdose of the medication and neither was the arrhythmia Torsade de Pointe which is associated with some drug-induced ventricular tachycardia. One can speculate that he had an area of the ventricle vulnerable to arrhythmia induction. However in the absence of significant cardiac conditions, central nervous system factors most likely played a role in the genesis of this arrhythmia. Stimulation of nerves that innervate the head and neck are well described to induce bradyarrhythmias [4] that can be profound [5] and are attributed to increases in parasympathetic nervous system activity [4, 5]. In contrast in this case, ventricular tachycardia occurred. The combination of both sudden arousal from sleep plus stimulation of nerves innervating the head and neck likely were a requirement for arrhythmia induction. In this case, the occurrence of ventricular tachyarrhythmia suggest a sympathetic nervous system mediated arrhythmia that is operative in part though the CNS [6]. Arousal from sleep has been implicated in generation of ventricular arrhythmias but it is usually attributed to the increase in catecholamines that occurs in the morning upon normal waking at usual waking hours [7]. This case suggests that it is the arousal from sleep rather than the time of day that is important in arrhythmogenesis. CNS endogenous opioids and neurotransmitters modulate catecholamine mediated arrhythmias. In the brain, some kappa-opioid receptor stimulation accentuates fatal ventricular arrhythmias induced by epinephrine [8] while other kinds of kappa opioid receptor stimulation do not [9]. Mu opioid receptor stimulation suppresses epinephrine-
4
S.W. Rabkin / International Journal of Cardiology 181 (2015) 3–4
Fig. 1. Continuous ECG recording from a 24 H ECG.
induced fatal ventricular arrhythmias [10]. It is interesting to speculate that a CNS kappa receptor subtype might have been involved in accentuating the occurrence of ventricular tachycardia in this case. In conclusion, this case demonstrates a first report of a specific stimulus and circumstance that can induce ventricular tachycardia. It contributes to our understanding of the brain–heart interconnections in the genesis of potentially fatal ventricular arrhythmias. Conflicts of interest None. References [1] W.P. Harvey, S.A. Levine, Paroxysmal ventricular tachycardia due to emotion: possible mechanism of death from fright, J. Am. Med. Assoc. 150 (1952) 479–480.
[2] S. Wolf, Forebrain involvement in fatal cardiac arrhythmia, Integr. Physiol. Behav. Sci. 30 (1995) 215–225. [3] J.A. Armour, J. Ardell, Neurocardiology, Oxford University Press, New York, 1995. [4] N.A. Barnard, R. Bainton, Bradycardia and the trigeminal nerve, J. Craniomaxillofac. Surg. 18 (1990) 359–360. [5] S. O'Donoghue, H. Abdallah, Asystole due to head scratching: a newly confirmed situational syncope, Heart Rhythm 10 (2013) 1728–1729. [6] M.J. Shen, D.P. Zipes, Role of the autonomic nervous system in modulating cardiac arrhythmias, Circ. Res. 114 (2014) 1004–1021. [7] R. Lampert, L. Rosenfeld, W. Batsford, F. Lee, C. McPherson, Circadian variation of sustained ventricular tachycardia in patients with coronary artery disease and implantable cardioverter-defibrillators, Circulation 90 (1994) 241–247. [8] S.W. Rabkin, The opioid agonist ethylketocyclazocine accentuates epinephrineinduced cardiac arrhythmias in the rat through an action in the brain, Brain Res. Bull. 31 (1993) 427–432. [9] S.W. Rabkin, Morphine and the endogenous opioid dynorphin in the brain attenuate digoxin-induced arrhythmias in guinea pigs, Pharmacol. Toxicol. 71 (1992) 353–360. [10] S.W. Rabkin, Morphine and morphiceptin increase the threshold for epinephrineinduced cardiac arrhythmias in the rat through brain mu opioid receptors, Clin. Exp. Pharmacol. Physiol. 20 (1993) 95–102.
