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Postexercise AV-block and syncope prevented by beta-blocker therapy
International Journal of Cardiology 173 (2014) e72–e73
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Postexercise AV-block and syncope prevented by beta-blocker therapy János Tomcsányi, Béla Bózsik, Tamás Frész ⁎ Department of Cardiology, Hospital of the Hospitaller Brothers of St. John of God, Budapest, Hungary
a r t i c l e
i n f o
Article history: Received 8 February 2014 Accepted 22 March 2014 Available online 28 March 2014 Keywords: Postexercise Syncope AV-block Beta-blocker therapy
Postexercise syncope or near-syncope is due to an abnormality in the autonomic regulation of vascular tone or heart rate resulting in symptomatic hypotension or bradycardia [1]. Most reports of postexercise syncope are likely to be incidences of neurally mediated syncope [2]. However, syncope after exercise can be a sign of significant pathophysiology, therefore requires thorough clinical evaluation. A 42-year-old woman experienced attacks of syncope or near syncope after vigorous exercise or after mental stress, which had been occurring for ten years. She denied reduced orthostatic tolerance. During the initial evaluation, the patient was otherwise well and her medical history was also unremarkable. An exercise test had been performed one year earlier. In the recovery phase, complete AV-block developed with syncope and a pacemaker was implanted without any further investigations. However, the patient still experienced attacks of syncope or near syncope after vigorous exercise. A repeat exercise test was done, which ended with near syncope. She was able to reach 10 METS with the Bruce protocol. The maximum heart rate and blood pressure were 186 bpm and 180/90 mmHg, respectively. Shortly after the end of the exercise, complete AV-block developed with a pacemaker escape beat and then pacemaker rhythm (Fig. 1A). Blood pressure dropped to 80/50 mmHg. After the normal blood pressure resumed, the patient was given 50 mg metoprolol orally, and half an hour later the exercise was repeated with the same settings. The patient had neither AV-block nor syncope or presyncope (see Fig. 1B). Blood pressure values at peak exercise, 2 min into recovery and 4 min into recovery were 150/80 mmHg, 140/80 mmHg and 120/80 mmHg, respectively. As the patient suffers
⁎ Corresponding author at: Árpád fejedelm útja 7, Budapest 1027, Hungary. Tel.: +36 14388560; fax: +36 14388561. E-mail address: [email protected] (T. Frész).
http://dx.doi.org/10.1016/j.ijcard.2014.03.147 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
from psoriasis, the pill-in-the-pocket strategy was recommended with 50 mg metoprolol before exercise. The patient had no more attacks of syncope and the repeated exercise was negative. The exact underlying mechanisms of neurally mediated syncope are not fully understood. What is clear is that cardiovascular reflexes that are normally useful in controlling the circulation become intermittently inappropriate, in response to a trigger, resulting in vasodilatation and/or bradycardia and thereby in a significant fall in arterial blood pressure and global cerebral perfusion. Postexercise hypotension is one of the several possible triggers [3]. Furthermore, to find the successful treatment remains a common clinical dilemma in these situations. Physical counter-manoeuvres designed to engage the muscle pump and augment venous return have the class I indication in neurally mediated syncope. Efficacy of medical treatment (e.g. midodrine, fludrocortisone) and the role of pacemaker implantation are debatable. Beta-blockers have been presumed to lessen the degree of ventricular mechanoreceptor activation owing to their negative inotropic effect in reflex syncope. This theory has not been supported by the outcome of randomised clinical trials [3]. McCord et al. tested the effectiveness of H1 receptor antagonism in preventing postexercise syncope and found the magnitude of the arterial pressure drop blunted [4]. However, beta blockers are not recommended routinely anymore in neurally mediated syncope, this case demonstrates that beta-blockers should at least be considered in the setting of postexercise syncope when other therapeutic measures fail. This case is further supported that in most patients hypotension and syncope cannot be avoided by pacing [5]. References [1] Osswald S, Brooks R, ONunain SS, et al. Asystole after exercise in healthy persons. Ann Intern Med 1994;120:1008–11. [2] Halliwill JR, Buck TM, Lacewell AN, Romero SA. Postexercise hypotension and sustained postexercise vasodilatation: what happens after we exercise? Exp Physiol 2013 Jan;98(1):7–18. [3] Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology; European Heart Rhythm Association; Heart Failure Association; Heart Rhythm SocietyMoya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30:2631–71. [4] McCord JL, Pellinger TK, Lynn BM, Halliwill JR. Potential benefit from an H1-receptor antagonist on postexercise syncope in the heat. Med Sci Sports Exerc 2008;40:1953–61. [5] Sra JS, Jazayeri MR, Avitall B, Dhala A, Deshpande S, Blanck Z. Comparison of cardiac pacing with drug therapy in the treatment of neurocardiogenic (vasovagal) syncope with bradycardia or asystolia. N Engl J Med 1993;328:1085–90.
J. Tomcsányi et al. / International Journal of Cardiology 173 (2014) e72–e73
e73
Fig. 1. A. After 10 MET exercise complete AV-block and pacemaker escape rhythm with hypotension. B. After metoprolol administration and exercise (10 MET) slowing of the heart rate without AV-block on the Holter monitoring.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Postexercise AV-block and syncope prevented by beta-blocker therapy János Tomcsányi, Béla Bózsik, Tamás Frész ⁎ Department of Cardiology, Hospital of the Hospitaller Brothers of St. John of God, Budapest, Hungary
a r t i c l e
i n f o
Article history: Received 8 February 2014 Accepted 22 March 2014 Available online 28 March 2014 Keywords: Postexercise Syncope AV-block Beta-blocker therapy
Postexercise syncope or near-syncope is due to an abnormality in the autonomic regulation of vascular tone or heart rate resulting in symptomatic hypotension or bradycardia [1]. Most reports of postexercise syncope are likely to be incidences of neurally mediated syncope [2]. However, syncope after exercise can be a sign of significant pathophysiology, therefore requires thorough clinical evaluation. A 42-year-old woman experienced attacks of syncope or near syncope after vigorous exercise or after mental stress, which had been occurring for ten years. She denied reduced orthostatic tolerance. During the initial evaluation, the patient was otherwise well and her medical history was also unremarkable. An exercise test had been performed one year earlier. In the recovery phase, complete AV-block developed with syncope and a pacemaker was implanted without any further investigations. However, the patient still experienced attacks of syncope or near syncope after vigorous exercise. A repeat exercise test was done, which ended with near syncope. She was able to reach 10 METS with the Bruce protocol. The maximum heart rate and blood pressure were 186 bpm and 180/90 mmHg, respectively. Shortly after the end of the exercise, complete AV-block developed with a pacemaker escape beat and then pacemaker rhythm (Fig. 1A). Blood pressure dropped to 80/50 mmHg. After the normal blood pressure resumed, the patient was given 50 mg metoprolol orally, and half an hour later the exercise was repeated with the same settings. The patient had neither AV-block nor syncope or presyncope (see Fig. 1B). Blood pressure values at peak exercise, 2 min into recovery and 4 min into recovery were 150/80 mmHg, 140/80 mmHg and 120/80 mmHg, respectively. As the patient suffers
⁎ Corresponding author at: Árpád fejedelm útja 7, Budapest 1027, Hungary. Tel.: +36 14388560; fax: +36 14388561. E-mail address: [email protected] (T. Frész).
http://dx.doi.org/10.1016/j.ijcard.2014.03.147 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
from psoriasis, the pill-in-the-pocket strategy was recommended with 50 mg metoprolol before exercise. The patient had no more attacks of syncope and the repeated exercise was negative. The exact underlying mechanisms of neurally mediated syncope are not fully understood. What is clear is that cardiovascular reflexes that are normally useful in controlling the circulation become intermittently inappropriate, in response to a trigger, resulting in vasodilatation and/or bradycardia and thereby in a significant fall in arterial blood pressure and global cerebral perfusion. Postexercise hypotension is one of the several possible triggers [3]. Furthermore, to find the successful treatment remains a common clinical dilemma in these situations. Physical counter-manoeuvres designed to engage the muscle pump and augment venous return have the class I indication in neurally mediated syncope. Efficacy of medical treatment (e.g. midodrine, fludrocortisone) and the role of pacemaker implantation are debatable. Beta-blockers have been presumed to lessen the degree of ventricular mechanoreceptor activation owing to their negative inotropic effect in reflex syncope. This theory has not been supported by the outcome of randomised clinical trials [3]. McCord et al. tested the effectiveness of H1 receptor antagonism in preventing postexercise syncope and found the magnitude of the arterial pressure drop blunted [4]. However, beta blockers are not recommended routinely anymore in neurally mediated syncope, this case demonstrates that beta-blockers should at least be considered in the setting of postexercise syncope when other therapeutic measures fail. This case is further supported that in most patients hypotension and syncope cannot be avoided by pacing [5]. References [1] Osswald S, Brooks R, ONunain SS, et al. Asystole after exercise in healthy persons. Ann Intern Med 1994;120:1008–11. [2] Halliwill JR, Buck TM, Lacewell AN, Romero SA. Postexercise hypotension and sustained postexercise vasodilatation: what happens after we exercise? Exp Physiol 2013 Jan;98(1):7–18. [3] Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology; European Heart Rhythm Association; Heart Failure Association; Heart Rhythm SocietyMoya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30:2631–71. [4] McCord JL, Pellinger TK, Lynn BM, Halliwill JR. Potential benefit from an H1-receptor antagonist on postexercise syncope in the heat. Med Sci Sports Exerc 2008;40:1953–61. [5] Sra JS, Jazayeri MR, Avitall B, Dhala A, Deshpande S, Blanck Z. Comparison of cardiac pacing with drug therapy in the treatment of neurocardiogenic (vasovagal) syncope with bradycardia or asystolia. N Engl J Med 1993;328:1085–90.
J. Tomcsányi et al. / International Journal of Cardiology 173 (2014) e72–e73
e73
Fig. 1. A. After 10 MET exercise complete AV-block and pacemaker escape rhythm with hypotension. B. After metoprolol administration and exercise (10 MET) slowing of the heart rate without AV-block on the Holter monitoring.