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Hyponatremia-induced stress cardiomyopathy due to psychogenic polydipsia
International Journal of Cardiology 202 (2016) 618–620
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Hyponatremia-induced stress cardiomyopathy due to psychogenic polydipsia☆ Alberto Cecconi a,c, Eduardo Franco b, Jose Alberto de Agustín a, Jean Paul Vilchez a,c, Julián Palacios-Rubio a, Cristina Sánchez-Enrique a, Antonio Fernández-Ortiz a,c, Carlos Macaya a, Rodrigo Fernández-Jiménez a,c,⁎ a b c
Department of Cardiology, Hospital Universitario Clínico San Carlos, Madrid, Spain Department of Cardiology, Hospital Universitario Ramón y Cajal, Madrid, Spain Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain
a r t i c l e
i n f o
Article history: Received 8 September 2015 Accepted 29 September 2015 Available online 6 October 2015 Keywords: Stress cardiomyopathy Hyponatremia Ventriculography Contrast echocardiogram
Dear Editor, A 41-years-old male was admitted to the Psychiatric Department for violent behaviour of abrupt onset. He had a previous diagnosis of psychogenic polydipsia and severe obsessive–compulsive disorder treated by an implanted brain stimulator, aripiprazole and clomipramine. Twenty-four hours after admission, he presented with typical chest pain. Vital signs and physical examination were unremarkable. A 12lead electrocardiogram (ECG) was performed showing ST-segment elevation in precordial leads and mirrored ST-segment depression in inferior leads (Fig. 1A). Urgent coronary angiography was immediately performed which revealed normal coronary arteries (Fig. 1B). A contrast left ventriculography was as well performed which showed regional mid-ventricular wall akinesia (Fig. 1C). Blood analysis documented a serum sodium concentration of 113 mmol/L (normal range: 135–145 mmol/L) which was related to an acute episode of psychogenic polydipsia. Apart from the vio-
☆ All authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation. The authors report no relationships that could be construed as a conflict of interest. ⁎ Corresponding author at: Translational Laboratory for Cardiovascular Imaging and Therapy, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro, 3, 28029 Madrid, Spain. E-mail address: [email protected] (R. Fernández-Jiménez).
http://dx.doi.org/10.1016/j.ijcard.2015.09.123 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
lent behaviour, no other hyponatremia-related neurological symptoms or seizures were present. Hemogram, potassium, renal function, thyroid hormones and inflammatory markers were within normal range. Peak values of troponin I and creatine kinase were 1.76 ng/mL (upper limit b 0.05 ng/mL) and 420 UI/L (upper limit b 170 UI/L), respectively. Oral fluid restriction and infusion of hypertonic saline solution were started, reaching normal serum concentration of sodium and balanced mental status within 48 h. A follow-up contrast echocardiogram was performed three days later and showed no regional left ventricle wall motion abnormalities (Fig. 2). The patient had an unremarkable course thereafter and was discharged after dosage adjustment of psychiatric medication. Stress cardiomyopathy is typically presented with transient leftventricular wall motion abnormalities related to a physical or emotional stress. The most common clinical presentation is chest pain associated with ST-segment elevation in the ECG, mimicking the presentation of an acute myocardial infarction. Conversely, coronary angiography typically shows absence of obstructive coronary disease and full recovery of myocardial motion occurs during follow-up in most cases [1]. The precise physiopathology is unclear. While catecholamine toxicity has been widely proposed as playing a key role in the disease [2], the list of triggers or predisposing factors keeps growing. In this occasion, we present a case of hyponatremia-induced stress cardiomyopathy due to psychogenic polydipsia. Asymptomatic mild hyponatremia is the most common electrolyte disorder encountered in clinical practice and do not usually requires intensive treatment. Conversely, acute severe symptomatic hyponatremia is a medical emergency which requires a rapid correction [3]. It has been reported that severe hyponatremia can be an uncommon precipitating factor for stress cardiomyopathy [4–8]. In all these previous reports, diuretic treatment and syndrome of inappropriate secretion of antidiuretic hormone were considered the likely causes of electrolyte imbalance, and typical apical motion abnormalities were documented during acute presentation. To the best of our knowledge, this is the first case in demonstrating an atypical form of stress cardiomyopathy precipitated by severe hyponatremia due to psychogenic polydipsia. The mechanistic link between hyponatremia and stress cardiomyopathy is unknown. It has been shown that the presence of hyponatremia at admission, psychiatric disorders or younger ages are more frequent in patients with a final diagnosis of stress cardiomyopathy [9] than those
Correspondence
619
Fig. 1. (A) A 12-lead electrocardiogram was performed during the acute episode of typical chest pain and showed ST-segment elevation in V1 to V3 and aVL, with mirrored ST-segment depression in inferior leads. (B) Urgent angiography showed absence of significant coronary stenosis in the right coronary artery and left coronary tree. (C) Contrast left ventriculography documented a regional mid-ventricular wall akinesia. End-diastolic and end-systolic frames are shown.
with primary acute myocardial infarction. Abnormal central nervous system function secondary to hyponatremia may produce an excessive catecholamine release, therefore triggering stress cardiomyopathy. In addition, it has been speculated that low sodium levels may increase the release of antidiuretic hormone, which is considered a stress hormone itself and might help to exacerbate this clinical syndrome [10]. These reasons can explain the relative high prevalence of hyponatremia in the context of stress cardiomyopathy, which might play a role in
stress cardiomyopathy. However, further investigations are needed to understand its specific physiological role in this disease. Acknowledgements The authors of this manuscript have certified that they comply with the principles of ethical publishing in the International Journal of Cardiology.
620
Correspondence
Fig. 2. Contrast-enhanced echocardiogram performed three days after the acute event. From top to bottom: apical 4-chamber view, apical 2-chamber view and apical 3-chamber view. End-diastolic (left panels) and end-systolic frames (right panels) are shown. No left ventricle wall motion abnormalities were detected.
References [1] T.M. Pilgrim, T.R. Wyss, Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review, Int. J. Cardiol. 124 (2008) 283–292. [2] I.S. Wittstein, D.R. Thiemann, J.A. Lima, K.L. Baughman, S.P. Schulman, G. Gerstenblith, et al., Neurohumoral features of myocardial stunning due to sudden emotional stress, N. Engl. J. Med. 352 (2005) 539–548. [3] J.G. Verbalis, S.R. Goldsmith, A. Greenberg, C. Korzelius, R.W. Schrier, R.H. Sterns, et al., Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations, Am. J. Med. 126 (2013) S1–S42. [4] M.I. Worthley, T.J. Anderson, Transient left ventricular apical ballooning syndrome following a hyponatraemic seizure, Int. J. Cardiol. 115 (2007) e102–e104. [5] D.M. Lemke, S.I. Hussain, T.J. Wolfe, M.A. Torbey, J.R. Lynch, A. Carlin, et al., Takotsubo cardiomyopathy associated with seizures, Neurocrit. Care. 9 (2008) 112–117.
[6] O. AbouEzzeddine, A. Prasad, Apical ballooning syndrome precipitated by hyponatremia, Int. J. Cardiol. 145 (2010) e26–e29. [7] H. Kawano, Y. Matsumoto, S. Arakawa, M. Hayano, H. Fijisawa, Takotsubo cardiomyopathy in a patient with severe hyponatremia associated with syndrome of inappropriate antidiuretic hormone, Intern. Med. 50 (2011) 727–732. [8] A. Chikata, W. Omi, T. Saeki, H. Nagai, S. Sakagami, Repeated pacemaker dysfunction in a patient with recurrent Takotsubo cardiomyopathy precipitated by hyponatremia, Int. J. Cardiol. 170 (2014) 443–444. [9] M. Falola, W. Fonbah, G. McGwin Jr., Takotsubo cardiomyopathy versus ST-elevation myocardial infarction in a large case–control study: proposing a new mechanism, Int. J. Cardiol. 167 (2013) 1079–1081. [10] D. Clich, Syndrome of inappropriate antidiuretic hormone secretion associated with stress, Lancet 1 (1982) 1131–1132.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Hyponatremia-induced stress cardiomyopathy due to psychogenic polydipsia☆ Alberto Cecconi a,c, Eduardo Franco b, Jose Alberto de Agustín a, Jean Paul Vilchez a,c, Julián Palacios-Rubio a, Cristina Sánchez-Enrique a, Antonio Fernández-Ortiz a,c, Carlos Macaya a, Rodrigo Fernández-Jiménez a,c,⁎ a b c
Department of Cardiology, Hospital Universitario Clínico San Carlos, Madrid, Spain Department of Cardiology, Hospital Universitario Ramón y Cajal, Madrid, Spain Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain
a r t i c l e
i n f o
Article history: Received 8 September 2015 Accepted 29 September 2015 Available online 6 October 2015 Keywords: Stress cardiomyopathy Hyponatremia Ventriculography Contrast echocardiogram
Dear Editor, A 41-years-old male was admitted to the Psychiatric Department for violent behaviour of abrupt onset. He had a previous diagnosis of psychogenic polydipsia and severe obsessive–compulsive disorder treated by an implanted brain stimulator, aripiprazole and clomipramine. Twenty-four hours after admission, he presented with typical chest pain. Vital signs and physical examination were unremarkable. A 12lead electrocardiogram (ECG) was performed showing ST-segment elevation in precordial leads and mirrored ST-segment depression in inferior leads (Fig. 1A). Urgent coronary angiography was immediately performed which revealed normal coronary arteries (Fig. 1B). A contrast left ventriculography was as well performed which showed regional mid-ventricular wall akinesia (Fig. 1C). Blood analysis documented a serum sodium concentration of 113 mmol/L (normal range: 135–145 mmol/L) which was related to an acute episode of psychogenic polydipsia. Apart from the vio-
☆ All authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation. The authors report no relationships that could be construed as a conflict of interest. ⁎ Corresponding author at: Translational Laboratory for Cardiovascular Imaging and Therapy, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro, 3, 28029 Madrid, Spain. E-mail address: [email protected] (R. Fernández-Jiménez).
http://dx.doi.org/10.1016/j.ijcard.2015.09.123 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
lent behaviour, no other hyponatremia-related neurological symptoms or seizures were present. Hemogram, potassium, renal function, thyroid hormones and inflammatory markers were within normal range. Peak values of troponin I and creatine kinase were 1.76 ng/mL (upper limit b 0.05 ng/mL) and 420 UI/L (upper limit b 170 UI/L), respectively. Oral fluid restriction and infusion of hypertonic saline solution were started, reaching normal serum concentration of sodium and balanced mental status within 48 h. A follow-up contrast echocardiogram was performed three days later and showed no regional left ventricle wall motion abnormalities (Fig. 2). The patient had an unremarkable course thereafter and was discharged after dosage adjustment of psychiatric medication. Stress cardiomyopathy is typically presented with transient leftventricular wall motion abnormalities related to a physical or emotional stress. The most common clinical presentation is chest pain associated with ST-segment elevation in the ECG, mimicking the presentation of an acute myocardial infarction. Conversely, coronary angiography typically shows absence of obstructive coronary disease and full recovery of myocardial motion occurs during follow-up in most cases [1]. The precise physiopathology is unclear. While catecholamine toxicity has been widely proposed as playing a key role in the disease [2], the list of triggers or predisposing factors keeps growing. In this occasion, we present a case of hyponatremia-induced stress cardiomyopathy due to psychogenic polydipsia. Asymptomatic mild hyponatremia is the most common electrolyte disorder encountered in clinical practice and do not usually requires intensive treatment. Conversely, acute severe symptomatic hyponatremia is a medical emergency which requires a rapid correction [3]. It has been reported that severe hyponatremia can be an uncommon precipitating factor for stress cardiomyopathy [4–8]. In all these previous reports, diuretic treatment and syndrome of inappropriate secretion of antidiuretic hormone were considered the likely causes of electrolyte imbalance, and typical apical motion abnormalities were documented during acute presentation. To the best of our knowledge, this is the first case in demonstrating an atypical form of stress cardiomyopathy precipitated by severe hyponatremia due to psychogenic polydipsia. The mechanistic link between hyponatremia and stress cardiomyopathy is unknown. It has been shown that the presence of hyponatremia at admission, psychiatric disorders or younger ages are more frequent in patients with a final diagnosis of stress cardiomyopathy [9] than those
Correspondence
619
Fig. 1. (A) A 12-lead electrocardiogram was performed during the acute episode of typical chest pain and showed ST-segment elevation in V1 to V3 and aVL, with mirrored ST-segment depression in inferior leads. (B) Urgent angiography showed absence of significant coronary stenosis in the right coronary artery and left coronary tree. (C) Contrast left ventriculography documented a regional mid-ventricular wall akinesia. End-diastolic and end-systolic frames are shown.
with primary acute myocardial infarction. Abnormal central nervous system function secondary to hyponatremia may produce an excessive catecholamine release, therefore triggering stress cardiomyopathy. In addition, it has been speculated that low sodium levels may increase the release of antidiuretic hormone, which is considered a stress hormone itself and might help to exacerbate this clinical syndrome [10]. These reasons can explain the relative high prevalence of hyponatremia in the context of stress cardiomyopathy, which might play a role in
stress cardiomyopathy. However, further investigations are needed to understand its specific physiological role in this disease. Acknowledgements The authors of this manuscript have certified that they comply with the principles of ethical publishing in the International Journal of Cardiology.
620
Correspondence
Fig. 2. Contrast-enhanced echocardiogram performed three days after the acute event. From top to bottom: apical 4-chamber view, apical 2-chamber view and apical 3-chamber view. End-diastolic (left panels) and end-systolic frames (right panels) are shown. No left ventricle wall motion abnormalities were detected.
References [1] T.M. Pilgrim, T.R. Wyss, Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review, Int. J. Cardiol. 124 (2008) 283–292. [2] I.S. Wittstein, D.R. Thiemann, J.A. Lima, K.L. Baughman, S.P. Schulman, G. Gerstenblith, et al., Neurohumoral features of myocardial stunning due to sudden emotional stress, N. Engl. J. Med. 352 (2005) 539–548. [3] J.G. Verbalis, S.R. Goldsmith, A. Greenberg, C. Korzelius, R.W. Schrier, R.H. Sterns, et al., Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations, Am. J. Med. 126 (2013) S1–S42. [4] M.I. Worthley, T.J. Anderson, Transient left ventricular apical ballooning syndrome following a hyponatraemic seizure, Int. J. Cardiol. 115 (2007) e102–e104. [5] D.M. Lemke, S.I. Hussain, T.J. Wolfe, M.A. Torbey, J.R. Lynch, A. Carlin, et al., Takotsubo cardiomyopathy associated with seizures, Neurocrit. Care. 9 (2008) 112–117.
[6] O. AbouEzzeddine, A. Prasad, Apical ballooning syndrome precipitated by hyponatremia, Int. J. Cardiol. 145 (2010) e26–e29. [7] H. Kawano, Y. Matsumoto, S. Arakawa, M. Hayano, H. Fijisawa, Takotsubo cardiomyopathy in a patient with severe hyponatremia associated with syndrome of inappropriate antidiuretic hormone, Intern. Med. 50 (2011) 727–732. [8] A. Chikata, W. Omi, T. Saeki, H. Nagai, S. Sakagami, Repeated pacemaker dysfunction in a patient with recurrent Takotsubo cardiomyopathy precipitated by hyponatremia, Int. J. Cardiol. 170 (2014) 443–444. [9] M. Falola, W. Fonbah, G. McGwin Jr., Takotsubo cardiomyopathy versus ST-elevation myocardial infarction in a large case–control study: proposing a new mechanism, Int. J. Cardiol. 167 (2013) 1079–1081. [10] D. Clich, Syndrome of inappropriate antidiuretic hormone secretion associated with stress, Lancet 1 (1982) 1131–1132.