Letters to the Editor
443
Repeated pacemaker dysfunction in a patient with recurrent takotsubo cardiomyopathy precipitated by hyponatremia Akio Chikata ⁎, Wataru Omi, Takahiro Saeki, Hideo Nagai, Satoru Sakagami Department of Cardiology, National Hospital Organization, Kanazawa Medical Center, Kanazawa, Japan
a r t i c l e
i n f o
Article history: Received 16 August 2013 Accepted 23 November 2013 Available online 4 December 2013 Keywords: Pacemaker dysfunction Takotsubo cardiomyopathy Hyponatremia
Left ventricular (LV) apical involvement has been recognized as a feature of takotsubo cardiomyopathy (TTC). However, variants of TTC characterized by transient LV wall motion abnormalities in regions other than the LV apex have been reported [1], and studies have also demonstrated that right ventricular (RV) involvement is not rare in TTC [2,3]. In patients who have undergone pacemaker implantation, mechanical and electrophysiological abnormalities in the RV apex caused by TTC can lead to pacemaker dysfunction [4]. Although TTC is often triggered by emotional or physiological stress, it is believed that hyponatremia can be an uncommon precipitating factor for TTC [5,6]. Here we describe a case of repeated pacemaker dysfunction in a patient with TTC precipitated by hyponatremia and recurrent RV involvement. An 80-year-old woman was referred to the emergency room on account of general malaise and weakness. When she was 77 years old, the patient had undergone permanent dual-chamber pacemaker implantation because of advanced atrioventricular block. The ventricular lead was placed in the RV apex. She drank 3–4 L of water per day before admission. The patient's Glasgow coma scale was E3V5M6 and she was slightly drowsy. Her blood pressure was 128/ 64 mm Hg, pulse rate was 84 beats per minute, and oxygen saturation was 100% on room air. Her lung and heart sounds were normal on
auscultation. A neurological examination revealed no palsy. Chest Xray showed no cardiomegaly or pulmonary congestion. A 12-lead electrocardiogram (ECG) showed sinus regular rhythm and ventricular pacing, and QRS complexes were similar to those previously recorded. Blood and chemical tests revealed hyponatremia (sodium levels: 116 mEq/L). Renal function, potassium levels, adrenal function, and thyroid function were normal. No acidosis or alkalosis was observed on blood gas analysis. Troponin T was negative and brain natriuretic peptide (BNP) levels were slightly elevated (22.9 pg/mL), although they were lower than those measured previously when the patient was in a stable condition. We considered that the patient's somnolent status and malaise were caused by severe hyponatremia due to psychogenic polydipsia; therefore, hypertonic saline was administered. Several hours later, lung wheezing became overt, and ECG showed negative T wave in precordial leads with QT prolongation. Echocardiography revealed apical dyskinesis and basal hyperkinesis of the LV (Fig. 1A). Coronary angiography revealed no significant stenosis. We diagnosed TTC, and intravenous infusion of furosemide and oxygen inhalation were initiated and fluid intake was restricted. On her second hospital day, BNP levels increased to 607.4 pg/mL and serum sodium levels returned to the normal range. In the evening of the second hospital day, ECG showed intermittent failure of RV pacing (Fig. 2). Although the baseline RV pacing threshold in her stable condition was high (3.12 V at 0.4 ms, unipolar), interrogation showed that the RV pacing threshold increased to 6.0 V at 0.4 ms (unipolar), and lead impedance was unchanged. The atrial pacing threshold and lead impedance were similar. We gained stable pacing with increased output and prolongation of pacing pulse (6.0 V, 1.2 ms). The RV pacing threshold tended to improve since the fourth hospital day, and returned to the baseline on the sixth hospital day. LV wall motion recovered to almost normal on the fifth hospital day (Fig. 1B). Nine months later, she was readmitted to our hospital on account of general malaise and hyponatremia. After admission, she again
Fig. 1. Echocardiogram on the second (A) and fifth hospital day (B) (four chamber view in systole). Apical ballooning (arrows) observed on the second day disappeared on the fifth day.
⁎ Corresponding author at: Department of Cardiology, National Hospital Organization, Kanazawa Medical Center, 1-1 Shimo-ishibimki-machi, Kanazawa 920-8650, Japan. Tel.: + 81 76 262 4161; fax: + 81 76 222 2758. E-mail address: [email protected] (A. Chikata).
444
Letters to the Editor
Fig. 2. Electrocardiogram in the evening on the second hospital day. The pacing rate was 80 beats per minute. Intermittent ventricular pacing failure, negative T wave, and QT prolongation were observed, particularly in escape junctional beats.
developed TTC and was treated with intravenous infusion of furosemide and oxygen inhalation with fluid restriction. Transient pacemaker dysfunction also occurred and bradycardia induced torsade de pointes. TTC is characterized by distinctive transient LV wall motion abnormalities without significant coronary artery stenosis, and in its classical form, the LV apex is affected. However, variants of TTC characterized by transient LV wall motion abnormalities in regions other than the LV apex have been reported [1]. Recent reports have also suggested that RV involvement is not rare in TTC [2]. RV dysfunction has been associated with lower LV ejection fraction, longer hospitalizations, and more complications [3]. Wissner et al. reported reversible pacemaker dysfunction in a patient with TTC; they suggested that loss of capture was induced by RV mechanical and electrophysiological abnormalities caused by TTC [4]. Metabolic or electrolyte derangement can lead to an increase in the capture threshold. For example, hyperkalemia has been reported to cause failure of atrial and ventricular capture due to pacemaker exit block [7]. Severe acid–base imbalance, hypoxemia, hypercarbia, and severe hyperglycemia can also cause pacemaker dysfunction. In our case, serum potassium levels, carbon dioxide concentrations, and glucose levels of the patient were in the normal range, and there were no acidosis or alkalosis. The patient's oxygen saturation was also sufficient. Although serum sodium levels were low, changes in serum sodium levels were not parallel with the changes in the pacing threshold. No other etiology could explain the reversible nature of ventricular pacing abnormalities. Normalization of the ventricular pacing threshold was coincident with the resolution of apical wall motion abnormalities, and recurrent TTC reproducibly induced pacing failure. These results suggest that mechanical and electrophysiological abnormalities in the RV apex caused by TTC led to a transient increase in the capture threshold. It has been reported that severe hyponatremia can be an uncommon precipitating factor for TTC. The mechanistic link
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.11.062
between hyponatremia and TTC is not immediately evident, but it has been speculated that excessive catecholamine release secondary to the associated abnormal central nervous system may cause myocardial injury [5,6]. In our case, serum sodium levels of the patient on admission were 116 mEq/L. Although low cardiac output states caused by TTC could induce nonosmotic release of Antidiuretic hormone (ADH), we believe that severe hyponatremia precipitated TTC because the patient had no cardiac manifestation and her laboratory date showed no elevation of troponin T or BNP levels on admission. This is the first case demonstrating repeated pacemaker dysfunction in a patient with recurrent TTC that appeared to be precipitated by hyponatremia. This case highlights the need for careful observation for abrupt changes in the pacing threshold in patients with TTC who have undergone temporary or permanent pacing.
References [1] Hurst RT, Askew JW, Reuss CS, et al. Transient midventricular ballooning syndrome: a new variant. J Am Coll Cardiol 2006;48:579–83. [2] Elesber AA, Prasad A, Bybee KA, et al. Transient cardiac apical ballooning syndrome: prevalence and clinical implications of right ventricular involvement. J Am Coll Cardiol 2006;47:1082–3. [3] Haghi D, Athanasiadis A, Papavassiliu T, et al. Right ventricular involvement in Takotsubo cardiomyopathy. Eur Heart J 2006;27:2433–9. [4] Wissner E, Fortuin FD, Scott LR, Altemose GT. Reversible pacemaker dysfunction in a patient with transient cardiac apical ballooning syndrome: a case report. Europace 2008;10:1105–7. [5] Worthley MI, Anderson TJ. Transient left ventricular apical ballooning syndrome following a hyponatraemic seizure. Int J Cardiol 2007;115:e102–4. [6] AbouEzzeddine O, Prasad A. Apical ballooning syndrome precipitated by hyponatremia. Int J Cardiol 2010;145:e26–9. [7] Kahloon MU, Aslam AK, Aslam AF, Wilbur SL, Vasavada BC, Khan IA. Hyperkalemia induced failure of atrial and ventricular pacemaker capture. Int J Cardiol 2005;105:224–6.
443
Repeated pacemaker dysfunction in a patient with recurrent takotsubo cardiomyopathy precipitated by hyponatremia Akio Chikata ⁎, Wataru Omi, Takahiro Saeki, Hideo Nagai, Satoru Sakagami Department of Cardiology, National Hospital Organization, Kanazawa Medical Center, Kanazawa, Japan
a r t i c l e
i n f o
Article history: Received 16 August 2013 Accepted 23 November 2013 Available online 4 December 2013 Keywords: Pacemaker dysfunction Takotsubo cardiomyopathy Hyponatremia
Left ventricular (LV) apical involvement has been recognized as a feature of takotsubo cardiomyopathy (TTC). However, variants of TTC characterized by transient LV wall motion abnormalities in regions other than the LV apex have been reported [1], and studies have also demonstrated that right ventricular (RV) involvement is not rare in TTC [2,3]. In patients who have undergone pacemaker implantation, mechanical and electrophysiological abnormalities in the RV apex caused by TTC can lead to pacemaker dysfunction [4]. Although TTC is often triggered by emotional or physiological stress, it is believed that hyponatremia can be an uncommon precipitating factor for TTC [5,6]. Here we describe a case of repeated pacemaker dysfunction in a patient with TTC precipitated by hyponatremia and recurrent RV involvement. An 80-year-old woman was referred to the emergency room on account of general malaise and weakness. When she was 77 years old, the patient had undergone permanent dual-chamber pacemaker implantation because of advanced atrioventricular block. The ventricular lead was placed in the RV apex. She drank 3–4 L of water per day before admission. The patient's Glasgow coma scale was E3V5M6 and she was slightly drowsy. Her blood pressure was 128/ 64 mm Hg, pulse rate was 84 beats per minute, and oxygen saturation was 100% on room air. Her lung and heart sounds were normal on
auscultation. A neurological examination revealed no palsy. Chest Xray showed no cardiomegaly or pulmonary congestion. A 12-lead electrocardiogram (ECG) showed sinus regular rhythm and ventricular pacing, and QRS complexes were similar to those previously recorded. Blood and chemical tests revealed hyponatremia (sodium levels: 116 mEq/L). Renal function, potassium levels, adrenal function, and thyroid function were normal. No acidosis or alkalosis was observed on blood gas analysis. Troponin T was negative and brain natriuretic peptide (BNP) levels were slightly elevated (22.9 pg/mL), although they were lower than those measured previously when the patient was in a stable condition. We considered that the patient's somnolent status and malaise were caused by severe hyponatremia due to psychogenic polydipsia; therefore, hypertonic saline was administered. Several hours later, lung wheezing became overt, and ECG showed negative T wave in precordial leads with QT prolongation. Echocardiography revealed apical dyskinesis and basal hyperkinesis of the LV (Fig. 1A). Coronary angiography revealed no significant stenosis. We diagnosed TTC, and intravenous infusion of furosemide and oxygen inhalation were initiated and fluid intake was restricted. On her second hospital day, BNP levels increased to 607.4 pg/mL and serum sodium levels returned to the normal range. In the evening of the second hospital day, ECG showed intermittent failure of RV pacing (Fig. 2). Although the baseline RV pacing threshold in her stable condition was high (3.12 V at 0.4 ms, unipolar), interrogation showed that the RV pacing threshold increased to 6.0 V at 0.4 ms (unipolar), and lead impedance was unchanged. The atrial pacing threshold and lead impedance were similar. We gained stable pacing with increased output and prolongation of pacing pulse (6.0 V, 1.2 ms). The RV pacing threshold tended to improve since the fourth hospital day, and returned to the baseline on the sixth hospital day. LV wall motion recovered to almost normal on the fifth hospital day (Fig. 1B). Nine months later, she was readmitted to our hospital on account of general malaise and hyponatremia. After admission, she again
Fig. 1. Echocardiogram on the second (A) and fifth hospital day (B) (four chamber view in systole). Apical ballooning (arrows) observed on the second day disappeared on the fifth day.
⁎ Corresponding author at: Department of Cardiology, National Hospital Organization, Kanazawa Medical Center, 1-1 Shimo-ishibimki-machi, Kanazawa 920-8650, Japan. Tel.: + 81 76 262 4161; fax: + 81 76 222 2758. E-mail address: [email protected] (A. Chikata).
444
Letters to the Editor
Fig. 2. Electrocardiogram in the evening on the second hospital day. The pacing rate was 80 beats per minute. Intermittent ventricular pacing failure, negative T wave, and QT prolongation were observed, particularly in escape junctional beats.
developed TTC and was treated with intravenous infusion of furosemide and oxygen inhalation with fluid restriction. Transient pacemaker dysfunction also occurred and bradycardia induced torsade de pointes. TTC is characterized by distinctive transient LV wall motion abnormalities without significant coronary artery stenosis, and in its classical form, the LV apex is affected. However, variants of TTC characterized by transient LV wall motion abnormalities in regions other than the LV apex have been reported [1]. Recent reports have also suggested that RV involvement is not rare in TTC [2]. RV dysfunction has been associated with lower LV ejection fraction, longer hospitalizations, and more complications [3]. Wissner et al. reported reversible pacemaker dysfunction in a patient with TTC; they suggested that loss of capture was induced by RV mechanical and electrophysiological abnormalities caused by TTC [4]. Metabolic or electrolyte derangement can lead to an increase in the capture threshold. For example, hyperkalemia has been reported to cause failure of atrial and ventricular capture due to pacemaker exit block [7]. Severe acid–base imbalance, hypoxemia, hypercarbia, and severe hyperglycemia can also cause pacemaker dysfunction. In our case, serum potassium levels, carbon dioxide concentrations, and glucose levels of the patient were in the normal range, and there were no acidosis or alkalosis. The patient's oxygen saturation was also sufficient. Although serum sodium levels were low, changes in serum sodium levels were not parallel with the changes in the pacing threshold. No other etiology could explain the reversible nature of ventricular pacing abnormalities. Normalization of the ventricular pacing threshold was coincident with the resolution of apical wall motion abnormalities, and recurrent TTC reproducibly induced pacing failure. These results suggest that mechanical and electrophysiological abnormalities in the RV apex caused by TTC led to a transient increase in the capture threshold. It has been reported that severe hyponatremia can be an uncommon precipitating factor for TTC. The mechanistic link
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.11.062
between hyponatremia and TTC is not immediately evident, but it has been speculated that excessive catecholamine release secondary to the associated abnormal central nervous system may cause myocardial injury [5,6]. In our case, serum sodium levels of the patient on admission were 116 mEq/L. Although low cardiac output states caused by TTC could induce nonosmotic release of Antidiuretic hormone (ADH), we believe that severe hyponatremia precipitated TTC because the patient had no cardiac manifestation and her laboratory date showed no elevation of troponin T or BNP levels on admission. This is the first case demonstrating repeated pacemaker dysfunction in a patient with recurrent TTC that appeared to be precipitated by hyponatremia. This case highlights the need for careful observation for abrupt changes in the pacing threshold in patients with TTC who have undergone temporary or permanent pacing.
References [1] Hurst RT, Askew JW, Reuss CS, et al. Transient midventricular ballooning syndrome: a new variant. J Am Coll Cardiol 2006;48:579–83. [2] Elesber AA, Prasad A, Bybee KA, et al. Transient cardiac apical ballooning syndrome: prevalence and clinical implications of right ventricular involvement. J Am Coll Cardiol 2006;47:1082–3. [3] Haghi D, Athanasiadis A, Papavassiliu T, et al. Right ventricular involvement in Takotsubo cardiomyopathy. Eur Heart J 2006;27:2433–9. [4] Wissner E, Fortuin FD, Scott LR, Altemose GT. Reversible pacemaker dysfunction in a patient with transient cardiac apical ballooning syndrome: a case report. Europace 2008;10:1105–7. [5] Worthley MI, Anderson TJ. Transient left ventricular apical ballooning syndrome following a hyponatraemic seizure. Int J Cardiol 2007;115:e102–4. [6] AbouEzzeddine O, Prasad A. Apical ballooning syndrome precipitated by hyponatremia. Int J Cardiol 2010;145:e26–9. [7] Kahloon MU, Aslam AK, Aslam AF, Wilbur SL, Vasavada BC, Khan IA. Hyperkalemia induced failure of atrial and ventricular pacemaker capture. Int J Cardiol 2005;105:224–6.
