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Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes?
American Journal of Emergency Medicine xxx (2015) xxx–xxx
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of literature☆,☆☆,★ Abstract Lithium is the drug of choice for bipolar disorder and has been in use for more than 50 years. Lithium is known to cause cardiac toxicity in humans including conduction disturbances, bradycardia, and repolarization abnormalities but has rarely been reported to cause left ventricular dysfunction. We report a patient with typical features of lithium toxicity including sinus bradycardia and junctional rhythm, who, in addition, presented atypical features with diffuse T-wave inversions, QT prolongation, and acute left ventricular systolic dysfunction with serum cardiac marker elevation. After excluding other causes of cardiomyopathy including coronary thrombosis, stress cardiomyopathy, and sepsis, a highly probable explanation for our patient’s acute left ventricular systolic dysfunction was lithium toxicity causing transient myocarditis. Extensive review of literature showed a few case reports of cardiac dysfunction associated with lithium, but acute left ventricular dysfunction caused by lithium has not been reported. Lithium has been in use as a long-term mood stabilizer for greater than 50 years [1]. It is the preferred drug for bipolar disorders, alone or in combination with other anticonvulsants [2]. Lithium has been shown to cause a variety of cardiac conduction disturbances including sinus bradycardia, atrioventricular nodal block, premature atrial and ventricular beats, and junctional arrhythmias [3]; but myocardial dysfunction associated with lithium has rarely been reported in humans [4]. We did an extensive review of literature to find possible cardiotoxic effects of lithium. A 35-year-old African-American woman with history of bipolar disorder and multiple prior suicidal attempts was brought to the emergency department (ED) after she was found unresponsive at home. In the ED, her Glasgow Coma Scale was 10; and her initial vitals revealed sinus rhythm of 35 beats per minute, respiratory rate of 10/min, blood pressure of 90/63 mm Hg, temperature of 97°F, and oxygen saturation of 80% on room air. A venous blood draw showed hypoxia with metabolic acidosis. Cardiovascular examination revealed significant bradycardia without any extra sounds, murmurs, or gallops. The remainder of the physical examination was unremarkable. Initial electrocardiogram showed severe bradycardia with junctional rhythm with a heart rate of 34 beats per minute (Fig. 1). Her troponins were elevated at 3.14 ng/mL (reference range, b 0.04ng/mL), with creatine kinase of 146 U/L and creatine kinase–MB of 6 ng/L with relative index of 5.76. Serum lithium level was significantly elevated at 3.7 mEq/L; and her ☆ Conflict of interest: none. ☆☆ Financial disclosures: none. ★ Acknowledgements: none.
creatinine level was 1.7 mg/dL. The results of the remainder of her laboratory tests were within normal limits. Echocardiography showed severe left ventricular systolic dysfunction with an ejection fraction of 15% with severe global hypokinesis without regional wall motion abnormalities (Fig. 2). Because of altered mental status and hypoxic respiratory failure, she was intubated. She was started on broad-spectrum antibiotics and received inotropes for circulatory support. She continued to deteriorate, remaining hypotensive and bradycardiac with heart rates in the low 30s. Hemodialysis was initiated. Her heart rates steadily improved, but she developed diffuse T-wave inversions with QT prolongation (Fig. 3) with a QTc of 531 milliseconds. Following dialysis, her lithium level was 0.55 mEq/L. She showed marked hemodynamic improvement and was weaned off inotropes and was extubated. Blood cultures were negative. A nuclear stress study showed no evidence of reversible ischemia or infarction with an ejection fraction of 61% (Fig. 4). Repeat echocardiogram in 4 days demonstrated significant improvement in ejection fraction to 60% to 65% (Fig. 5). She was discharged home in a stable condition. Lithium is most commonly prescribed as lithium carbonate followed by lithium citrate [2]. It has a narrow therapeutic index and should be used with caution in patients with renal failure [5,6]. The optimum recommended plasma concentration varies according to different guidelines, with American Psychiatry Association [7] recommending 0.5 to 1.2 mmol/L and 0.6 to 0.8 mmol/L for initiation and maintenance, respectively. Lithium exerts its therapeutic effect through multiple mechanisms, including modulation of neurotransmission [8], serotonin release [9], and inhibition of ionositol monophosphatase, thereby increasing ionositol triphosphate [8]. Earlier reports on animal studies have shown that lithium affects cardiac conduction and, in larger doses, could depress myocardial systolic function, lowering blood pressure and resulting in diastolic cardiac arrest [10]. Lithium enters cardiac myocyte, displaces positively charged monovalent cations (Na+), and creates intracellular metabolic changes. Although its entry into cardiac myocytes is similar to Na+, it is not removed as efficiently as sodium ions [11]. Lithium overdose mainly causes neurologic effects; however, cardiac toxicity has been reported, most commonly as bradycardia without hypotension [12]. Cardiac complications are reported in 6% of all hospitalized lithium overdose cases [12]. Serious cardiac toxicity due to lithium toxicity is uncommon and generally occurs in individuals with underlying heart disease [13]. Medications including angiotensin-converting enzyme, diuretics, inhibitors, and nonsteroidal anti-inflammatory drugs, which cause dehydration or renal impairment, could precipitate lithium toxicity [14]. Lithium overdose has been shown to cause a wide range of electrocardiographic changes, the most common being T-wave flattening without inversion [15,16]. Other presentations include atrioventricular
0735-6757/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
2
M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Fig. 1. Initial electrocardiogram showing bradycardia with junctional rhythm.
dissociation, junctional rhythm, and sinus node dysfunction secondary to decreased depolarization rate of sinus node [17,18]. Direct myocyte injury causing left ventricular dysfunction or elevation of cardiac biomarkers has rarely been reported in humans [4]. Of the 745 cases of lithium overdose reported in the French Pharmaco-Vigilance Database, only 3 presented with dilated cardiomyopathy [4]. Extensive review of literature did not reveal any cases except 2 case reports of possible cardiomyopathy associated with lithium; however, the first patient had a long-term use of lithium rather than acute toxicity [19], and the second one was lithium-induced Takotsubo cardiomyopathy [20], which was unlikely to be the cause in our patient. Using the Bayesian confidence propagation network in the WHO database, Coulter et al [21] found a probable link that needed more investigation for association between lithium exposure and cardiomyopathy. Our patient had typical presentation of lithium toxicity ranging from sinus bradycardia to bradycardia with junctional rhythm; what is unusual about her presentation was diffuse T-wave inversions with QTc prolongation and severe left ventricular dysfunction associated with elevated cardiac markers. The differential diagnosis included acute coronary syndrome, stress cardiomyopathy, viral myocarditis, and
myocarditis secondary to sepsis. Her global hypokinesis with negative nuclear stress test result excludes coronary artery disease as the cause. She did not have apical or basal ballooning to suggest stress cardiomyopathy [22,23]. She was not septic; therefore, toxic myocarditis secondary to lactic acidosis is unlikely [24]. The transient nature of left ventricular dysfunction would exclude viral myocarditis. The rapid recovery of ejection fraction and normal lithium level after dialysis would support transient myocardial injury caused by lithium as the etiology of global hypokinesis with elevated cardiac markers. Thus, it is important to recognize the acute cardiac effects of lithium toxicity including possible direct myocardial injury and to treat accordingly. Mahesh Anantha Narayanan MD ⁎ Toufik Mahfood Haddad MD Department of Internal Medicine, CHI Health Creighton University Medical Center, Creighton University School of Medicine ⁎Corresponding author at: Department of Internal Medicine 601 North 30th St #5800, Omaha, NE 68131 Tel.: +1 507 319 2446; fax: +1 402 717 0770 E-mail address: [email protected] Ojas Bansal MD Cardiac Center of Creighton University, CHI Health Creighton University Medical Center, Creighton University School of Medicine Janani Baskaran MBBS University of Texas Health Science Center at San Antonio Muhammad S. Azzouz MD Abhilash Akinapelli MD Dennis J. Esterbrooks MD Cardiac Center of Creighton University, CHI Health Creighton University Medical Center, Creighton University School of Medicine http://dx.doi.org/10.1016/j.ajem.2015.03.023 References
Fig. 2. Initial echocardiogram showing dilated left ventricle with low ejection fraction.
[1] Belmaker RH. Bipolar disorder. N Engl J Med 2004;351(5):476–86. [2] Oruch R, Elderbi MA, Khattab HA, Pryme IF, Lund A. Lithium: a review of pharmacology, clinical uses, and toxicity. Eur J Pharmacol 2014;740:464–73. [3] Brady HR, Horgan JH. Lithium and the heart. Unanswered questions. Chest 1988; 93(1):166–9.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
3
Fig. 3. Repeat electrocardiogram showing diffuse T-wave inversions and QT prolongation.
[4] Montastruc G, Favreliere S, Sommet A, Pathak A, Lapeyre-Mestre M, Perault-Pochat MC, et al. Drugs and dilated cardiomyopathies: a case/noncase study in the French PharmacoVigilance database. Br J Clin Pharmacol 2010;69(3):287–94. [5] Deligiannidis KM, Byatt N, Freeman MP. Pharmacotherapy for mood disorders in pregnancy: a review of pharmacokinetic changes and clinical recommendations for therapeutic drug monitoring. J Clin Psychopharmacol 2014;34(2):244–55. [6] Wijeratne C, Draper B. Reformulation of current recommendations for target serum lithium concentration according to clinical indication, age and physical comorbidity. Aust N Z J Psychiatry 2011;45(12):1026–32. [7] Practice guideline for the treatment of patients with bipolar disorder. American Psychiatric Association. Am J Psychiatry 1994;151(12 Suppl.):1–36. [8] Jope RS. Anti-bipolar therapy: mechanism of action of lithium. Mol Psychiatry 1999; 4(2):117–28. [9] Massot O, Rousselle JC, Fillion MP, Januel D, Plantefol M, Fillion G. 5-HT1B receptors: a novel target for lithium. possible involvement in mood disorders. Neuropsychopharmacology 1999;21(4):530–41. [10] Talati SN, Aslam AF, Vasavada B. Sinus node dysfunction in association with chronic lithium therapy: a case report and review of literature. Am J Ther 2009;16(3):274–8. [11] Singer I, Rotenberg D. Mechanisms of lithium action. N Engl J Med 1973;289(5):254–60. [12] Offerman SR, Alsop JA, Lee J, Holmes JF. Hospitalized lithium overdose cases reported to the California Poison Control System. Clin Toxicol (Phila) 2010;48(5):443–8. [13] Serinken M, Karcioglu O, Korkmaz A. Rarely seen cardiotoxicity of lithium overdose: complete heart block. Int J Cardiol 2009;132(2):276–8. [14] Phelan KM, Mosholder AD, Lu S. Lithium interaction with the cyclooxygenase 2 inhibitors rofecoxib and celecoxib and other nonsteroidal anti-inflammatory drugs. J Clin Psychiatry 2003;64(11):1328–34.
[15] Demers RG, Heninger GR. Electrocardiographic T-wave changes during lithium carbonate treatment. JAMA 1971;218(3):381–6. [16] Bucht G, Smigan L, Wahlin A, Eriksson P. ECG changes during lithium therapy. A prospective study. Acta Med Scand 1984;216(1):101–4. [17] Mitchell JE, Mackenzie TB. Cardiac effects of lithium therapy in man: a review. J Clin Psychiatry 1982;43(2):47–51. [18] Tilkian AG, Schroeder JS, Kao JJ, Hultgren HN. The cardiovascular effects of lithium in man. A review of the literature. Am J Med 1976;61(5):665–70. [19] Aichhorn W, Huber R, Stuppaeck C, Whitworth AB. Cardiomyopathy after long-term treatment with lithium—more than a coincidence? J Psychopharmacol 2006;20(4): 589–91. [20] Kitami M, Oizumi H, Kish SJ, Furukawa Y. Takotsubo cardiomyopathy associated with lithium intoxication in bipolar disorder: a case report. J Clin Psychopharmacol 2014;34(3):410–1. [21] Coulter DM, Bate A, Meyboom RH, Lindquist M, Edwards IR. Antipsychotic drugs and heart muscle disorder in international pharmacovigilance: data mining study. BMJ 2001;322(7296):1207–9. [22] Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (tako-tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J 2008;155(3): 408–17. [23] Anantha Narayanan M, Kandasamy VV, Chandraprakasam S, Mooss A. Reversible stress cardiomyopathy presenting as acute coronary syndrome with elevated troponin in the absence of regional wall motion abnormalities: a forme fruste of stress cardiomyopathy? Case Rep Med 2014;2014:796202. [24] Weisel RD, Vito L, Dennis RC, Valeri CR, Hechtman HB. Myocardial depression during sepsis. Am J Surg 1977;133(4):512–21.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
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M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Fig. 4. Nuclear stress imaging showing no reversible or fixed defect.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Fig. 5. Repeat echocardiogram in 4 days showing normal left ventricular size.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
5
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of literature☆,☆☆,★ Abstract Lithium is the drug of choice for bipolar disorder and has been in use for more than 50 years. Lithium is known to cause cardiac toxicity in humans including conduction disturbances, bradycardia, and repolarization abnormalities but has rarely been reported to cause left ventricular dysfunction. We report a patient with typical features of lithium toxicity including sinus bradycardia and junctional rhythm, who, in addition, presented atypical features with diffuse T-wave inversions, QT prolongation, and acute left ventricular systolic dysfunction with serum cardiac marker elevation. After excluding other causes of cardiomyopathy including coronary thrombosis, stress cardiomyopathy, and sepsis, a highly probable explanation for our patient’s acute left ventricular systolic dysfunction was lithium toxicity causing transient myocarditis. Extensive review of literature showed a few case reports of cardiac dysfunction associated with lithium, but acute left ventricular dysfunction caused by lithium has not been reported. Lithium has been in use as a long-term mood stabilizer for greater than 50 years [1]. It is the preferred drug for bipolar disorders, alone or in combination with other anticonvulsants [2]. Lithium has been shown to cause a variety of cardiac conduction disturbances including sinus bradycardia, atrioventricular nodal block, premature atrial and ventricular beats, and junctional arrhythmias [3]; but myocardial dysfunction associated with lithium has rarely been reported in humans [4]. We did an extensive review of literature to find possible cardiotoxic effects of lithium. A 35-year-old African-American woman with history of bipolar disorder and multiple prior suicidal attempts was brought to the emergency department (ED) after she was found unresponsive at home. In the ED, her Glasgow Coma Scale was 10; and her initial vitals revealed sinus rhythm of 35 beats per minute, respiratory rate of 10/min, blood pressure of 90/63 mm Hg, temperature of 97°F, and oxygen saturation of 80% on room air. A venous blood draw showed hypoxia with metabolic acidosis. Cardiovascular examination revealed significant bradycardia without any extra sounds, murmurs, or gallops. The remainder of the physical examination was unremarkable. Initial electrocardiogram showed severe bradycardia with junctional rhythm with a heart rate of 34 beats per minute (Fig. 1). Her troponins were elevated at 3.14 ng/mL (reference range, b 0.04ng/mL), with creatine kinase of 146 U/L and creatine kinase–MB of 6 ng/L with relative index of 5.76. Serum lithium level was significantly elevated at 3.7 mEq/L; and her ☆ Conflict of interest: none. ☆☆ Financial disclosures: none. ★ Acknowledgements: none.
creatinine level was 1.7 mg/dL. The results of the remainder of her laboratory tests were within normal limits. Echocardiography showed severe left ventricular systolic dysfunction with an ejection fraction of 15% with severe global hypokinesis without regional wall motion abnormalities (Fig. 2). Because of altered mental status and hypoxic respiratory failure, she was intubated. She was started on broad-spectrum antibiotics and received inotropes for circulatory support. She continued to deteriorate, remaining hypotensive and bradycardiac with heart rates in the low 30s. Hemodialysis was initiated. Her heart rates steadily improved, but she developed diffuse T-wave inversions with QT prolongation (Fig. 3) with a QTc of 531 milliseconds. Following dialysis, her lithium level was 0.55 mEq/L. She showed marked hemodynamic improvement and was weaned off inotropes and was extubated. Blood cultures were negative. A nuclear stress study showed no evidence of reversible ischemia or infarction with an ejection fraction of 61% (Fig. 4). Repeat echocardiogram in 4 days demonstrated significant improvement in ejection fraction to 60% to 65% (Fig. 5). She was discharged home in a stable condition. Lithium is most commonly prescribed as lithium carbonate followed by lithium citrate [2]. It has a narrow therapeutic index and should be used with caution in patients with renal failure [5,6]. The optimum recommended plasma concentration varies according to different guidelines, with American Psychiatry Association [7] recommending 0.5 to 1.2 mmol/L and 0.6 to 0.8 mmol/L for initiation and maintenance, respectively. Lithium exerts its therapeutic effect through multiple mechanisms, including modulation of neurotransmission [8], serotonin release [9], and inhibition of ionositol monophosphatase, thereby increasing ionositol triphosphate [8]. Earlier reports on animal studies have shown that lithium affects cardiac conduction and, in larger doses, could depress myocardial systolic function, lowering blood pressure and resulting in diastolic cardiac arrest [10]. Lithium enters cardiac myocyte, displaces positively charged monovalent cations (Na+), and creates intracellular metabolic changes. Although its entry into cardiac myocytes is similar to Na+, it is not removed as efficiently as sodium ions [11]. Lithium overdose mainly causes neurologic effects; however, cardiac toxicity has been reported, most commonly as bradycardia without hypotension [12]. Cardiac complications are reported in 6% of all hospitalized lithium overdose cases [12]. Serious cardiac toxicity due to lithium toxicity is uncommon and generally occurs in individuals with underlying heart disease [13]. Medications including angiotensin-converting enzyme, diuretics, inhibitors, and nonsteroidal anti-inflammatory drugs, which cause dehydration or renal impairment, could precipitate lithium toxicity [14]. Lithium overdose has been shown to cause a wide range of electrocardiographic changes, the most common being T-wave flattening without inversion [15,16]. Other presentations include atrioventricular
0735-6757/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
2
M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Fig. 1. Initial electrocardiogram showing bradycardia with junctional rhythm.
dissociation, junctional rhythm, and sinus node dysfunction secondary to decreased depolarization rate of sinus node [17,18]. Direct myocyte injury causing left ventricular dysfunction or elevation of cardiac biomarkers has rarely been reported in humans [4]. Of the 745 cases of lithium overdose reported in the French Pharmaco-Vigilance Database, only 3 presented with dilated cardiomyopathy [4]. Extensive review of literature did not reveal any cases except 2 case reports of possible cardiomyopathy associated with lithium; however, the first patient had a long-term use of lithium rather than acute toxicity [19], and the second one was lithium-induced Takotsubo cardiomyopathy [20], which was unlikely to be the cause in our patient. Using the Bayesian confidence propagation network in the WHO database, Coulter et al [21] found a probable link that needed more investigation for association between lithium exposure and cardiomyopathy. Our patient had typical presentation of lithium toxicity ranging from sinus bradycardia to bradycardia with junctional rhythm; what is unusual about her presentation was diffuse T-wave inversions with QTc prolongation and severe left ventricular dysfunction associated with elevated cardiac markers. The differential diagnosis included acute coronary syndrome, stress cardiomyopathy, viral myocarditis, and
myocarditis secondary to sepsis. Her global hypokinesis with negative nuclear stress test result excludes coronary artery disease as the cause. She did not have apical or basal ballooning to suggest stress cardiomyopathy [22,23]. She was not septic; therefore, toxic myocarditis secondary to lactic acidosis is unlikely [24]. The transient nature of left ventricular dysfunction would exclude viral myocarditis. The rapid recovery of ejection fraction and normal lithium level after dialysis would support transient myocardial injury caused by lithium as the etiology of global hypokinesis with elevated cardiac markers. Thus, it is important to recognize the acute cardiac effects of lithium toxicity including possible direct myocardial injury and to treat accordingly. Mahesh Anantha Narayanan MD ⁎ Toufik Mahfood Haddad MD Department of Internal Medicine, CHI Health Creighton University Medical Center, Creighton University School of Medicine ⁎Corresponding author at: Department of Internal Medicine 601 North 30th St #5800, Omaha, NE 68131 Tel.: +1 507 319 2446; fax: +1 402 717 0770 E-mail address: [email protected] Ojas Bansal MD Cardiac Center of Creighton University, CHI Health Creighton University Medical Center, Creighton University School of Medicine Janani Baskaran MBBS University of Texas Health Science Center at San Antonio Muhammad S. Azzouz MD Abhilash Akinapelli MD Dennis J. Esterbrooks MD Cardiac Center of Creighton University, CHI Health Creighton University Medical Center, Creighton University School of Medicine http://dx.doi.org/10.1016/j.ajem.2015.03.023 References
Fig. 2. Initial echocardiogram showing dilated left ventricle with low ejection fraction.
[1] Belmaker RH. Bipolar disorder. N Engl J Med 2004;351(5):476–86. [2] Oruch R, Elderbi MA, Khattab HA, Pryme IF, Lund A. Lithium: a review of pharmacology, clinical uses, and toxicity. Eur J Pharmacol 2014;740:464–73. [3] Brady HR, Horgan JH. Lithium and the heart. Unanswered questions. Chest 1988; 93(1):166–9.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
3
Fig. 3. Repeat electrocardiogram showing diffuse T-wave inversions and QT prolongation.
[4] Montastruc G, Favreliere S, Sommet A, Pathak A, Lapeyre-Mestre M, Perault-Pochat MC, et al. Drugs and dilated cardiomyopathies: a case/noncase study in the French PharmacoVigilance database. Br J Clin Pharmacol 2010;69(3):287–94. [5] Deligiannidis KM, Byatt N, Freeman MP. Pharmacotherapy for mood disorders in pregnancy: a review of pharmacokinetic changes and clinical recommendations for therapeutic drug monitoring. J Clin Psychopharmacol 2014;34(2):244–55. [6] Wijeratne C, Draper B. Reformulation of current recommendations for target serum lithium concentration according to clinical indication, age and physical comorbidity. Aust N Z J Psychiatry 2011;45(12):1026–32. [7] Practice guideline for the treatment of patients with bipolar disorder. American Psychiatric Association. Am J Psychiatry 1994;151(12 Suppl.):1–36. [8] Jope RS. Anti-bipolar therapy: mechanism of action of lithium. Mol Psychiatry 1999; 4(2):117–28. [9] Massot O, Rousselle JC, Fillion MP, Januel D, Plantefol M, Fillion G. 5-HT1B receptors: a novel target for lithium. possible involvement in mood disorders. Neuropsychopharmacology 1999;21(4):530–41. [10] Talati SN, Aslam AF, Vasavada B. Sinus node dysfunction in association with chronic lithium therapy: a case report and review of literature. Am J Ther 2009;16(3):274–8. [11] Singer I, Rotenberg D. Mechanisms of lithium action. N Engl J Med 1973;289(5):254–60. [12] Offerman SR, Alsop JA, Lee J, Holmes JF. Hospitalized lithium overdose cases reported to the California Poison Control System. Clin Toxicol (Phila) 2010;48(5):443–8. [13] Serinken M, Karcioglu O, Korkmaz A. Rarely seen cardiotoxicity of lithium overdose: complete heart block. Int J Cardiol 2009;132(2):276–8. [14] Phelan KM, Mosholder AD, Lu S. Lithium interaction with the cyclooxygenase 2 inhibitors rofecoxib and celecoxib and other nonsteroidal anti-inflammatory drugs. J Clin Psychiatry 2003;64(11):1328–34.
[15] Demers RG, Heninger GR. Electrocardiographic T-wave changes during lithium carbonate treatment. JAMA 1971;218(3):381–6. [16] Bucht G, Smigan L, Wahlin A, Eriksson P. ECG changes during lithium therapy. A prospective study. Acta Med Scand 1984;216(1):101–4. [17] Mitchell JE, Mackenzie TB. Cardiac effects of lithium therapy in man: a review. J Clin Psychiatry 1982;43(2):47–51. [18] Tilkian AG, Schroeder JS, Kao JJ, Hultgren HN. The cardiovascular effects of lithium in man. A review of the literature. Am J Med 1976;61(5):665–70. [19] Aichhorn W, Huber R, Stuppaeck C, Whitworth AB. Cardiomyopathy after long-term treatment with lithium—more than a coincidence? J Psychopharmacol 2006;20(4): 589–91. [20] Kitami M, Oizumi H, Kish SJ, Furukawa Y. Takotsubo cardiomyopathy associated with lithium intoxication in bipolar disorder: a case report. J Clin Psychopharmacol 2014;34(3):410–1. [21] Coulter DM, Bate A, Meyboom RH, Lindquist M, Edwards IR. Antipsychotic drugs and heart muscle disorder in international pharmacovigilance: data mining study. BMJ 2001;322(7296):1207–9. [22] Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (tako-tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J 2008;155(3): 408–17. [23] Anantha Narayanan M, Kandasamy VV, Chandraprakasam S, Mooss A. Reversible stress cardiomyopathy presenting as acute coronary syndrome with elevated troponin in the absence of regional wall motion abnormalities: a forme fruste of stress cardiomyopathy? Case Rep Med 2014;2014:796202. [24] Weisel RD, Vito L, Dennis RC, Valeri CR, Hechtman HB. Myocardial depression during sepsis. Am J Surg 1977;133(4):512–21.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
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M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Fig. 4. Nuclear stress imaging showing no reversible or fixed defect.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
M. Anantha Narayanan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Fig. 5. Repeat echocardiogram in 4 days showing normal left ventricular size.
Please cite this article as: Anantha Narayanan M, et al, Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? A case report and review of lite..., Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.03.023
5