American Journal of Emergency Medicine xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Correspondence
Stress-induced cardiomyopathy in pheochromocytoma: the way we treat and the way we think To the Editor,
We thank the authors for the relevant comment to our case report; their thoughtful input gives us the opportunity to specify some concepts. First of all, as stated by modified Mayo Clinic diagnostic criteria for Tako-tsubo cardiomyopathy [1] and new diagnostic criteria proposed by Tako-tsubo Italian Network [2], once Tako-tsubo cardiomyopathy has been suspected, a diagnostic work-up to rule out pheochromocytoma should be systematically performed. Owing to its transient left ventricular dysfunction [3], the treatment of stress-related cardiomyopathy (SRC) is mainly supportive, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, and β-blockers. Diuretics are indicated especially when acute heart failure occurs. β-Blockers should be used with caution in case of cardiogenic shock and only if the left ventricular outflow tract obstruction is associated [4]. In this case, an excessive dehydration has to be avoided. Because of the high catecholamine spillover in the pathophysiology of SRC, inotropic agents can have deleterious effects and are not indicated. Thus, in case of hemodynamic instability, intra-aortic balloon pump should be preferred. Stress-related cardiomyopathy, in the acute phase, is characterized by low cardiac output and low preload, so in our opinion, a pharmacologic treatment with α-adrenergic blockers that further reduce the peripheral vascular resistance do not seem helpful. Moreover, in the pathophysiology of SRC, the direct effects of catecholamines on the myocardium is related to negative inotropic effects of epinephrine via stimulation of the cardioprotective β2-adrenergic receptors–Gi signaling pathway [5], whereas α-adrenergic receptors do not seem to play a prominent role. On the other hand, α-blockade is the first choice for the management of pheochromocytoma crisis [6] and to reduce the risk of hypertensive crises in patients with biochemically active pheochromocytoma [7]. α-Blockade should be started before β-blockade because stimulation of α-adrenoceptors unopposed by β-adrenoceptor vasodilation can result in hypertensive crises [6,7]. Vasculitis is a well-described but rare autoimmune complication of pheochromocytoma, triggered by an excess of cathecolamine levels [8]. Cathecolamine-induced vascular damage is characterized by irregularities of vascular wall, stenosis or aneurysms, generally detected by angiography or computed tomography angiography [9]. Arterial caliper variation resembling vasculitis or vasospasm has been reported without histopathologic changes of intraluminal thrombosis or vasculitis, for this reason, named pseudovasculitis [10]. Isolated arterial thrombosis is not a characteristic complication of cathecolamine-induced vasculitis. In our patient, with the exception
leukocytosis, a very frequent finding in pheochromocytoma, there was no clinical, instrumental, or laboratory findings that could suggest a vasculitis. The sudden onset of clinical symptoms of popliteal artery occlusion as well as the abrupt interruption of flow at computed tomography angiography in a context of regular intimal profile of the artery and in absence of other specific abnormalities of other vascular districts are more suggestive of an acute thrombotic occlusion than a vasculitis complication. We have to keep in mind that the excess of catecholaminergic stimulation predisposes to a hypercoagulability state that, in turn, favors arterial thrombosis [11]. Furthermore, some cases of arterial thrombosis and a case of ventricular thrombus in patients with well-documented pheochromocytoma are recently reported [12-14]. This possible complication arise another challenging question about the opportunity to use anticoagulant agents in patients with persistent severe left ventricular systolic dysfunction and pheochromocytoma.
Marco Di Maio, MD ⁎ Maria Vincenza Polito, MD Heart Department University Hospital “San Giovanni di Dio e Ruggi d’Aragona” Salerno, Italy Department of Medicine and Surgery University of Salerno Salerno, Italy ⁎Corresponding author. E-mail addresses: [email protected] [email protected] Rodolfo Citro, MD Heart Department University Hospital “San Giovanni di Dio e Ruggi d’Aragona” Salerno, Italy E-mail address: [email protected] Federico Piscione, MD Heart Department University Hospital “San Giovanni di Dio e Ruggi d’Aragona” Salerno, Italy Department of Medicine and Surgery University of Salerno Salerno, Italy E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.04.040
0735-6757/© 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Di Maio M, et al, Stress-induced cardiomyopathy in pheochromocytoma: the way we treat and the way we think, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.040
2
Correspondence
References [1] 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. [2] Parodi G, Citro R, Bellandi B, Provenza G, Marrani M, Bossone E. Revised clinical diagnostic criteria for Tako-tsubo syndrome: the Tako-tsubo Italian Network proposal. Int J Cardiol 2014;172(1):282–3. [3] Citro R, Rigo F, Ciampi Q, et al. Echocardiographic assessment of regional left ventricular wall motion abnormalities in patients with tako-tsubo cardiomyopathy: comparison with anterior myocardial infarction. Eur J Echocardiogr 2011;12(7):542–9. [4] Citro R, Rigo F, D'Andrea A, et al. Echocardiographic correlates of acute heart failure, cardiogenic shock, and in-hospital mortality in tako-tsubo cardiomyopathy. JACC Cardiovasc Imaging 2014;7(2):119–29. [5] Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy—a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008;5(1):22–9.
[6] Scholten A, Cisco RM, Vriens MR, et al. Pheochromocytoma crisis is not a surgical emergency. J Clin Endocrinol Metab 2013;98:581–91. [7] Martucci VL, Pacak K. Pheochromocytoma and paraganglioma: diagnosis, genetics, management, and treatment. Curr Probl Cancer 2014;38:7–41. [8] Sarathi V, Lila AR, Bandgar TR, Shah NS. Aortoarteritis: could it be a form of catecholamine-induced vasculitis? Indian J Endocrinol Metab 2013;17:163–6. [9] Pontes Tde C, Rufino GP, Gurgel MG, Medeiros AC, Freire EA. Fibromuscular dysplasia: a differential diagnosis of vasculitis. Rev Bras Reumatol 2012;52(1):70–4. [10] Razavi M, Bendixen B, Maley JE, et al. CNS pseudovasculitis in a patient with pheochromocytoma. Neurology 1999;52(5):1088–90. [11] Van Zaane B, Stuijver DJ, Squizzato A, Gerdes VE. Arterial and venous thrombosis in endocrine diseases. Semin Thromb Hemost 2013;39(5):489–95. [12] Kaiser S, Chronakos J, Dietzek AM. Acute upper extremity arterial thrombosis and stroke in an unresected pheochromocytoma. J Vasc Surg 2013;58:1069–72. [13] Vindenes T, Crump N, Casenas R, Wood K. Pheochromocytoma causing cardiomyopathy, ischemic stroke and acute arterial thrombosis: a case report and review of the literature. Conn Med 2013;77(2):95–8. [14] Hou R, Leathersich AM, Ruud BT. Pheochromocytoma presenting with arterial and intracardiac thrombus in a 47-year-old woman: a case report. J Med Case Rep 2011;5:310.
Please cite this article as: Di Maio M, et al, Stress-induced cardiomyopathy in pheochromocytoma: the way we treat and the way we think, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.040
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Correspondence
Stress-induced cardiomyopathy in pheochromocytoma: the way we treat and the way we think To the Editor,
We thank the authors for the relevant comment to our case report; their thoughtful input gives us the opportunity to specify some concepts. First of all, as stated by modified Mayo Clinic diagnostic criteria for Tako-tsubo cardiomyopathy [1] and new diagnostic criteria proposed by Tako-tsubo Italian Network [2], once Tako-tsubo cardiomyopathy has been suspected, a diagnostic work-up to rule out pheochromocytoma should be systematically performed. Owing to its transient left ventricular dysfunction [3], the treatment of stress-related cardiomyopathy (SRC) is mainly supportive, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, and β-blockers. Diuretics are indicated especially when acute heart failure occurs. β-Blockers should be used with caution in case of cardiogenic shock and only if the left ventricular outflow tract obstruction is associated [4]. In this case, an excessive dehydration has to be avoided. Because of the high catecholamine spillover in the pathophysiology of SRC, inotropic agents can have deleterious effects and are not indicated. Thus, in case of hemodynamic instability, intra-aortic balloon pump should be preferred. Stress-related cardiomyopathy, in the acute phase, is characterized by low cardiac output and low preload, so in our opinion, a pharmacologic treatment with α-adrenergic blockers that further reduce the peripheral vascular resistance do not seem helpful. Moreover, in the pathophysiology of SRC, the direct effects of catecholamines on the myocardium is related to negative inotropic effects of epinephrine via stimulation of the cardioprotective β2-adrenergic receptors–Gi signaling pathway [5], whereas α-adrenergic receptors do not seem to play a prominent role. On the other hand, α-blockade is the first choice for the management of pheochromocytoma crisis [6] and to reduce the risk of hypertensive crises in patients with biochemically active pheochromocytoma [7]. α-Blockade should be started before β-blockade because stimulation of α-adrenoceptors unopposed by β-adrenoceptor vasodilation can result in hypertensive crises [6,7]. Vasculitis is a well-described but rare autoimmune complication of pheochromocytoma, triggered by an excess of cathecolamine levels [8]. Cathecolamine-induced vascular damage is characterized by irregularities of vascular wall, stenosis or aneurysms, generally detected by angiography or computed tomography angiography [9]. Arterial caliper variation resembling vasculitis or vasospasm has been reported without histopathologic changes of intraluminal thrombosis or vasculitis, for this reason, named pseudovasculitis [10]. Isolated arterial thrombosis is not a characteristic complication of cathecolamine-induced vasculitis. In our patient, with the exception
leukocytosis, a very frequent finding in pheochromocytoma, there was no clinical, instrumental, or laboratory findings that could suggest a vasculitis. The sudden onset of clinical symptoms of popliteal artery occlusion as well as the abrupt interruption of flow at computed tomography angiography in a context of regular intimal profile of the artery and in absence of other specific abnormalities of other vascular districts are more suggestive of an acute thrombotic occlusion than a vasculitis complication. We have to keep in mind that the excess of catecholaminergic stimulation predisposes to a hypercoagulability state that, in turn, favors arterial thrombosis [11]. Furthermore, some cases of arterial thrombosis and a case of ventricular thrombus in patients with well-documented pheochromocytoma are recently reported [12-14]. This possible complication arise another challenging question about the opportunity to use anticoagulant agents in patients with persistent severe left ventricular systolic dysfunction and pheochromocytoma.
Marco Di Maio, MD ⁎ Maria Vincenza Polito, MD Heart Department University Hospital “San Giovanni di Dio e Ruggi d’Aragona” Salerno, Italy Department of Medicine and Surgery University of Salerno Salerno, Italy ⁎Corresponding author. E-mail addresses: [email protected] [email protected] Rodolfo Citro, MD Heart Department University Hospital “San Giovanni di Dio e Ruggi d’Aragona” Salerno, Italy E-mail address: [email protected] Federico Piscione, MD Heart Department University Hospital “San Giovanni di Dio e Ruggi d’Aragona” Salerno, Italy Department of Medicine and Surgery University of Salerno Salerno, Italy E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.04.040
0735-6757/© 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Di Maio M, et al, Stress-induced cardiomyopathy in pheochromocytoma: the way we treat and the way we think, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.040
2
Correspondence
References [1] 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. [2] Parodi G, Citro R, Bellandi B, Provenza G, Marrani M, Bossone E. Revised clinical diagnostic criteria for Tako-tsubo syndrome: the Tako-tsubo Italian Network proposal. Int J Cardiol 2014;172(1):282–3. [3] Citro R, Rigo F, Ciampi Q, et al. Echocardiographic assessment of regional left ventricular wall motion abnormalities in patients with tako-tsubo cardiomyopathy: comparison with anterior myocardial infarction. Eur J Echocardiogr 2011;12(7):542–9. [4] Citro R, Rigo F, D'Andrea A, et al. Echocardiographic correlates of acute heart failure, cardiogenic shock, and in-hospital mortality in tako-tsubo cardiomyopathy. JACC Cardiovasc Imaging 2014;7(2):119–29. [5] Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy—a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008;5(1):22–9.
[6] Scholten A, Cisco RM, Vriens MR, et al. Pheochromocytoma crisis is not a surgical emergency. J Clin Endocrinol Metab 2013;98:581–91. [7] Martucci VL, Pacak K. Pheochromocytoma and paraganglioma: diagnosis, genetics, management, and treatment. Curr Probl Cancer 2014;38:7–41. [8] Sarathi V, Lila AR, Bandgar TR, Shah NS. Aortoarteritis: could it be a form of catecholamine-induced vasculitis? Indian J Endocrinol Metab 2013;17:163–6. [9] Pontes Tde C, Rufino GP, Gurgel MG, Medeiros AC, Freire EA. Fibromuscular dysplasia: a differential diagnosis of vasculitis. Rev Bras Reumatol 2012;52(1):70–4. [10] Razavi M, Bendixen B, Maley JE, et al. CNS pseudovasculitis in a patient with pheochromocytoma. Neurology 1999;52(5):1088–90. [11] Van Zaane B, Stuijver DJ, Squizzato A, Gerdes VE. Arterial and venous thrombosis in endocrine diseases. Semin Thromb Hemost 2013;39(5):489–95. [12] Kaiser S, Chronakos J, Dietzek AM. Acute upper extremity arterial thrombosis and stroke in an unresected pheochromocytoma. J Vasc Surg 2013;58:1069–72. [13] Vindenes T, Crump N, Casenas R, Wood K. Pheochromocytoma causing cardiomyopathy, ischemic stroke and acute arterial thrombosis: a case report and review of the literature. Conn Med 2013;77(2):95–8. [14] Hou R, Leathersich AM, Ruud BT. Pheochromocytoma presenting with arterial and intracardiac thrombus in a 47-year-old woman: a case report. J Med Case Rep 2011;5:310.
Please cite this article as: Di Maio M, et al, Stress-induced cardiomyopathy in pheochromocytoma: the way we treat and the way we think, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.040
