International Journal of Cardiology 177 (2014) 162–165
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Cardiac rupture in a patient with Takotsubo syndrome triggered by acute myocardial infarction: Two messages Shams Y-Hassan ⁎ Karolinska University Hospital, Huddinge, Department of Cardiology, S-141 86 Stockholm, Sweden
a r t i c l e
i n f o
Article history: Received 1 September 2014 Accepted 20 September 2014 Available online 28 September 2014 Keywords: Acute coronary syndrome Myocardial infarction Myocardial stunning Takotsubo Broken heart syndrome Cardiac rupture
A transient episode of coronary ischemia may induce prolonged but reversible left ventricular dysfunction. This condition has been termed post-ischemic myocardial stunning (PIMS). PIMS has been identified following acute coronary syndrome (ACS), reperfusion, exercise induced angina, angioplasty, ischemic stress induced by dobutamine or dipyridamole, and cardiac surgery [1]. Takotsubo syndrome (TS) is characterized by a transient circumferential (bi-) left ventricular wall motion abnormality resulting in a conspicuous ballooning of the left ventricle during systole [2,3]. One of the serious complications of acute myocardial infarction (AMI) and TS is the left ventricular free wall rupture [4,5]. Myriads of emotional and physical stress factors may trigger TS. In spite of being a strong physical stress factor, ACS including AMI is still regarded as an exclusion criterion for TS [6]. In this report, a case of TS triggered by AMI and complicated by left ventricular free wall rupture at the infarction site is described. Furthermore, the relationship between ACS and TS and the probable cause of cardiac rupture in TS are described. A 73-year-old man presented with a clinical picture of acute pulmonary oedema. He had history of hypertension and diabetes mellitus treated with oral drugs. The patient has been under investigation for amnesia during the last month before the index presentation. He presented with two days of increasing dry cough and breathlessness and admitted with clinical symptoms and signs of pulmonary oedema, which was confirmed with chest X-ray. The patient did not experience ⁎ Tel.: +46 8 58582805; fax: +46 8 58586710. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.09.108 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
chest pain and had no fever. The heart rate was 127/min and blood pressure was normal 120/70 mm Hg. The electrocardiogram showed sinus tachycardia with Q-waves and ST elevation over the inferior leads. There was ST-depression over the anterolateral leads (Fig. 1A). Conventional treatment of pulmonary oedema was initiated. Sex to 8 h after admission, the patient worsened and the blood pressure decreased to systolic 90 mm Hg. Emergency coronary angiography revealed dominant left coronary artery and hypoplastic right coronary artery with tight stenoses in all the three major coronary arteries (white arrows in Fig. 1B, C, D, and E). There was no sign of ongoing coronary occlusion. Left ventriculography showed akinesia in the middle and basal inferior wall and in a broad band of the mid-anterior, mid-lateral and midseptal parts of the left ventricle. There was good contraction of the anterior-basal region and the outermost apical region of the left ventricle (Fig. 2A, B, C and D arrows and asterisks). There was a marked elevation of the high sensitive troponin T (2840 nanog/L) and plasma NTproBNP (3710 ng/L). Treatment with levosimendan was initiated in order to optimize the medical treatment before surgical cardiac revascularization. One day after coronary angiography, the clinical condition of the patient deteriorated with severe hypotension. Emergent bedside echocardiography showed pericardial effusion with signs of cardiac tamponade. The patient died in spite of pericardiocentesis and cardiac resuscitation. Postmortem examination of the heart showed signs of hemopericardium, perforation of the left ventricular free wall at the upper posterior part of the left ventricle with gross signs of acute myocardial infarction in small region around the rupture site (Fig. 3A). There was a sign of old myocardial infarction above the posterior apical region. No remarkable macroscopic change was seen at the anterior, lateral and septal regions of the left ventricle (Fig. 3B). The current case had clear signs of acute inferior myocardial infarction (MI) with new inferior ST-elevations and Q-waves, marked elevation of the high sensitive troponin T, akinesia in the inferior and basal-inferior parts of the left ventricle with macroscopic signs of new infarction and cardiac rupture in the same region on post-mortem examination. However, the left ventricular dysfunction (LVD) extended beyond the inferior part of the left ventricle to involve a broad band of the middle parts of the anterior, lateral and septal regions with hyperkinesia in the basal region of anterior and lateral walls and normal contraction of the outermost apical region (Fig. 2B and D). This pattern of wall motion abnormality resulted in an eye-catching ballooning of the left ventricle during systole (Fig. 2B). The reversibility of the LVD could not be determined because the patient died one day after coronary angiography. However, gross postmortem examination of the anterior, lateral and
S. Y-Hassan / International Journal of Cardiology 177 (2014) 162–165
163
Fig. 1. A, twelve lead electrocardiogram reveals Q-wave and inferior ST-elevations and anterolateral ST-depressions. B, C, D, and E, coronary angiogram showing advanced three-vessel disease with multiple stenosis but no ongoing coronary occlusion. LCA, left coronary artery; RCA, right coronary artery.
septal parts of the left ventricle was completely normal and showed no signs of new or old infarction. The patient has advanced three-vessel disease but no ongoing coronary occlusion. The a-, hypokinesia in the inferior-basal and inferior regions could be accounted by the new and old myocardial infarction but the remainder akinetic parts of the left ventricle did not follow a single or multiple vascular supply region because of normal contractions in the outermost apical region. Consequently the LVD in the present patient is deemed to be caused partly by the acute inferior myocardial infarction and partly by PIMS induced by an ischemic insult. This PIMS has also the characteristic features of TS. The LVD caused by the ballooned stunned myocardium was in fact much more extensive than the limited inferior basal part which was caused by the infarcted myocardium. The pulmonary oedema was most probably caused by the stunned myocardium and the death of the patient was caused by the cardiac rupture at the infarction site. Two important findings in the current case deserve discussion. First: ACS and TS may coexist and ACS including AMI may trigger TS. An acute coronary ischemic event including AMI may “cause” prolonged but reversible LVD which is termed PIMS [1]. There are substantial data supporting the fact that the left ventricular dysfunction in PIMS and TS have the same clinical presentation and course, ECG, cardiac image, scintigraphic, and histopathologic changes and findings [7]. TS has a clinical presentation, which is identical to that of ACS. The development of evolutionary giant T-wave inversions and prolongation of QTc is a typical finding in some of the cases in both PIMS and TS. In both conditions the LVD is reversible during a period of days or weeks [3,6]. The stunned myocardium in PIMS may be “awakened” with the improvement of LVD at least
transiently during inotropic stimulation. Low dose dobutamine stress echocardiography has also shown improvement of LVD in TS [8]. The perfusion, metabolic and innervation scintigraphic examination of the left ventricle in patients with TS has shown normal perfusion, decreased metabolic and innervations uptake [9]. These scintigraphic findings are typical for myocardial stunning. Contraction band necrosis is a well-recognized histopathological finding in successful coronary reperfusion. Coagulative myocytolysis (contraction band necrosis) and colliquative myocytolysis (vacuolization) may be observed in some patients with myocardial infarction [10]. These findings are typically located outside the infarcted region and sometimes remote from the infarcted regions. Contraction band necrosis and vacuolization are also constant histopathological findings in TS [11]. Furthermore, during the last few years, several cases of typical TS, triggered by ACS and coronary spasm, have been reported [12]. The LVD in those cases is actually PIMS. Also in some typical cases of TS, cardiac magnetic resonance (CMR) imaging has shown findings suggestive of myocardial infarction. This may indicate that the myocardial infarction has triggered TS. Eitel et al. [13] studied 59 patients with left ventricular apical ballooning and normal coronary arteries with CMR imaging. The CMR imaging revealed findings suggestive of myocardial infarction in 13 patients (22%). Muellerleile et al. [14] have studied 14 patients having clinically TS with CMR imaging. They found delayed gadolinium enhancement in 6 out of 14 patients. These findings indicate that the delayed enhancement seen in some patients may be either a hitherto unknown feature of TS or it is a sign of myocardial infarction that had triggered TS. Chao et al. [15]
164
S. Y-Hassan / International Journal of Cardiology 177 (2014) 162–165
Fig. 2. Left ventriculography in RAO projection during diastole (A) and systole (B). In this projection, the left mid-ventricular ballooning induced by takotsubo (asterisks and red arrows) and the inferior and inferior-basal akinesia caused by myocardial infarction (thick white arrows) is obvious. Left ventriculography in cranial LAO projection during diastole (C) and systole (D) shows clearly left mid-ventricular ballooning. RAO, right anterior oblique: LAO, left anterior oblique. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
reported on the pattern of left ventricular dysfunction in acute occlusion of the left anterior descending artery (LAD). They found that 26% of patients with acute LAD occlusion had left ventricular contraction pattern typical for TS. Interestingly, the majority of these patients were females. A myriad of physical stress factors, extending from the most serious diseases like subarachnoid hemorrhage and septicemia to the most physiological processes like physical exercise and sexual intercourse, have been reported to precipitate TS [3,6, 16]. Acute myocardial infarction is really a major physical stress factor. It will be unreasonable not to believe that the stress of an ACS and other acute cardiac diseases could also trigger TS. Second: Cardiac rupture in the current case occurred in a patient with TS triggered by AMI. Rupture of the left ventricular free wall is a well-known life threatening and a leading cause of death in patients with AMI [17]. This complication has also been reported in patients with TS [5]. Female gender and old age have been shown to be associated with cardiac rupture in both acute myocardial infarction and TS. In the current case, the cardiac rupture occurred at the myocardial infarction site. Other investigators have also identified signs of myocardial infarction at the site of cardiac rupture in patients with TS. Sacha et al. [18] described a case of left ventricular apical rupture in a patient with TS with fatal outcome. Microscopic examination revealed transmural myocardial necrosis with hemorrhage and mild focal polymorphonuclear leucocyte infiltration at the rupture site. Izumi et al. [19] reported on a
case of TS complicated by ventricular septal perforation. On pathological examination, the ventricular septum showed relatively new signs of myocardial infarction, in which only nuclei were lost, and an old infarct lesion accompanied by hemosiderin deposition was present in the root of the papillary muscle. Kumar et al. [20] have described a case of TS in which the patient developed free left ventricular wall rupture leading to death. Microscopic examination of the rupture site showed necrotic fibers, exhibiting increased eosinophilic staining, contraction band necrosis along with polymorphonuclear cell infiltration and bundles of wavy myocardial fibers. Surrounding the tear, diffuse, patchy infarction of myocardial fibers was seen in that case. This may indicate that some cases of TS complicated by cardiac rupture may have been triggered by AMI where the rupture may actually have been caused by myocardial infarction. In conclusion, a case of TS triggered by AMI and complicated by a cardiac rupture at the infarction site leading to death of the patient is described. The findings in this case indicate that AMI may trigger rather than exclude TS. Furthermore, cardiac rupture in TS may indicate an underlying myocardial infarction as a trigger factor for TS. Conflict of interest The author reports no relationships that could be construed as a conflict of interest.
S. Y-Hassan / International Journal of Cardiology 177 (2014) 162–165
Fig. 3. Postmortem examination of the heart showed 1.2 cm long perforation at the infarcted infero-basal region (A thick black arrow). Gross examination of the anterior, lateral and apical regions of the heart was quite normal (B).
References [1] Kloner RA, Arimie RB, Kay GL, Cannom D, Matthews R, Bhandari A, et al. Evidence for stunned myocardium in humans: a 2001 update. Coron Artery Dis 2001;12:349–56.
165
[2] Y-Hassan S, Yamasaki K. History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies. Int J Cardiol 2013;166: 736–7. [3] Kawai S, Suzuki H, Yamaguchi H, Tanaka K, Sawada H, Aizawa T, et al. Ampulla cardiomyopathy (‘takotusbo’ cardiomyopathy)—reversible left ventricular dysfunction: with ST segment elevation. Jpn Circ J 2000;64:156–9. [4] Wilansky S, Moreno CA, Lester SJ. Complications of myocardial infarction. Crit Care Med 2007;35:S348–54. [5] Kumar S, Kaushik S, Nautiyal A, Choudhary SK, Kayastha BL, Mostow N, et al. Cardiac rupture in takotsubo cardiomyopathy: a systematic review. Clin Cardiol 2011;34: 672–6. [6] 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: 408–17. [7] Y-Hassan S, Jernberg T. Bromocriptine-induced coronary spasm caused acute coronary syndrome, which triggered its own clinical twin—takotsubo syndrome. Cardiology 2011;119:1–6. [8] Uznanska B, Plewka M, Wierzbowska-Drabik K, Chrzanowski L, Kasprzak JD. Early prediction of ventricular recovery in takotsubo syndrome using stress and contrast echocardiography. Med Sci Monit 2009;15:CS89–94. [9] Uchida Y, Nanjo S, Fujimoto S, Yamashina S, Wagatsma K, Nakano H, et al. Scintigraphic studies on the etiology of ampulla cardiomyopathy. J Cardiol 2008;51: 121–30. [10] Samuels MA. Neurogenic heart disease: a unifying hypothesis. Am J Cardiol 1987;60: 15J–9J. [11] Nef HM, Mollmann H, Kostin S, Troidl C, Voss S, Weber M, et al. Tako-tsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery. Eur Heart J 2007;28:2456–64. [12] Y-Hassan S, Henareh L. Spontaneous coronary artery dissection triggered postischemic myocardial stunning and takotsubo syndrome: Two different names for the same condition. Cardiovasc Revasc Med 2013;14:109–12. [13] Eitel I, Behrendt F, Schindler K, Kivelitz D, Gutberlet M, Schuler G, et al. Differential diagnosis of suspected apical ballooning syndrome using contrast-enhanced magnetic resonance imaging. Eur Heart J 2008;29:2651–9. [14] Muellerleile K, Lund G, Groth M, Barmeyer A, Sultan A, Heitzer T, et al. Delayedenhancement magnetic resonance imaging in patients with clinically suspected stress cardiomyopathy (tako-tsubo). Rofo 2010;182:29–35. [15] Chao T, Lindsay J, Collins S, Woldeyes L, Joshi SB, Steinberg DH, et al. Can acute occlusion of the left anterior descending coronary artery produce a typical “takotsubo” left ventricular contraction pattern? Am J Cardiol 2009;104:202–4. [16] Y-Hassan S, Settergren M, Henareh L. Sepsis-induced myocardial depression and takotsubo syndrome. Acute Card Care 2014:1–8. [17] Wehrens XH, Doevendans PA. Cardiac rupture complicating myocardial infarction. Int J Cardiol 2004;95:285–92. [18] Sacha J, Maselko J, Wester A, Szudrowicz Z, Pluta W. Left ventricular apical rupture caused by takotsubo cardiomyopathy—comprehensive pathological heart investigation. Circ J 2007;71:982–5. [19] Izumi K, Tada S, Yamada T. A case of takotsubo cardiomyopathy complicated by ventricular septal perforation. Circ J 2008;72:1540–3. [20] Kumar S, Kaushik S, Nautiyal A, Mostow N, Lazar JM. Pathology findings mimicking acute myocardial infarction in a case of takotsubo cardiomyopathy complicated by cardiac rupture. J Cardiovasc Med 2012;13:478–80.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Cardiac rupture in a patient with Takotsubo syndrome triggered by acute myocardial infarction: Two messages Shams Y-Hassan ⁎ Karolinska University Hospital, Huddinge, Department of Cardiology, S-141 86 Stockholm, Sweden
a r t i c l e
i n f o
Article history: Received 1 September 2014 Accepted 20 September 2014 Available online 28 September 2014 Keywords: Acute coronary syndrome Myocardial infarction Myocardial stunning Takotsubo Broken heart syndrome Cardiac rupture
A transient episode of coronary ischemia may induce prolonged but reversible left ventricular dysfunction. This condition has been termed post-ischemic myocardial stunning (PIMS). PIMS has been identified following acute coronary syndrome (ACS), reperfusion, exercise induced angina, angioplasty, ischemic stress induced by dobutamine or dipyridamole, and cardiac surgery [1]. Takotsubo syndrome (TS) is characterized by a transient circumferential (bi-) left ventricular wall motion abnormality resulting in a conspicuous ballooning of the left ventricle during systole [2,3]. One of the serious complications of acute myocardial infarction (AMI) and TS is the left ventricular free wall rupture [4,5]. Myriads of emotional and physical stress factors may trigger TS. In spite of being a strong physical stress factor, ACS including AMI is still regarded as an exclusion criterion for TS [6]. In this report, a case of TS triggered by AMI and complicated by left ventricular free wall rupture at the infarction site is described. Furthermore, the relationship between ACS and TS and the probable cause of cardiac rupture in TS are described. A 73-year-old man presented with a clinical picture of acute pulmonary oedema. He had history of hypertension and diabetes mellitus treated with oral drugs. The patient has been under investigation for amnesia during the last month before the index presentation. He presented with two days of increasing dry cough and breathlessness and admitted with clinical symptoms and signs of pulmonary oedema, which was confirmed with chest X-ray. The patient did not experience ⁎ Tel.: +46 8 58582805; fax: +46 8 58586710. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.09.108 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
chest pain and had no fever. The heart rate was 127/min and blood pressure was normal 120/70 mm Hg. The electrocardiogram showed sinus tachycardia with Q-waves and ST elevation over the inferior leads. There was ST-depression over the anterolateral leads (Fig. 1A). Conventional treatment of pulmonary oedema was initiated. Sex to 8 h after admission, the patient worsened and the blood pressure decreased to systolic 90 mm Hg. Emergency coronary angiography revealed dominant left coronary artery and hypoplastic right coronary artery with tight stenoses in all the three major coronary arteries (white arrows in Fig. 1B, C, D, and E). There was no sign of ongoing coronary occlusion. Left ventriculography showed akinesia in the middle and basal inferior wall and in a broad band of the mid-anterior, mid-lateral and midseptal parts of the left ventricle. There was good contraction of the anterior-basal region and the outermost apical region of the left ventricle (Fig. 2A, B, C and D arrows and asterisks). There was a marked elevation of the high sensitive troponin T (2840 nanog/L) and plasma NTproBNP (3710 ng/L). Treatment with levosimendan was initiated in order to optimize the medical treatment before surgical cardiac revascularization. One day after coronary angiography, the clinical condition of the patient deteriorated with severe hypotension. Emergent bedside echocardiography showed pericardial effusion with signs of cardiac tamponade. The patient died in spite of pericardiocentesis and cardiac resuscitation. Postmortem examination of the heart showed signs of hemopericardium, perforation of the left ventricular free wall at the upper posterior part of the left ventricle with gross signs of acute myocardial infarction in small region around the rupture site (Fig. 3A). There was a sign of old myocardial infarction above the posterior apical region. No remarkable macroscopic change was seen at the anterior, lateral and septal regions of the left ventricle (Fig. 3B). The current case had clear signs of acute inferior myocardial infarction (MI) with new inferior ST-elevations and Q-waves, marked elevation of the high sensitive troponin T, akinesia in the inferior and basal-inferior parts of the left ventricle with macroscopic signs of new infarction and cardiac rupture in the same region on post-mortem examination. However, the left ventricular dysfunction (LVD) extended beyond the inferior part of the left ventricle to involve a broad band of the middle parts of the anterior, lateral and septal regions with hyperkinesia in the basal region of anterior and lateral walls and normal contraction of the outermost apical region (Fig. 2B and D). This pattern of wall motion abnormality resulted in an eye-catching ballooning of the left ventricle during systole (Fig. 2B). The reversibility of the LVD could not be determined because the patient died one day after coronary angiography. However, gross postmortem examination of the anterior, lateral and
S. Y-Hassan / International Journal of Cardiology 177 (2014) 162–165
163
Fig. 1. A, twelve lead electrocardiogram reveals Q-wave and inferior ST-elevations and anterolateral ST-depressions. B, C, D, and E, coronary angiogram showing advanced three-vessel disease with multiple stenosis but no ongoing coronary occlusion. LCA, left coronary artery; RCA, right coronary artery.
septal parts of the left ventricle was completely normal and showed no signs of new or old infarction. The patient has advanced three-vessel disease but no ongoing coronary occlusion. The a-, hypokinesia in the inferior-basal and inferior regions could be accounted by the new and old myocardial infarction but the remainder akinetic parts of the left ventricle did not follow a single or multiple vascular supply region because of normal contractions in the outermost apical region. Consequently the LVD in the present patient is deemed to be caused partly by the acute inferior myocardial infarction and partly by PIMS induced by an ischemic insult. This PIMS has also the characteristic features of TS. The LVD caused by the ballooned stunned myocardium was in fact much more extensive than the limited inferior basal part which was caused by the infarcted myocardium. The pulmonary oedema was most probably caused by the stunned myocardium and the death of the patient was caused by the cardiac rupture at the infarction site. Two important findings in the current case deserve discussion. First: ACS and TS may coexist and ACS including AMI may trigger TS. An acute coronary ischemic event including AMI may “cause” prolonged but reversible LVD which is termed PIMS [1]. There are substantial data supporting the fact that the left ventricular dysfunction in PIMS and TS have the same clinical presentation and course, ECG, cardiac image, scintigraphic, and histopathologic changes and findings [7]. TS has a clinical presentation, which is identical to that of ACS. The development of evolutionary giant T-wave inversions and prolongation of QTc is a typical finding in some of the cases in both PIMS and TS. In both conditions the LVD is reversible during a period of days or weeks [3,6]. The stunned myocardium in PIMS may be “awakened” with the improvement of LVD at least
transiently during inotropic stimulation. Low dose dobutamine stress echocardiography has also shown improvement of LVD in TS [8]. The perfusion, metabolic and innervation scintigraphic examination of the left ventricle in patients with TS has shown normal perfusion, decreased metabolic and innervations uptake [9]. These scintigraphic findings are typical for myocardial stunning. Contraction band necrosis is a well-recognized histopathological finding in successful coronary reperfusion. Coagulative myocytolysis (contraction band necrosis) and colliquative myocytolysis (vacuolization) may be observed in some patients with myocardial infarction [10]. These findings are typically located outside the infarcted region and sometimes remote from the infarcted regions. Contraction band necrosis and vacuolization are also constant histopathological findings in TS [11]. Furthermore, during the last few years, several cases of typical TS, triggered by ACS and coronary spasm, have been reported [12]. The LVD in those cases is actually PIMS. Also in some typical cases of TS, cardiac magnetic resonance (CMR) imaging has shown findings suggestive of myocardial infarction. This may indicate that the myocardial infarction has triggered TS. Eitel et al. [13] studied 59 patients with left ventricular apical ballooning and normal coronary arteries with CMR imaging. The CMR imaging revealed findings suggestive of myocardial infarction in 13 patients (22%). Muellerleile et al. [14] have studied 14 patients having clinically TS with CMR imaging. They found delayed gadolinium enhancement in 6 out of 14 patients. These findings indicate that the delayed enhancement seen in some patients may be either a hitherto unknown feature of TS or it is a sign of myocardial infarction that had triggered TS. Chao et al. [15]
164
S. Y-Hassan / International Journal of Cardiology 177 (2014) 162–165
Fig. 2. Left ventriculography in RAO projection during diastole (A) and systole (B). In this projection, the left mid-ventricular ballooning induced by takotsubo (asterisks and red arrows) and the inferior and inferior-basal akinesia caused by myocardial infarction (thick white arrows) is obvious. Left ventriculography in cranial LAO projection during diastole (C) and systole (D) shows clearly left mid-ventricular ballooning. RAO, right anterior oblique: LAO, left anterior oblique. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
reported on the pattern of left ventricular dysfunction in acute occlusion of the left anterior descending artery (LAD). They found that 26% of patients with acute LAD occlusion had left ventricular contraction pattern typical for TS. Interestingly, the majority of these patients were females. A myriad of physical stress factors, extending from the most serious diseases like subarachnoid hemorrhage and septicemia to the most physiological processes like physical exercise and sexual intercourse, have been reported to precipitate TS [3,6, 16]. Acute myocardial infarction is really a major physical stress factor. It will be unreasonable not to believe that the stress of an ACS and other acute cardiac diseases could also trigger TS. Second: Cardiac rupture in the current case occurred in a patient with TS triggered by AMI. Rupture of the left ventricular free wall is a well-known life threatening and a leading cause of death in patients with AMI [17]. This complication has also been reported in patients with TS [5]. Female gender and old age have been shown to be associated with cardiac rupture in both acute myocardial infarction and TS. In the current case, the cardiac rupture occurred at the myocardial infarction site. Other investigators have also identified signs of myocardial infarction at the site of cardiac rupture in patients with TS. Sacha et al. [18] described a case of left ventricular apical rupture in a patient with TS with fatal outcome. Microscopic examination revealed transmural myocardial necrosis with hemorrhage and mild focal polymorphonuclear leucocyte infiltration at the rupture site. Izumi et al. [19] reported on a
case of TS complicated by ventricular septal perforation. On pathological examination, the ventricular septum showed relatively new signs of myocardial infarction, in which only nuclei were lost, and an old infarct lesion accompanied by hemosiderin deposition was present in the root of the papillary muscle. Kumar et al. [20] have described a case of TS in which the patient developed free left ventricular wall rupture leading to death. Microscopic examination of the rupture site showed necrotic fibers, exhibiting increased eosinophilic staining, contraction band necrosis along with polymorphonuclear cell infiltration and bundles of wavy myocardial fibers. Surrounding the tear, diffuse, patchy infarction of myocardial fibers was seen in that case. This may indicate that some cases of TS complicated by cardiac rupture may have been triggered by AMI where the rupture may actually have been caused by myocardial infarction. In conclusion, a case of TS triggered by AMI and complicated by a cardiac rupture at the infarction site leading to death of the patient is described. The findings in this case indicate that AMI may trigger rather than exclude TS. Furthermore, cardiac rupture in TS may indicate an underlying myocardial infarction as a trigger factor for TS. Conflict of interest The author reports no relationships that could be construed as a conflict of interest.
S. Y-Hassan / International Journal of Cardiology 177 (2014) 162–165
Fig. 3. Postmortem examination of the heart showed 1.2 cm long perforation at the infarcted infero-basal region (A thick black arrow). Gross examination of the anterior, lateral and apical regions of the heart was quite normal (B).
References [1] Kloner RA, Arimie RB, Kay GL, Cannom D, Matthews R, Bhandari A, et al. Evidence for stunned myocardium in humans: a 2001 update. Coron Artery Dis 2001;12:349–56.
165
[2] Y-Hassan S, Yamasaki K. History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies. Int J Cardiol 2013;166: 736–7. [3] Kawai S, Suzuki H, Yamaguchi H, Tanaka K, Sawada H, Aizawa T, et al. Ampulla cardiomyopathy (‘takotusbo’ cardiomyopathy)—reversible left ventricular dysfunction: with ST segment elevation. Jpn Circ J 2000;64:156–9. [4] Wilansky S, Moreno CA, Lester SJ. Complications of myocardial infarction. Crit Care Med 2007;35:S348–54. [5] Kumar S, Kaushik S, Nautiyal A, Choudhary SK, Kayastha BL, Mostow N, et al. Cardiac rupture in takotsubo cardiomyopathy: a systematic review. Clin Cardiol 2011;34: 672–6. [6] 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: 408–17. [7] Y-Hassan S, Jernberg T. Bromocriptine-induced coronary spasm caused acute coronary syndrome, which triggered its own clinical twin—takotsubo syndrome. Cardiology 2011;119:1–6. [8] Uznanska B, Plewka M, Wierzbowska-Drabik K, Chrzanowski L, Kasprzak JD. Early prediction of ventricular recovery in takotsubo syndrome using stress and contrast echocardiography. Med Sci Monit 2009;15:CS89–94. [9] Uchida Y, Nanjo S, Fujimoto S, Yamashina S, Wagatsma K, Nakano H, et al. Scintigraphic studies on the etiology of ampulla cardiomyopathy. J Cardiol 2008;51: 121–30. [10] Samuels MA. Neurogenic heart disease: a unifying hypothesis. Am J Cardiol 1987;60: 15J–9J. [11] Nef HM, Mollmann H, Kostin S, Troidl C, Voss S, Weber M, et al. Tako-tsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery. Eur Heart J 2007;28:2456–64. [12] Y-Hassan S, Henareh L. Spontaneous coronary artery dissection triggered postischemic myocardial stunning and takotsubo syndrome: Two different names for the same condition. Cardiovasc Revasc Med 2013;14:109–12. [13] Eitel I, Behrendt F, Schindler K, Kivelitz D, Gutberlet M, Schuler G, et al. Differential diagnosis of suspected apical ballooning syndrome using contrast-enhanced magnetic resonance imaging. Eur Heart J 2008;29:2651–9. [14] Muellerleile K, Lund G, Groth M, Barmeyer A, Sultan A, Heitzer T, et al. Delayedenhancement magnetic resonance imaging in patients with clinically suspected stress cardiomyopathy (tako-tsubo). Rofo 2010;182:29–35. [15] Chao T, Lindsay J, Collins S, Woldeyes L, Joshi SB, Steinberg DH, et al. Can acute occlusion of the left anterior descending coronary artery produce a typical “takotsubo” left ventricular contraction pattern? Am J Cardiol 2009;104:202–4. [16] Y-Hassan S, Settergren M, Henareh L. Sepsis-induced myocardial depression and takotsubo syndrome. Acute Card Care 2014:1–8. [17] Wehrens XH, Doevendans PA. Cardiac rupture complicating myocardial infarction. Int J Cardiol 2004;95:285–92. [18] Sacha J, Maselko J, Wester A, Szudrowicz Z, Pluta W. Left ventricular apical rupture caused by takotsubo cardiomyopathy—comprehensive pathological heart investigation. Circ J 2007;71:982–5. [19] Izumi K, Tada S, Yamada T. A case of takotsubo cardiomyopathy complicated by ventricular septal perforation. Circ J 2008;72:1540–3. [20] Kumar S, Kaushik S, Nautiyal A, Mostow N, Lazar JM. Pathology findings mimicking acute myocardial infarction in a case of takotsubo cardiomyopathy complicated by cardiac rupture. J Cardiovasc Med 2012;13:478–80.
