American Journal of Emergency Medicine 33 (2015) 983.e1–983.e4
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Role of cardiac magnetic resonance in the differential diagnosis of Takotsubo cardiomyopathy Abstract Takotsubo cardiomyopathy (TTC) is a transient form of acute heart failure triggered by stressful events and associated with a typical left ventricular ballooning. Cardiac magnetic resonance imaging may be helpful in the diagnosis of this syndrome, particularly when differential diagnosis with acute coronary syndrome (ACS) is not easy. We report 2 cases in which the distinction between TTC and ACS was required because of overlapping clinical presentation and presence of normal coronary angiography. Cardiac magnetic resonance imaging was therefore performed with the aim to distinguish the 2 clinical entities. The presence of localized edema in the midbasal segments of the lateral wall and the presence of subendocardial late enhancement in the basal segment of the inferolateral wall in case 1 were likely to be indicative of myocardial infarction in normal epicardial coronary arteries and microcirculation disease. The typical localization of edema to midapical segments of the left ventricle in the absence of late enhancement in case 2 was indicative of TTC. The evaluation with cardiac magnetic resonance imaging of myocardial edema and myocardial scar/fibrosis allowed the prompt distinction between acute ischemic heart disease and TTC. Cardiac magnetic resonance imaging at admission may provide relevant functional and tissue information that might be useful in the diagnosis of TTC and in differential diagnosis with ACS.
Takotsubo cardiomyopathy (TTC), also known as “apical ballooning” or “broken heart” syndrome is a medical condition firstly described in 1990 by Satoh et al [1-3]. Cardiac magnetic resonance imaging (cMRI) is particularly suitable for the study of patients with TTC, both for the accurate assessment of left and right ventricular function, the evaluation of the kinetics, and the possibility to exclude the presence of thrombi. In addition, cMRI allows a functional approach, by the identification of myocardial edema or possible signs of irreversible myocardial damage (fibrosis/necrosis), thus ruling out other diseases such as acute cardiac myocarditis or acute coronary syndromes (ACS). In this article, we report 2 cases in which cMRI allowed the prompt distinction between acute ischemic heart disease and TTC. Case 1: A 64-year-old woman (RO) affected by hypertension and persistent atrial fibrillation was referred to emergency department for typical chest pain, dyspnea, and sweating. Electrocardiogram (ECG) showed sinus rhythm with poor R-wave progression and negative T waves in the precordial leads and long QT interval. Blood pressure at admission was 170/120 mm Hg; troponin I values, 0.25 ng/mL; serum creatinine, 1.44 mg/dL; total cholesterol, 252 mg/dL; and blood glucose, 144 mg/dL. The patient was therefore admitted to the acute cardiac care unit with a diagnosis of suspected ACS. Echocardiogram, however, showed severe left ventricular (LV) dysfunction (LV ejection fraction [EF], 30%)
Fig. 1. Left, Cine balanced turbo field echo 4-chamber view (end-systolic phase): the arrow shows the akinesis of the right ventricular apex.
Fig. 2. Right, Black-blood-T2-short-tau-inversion recovery short axis view: signal hyperintensity of lateral wall and expression of myocardial edema (arrows).
0735-6757/© 2014 Elsevier Inc. All rights reserved.
983.e2
G. Casavecchia et al. / American Journal of Emergency Medicine 33 (2015) 983.e1–983.e4
Fig. 3. Phase-sensitive inversion recovery turbo field echo 4-chamber and short axis view: subendocardial LGE of the basal segment of the inferolateral wall (arrows).
(Fig. 1; Video 1); and hypokinesis of the remaining segments. The black-blood-T2-short-tau-inversion recovery (BB-T2-STIR) sequences showed transmural myocardial edema in midbasal segments of the lateral wall (Fig. 2) with presence, at phase-sensitive inversion recovery turbo field echo sequences, of subendocardial late enhancement at the basal segment of the inferolateral wall (Fig. 3). One week later, however, echocardiogram examination showed a partial recovery of LVEF (48%) with LV inferior wall hypokinesis.
Fig. 4. Left, Cine balanced turbo field echo 4-chamber view (end-systolic phase): recovery of apical right ventricular akinesis.
with apical akinesis and hypokinesis of the remaining segments. Coronary angiography showed normal coronary arteries. The patient underwent cMRI, which showed a 37% LVEF; indexed end-diastolic volume, 81 mL/m 2; indexed end-systolic volume (iESV), 51 mL/m 2; LV apical akinesis; involvement of right ventricular apex
Five months later, the patient underwent cMRI control, with evidence of partial recovery of LVEF (47%; indexed end-diastolic volume, 88 mL/m 2; iESV, 47 mL/m2), hypokinesis of the lateral wall with recovery of previously akinetic right ventricular apex (Figs. 4 and 5; Video 2). No alterations of the signal in the sequences BB-T2-STIR were found, whereas in phase-sensitive inversion recovery turbo field echo sequences, subendocardial late enhancement of the basal segment of the inferolateral wall was confirmed (Fig. 6). Case 2: A 72-year-old woman (SI) affected by hypertension, dyslipidemia, psoriatic arthritis, hypothyroidism, history of recurrent atypical chest pain treated with paracetamol, and in the week before hospitalization, finding of low blood pressure, presented to the emergency department with weakness and hypotension (80/50 mm Hg). Blood tests showed a rise in troponin I levels (2.52 ng/mL). The ECG showed sinus tachycardia with ST-elevation in V2 to V5 leads and prolonged QT, and echocardiography a severe LV dysfunction (LVEF, 25%) with typical “apical ballooning.” Coronary angiography, again, was normal. Cardiac magnetic resonance imaging showed LV dysfunction (LVEF, 33%; iESV, 41.5 mL/m 2 ), akinetic LV midapical segments,
Fig. 5. Right, Cine balanced turbo field echo right ventricle 2-chamber view (systolic and diastolic phase): recovery of apical right ventricular akinesis.
G. Casavecchia et al. / American Journal of Emergency Medicine 33 (2015) 983.e1–983.e4
983.e3
Fig. 6. Phase-sensitive inversion recovery turbo field echo 4-chamber and short axis view: subendocardial LGE of basal segment of inferolateral wall (arrows).
Fig. 7. Cine balanced turbo field echo 2-chamber view (diastolic phase to left and systolic phase to right): typical apical ballooning in Takotsubo syndrome.
and basal hyperkinesis (Fig. 7; Video 3). The BB-T2-STIR sequences showed transmural myocardial edema at LV midapical segments (Fig. 8) in the absence, at phase-sensitive inversion recovery turbo field echo (PSIR-TFE) sequences, of late enhancement (Fig. 9). The echocardiogram at discharge showed partial recovery of LVEF (38%). Six months later, a follow-up cMRI showed complete recovery of LVEF (57%) and normal segmental kinetics (Fig. 10; Video 4). The BB-
T2-STIR sequences did not show signal anomalies, and PSIR-TFE did not document myocardial fibrosis/scar. Differential diagnosis of TTC is crucial for avoiding unnecessary potential harmful therapies. The diagnosis is mainly based on the exclusion of signs suggestive for ACS (demonstration of normal coronary arteries at angiography). Echocardiography is ideal in detecting ventricular (apical) ballooning, a landmark in the diagnosis of TTC although not absolutely specific.
Fig. 8. Left, Black-blood-T2-short-tau-inversion recovery short axis: signal hyperintensity in the midsegments of left ventricle.
Fig. 9. Right, Phase-sensitive inversion recovery turbo field echo 4-chamber view: absence of late enhancement.
983.e4
G. Casavecchia et al. / American Journal of Emergency Medicine 33 (2015) 983.e1–983.e4
Fig. 10. Cine balanced turbo field echo 2-chamber view (diastolic phase to left and systolic phase to right): complete recovery of LV contractility.
Cardiac magnetic resonance imaging is a noninvasive imaging technique that allows the distinction of different clinical entities presenting as a suspected ACS. A peculiar aspect of TTC is the absence of late gadolinium enhancement (LGE) [4], although some reports describe small areas of LGE in apical segments [5]. Experimental data show that delayed washout of gadolinium may be caused not only by permanent myocardial necrosis/ fibrosis but also by increased interstitial water content such that associated with transient myocardial edema [6]. The subtle changes are called myocardial edema-related late myocardial enhancement and not true scarring. The signal hyperintensity on BB-T2-STIR correlates with the water content in the myocardial wall: in TTC, this sequence shows a typical distribution of the edema in the midapical segments [7]. The sequences for the study of dynamic first pass perfusion generally do not show abnormalities, although some authors have reported perfusion defects consistent with abnormal microvascular flow [8]. The cMRI can also highlight some of the complications of this syndrome such as LV apical thrombosis. The clinical presentation of case 1 and the risk factors present were highly suspected for ACS; in spite of that, ECG anomalies, apical ballooning, and the absence of coronary artery disease were suggestive for TTC. Main discordant note was the absence at echocardiography of basal hyperkinesis, another landmark of TTC. In such a case, cMRI showed its additional diagnostic value, not confirming the first provisional diagnosis of TTC. The presence of localized edema in the midbasal segments of the lateral wall and the presence of subendocardial late enhancement in the basal segment of the inferolateral wall, in the absence of epicardial coronary stenosis, were likely to be indicative of myocardial infarction in normal epicardial coronary arteries [9] and impaired microcirculation, which resulted in myocardial stunning with subsequent recovery in the following months. In case 2, instead, the clinical and instrumental data were suggestive for a TTC, further confirmed at cMRI based on typical localized edema to midapical segments of the left ventricle, in the absence of late enhancement. Cardiac magnetic resonance imaging may provide incremental diagnostic information and could allow the detection of relevant functional and tissue changes useful for the diagnostic work up of TTC. The combination of typical regional wall motion abnormalities and presence of reversible myocardial injury/absence of significant irreversible tissue injury may be helpful in differentiation of TTC from ACS in overlapping clinical presentations. Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ajem.2014.11.040.
Graziapia Casavecchia, MD Cardiologia Universitaria, Ospedali Riuniti, Foggia, Italy Matteo Gravina, MD Radiologia Universitaria, Ospedali Riuniti, Foggia, Italy
Antonio Totaro, MD Deparment of Medical & Surgical Sciences University of Foggia, Foggia, Italy Riccardo Ieva, MD Cardiologia Universitaria, Ospedali Riuniti, Foggia, Italy Roberta Vinci, MD Luca Macarini, MD Deparment of Medical & Surgical Sciences, University of Foggia, Italy Matteo Di Biase, MD Natale Daniele Brunetti, MD, PhD⁎ Department of Medical & Surgical Sciences University of Foggia, Foggia, Italy ⁎Corresponding author. Viale Pinto 1, 71100 Foggia, Italy Tel.:+393389112358; Fax:+390881745424 E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.11.040
References [1] Satoh H, Tateishi H, Uchida T, Dote K, Ishihara M. Stunned myocardium with specific tsubo-type left ventriculographic configuration due to multi vessel spasm. In: Kodama K, Haze K, Hon M, editors. Clinical aspects of myocardial injury: from ischemia to heart failure. Tokyo: Kagakuhyouronsya Co.; 1990. p. 56–64. [2] Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41: 737–42. [3] Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation 2008;118:2754–27623. [4] Assomull RG, Lyne JC, Keenan N, Gulati A, Bunce NH, Davies SW, et al. The role of cardiovascular magnetic resonance in patients presenting with chest pain, raised troponin, and unobstructed coronary arteries. Eur Heart J 2007;28: 1242–9. [5] Naruse Y, Sato A, Kasahara K, Makino K, Sano M, Takeuchi Y, et al. The clinical impact of late gadolinium enhancement in Takotsubo cardiomyopathy: serial analysis of cardiovascular magnetic resonance images. J Cardiovasc Magn Reson 2011;13:67. [6] Inoue S, Murakami Y, Ochiai K, Kitamura J, Ishibashi Y, Kawamitsu H, et al. The contributory role of interstitial water in Gd-DTPA-enhanced MRI in myocardial infarction. J Magn Reson Imaging 1999;9:215–9. [7] Otsuka Y, Noguchi T, Goto Y, Nonogi H, Yamada N. Hyperintensity on T2-weighted magnetic resonance imaging in Takotsubo cardiomyopathy. Int J Cardiol 2008;130: 113–6. [8] Elesber A, Bybee KA, Prasad A, Wright RS, Lerman A, Rihal CS. Myocardial perfusion in apical ballooning syndrome correlate of myocardial injury. Am Heart J 2006;152: 469.e9–469.e13. [9] Niccoli G, Scalone G, Crea F. L'infarto miocardico acuto a coronarie normali: cosa ci sfugge? G Ital Cardiol 2013;14:817–27.
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Role of cardiac magnetic resonance in the differential diagnosis of Takotsubo cardiomyopathy Abstract Takotsubo cardiomyopathy (TTC) is a transient form of acute heart failure triggered by stressful events and associated with a typical left ventricular ballooning. Cardiac magnetic resonance imaging may be helpful in the diagnosis of this syndrome, particularly when differential diagnosis with acute coronary syndrome (ACS) is not easy. We report 2 cases in which the distinction between TTC and ACS was required because of overlapping clinical presentation and presence of normal coronary angiography. Cardiac magnetic resonance imaging was therefore performed with the aim to distinguish the 2 clinical entities. The presence of localized edema in the midbasal segments of the lateral wall and the presence of subendocardial late enhancement in the basal segment of the inferolateral wall in case 1 were likely to be indicative of myocardial infarction in normal epicardial coronary arteries and microcirculation disease. The typical localization of edema to midapical segments of the left ventricle in the absence of late enhancement in case 2 was indicative of TTC. The evaluation with cardiac magnetic resonance imaging of myocardial edema and myocardial scar/fibrosis allowed the prompt distinction between acute ischemic heart disease and TTC. Cardiac magnetic resonance imaging at admission may provide relevant functional and tissue information that might be useful in the diagnosis of TTC and in differential diagnosis with ACS.
Takotsubo cardiomyopathy (TTC), also known as “apical ballooning” or “broken heart” syndrome is a medical condition firstly described in 1990 by Satoh et al [1-3]. Cardiac magnetic resonance imaging (cMRI) is particularly suitable for the study of patients with TTC, both for the accurate assessment of left and right ventricular function, the evaluation of the kinetics, and the possibility to exclude the presence of thrombi. In addition, cMRI allows a functional approach, by the identification of myocardial edema or possible signs of irreversible myocardial damage (fibrosis/necrosis), thus ruling out other diseases such as acute cardiac myocarditis or acute coronary syndromes (ACS). In this article, we report 2 cases in which cMRI allowed the prompt distinction between acute ischemic heart disease and TTC. Case 1: A 64-year-old woman (RO) affected by hypertension and persistent atrial fibrillation was referred to emergency department for typical chest pain, dyspnea, and sweating. Electrocardiogram (ECG) showed sinus rhythm with poor R-wave progression and negative T waves in the precordial leads and long QT interval. Blood pressure at admission was 170/120 mm Hg; troponin I values, 0.25 ng/mL; serum creatinine, 1.44 mg/dL; total cholesterol, 252 mg/dL; and blood glucose, 144 mg/dL. The patient was therefore admitted to the acute cardiac care unit with a diagnosis of suspected ACS. Echocardiogram, however, showed severe left ventricular (LV) dysfunction (LV ejection fraction [EF], 30%)
Fig. 1. Left, Cine balanced turbo field echo 4-chamber view (end-systolic phase): the arrow shows the akinesis of the right ventricular apex.
Fig. 2. Right, Black-blood-T2-short-tau-inversion recovery short axis view: signal hyperintensity of lateral wall and expression of myocardial edema (arrows).
0735-6757/© 2014 Elsevier Inc. All rights reserved.
983.e2
G. Casavecchia et al. / American Journal of Emergency Medicine 33 (2015) 983.e1–983.e4
Fig. 3. Phase-sensitive inversion recovery turbo field echo 4-chamber and short axis view: subendocardial LGE of the basal segment of the inferolateral wall (arrows).
(Fig. 1; Video 1); and hypokinesis of the remaining segments. The black-blood-T2-short-tau-inversion recovery (BB-T2-STIR) sequences showed transmural myocardial edema in midbasal segments of the lateral wall (Fig. 2) with presence, at phase-sensitive inversion recovery turbo field echo sequences, of subendocardial late enhancement at the basal segment of the inferolateral wall (Fig. 3). One week later, however, echocardiogram examination showed a partial recovery of LVEF (48%) with LV inferior wall hypokinesis.
Fig. 4. Left, Cine balanced turbo field echo 4-chamber view (end-systolic phase): recovery of apical right ventricular akinesis.
with apical akinesis and hypokinesis of the remaining segments. Coronary angiography showed normal coronary arteries. The patient underwent cMRI, which showed a 37% LVEF; indexed end-diastolic volume, 81 mL/m 2; indexed end-systolic volume (iESV), 51 mL/m 2; LV apical akinesis; involvement of right ventricular apex
Five months later, the patient underwent cMRI control, with evidence of partial recovery of LVEF (47%; indexed end-diastolic volume, 88 mL/m 2; iESV, 47 mL/m2), hypokinesis of the lateral wall with recovery of previously akinetic right ventricular apex (Figs. 4 and 5; Video 2). No alterations of the signal in the sequences BB-T2-STIR were found, whereas in phase-sensitive inversion recovery turbo field echo sequences, subendocardial late enhancement of the basal segment of the inferolateral wall was confirmed (Fig. 6). Case 2: A 72-year-old woman (SI) affected by hypertension, dyslipidemia, psoriatic arthritis, hypothyroidism, history of recurrent atypical chest pain treated with paracetamol, and in the week before hospitalization, finding of low blood pressure, presented to the emergency department with weakness and hypotension (80/50 mm Hg). Blood tests showed a rise in troponin I levels (2.52 ng/mL). The ECG showed sinus tachycardia with ST-elevation in V2 to V5 leads and prolonged QT, and echocardiography a severe LV dysfunction (LVEF, 25%) with typical “apical ballooning.” Coronary angiography, again, was normal. Cardiac magnetic resonance imaging showed LV dysfunction (LVEF, 33%; iESV, 41.5 mL/m 2 ), akinetic LV midapical segments,
Fig. 5. Right, Cine balanced turbo field echo right ventricle 2-chamber view (systolic and diastolic phase): recovery of apical right ventricular akinesis.
G. Casavecchia et al. / American Journal of Emergency Medicine 33 (2015) 983.e1–983.e4
983.e3
Fig. 6. Phase-sensitive inversion recovery turbo field echo 4-chamber and short axis view: subendocardial LGE of basal segment of inferolateral wall (arrows).
Fig. 7. Cine balanced turbo field echo 2-chamber view (diastolic phase to left and systolic phase to right): typical apical ballooning in Takotsubo syndrome.
and basal hyperkinesis (Fig. 7; Video 3). The BB-T2-STIR sequences showed transmural myocardial edema at LV midapical segments (Fig. 8) in the absence, at phase-sensitive inversion recovery turbo field echo (PSIR-TFE) sequences, of late enhancement (Fig. 9). The echocardiogram at discharge showed partial recovery of LVEF (38%). Six months later, a follow-up cMRI showed complete recovery of LVEF (57%) and normal segmental kinetics (Fig. 10; Video 4). The BB-
T2-STIR sequences did not show signal anomalies, and PSIR-TFE did not document myocardial fibrosis/scar. Differential diagnosis of TTC is crucial for avoiding unnecessary potential harmful therapies. The diagnosis is mainly based on the exclusion of signs suggestive for ACS (demonstration of normal coronary arteries at angiography). Echocardiography is ideal in detecting ventricular (apical) ballooning, a landmark in the diagnosis of TTC although not absolutely specific.
Fig. 8. Left, Black-blood-T2-short-tau-inversion recovery short axis: signal hyperintensity in the midsegments of left ventricle.
Fig. 9. Right, Phase-sensitive inversion recovery turbo field echo 4-chamber view: absence of late enhancement.
983.e4
G. Casavecchia et al. / American Journal of Emergency Medicine 33 (2015) 983.e1–983.e4
Fig. 10. Cine balanced turbo field echo 2-chamber view (diastolic phase to left and systolic phase to right): complete recovery of LV contractility.
Cardiac magnetic resonance imaging is a noninvasive imaging technique that allows the distinction of different clinical entities presenting as a suspected ACS. A peculiar aspect of TTC is the absence of late gadolinium enhancement (LGE) [4], although some reports describe small areas of LGE in apical segments [5]. Experimental data show that delayed washout of gadolinium may be caused not only by permanent myocardial necrosis/ fibrosis but also by increased interstitial water content such that associated with transient myocardial edema [6]. The subtle changes are called myocardial edema-related late myocardial enhancement and not true scarring. The signal hyperintensity on BB-T2-STIR correlates with the water content in the myocardial wall: in TTC, this sequence shows a typical distribution of the edema in the midapical segments [7]. The sequences for the study of dynamic first pass perfusion generally do not show abnormalities, although some authors have reported perfusion defects consistent with abnormal microvascular flow [8]. The cMRI can also highlight some of the complications of this syndrome such as LV apical thrombosis. The clinical presentation of case 1 and the risk factors present were highly suspected for ACS; in spite of that, ECG anomalies, apical ballooning, and the absence of coronary artery disease were suggestive for TTC. Main discordant note was the absence at echocardiography of basal hyperkinesis, another landmark of TTC. In such a case, cMRI showed its additional diagnostic value, not confirming the first provisional diagnosis of TTC. The presence of localized edema in the midbasal segments of the lateral wall and the presence of subendocardial late enhancement in the basal segment of the inferolateral wall, in the absence of epicardial coronary stenosis, were likely to be indicative of myocardial infarction in normal epicardial coronary arteries [9] and impaired microcirculation, which resulted in myocardial stunning with subsequent recovery in the following months. In case 2, instead, the clinical and instrumental data were suggestive for a TTC, further confirmed at cMRI based on typical localized edema to midapical segments of the left ventricle, in the absence of late enhancement. Cardiac magnetic resonance imaging may provide incremental diagnostic information and could allow the detection of relevant functional and tissue changes useful for the diagnostic work up of TTC. The combination of typical regional wall motion abnormalities and presence of reversible myocardial injury/absence of significant irreversible tissue injury may be helpful in differentiation of TTC from ACS in overlapping clinical presentations. Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ajem.2014.11.040.
Graziapia Casavecchia, MD Cardiologia Universitaria, Ospedali Riuniti, Foggia, Italy Matteo Gravina, MD Radiologia Universitaria, Ospedali Riuniti, Foggia, Italy
Antonio Totaro, MD Deparment of Medical & Surgical Sciences University of Foggia, Foggia, Italy Riccardo Ieva, MD Cardiologia Universitaria, Ospedali Riuniti, Foggia, Italy Roberta Vinci, MD Luca Macarini, MD Deparment of Medical & Surgical Sciences, University of Foggia, Italy Matteo Di Biase, MD Natale Daniele Brunetti, MD, PhD⁎ Department of Medical & Surgical Sciences University of Foggia, Foggia, Italy ⁎Corresponding author. Viale Pinto 1, 71100 Foggia, Italy Tel.:+393389112358; Fax:+390881745424 E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.11.040
References [1] Satoh H, Tateishi H, Uchida T, Dote K, Ishihara M. Stunned myocardium with specific tsubo-type left ventriculographic configuration due to multi vessel spasm. In: Kodama K, Haze K, Hon M, editors. Clinical aspects of myocardial injury: from ischemia to heart failure. Tokyo: Kagakuhyouronsya Co.; 1990. p. 56–64. [2] Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41: 737–42. [3] Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation 2008;118:2754–27623. [4] Assomull RG, Lyne JC, Keenan N, Gulati A, Bunce NH, Davies SW, et al. The role of cardiovascular magnetic resonance in patients presenting with chest pain, raised troponin, and unobstructed coronary arteries. Eur Heart J 2007;28: 1242–9. [5] Naruse Y, Sato A, Kasahara K, Makino K, Sano M, Takeuchi Y, et al. The clinical impact of late gadolinium enhancement in Takotsubo cardiomyopathy: serial analysis of cardiovascular magnetic resonance images. J Cardiovasc Magn Reson 2011;13:67. [6] Inoue S, Murakami Y, Ochiai K, Kitamura J, Ishibashi Y, Kawamitsu H, et al. The contributory role of interstitial water in Gd-DTPA-enhanced MRI in myocardial infarction. J Magn Reson Imaging 1999;9:215–9. [7] Otsuka Y, Noguchi T, Goto Y, Nonogi H, Yamada N. Hyperintensity on T2-weighted magnetic resonance imaging in Takotsubo cardiomyopathy. Int J Cardiol 2008;130: 113–6. [8] Elesber A, Bybee KA, Prasad A, Wright RS, Lerman A, Rihal CS. Myocardial perfusion in apical ballooning syndrome correlate of myocardial injury. Am Heart J 2006;152: 469.e9–469.e13. [9] Niccoli G, Scalone G, Crea F. L'infarto miocardico acuto a coronarie normali: cosa ci sfugge? G Ital Cardiol 2013;14:817–27.
