Left Ventricular Rupture Associated With Takotsubo Cardiomyopathy
2004; Elsevier BV; Volume: 79; Issue: 6 Linguagem: Inglês
10.4065/79.6.821
ISSN1942-5546
AutoresYoshihiro J. Akashi, Tamotsu Tejima, Harumizu Sakurada, Hisao Matsuda, Kengo Suzuki, Kensuke Kawasaki, Katsuhiko Tsuchiya, Nobuyuki Hashimoto, Haruki Musha, Masayoshi Sakakibara, Kiyoshi Nakazawa, Fumihiko Miyake,
Tópico(s)Cardiac Imaging and Diagnostics
ResumoA 70-year-old woman was admitted to the hospital with chest discomfort after quarreling with her neighbors. Electrocardiography revealed ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6. Coronary angiography demonstrated normal arteries, but left ventriculography showed apical akinesis and basal hyperkinesis. Takotsubo cardiomyopathy was diagnosed on the basis of these characteristic findings. The creatine kinase and creatine kinase-MB concentrations were elevated at admission and reached maximum levels 6 hours after admission. The plasma level of brain natriuretic peptide was 10.7 pg/mL (reference range, <18.4 pg/mL) on the first hospital day. ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6 persisted at 72 hours after admission. On the third hospital day, sudden rupture of the left ventricle occurred, and despite extensive resuscitation efforts, the patient died. Takotsubo cardiomyopathy presents in a manner similar to that of acute myocardial infarction, but ventricular systolic function usually returns to normal within a few weeks. To our knowledge, this is the first reported case of fatal left ventricular rupture associated with takotsubo cardiomyopathy. We suggest that takotsubo cardiomyopathy may be a newly recognized cause of sudden cardiac death. A 70-year-old woman was admitted to the hospital with chest discomfort after quarreling with her neighbors. Electrocardiography revealed ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6. Coronary angiography demonstrated normal arteries, but left ventriculography showed apical akinesis and basal hyperkinesis. Takotsubo cardiomyopathy was diagnosed on the basis of these characteristic findings. The creatine kinase and creatine kinase-MB concentrations were elevated at admission and reached maximum levels 6 hours after admission. The plasma level of brain natriuretic peptide was 10.7 pg/mL (reference range, <18.4 pg/mL) on the first hospital day. ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6 persisted at 72 hours after admission. On the third hospital day, sudden rupture of the left ventricle occurred, and despite extensive resuscitation efforts, the patient died. Takotsubo cardiomyopathy presents in a manner similar to that of acute myocardial infarction, but ventricular systolic function usually returns to normal within a few weeks. To our knowledge, this is the first reported case of fatal left ventricular rupture associated with takotsubo cardiomyopathy. We suggest that takotsubo cardiomyopathy may be a newly recognized cause of sudden cardiac death. Numerous reports have described a type of left ventricular dysfunction that resembles acute myocardial infarction but in which cardiac catheterization reveals normal coronary arteries and the left ventricle is shaped like a takotsubo1–18 (the Japanese word for an octopus fishing pot with a round bottom and a narrow neck). Hence, this syndrome is frequently referred to as takotsubo cardiomyopathy.1Kawai S Suzuki H Yamaguchi H et al.Ampulla cardiomyopathy ('Takotsubo' cardiomyopathy)—reversible left ventricular dysfunction: with ST segment elevation [published correction appears in Jpn Circ J. 2000;64:237].Jpn Circ J. 2000; 64: 156-159Crossref PubMed Scopus (283) Google Scholar, 3Tsuchihashi K Ueshima K Uchida T Angina Pectoris-Myocardial Infarction Investigations in Japan et al.Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction.J Am Coll Cardiol. 2001; 38: 11-18Abstract Full Text Full Text PDF PubMed Scopus (1346) Google Scholar, 4Kurisu S Sato H Kawagoe T et al.Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction.Am Heart J. 2002; 143: 448-455Abstract Full Text Full Text PDF PubMed Scopus (731) Google Scholar, 5Ueyama T Kasamatsu K Hano T Yamamoto K Tsuruo Y Nishio I Emotional stress induces transient left ventricular hypocontraction in the rat via activation of cardiac adrenoceptors: a possible animal model of 'tako-tsubo' cardiomyopathy.Circ J. 2002; 66: 712-713Crossref PubMed Scopus (279) Google Scholar, 6Akashi YJ Sakakibara M Miyake F Reversible left ventricular dysfunction "takotsubo" cardiomyopathy associated with pneumothorax.Heart. 2002; 87: E1Crossref PubMed Scopus (59) Google Scholar, 7Akashi YJ Nakazawa K Sakakibara M Miyake F Sasaka K Reversible left ventricular dysfunction "takotsubo" cardiomyopathy related to catecholamine cardiotoxicity.J Electrocardiol. 2002; 35: 351-356Abstract Full Text PDF PubMed Scopus (84) Google Scholar, 8Abe 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: 737-742Abstract Full Text Full Text PDF PubMed Scopus (541) Google Scholar, 9Kurisu S Inoue I Kawagoe T et al.Myocardial perfusion and fatty acid metabolism in patients with tako-tsubo-like left ventricular dysfunction.J Am Coll Cardiol. 2003; 41: 743-748Abstract Full Text Full Text PDF PubMed Scopus (279) Google Scholar, 10Akashi YJ Nakazawa K Kida K et al.Reversible ventricular dysfunction (takotsubo cardiomyopathy) following polymorphic ventricular tachycardia.Can J Cardiol. 2003; 19: 449-451PubMed Google Scholar, 11Kurisu S Inoue I Kawagoe T et al.Left ventricular apical thrombus formation in a patient with suspected Tako-Tsubo-like left ventricular dysfunction.Circ J. 2003; 67: 556-558Crossref PubMed Scopus (63) Google Scholar, 12Akashi YJ Nakazawa K Sakakibara M Miyake F Koike J Sasaka K The clinical features of takotsubo cardiomyopathy.QJM. 2003; 96: 563-573Crossref PubMed Scopus (272) Google Scholar Typically, left ventricular function normalizes within a few weeks. This type of cardiomyopathy has been observed predominantly in women older than 60 years. Physical or emotional stress usually precedes the onset of symptoms. The pathogenesis has not been fully clarified, but catecholamine cardiotoxicity and adrenoceptor hyperreactivity have been suggested as potential causes.10Akashi YJ Nakazawa K Kida K et al.Reversible ventricular dysfunction (takotsubo cardiomyopathy) following polymorphic ventricular tachycardia.Can J Cardiol. 2003; 19: 449-451PubMed Google Scholar, 12Akashi YJ Nakazawa K Sakakibara M Miyake F Koike J Sasaka K The clinical features of takotsubo cardiomyopathy.QJM. 2003; 96: 563-573Crossref PubMed Scopus (272) Google Scholar, 16Salathe M Weiss P Ritz R Rapid reversal of heart failure in a patient with phaeochromocytoma and catecholamine-induced cardiomyopathy who was treated with captopril.Br Heart J. 1992; 68: 527-528Crossref PubMed Scopus (68) Google Scholar, 19Ueyama T Senba E Kasamatsu K et al.Molecular mechanism of emotional stress-induced and catecholamine-induced heart attack.J Cardiovasc Pharmacol. 2003; 41: S115-S118PubMed Google Scholar We describe a case of takotsubo cardiomyopathy associated with fatal rupture of the left ventricle. A 70-year-old woman was admitted to our hospital with continuous chest discomfort 2 hours after a quarrel with her neighbors. She had had untreated hypertension and hyperlipidemia for several years but had no history of similar chest symptoms and no family history of heart disease, including sudden cardiac death. At her annual medical checkup 2 weeks before admission, electrocardiography (ECG) revealed normal findings (Figure 1). On admission, the patient's pulse rate was 81/min, her blood pressure was 171/95 mm Hg, and her temperature was 35.8°C. Routine laboratory studies disclosed the following values (reference ranges shown parenthetically): leukocyte count, 12.4 × 109/L; hemoglobin, 13.5 g/dL; platelet count, 209 × 109/L; aspartate aminotransferase, 69 U/L; lactate dehydrogenase, 294 U/L; creatine kinase, 546 U/L (16-129 U/L); creatine kinase-MB isoenzyme, 61 U/L (<25 U/L); potassium, 4.3 mEq/L; calcium, 9.2 mg/dL; and C-reactive protein, 1.44 mg/dL. The plasma level of brain natriuretic peptide was 10.7 pg/mL (<18.4 pg/mL). Electrocardiography revealed normal sinus rhythm (72 beats/min) with ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6. Pathologic Q waves were present in leads V1 through V5, which represented a change from her preadmission ECG (Figure 1). Echocardiography revealed akinesis of the left ventricle, except in the basal region (the apical wall thickness was 6 mm). Left ventricular outflow tract obstruction was not present on Doppler echocardiographic examination. Emergent cardiac catheterization was performed within 30 minutes of admission. Coronary angiography showed normal arteries with TIMI (Thrombolysis in Myocardial Infarction) grade 3 flow (Figure 2, top), but left ventriculography revealed abnormal wall motion with apical akinesis and basal hyperkinesis (Figure 2, bottom). The left ventricular ejection fraction, calculated using the Simpson method,20Chapman CB Baker O Reynolds J Bonte FJ Use of biplane cinefluorography for measurement of ventricular volume.Circulation. 1958; 18: 1105-1117Crossref PubMed Scopus (226) Google Scholar was 51%. The left ventricular end-systolic pressure was 102 mm Hg, and the left ventricular end-diastolic pressure was 12 mm Hg. There were no pressure gradients between the left ventricular apex, midportion, and outflow tract. Provocation testing for coronary spasm was not performed. Echocardiography showed no evidence of pericardial effusion in the acute phase. The patient's symptoms subsided soon after admission with infusion of isosorbide dinitrate and administration of a mild sedative. Because of the aneurysmal change in the left ventricular apex, anticoagulant therapy was initiated (10,000 U/d of heparin intravenously). Six hours after admission, the creatine kinase and creatine kinase-MB concentrations reached maximum values of 748 U/L and 72 U/L, respectively. Twenty-four hours after admission, ECG showed increased ST-segment elevation in leads II, III, aVF, and V2 through V6, which persisted at 72 hours (Figure 1). However, none of the patient's laboratory values indicated a worsening condition, and she was fully conscious and oriented. During repeated echocardiography 73 hours after admission, the patient complained of chest discomfort and suddenly lost consciousness; she had no measurable blood pressure. Echocardiography showed a large anechoic zone around the heart, suggesting pericardial effusion due to cardiac rupture. We attempted resuscitation with percutaneous cardiopulmonary support, intra-aortic balloon counterpulsation, and temporary cardiac pacing in the coronary care unit. Because the patient's hemodynamics remained unstable, median sternotomy was performed to attempt direct suture of the cardiac rupture. A rupture measuring 5 mm was identified 20 mm from the left ventricular apex, but it could not be closed completely. The patient died 75 hours after admission. In accordance with her family's wishes, an autopsy was not performed. Numerous reports have described patients with reversible left ventricular dysfunction and symptoms similar to those of acute myocardial infarction without coronary artery stenoses.1Kawai S Suzuki H Yamaguchi H et al.Ampulla cardiomyopathy ('Takotsubo' cardiomyopathy)—reversible left ventricular dysfunction: with ST segment elevation [published correction appears in Jpn Circ J. 2000;64:237].Jpn Circ J. 2000; 64: 156-159Crossref PubMed Scopus (283) Google Scholar, 2Villareal RP Achari A Wilansky S Wilson JM Anteroapical stunning and left ventricular outflow tract obstruction.Mayo Clin Proc. 2001; 76: 79-83Abstract Full Text Full Text PDF PubMed Scopus (182) Google Scholar, 3Tsuchihashi K Ueshima K Uchida T Angina Pectoris-Myocardial Infarction Investigations in Japan et al.Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction.J Am Coll Cardiol. 2001; 38: 11-18Abstract Full Text Full Text PDF PubMed Scopus (1346) Google Scholar, 4Kurisu S Sato H Kawagoe T et al.Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction.Am Heart J. 2002; 143: 448-455Abstract Full Text Full Text PDF PubMed Scopus (731) Google Scholar, 5Ueyama T Kasamatsu K Hano T Yamamoto K Tsuruo Y Nishio I Emotional stress induces transient left ventricular hypocontraction in the rat via activation of cardiac adrenoceptors: a possible animal model of 'tako-tsubo' cardiomyopathy.Circ J. 2002; 66: 712-713Crossref PubMed Scopus (279) Google Scholar, 6Akashi YJ Sakakibara M Miyake F Reversible left ventricular dysfunction "takotsubo" cardiomyopathy associated with pneumothorax.Heart. 2002; 87: E1Crossref PubMed Scopus (59) Google Scholar, 7Akashi YJ Nakazawa K Sakakibara M Miyake F Sasaka K Reversible left ventricular dysfunction "takotsubo" cardiomyopathy related to catecholamine cardiotoxicity.J Electrocardiol. 2002; 35: 351-356Abstract Full Text PDF PubMed Scopus (84) Google Scholar, 8Abe 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: 737-742Abstract Full Text Full Text PDF PubMed Scopus (541) Google Scholar, 9Kurisu S Inoue I Kawagoe T et al.Myocardial perfusion and fatty acid metabolism in patients with tako-tsubo-like left ventricular dysfunction.J Am Coll Cardiol. 2003; 41: 743-748Abstract Full Text Full Text PDF PubMed Scopus (279) Google Scholar, 10Akashi YJ Nakazawa K Kida K et al.Reversible ventricular dysfunction (takotsubo cardiomyopathy) following polymorphic ventricular tachycardia.Can J Cardiol. 2003; 19: 449-451PubMed Google Scholar, 11Kurisu S Inoue I Kawagoe T et al.Left ventricular apical thrombus formation in a patient with suspected Tako-Tsubo-like left ventricular dysfunction.Circ J. 2003; 67: 556-558Crossref PubMed Scopus (63) Google Scholar, 12Akashi YJ Nakazawa K Sakakibara M Miyake F Koike J Sasaka K The clinical features of takotsubo cardiomyopathy.QJM. 2003; 96: 563-573Crossref PubMed Scopus (272) Google Scholar, 13Girod JP Messerli AW Frank Z Tang WH Brener SJ Takotsubo-like transient left ventricular dysfunction.Circulation. 2003; 107: e120-e121Crossref PubMed Google Scholar, 14Braunwald E Kloner RA The stunned myocardium: prolonged, postischemic ventricular dysfunction.Circulation. 1982; 66: 1146-1149Crossref PubMed Scopus (2389) Google Scholar, 15Pollick C Cujec B Parker S Tator C Left ventricular wall motion abnormalities in subarachnoid hemorrhage: an echocardiographic study.J Am Coll Cardiol. 1988; 12: 600-605Abstract Full Text PDF PubMed Scopus (192) Google Scholar, 16Salathe M Weiss P Ritz R Rapid reversal of heart failure in a patient with phaeochromocytoma and catecholamine-induced cardiomyopathy who was treated with captopril.Br Heart J. 1992; 68: 527-528Crossref PubMed Scopus (68) Google Scholar, 17Scott IU Guttermann DD Pheochromocytoma with reversible focal cardiac dysfunction.Am Heart J. 1995; 130: 909-911Abstract Full Text PDF PubMed Scopus (48) Google Scholar, 18Lee C Wolfe KB Rabson JL Reversible biventricular dysfunction secondary to ischemia in a patient with acute airway obstruction: a case report and review of the literature on reversible causes of acute ventricular dysfunction.Can J Cardiol. 1999; 15: 705-708PubMed Google Scholar The reversibility of ventricular dysfunction in these patients is reminiscent of ischemic myocardial stunning,1Kawai S Suzuki H Yamaguchi H et al.Ampulla cardiomyopathy ('Takotsubo' cardiomyopathy)—reversible left ventricular dysfunction: with ST segment elevation [published correction appears in Jpn Circ J. 2000;64:237].Jpn Circ J. 2000; 64: 156-159Crossref PubMed Scopus (283) Google Scholar, 6Akashi YJ Sakakibara M Miyake F Reversible left ventricular dysfunction "takotsubo" cardiomyopathy associated with pneumothorax.Heart. 2002; 87: E1Crossref PubMed Scopus (59) Google Scholar, 21Kloner RA Przyklenk K Patel B Altered myocardial states: the stunned and hibernating myocardium.Am J Med. 1989; 86: 14-22Abstract Full Text PDF PubMed Scopus (159) Google Scholar but takotsubo cardiomyopathy is associated with patent coronary arteries even during the acute phase when ST-segment elevation occurs. We have seen about 20 cases of takotsubo cardiomyopathy at our 3 institutions during the past 5 years. The ECG changes usually are not specific to any lead configuration. In most cases, ST-segment elevation persists in the limb leads for 1 week or more, and pathologic Q waves and inverted T waves ultimately develop in the leads that initially show ST-segment elevation.12Akashi YJ Nakazawa K Sakakibara M Miyake F Koike J Sasaka K The clinical features of takotsubo cardiomyopathy.QJM. 2003; 96: 563-573Crossref PubMed Scopus (272) Google Scholar Although ECG recordings were available for only 72 hours in our fatal case, prolonged ST-segment elevation was observed in most precordial leads. Moreover, this patient had the highest level of creatine kinase-MB among our patients with takotsubo cardiomyopathy. These findings might be signs of impending rupture in takotsubo cardiomyopathy. Catecholamine cardiomyopathy or a high plasma level of norepinephrine can cause ST-segment and regional ventricular wall motion abnormalities.3Tsuchihashi K Ueshima K Uchida T Angina Pectoris-Myocardial Infarction Investigations in Japan et al.Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction.J Am Coll Cardiol. 2001; 38: 11-18Abstract Full Text Full Text PDF PubMed Scopus (1346) Google Scholar, 4Kurisu S Sato H Kawagoe T et al.Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction.Am Heart J. 2002; 143: 448-455Abstract Full Text Full Text PDF PubMed Scopus (731) Google Scholar, 5Ueyama T Kasamatsu K Hano T Yamamoto K Tsuruo Y Nishio I Emotional stress induces transient left ventricular hypocontraction in the rat via activation of cardiac adrenoceptors: a possible animal model of 'tako-tsubo' cardiomyopathy.Circ J. 2002; 66: 712-713Crossref PubMed Scopus (279) Google Scholar, 11Kurisu S Inoue I Kawagoe T et al.Left ventricular apical thrombus formation in a patient with suspected Tako-Tsubo-like left ventricular dysfunction.Circ J. 2003; 67: 556-558Crossref PubMed Scopus (63) Google Scholar, 12Akashi YJ Nakazawa K Sakakibara M Miyake F Koike J Sasaka K The clinical features of takotsubo cardiomyopathy.QJM. 2003; 96: 563-573Crossref PubMed Scopus (272) Google Scholar, 16Salathe M Weiss P Ritz R Rapid reversal of heart failure in a patient with phaeochromocytoma and catecholamine-induced cardiomyopathy who was treated with captopril.Br Heart J. 1992; 68: 527-528Crossref PubMed Scopus (68) Google Scholar Whether the increased plasma level of norepinephrine in our patients is specific for this type of cardiomyopathy or is a nonspecific consequence of heart failure with a low cardiac output is unclear. Mismatches between scintigraphy-imaged myocardial sympathetic nerve function and myocardial blood flow have been found in patients with traumatic stress.22Yamabe H Hanaoka J Funakoshi T et al.Deep negative T waves and abnormal cardiac sympathetic image (123I-MIBG) after the Great Hanshin Earthquake of 1995.Am J Med Sci. 1996; 311: 221-224Abstract Full Text PDF PubMed Google Scholar Such cardiac hypersensitivity to catecholamines is not necessarily related to myocardial ischemia; therefore, coronary microvascular inflammation and microneuropathy limited to the heart are unlikely causes of takotsubo cardiomyopathy. Apical thrombus formation has been reported in a patient with takotsubo-like left ventricular dysfunction,17Scott IU Guttermann DD Pheochromocytoma with reversible focal cardiac dysfunction.Am Heart J. 1995; 130: 909-911Abstract Full Text PDF PubMed Scopus (48) Google Scholar suggesting that transient ventricular dysfunction can lead to apical thrombosis. Although we do not usually administer anticoagulants to patients with takotsubo cardiomyopathy and have had no thrombotic complications, we initiated heparin therapy in the patient reported herein to prevent the development of thrombus. We used the same regimen that is used to prevent thrombi in patients with ventricular aneurysms as a complication of myocardial infarction. Takotsubo cardiomyopathy is well-known for its resemblance to acute myocardial infarction, but most patients recover without any complications. Our experience with the reported case suggests that takotsubo cardiomyopathy can cause ventricular rupture in a manner and time course similar to that of acute myocardial infarction, even if blood pressure and other physiologic parameters are well maintained. It remains unclear whether the coagulation system plays a role in this form of cardiomyopathy. In summary, the patient described herein is, to our knowledge, the first reported case of ruptured takotsubo cardiomyopathy. We previously reported a case of takotsubo cardiomyopathy associated with idiopathic ventricular tachycardia.10Akashi YJ Nakazawa K Kida K et al.Reversible ventricular dysfunction (takotsubo cardiomyopathy) following polymorphic ventricular tachycardia.Can J Cardiol. 2003; 19: 449-451PubMed Google Scholar In view of our previous experience and the findings in the current case, we suggest that takotsubo cardiomyopathy may be a newly recognized cause of sudden cardiac death due to left ventricular rupture similar to that seen with acute myocardial infarction due to obstructive epicardial coronary artery disease. Our experience suggests that patients with takotsubo cardiomyopathy should be monitored carefully for mechanical complications in a manner similar to that used in patients with myocardial infarction.
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