Takotsubo Cardiomyopathy: Expanding the Differential Diagnosis in Cardiothoracic Surgery
2006; Elsevier BV; Volume: 83; Issue: 1 Linguagem: Inglês
10.1016/j.athoracsur.2006.05.115
ISSN1552-6259
AutoresMarius Berman, Milton Sauté, Eyal Porat, Mordechai Vaturi, Leslie Paul-Kislin, Bernardo A. Vidne, Alexander Kogan,
Tópico(s)Pericarditis and Cardiac Tamponade
ResumoWe describe a case of takotsubo cardiomyopathy in a 69-year-old woman after right upper lobectomy, without cardiac antecedents. The immediate course of recovery was uneventful. On the first postoperative day, clinical symptoms of acute coronary syndrome developed in association with ischemic electrocardiographic changes and a mild elevation in creatinine phosphokinase levels. Echocardiography showed moderate left ventricular dysfunction, with a typical takotsubo pattern. Coronary angiography revealed no abnormalities. After 2 days of supportive treatment, the patient recovered completely. The clinical presentation, instrumental findings, additional cardiac and noncardiac diseases, and the potential pathomechanism of takotsubo cardiomyopathy are described according to the current medical literature. We describe a case of takotsubo cardiomyopathy in a 69-year-old woman after right upper lobectomy, without cardiac antecedents. The immediate course of recovery was uneventful. On the first postoperative day, clinical symptoms of acute coronary syndrome developed in association with ischemic electrocardiographic changes and a mild elevation in creatinine phosphokinase levels. Echocardiography showed moderate left ventricular dysfunction, with a typical takotsubo pattern. Coronary angiography revealed no abnormalities. After 2 days of supportive treatment, the patient recovered completely. The clinical presentation, instrumental findings, additional cardiac and noncardiac diseases, and the potential pathomechanism of takotsubo cardiomyopathy are described according to the current medical literature. Takotsubo cardiomyopathy is characterized by transient left ventricular dyssynergy, typically, apical ballooning with concomitant compensatory basal hyperkinesis. Dote and colleagues [1Dote K. Sato H. Tateishi H. Uchida T. Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases.J Cardiol. 1991; 21: 203-214PubMed Google Scholar], in 1991 were one of the first to describe the syndrome, and they named it takotsubo-like left ventricular dysfunction because of the resemblance of the dysfunction heart to the round-bottomed narrow-necked fishing pot used to trap octopus in Japan. Subsequent reports followed from the United States and Western Europe. The disease has also been called ampulla syndrome, broken heart syndrome, neurogenic stunned myocardium, and acute stress cardiomyopathy. We describe a case of takotsubo cardiomyopathy in a 69-years-old woman after right upper lobectomy.A 69-year-old woman was referred to our center for an elective right upper lobectomy after diagnosis of moderate differentiated adenocarcinoma, 3 cm in diameter, with negative findings on mediastinoscopy and positive findings on positron emission tomography-computed tomography. Her background included heavy smoking and peripheral vascular disease.The operation and immediate postoperative course were uneventful. On the first postoperative day, hemodynamic and respiratory instability were noted, but the clinical examination revealed no abnormality. The electrocardiogram showed extensive ST elevation in V1-V6, with a negative T wave in leads II, III, and aVF. The chest roentgenogram showed a normal-sized cardiac mass with fully inflated lower and middle right lobes, and no signs of bleeding, pneumothorax, or pulmonary edema. Peak serum creatinine kinase (CK) measured 1156 U/L, CK-MB was 162 U/L, and the peak level of troponin T was 0.022 ng/mL. Echocardiography showed moderate-to-severe left ventricular dysfunction with apical ballooning and compensatory basal hyperkinesis (Fig 1). Because of the patient’s low blood pressure that failed to respond to fluids, a medium dose of noradrenaline was started.Emergent coronary angiography showed only a nonsignificant lesion in the left anterior descending artery; the rest of the vessel was completely open (Fig. 2). The patient was transferred for further supportive care to the intensive cardiac care unit, where treatment consisted mainly of inotropic support, diuretic agents, anticoagulant therapy, and oxygen mask.Fig 2Coronary angiography left anterior oblique view, immediately after thoracotomy, shows normal left (A) and right (B) vessel anatomy.View Large Image Figure ViewerDownload (PPT)Arterial blood analysis showed slight respiratory acidosis, which was corrected later. After several hours, rapid supraventricular tachycardia developed that turned into rapid atrial fibrillation and subsequent conversion to sinus rhythm after a 300-mg dose of intravenous amiodarone. After 2 days of supportive measures, the patient’s status improved clinically, the ST elevation turned to a normal pattern, and the echocardiography showed normalization of myocardium function (Fig 3). The patient was discharged 2 days later.Fig 3Four-chamber view 48 hours after thoracotomy shows normal left ventricular anatomy.View Large Image Figure ViewerDownload (PPT)CommentTakotsubo cardiomyopathy, or transient left ventricular apical ballooning syndrome, is a unique disorder that has only recently been generally recognized [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar]. It resembles acute ST elevation myocardial infarction in presenting symptoms of chest pain or dyspnea, acute ischemic changes in the electrocardiogram, and elevated levels of cardiac biomarkers (CK and troponin T or I). At coronary angiography, however, patients have no sign of obstructive epicardial coronary atherothrombosis, despite the presence of left ventricular angiography of typical apical ballooning with compensatory basal hyperkinesis.The syndrome affects mainly postmenopausal women after an episode of acute emotional or physiologic stress, general surgery, hypoglycemia, and hyperthyroidism. The proposed Mayo Clinic criteria [3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar] for the clinical diagnosis of the takotsubo cardiomyopathy are:1transient akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments with regional wall-motion abnormalities extending beyond a single epicardial vascular distribution;2absence of obstructive coronary disease or angiographic evidence of acute plaque rupture;3new electrocardiographic abnormalities (either ST-segment elevation or T-wave inversion); and4absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, and hypertrophic cardiomyopathy.The most common reported clinical complication is left heart failure, which may require aggressive diuresis, inotropic drugs, and hemodynamic support. In addition, it is not uncommon for patients to acquire a hemodynamically significant dynamic left ventricular intracavitary obstruction due to the dyskinetic apical and midventricular segments with concomitant hyperdynamic basal segments. The distinction of a dynamic left ventricular intracavitary pressure gradient from hypotension due solely to pump failure has important implications for therapy.The management of the takotsubo cardiomyopathy, determined mainly from the limited literature, consists of β-blockers, angiotensin-converting enzyme inhibitors (in patients without an intracavitary gradient), aspirin, and intravenous diuretics, as needed. Hypotension is managed according to its cause. Dynamic intraventricular obstruction is managed by administration of β-blockers to increase diastolic ventricular filling time and left ventricular end-diastolic volume [4Kyuma M. Tsuchihashi K. Shinshi Y. Hase M. Nakata T. Ooiwa H. Effect of intravenous propranolol on left ventricular apical ballooning without coronary artery stenosis: three cases.Circ J. 2002; 66: 1181-1184Crossref PubMed Scopus (123) Google Scholar], phenylephrine to increase afterload with subsequent reduction of the intraventricular gradient [5Haley J.H. Sinak L.J. Tajik A.J. Ommen S.R. Oh J.K. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock.Mayo Clin Proc. 1999; 74: 901-906Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar], and fluid resuscitation in the absence of pulmonary congestion. If documented coronary vasospasm is suspected, a nondihydropyridine calcium-channel blocker, such as diltiazem or verapamil, may be considered. Short-term anticoagulation therapy should also be considered to prevent the formation of mural thrombus. Hemodynamic complications are also treated by intraaortic balloon counterpulsation [6Stollberger C. Finstere J. Schneider B. Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.Minerva Cardioangiol. 2005; 53: 139-145PubMed Google Scholar].The depressed left ventricular systolic function and characteristic left ventricular apical and midventricular regional wall-motion abnormalities are transient features of the syndrome and generally resolve within days to weeks after initial presentation. The overall prognosis seems to be favorable. The akinesia regresses after 5 to 10 days, and the electrocardiogram normalizes within 7 to 11 days, always later than the normalization of the ventricular contraction [6Stollberger C. Finstere J. Schneider B. Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.Minerva Cardioangiol. 2005; 53: 139-145PubMed Google Scholar].Reported complications [3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar] of the syndrome include left heart failure with and without pulmonary edema, cardiogenic shock, dynamic intraventricular obstruction with left ventricular intracavitary pressure gradient generation, mitral regurgitation resulting from chordal tethering, and systolic anterior motion of the mitral valve apparatus, ventricular arrhythmias, left ventricular mural thrombus formation, left ventricular free wall rupture, and death (<1%).Although more than 15 years have elapsed since the first case was published, the main pathophysiology of takotsubo syndrome remains unclear. The precedent physical or emotional stress, or both, in most cases might suggest a role for the sympathetic system. Several interesting findings have been reported so far:1Coronary vasospasm tests using ergonovine or acetylcholine induced a simple epicardial coronary spasm and a multi-vessel coronary spasm in only a few patients. When diffuse vasospasm was observed, there was no ST elevation.2Assessments of the coronary microcirculation by several techniques, such as contrast-enhanced echocardiography, intracoronary Doppler guide-wire, coronary flow reserve and thrombolysis in myocardial infarction frame count yielded contradictory results [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 7Abe 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 (539) Google Scholar].3The assessment of metabolic versus perfusion defects by myocardial single-photon emission computed tomography (using technecium-99m tetrofosmin or thallium-201) yielded no convincing results [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 7Abe 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 (539) Google Scholar].Morya and colleagues [8Moryia M. Mori H. Suzuki N. Hazama M. Yano K. Six month follow-up of tako-tsubo cardiomyopathy with I-123-beta-metyl-iodophenyl pentadecanoic acid and I-123-meta-iodobenzyl-guanidine myocardial scintigraphy.Intern Med. 2002; 41: 829-833Crossref PubMed Scopus (38) Google Scholar], in a study of sympathetic innervations and catecholamine levels, found a decreased in MIBG (iodine-131-meta-iodobenzylguanidine)-like guanethidine uptake (active uptake to neuron endings) in the apex, suggesting that the syndrome was due to discrepancy in sympathetic innervation in the apical and basal regions. This assumption was supported by Kurisu and colleagues [9Kurisu S. Sato Kawagoe H. Ishihara 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: 449-455Abstract Full Text Full Text PDF Scopus (730) Google Scholar], who found that catecholamine levels were normal or slightly elevated in patients with apical ballooning, not ruling out catecholamine oversensitivity.Merli and colleagues [10Merli E. Sutcliffe S. Gori M. Sutherland G. Tako-tsubo cardiomyopathy: new insights into he possible underlying pathophysiology.Eur J Echocardiography. 2006; 7: 53-61Crossref PubMed Scopus (190) Google Scholar] noted abnormal myocardial functional architecture in takotsubo cardiomyopathy, including localized midventricular septal thickening, which could cause severe transient midcavitary obstruction in the presence of dehydration, or raised catecholamine levels due to physical or emotional stress, or both. Specifically, the authors speculated that the midventricular septal thickening effectively divides the left ventricle into two functionally different chambers, with a marked increase in wall stress in the high-pressure distal apical chamber. Combined with the abnormally high circulating catecholamine levels, this induces widespread subendocardial ischemia that is unrelated to a specific coronary artery territory. With rehydration/fall in catecholamine levels, the interventricular gradient resolves, and distal function recovers.In conclusion, additional evaluations of takotsubo cardiomyopathy are needed, including a more precise assessment of its true incidence, identification of risk factors, potential preventive measures, risk stratification, and elucidation of the underlying pathophysiologic mechanisms. Takotsubo cardiomyopathy is characterized by transient left ventricular dyssynergy, typically, apical ballooning with concomitant compensatory basal hyperkinesis. Dote and colleagues [1Dote K. Sato H. Tateishi H. Uchida T. Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases.J Cardiol. 1991; 21: 203-214PubMed Google Scholar], in 1991 were one of the first to describe the syndrome, and they named it takotsubo-like left ventricular dysfunction because of the resemblance of the dysfunction heart to the round-bottomed narrow-necked fishing pot used to trap octopus in Japan. Subsequent reports followed from the United States and Western Europe. The disease has also been called ampulla syndrome, broken heart syndrome, neurogenic stunned myocardium, and acute stress cardiomyopathy. We describe a case of takotsubo cardiomyopathy in a 69-years-old woman after right upper lobectomy. A 69-year-old woman was referred to our center for an elective right upper lobectomy after diagnosis of moderate differentiated adenocarcinoma, 3 cm in diameter, with negative findings on mediastinoscopy and positive findings on positron emission tomography-computed tomography. Her background included heavy smoking and peripheral vascular disease. The operation and immediate postoperative course were uneventful. On the first postoperative day, hemodynamic and respiratory instability were noted, but the clinical examination revealed no abnormality. The electrocardiogram showed extensive ST elevation in V1-V6, with a negative T wave in leads II, III, and aVF. The chest roentgenogram showed a normal-sized cardiac mass with fully inflated lower and middle right lobes, and no signs of bleeding, pneumothorax, or pulmonary edema. Peak serum creatinine kinase (CK) measured 1156 U/L, CK-MB was 162 U/L, and the peak level of troponin T was 0.022 ng/mL. Echocardiography showed moderate-to-severe left ventricular dysfunction with apical ballooning and compensatory basal hyperkinesis (Fig 1). Because of the patient’s low blood pressure that failed to respond to fluids, a medium dose of noradrenaline was started. Emergent coronary angiography showed only a nonsignificant lesion in the left anterior descending artery; the rest of the vessel was completely open (Fig. 2). The patient was transferred for further supportive care to the intensive cardiac care unit, where treatment consisted mainly of inotropic support, diuretic agents, anticoagulant therapy, and oxygen mask. Arterial blood analysis showed slight respiratory acidosis, which was corrected later. After several hours, rapid supraventricular tachycardia developed that turned into rapid atrial fibrillation and subsequent conversion to sinus rhythm after a 300-mg dose of intravenous amiodarone. After 2 days of supportive measures, the patient’s status improved clinically, the ST elevation turned to a normal pattern, and the echocardiography showed normalization of myocardium function (Fig 3). The patient was discharged 2 days later. CommentTakotsubo cardiomyopathy, or transient left ventricular apical ballooning syndrome, is a unique disorder that has only recently been generally recognized [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar]. It resembles acute ST elevation myocardial infarction in presenting symptoms of chest pain or dyspnea, acute ischemic changes in the electrocardiogram, and elevated levels of cardiac biomarkers (CK and troponin T or I). At coronary angiography, however, patients have no sign of obstructive epicardial coronary atherothrombosis, despite the presence of left ventricular angiography of typical apical ballooning with compensatory basal hyperkinesis.The syndrome affects mainly postmenopausal women after an episode of acute emotional or physiologic stress, general surgery, hypoglycemia, and hyperthyroidism. The proposed Mayo Clinic criteria [3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar] for the clinical diagnosis of the takotsubo cardiomyopathy are:1transient akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments with regional wall-motion abnormalities extending beyond a single epicardial vascular distribution;2absence of obstructive coronary disease or angiographic evidence of acute plaque rupture;3new electrocardiographic abnormalities (either ST-segment elevation or T-wave inversion); and4absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, and hypertrophic cardiomyopathy.The most common reported clinical complication is left heart failure, which may require aggressive diuresis, inotropic drugs, and hemodynamic support. In addition, it is not uncommon for patients to acquire a hemodynamically significant dynamic left ventricular intracavitary obstruction due to the dyskinetic apical and midventricular segments with concomitant hyperdynamic basal segments. The distinction of a dynamic left ventricular intracavitary pressure gradient from hypotension due solely to pump failure has important implications for therapy.The management of the takotsubo cardiomyopathy, determined mainly from the limited literature, consists of β-blockers, angiotensin-converting enzyme inhibitors (in patients without an intracavitary gradient), aspirin, and intravenous diuretics, as needed. Hypotension is managed according to its cause. Dynamic intraventricular obstruction is managed by administration of β-blockers to increase diastolic ventricular filling time and left ventricular end-diastolic volume [4Kyuma M. Tsuchihashi K. Shinshi Y. Hase M. Nakata T. Ooiwa H. Effect of intravenous propranolol on left ventricular apical ballooning without coronary artery stenosis: three cases.Circ J. 2002; 66: 1181-1184Crossref PubMed Scopus (123) Google Scholar], phenylephrine to increase afterload with subsequent reduction of the intraventricular gradient [5Haley J.H. Sinak L.J. Tajik A.J. Ommen S.R. Oh J.K. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock.Mayo Clin Proc. 1999; 74: 901-906Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar], and fluid resuscitation in the absence of pulmonary congestion. If documented coronary vasospasm is suspected, a nondihydropyridine calcium-channel blocker, such as diltiazem or verapamil, may be considered. Short-term anticoagulation therapy should also be considered to prevent the formation of mural thrombus. Hemodynamic complications are also treated by intraaortic balloon counterpulsation [6Stollberger C. Finstere J. Schneider B. Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.Minerva Cardioangiol. 2005; 53: 139-145PubMed Google Scholar].The depressed left ventricular systolic function and characteristic left ventricular apical and midventricular regional wall-motion abnormalities are transient features of the syndrome and generally resolve within days to weeks after initial presentation. The overall prognosis seems to be favorable. The akinesia regresses after 5 to 10 days, and the electrocardiogram normalizes within 7 to 11 days, always later than the normalization of the ventricular contraction [6Stollberger C. Finstere J. Schneider B. Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.Minerva Cardioangiol. 2005; 53: 139-145PubMed Google Scholar].Reported complications [3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar] of the syndrome include left heart failure with and without pulmonary edema, cardiogenic shock, dynamic intraventricular obstruction with left ventricular intracavitary pressure gradient generation, mitral regurgitation resulting from chordal tethering, and systolic anterior motion of the mitral valve apparatus, ventricular arrhythmias, left ventricular mural thrombus formation, left ventricular free wall rupture, and death (<1%).Although more than 15 years have elapsed since the first case was published, the main pathophysiology of takotsubo syndrome remains unclear. The precedent physical or emotional stress, or both, in most cases might suggest a role for the sympathetic system. Several interesting findings have been reported so far:1Coronary vasospasm tests using ergonovine or acetylcholine induced a simple epicardial coronary spasm and a multi-vessel coronary spasm in only a few patients. When diffuse vasospasm was observed, there was no ST elevation.2Assessments of the coronary microcirculation by several techniques, such as contrast-enhanced echocardiography, intracoronary Doppler guide-wire, coronary flow reserve and thrombolysis in myocardial infarction frame count yielded contradictory results [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 7Abe 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 (539) Google Scholar].3The assessment of metabolic versus perfusion defects by myocardial single-photon emission computed tomography (using technecium-99m tetrofosmin or thallium-201) yielded no convincing results [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 7Abe 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 (539) Google Scholar].Morya and colleagues [8Moryia M. Mori H. Suzuki N. Hazama M. Yano K. Six month follow-up of tako-tsubo cardiomyopathy with I-123-beta-metyl-iodophenyl pentadecanoic acid and I-123-meta-iodobenzyl-guanidine myocardial scintigraphy.Intern Med. 2002; 41: 829-833Crossref PubMed Scopus (38) Google Scholar], in a study of sympathetic innervations and catecholamine levels, found a decreased in MIBG (iodine-131-meta-iodobenzylguanidine)-like guanethidine uptake (active uptake to neuron endings) in the apex, suggesting that the syndrome was due to discrepancy in sympathetic innervation in the apical and basal regions. This assumption was supported by Kurisu and colleagues [9Kurisu S. Sato Kawagoe H. Ishihara 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: 449-455Abstract Full Text Full Text PDF Scopus (730) Google Scholar], who found that catecholamine levels were normal or slightly elevated in patients with apical ballooning, not ruling out catecholamine oversensitivity.Merli and colleagues [10Merli E. Sutcliffe S. Gori M. Sutherland G. Tako-tsubo cardiomyopathy: new insights into he possible underlying pathophysiology.Eur J Echocardiography. 2006; 7: 53-61Crossref PubMed Scopus (190) Google Scholar] noted abnormal myocardial functional architecture in takotsubo cardiomyopathy, including localized midventricular septal thickening, which could cause severe transient midcavitary obstruction in the presence of dehydration, or raised catecholamine levels due to physical or emotional stress, or both. Specifically, the authors speculated that the midventricular septal thickening effectively divides the left ventricle into two functionally different chambers, with a marked increase in wall stress in the high-pressure distal apical chamber. Combined with the abnormally high circulating catecholamine levels, this induces widespread subendocardial ischemia that is unrelated to a specific coronary artery territory. With rehydration/fall in catecholamine levels, the interventricular gradient resolves, and distal function recovers.In conclusion, additional evaluations of takotsubo cardiomyopathy are needed, including a more precise assessment of its true incidence, identification of risk factors, potential preventive measures, risk stratification, and elucidation of the underlying pathophysiologic mechanisms. Takotsubo cardiomyopathy, or transient left ventricular apical ballooning syndrome, is a unique disorder that has only recently been generally recognized [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar]. It resembles acute ST elevation myocardial infarction in presenting symptoms of chest pain or dyspnea, acute ischemic changes in the electrocardiogram, and elevated levels of cardiac biomarkers (CK and troponin T or I). At coronary angiography, however, patients have no sign of obstructive epicardial coronary atherothrombosis, despite the presence of left ventricular angiography of typical apical ballooning with compensatory basal hyperkinesis. The syndrome affects mainly postmenopausal women after an episode of acute emotional or physiologic stress, general surgery, hypoglycemia, and hyperthyroidism. The proposed Mayo Clinic criteria [3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar] for the clinical diagnosis of the takotsubo cardiomyopathy are:1transient akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments with regional wall-motion abnormalities extending beyond a single epicardial vascular distribution;2absence of obstructive coronary disease or angiographic evidence of acute plaque rupture;3new electrocardiographic abnormalities (either ST-segment elevation or T-wave inversion); and4absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, and hypertrophic cardiomyopathy. The most common reported clinical complication is left heart failure, which may require aggressive diuresis, inotropic drugs, and hemodynamic support. In addition, it is not uncommon for patients to acquire a hemodynamically significant dynamic left ventricular intracavitary obstruction due to the dyskinetic apical and midventricular segments with concomitant hyperdynamic basal segments. The distinction of a dynamic left ventricular intracavitary pressure gradient from hypotension due solely to pump failure has important implications for therapy. The management of the takotsubo cardiomyopathy, determined mainly from the limited literature, consists of β-blockers, angiotensin-converting enzyme inhibitors (in patients without an intracavitary gradient), aspirin, and intravenous diuretics, as needed. Hypotension is managed according to its cause. Dynamic intraventricular obstruction is managed by administration of β-blockers to increase diastolic ventricular filling time and left ventricular end-diastolic volume [4Kyuma M. Tsuchihashi K. Shinshi Y. Hase M. Nakata T. Ooiwa H. Effect of intravenous propranolol on left ventricular apical ballooning without coronary artery stenosis: three cases.Circ J. 2002; 66: 1181-1184Crossref PubMed Scopus (123) Google Scholar], phenylephrine to increase afterload with subsequent reduction of the intraventricular gradient [5Haley J.H. Sinak L.J. Tajik A.J. Ommen S.R. Oh J.K. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock.Mayo Clin Proc. 1999; 74: 901-906Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar], and fluid resuscitation in the absence of pulmonary congestion. If documented coronary vasospasm is suspected, a nondihydropyridine calcium-channel blocker, such as diltiazem or verapamil, may be considered. Short-term anticoagulation therapy should also be considered to prevent the formation of mural thrombus. Hemodynamic complications are also treated by intraaortic balloon counterpulsation [6Stollberger C. Finstere J. Schneider B. Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.Minerva Cardioangiol. 2005; 53: 139-145PubMed Google Scholar]. The depressed left ventricular systolic function and characteristic left ventricular apical and midventricular regional wall-motion abnormalities are transient features of the syndrome and generally resolve within days to weeks after initial presentation. The overall prognosis seems to be favorable. The akinesia regresses after 5 to 10 days, and the electrocardiogram normalizes within 7 to 11 days, always later than the normalization of the ventricular contraction [6Stollberger C. Finstere J. Schneider B. Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.Minerva Cardioangiol. 2005; 53: 139-145PubMed Google Scholar]. Reported complications [3Bybee K.A. Kara T. Prasad A. et al.Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction.Ann Intern Med. 2004; 141: 858-865Crossref PubMed Scopus (1218) Google Scholar] of the syndrome include left heart failure with and without pulmonary edema, cardiogenic shock, dynamic intraventricular obstruction with left ventricular intracavitary pressure gradient generation, mitral regurgitation resulting from chordal tethering, and systolic anterior motion of the mitral valve apparatus, ventricular arrhythmias, left ventricular mural thrombus formation, left ventricular free wall rupture, and death (<1%). Although more than 15 years have elapsed since the first case was published, the main pathophysiology of takotsubo syndrome remains unclear. The precedent physical or emotional stress, or both, in most cases might suggest a role for the sympathetic system. Several interesting findings have been reported so far:1Coronary vasospasm tests using ergonovine or acetylcholine induced a simple epicardial coronary spasm and a multi-vessel coronary spasm in only a few patients. When diffuse vasospasm was observed, there was no ST elevation.2Assessments of the coronary microcirculation by several techniques, such as contrast-enhanced echocardiography, intracoronary Doppler guide-wire, coronary flow reserve and thrombolysis in myocardial infarction frame count yielded contradictory results [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 7Abe 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 (539) Google Scholar].3The assessment of metabolic versus perfusion defects by myocardial single-photon emission computed tomography (using technecium-99m tetrofosmin or thallium-201) yielded no convincing results [2Tsuchihashi K. Ueshima K. Uchida T. 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 (1340) Google Scholar, 7Abe 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 (539) Google Scholar]. Morya and colleagues [8Moryia M. Mori H. Suzuki N. Hazama M. Yano K. Six month follow-up of tako-tsubo cardiomyopathy with I-123-beta-metyl-iodophenyl pentadecanoic acid and I-123-meta-iodobenzyl-guanidine myocardial scintigraphy.Intern Med. 2002; 41: 829-833Crossref PubMed Scopus (38) Google Scholar], in a study of sympathetic innervations and catecholamine levels, found a decreased in MIBG (iodine-131-meta-iodobenzylguanidine)-like guanethidine uptake (active uptake to neuron endings) in the apex, suggesting that the syndrome was due to discrepancy in sympathetic innervation in the apical and basal regions. This assumption was supported by Kurisu and colleagues [9Kurisu S. Sato Kawagoe H. Ishihara 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: 449-455Abstract Full Text Full Text PDF Scopus (730) Google Scholar], who found that catecholamine levels were normal or slightly elevated in patients with apical ballooning, not ruling out catecholamine oversensitivity. Merli and colleagues [10Merli E. Sutcliffe S. Gori M. Sutherland G. Tako-tsubo cardiomyopathy: new insights into he possible underlying pathophysiology.Eur J Echocardiography. 2006; 7: 53-61Crossref PubMed Scopus (190) Google Scholar] noted abnormal myocardial functional architecture in takotsubo cardiomyopathy, including localized midventricular septal thickening, which could cause severe transient midcavitary obstruction in the presence of dehydration, or raised catecholamine levels due to physical or emotional stress, or both. Specifically, the authors speculated that the midventricular septal thickening effectively divides the left ventricle into two functionally different chambers, with a marked increase in wall stress in the high-pressure distal apical chamber. Combined with the abnormally high circulating catecholamine levels, this induces widespread subendocardial ischemia that is unrelated to a specific coronary artery territory. With rehydration/fall in catecholamine levels, the interventricular gradient resolves, and distal function recovers. In conclusion, additional evaluations of takotsubo cardiomyopathy are needed, including a more precise assessment of its true incidence, identification of risk factors, potential preventive measures, risk stratification, and elucidation of the underlying pathophysiologic mechanisms.
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