Transient left ventricular apical

Transcription

1 CoverArticle CEContinuing Education Transient Le f t Vent ricular Apical Ballooning Brenda McCulloch, RN, MSN, CNS Transient left ventricular apical ballooning, also known as takotsubo cardiomyopathy, is an unusual abnormality that may be the underlying cause of signs and symptoms of acute myocardial infarction (AMI) in a small number of patients. The signs and symptoms include chest pain, ST-segment changes, and the release of cardiac biomarkers. 1 Dyspnea and hypotension may also occur. Although these signs and symptoms are suggestive of AMI, they are not caused by ischemic coronary artery disease. This abrupt onset of extensive ballooning or dilatation of the left ventricle occurs most often in postmenopausal women after a traumatic psychosocial or physical stressor. 1 Although its onset is sudden and dramatic, apical ballooning is transient and reversible. Its cause is not known. It is increasingly recognized and reported in the medical literature. Because apical ballooning mimics the signs and symptoms of AMI, emergency department and critical care nurses may care for patients with this interesting and uncommon abnormality. In this article, I review the pathophysiology, clinical features, management, complications, and prognosis of apical ballooning. Three case reports are included to illustrate the growing experience with this abnormality. Apical ballooning was first described in the Japanese literature in the early 1990s and was attributed to simultaneous spasm of multiple coronary arteries. 2,3 The original name given to apical ballooning was takotsubo cardiomyopathy, which was derived from the shape of the narrow-necked bulging takotsubo container used by Japanese fisherman to trap octopus. The shape of the takotsubo pot resembles the distorted ballooning ventricle (Figure 1). Table 1 lists several other terms used in the medical literature to describe this ballooning. Additional reports of apical ballooning have come from many areas of the world, including Europe, 7-10 Australia, 11 South America, 12 and the United States Because of the increased recognition of this abnormality, in the International This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives: 1. Define transient left ventricular apical ballooning and examine triggers of this syndrome 2. Describe the clinical features of apical ballooning 3. Identify diagnostic findings common in apical ballooning Author Brenda McCulloch is a clinical nurse specialist for the Sutter Heart Institute in Sacramento, California. She has 25 years of experience in cardiovascular nursing, with a concentration in interventional cardiology. Corresponding author: Brenda McCulloch, RN, MSN, CNS, Sutter Heart Institute, Sutter Medical Center, Sacramento, 5301 F St, Suite 304, Sacramento, CA ( mccullb@sutterhealth.org). To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA Phone, (800) or (949) (ext 532); fax, (949) ; , reprints@aacn.org. 20 CRITICALCARENURSE Vol 27, No. 6, DECEMBER

2 Table 1 Synonyms for apical ballooning Ampulla cardiomyopathy 5 Broken-heart syndrome 5 Neurogenic stunned myocardium 6 Stress cardiomyopathy 6 Takotsubo cardiomyopathy 1,2 Transient left ventricular dysfunction 5 Classification of Diseases, Ninth Revision, the National Center for Health Statistics 17 established as the unique code for apical ballooning. Etiology, Incidence, and Precipitating Factors The precise etiology of apical ballooning is unclear. In Japan, 1% to 2% of patients who have signs and symptoms of AMI and undergo emergent coronary angiography actually have apical ballooning. 5 To date, a similar percentage of patients in the United States have these findings, suggesting that apical ballooning may be more common than initially thought. 14,15,18 The abnormality occurs most often in postmenopausal women, and the reason for this prevalence is also unclear. The preponderance of apical ballooning reportedly is 6 to 9 times higher in women than in men. 19 A Figure 1 A, Distored ballooning ventricle. B, Takotsubo pot used by Japanese fishermen to catch octopus. Reprinted from Kurisu et al, 4 with permission. Copyright Elsevier B Among women with signs and symptoms of AMI, 6% have apical ballooning. 19 Most patients with apical ballooning have experienced a marked psychosocial or physical stress that precipitates their signs and symptoms. 5,13-15,18-20 Examples of reported stressors are listed in Table 2. Pathophysiology Patients with apical ballooning have marked systolic ballooning of the ventricular apex, often associated with hypercontracility of the base of the heart. Although ballooning of the left ventricle is most common, the right ventricle can also be affected. 2,32 In the initial reports from Japan, the alterations in ventricular function were attributed to simultaneous multivessel coronary artery spasm. 1,2 The pathophysiological mechanism that initiates apical ballooning is not fully understood, but it is now thought to be related to stunning of the myocardium related to excessive catecholamines. 15,16 In most patients, the onset of signs and symptoms is preceded by increased psychosocial or physical stress, suggesting an association with increased activity of the sympathetic nervous system. Catechol - amines can have a toxic effect on the myocardium. 18 Markedly elevated serum levels of catecholamines have been reported in patients with apical ballooning, and it is postulated that these elevated levels lead to toxic myocardial effects and stunning of the ventricle. In one series of patients, 16 the levels of plasma catecholamines were several times higher than the levels in a group of patients who had AMI. Other suggested mechanisms include rupture of a nonobstructive plaque followed by spontaneous thrombolysis, 11 micro vascular coronary spasm or dysfunction, 16,23 transient obstruction to left ventricular outflow, 1 and acute myocarditis. 23 Why apical ballooning occurs most often in postmenopausal women is not known. The role of sex hormones and their impact on the sympathetic nervous system and catecholamine metabolism are not well understood. Postmenopausal alterations of endothelial function are also not well understood. 5 More research is necessary. In addition, a genetic component may be involved; apical ballooning has been reported in sisters. Some patients have had single or multiple recurrences of this abnormality. 15,16,21,33 Anatomically, an abnormally long left anterior descending artery that courses along the diaphragmatic surface of the left ventricle has been reported, but this finding is not a consistent one in apical ballooning. 34 Elevated levels of circulating CRITICALCARENURSE Vol 27, No. 6, DECEMBER

3 Table 2 Reported triggers of apical ballooning Unexpected death of a spouse, child, or close family member 14-16,18,21 Anniversary of death of a family member 14 Having a spouse leave for war 22 Witnessing an accident, being in an accident 1,16,21,23 House fire 1 Armed robbery 16 Excessive alcohol intake or alcohol/drug withdrawal 1,23 Surprise party, surprise reunion 16 Losing money in a casino, loss of life savings, financial instability 14,22,24 Court appearance, legal proceedings 18 Public performance, public speaking 18 Hypothermia 7 Loss of job, occupational stress 24,25 Lightning strike 26 Earthquake 27 Quarreling, fierce arguments 1,14,16,28 Domestic abuse 14 Vigorous exercise 1,28 catecholamines 16,32,35 and plasma brain natriuretic peptide have been reported. 21 In one report, 18 endomyocardial biopsy showed no significant inflammatory process. In another report, 24 biopsy did not suggest any specific heart disease, and myocarditis was ruled out as a causative factor. Some patients have a pressure gradient within the left ventricle, but this finding is not consistent. 20 Results of thallium nuclear scanning are usually normal or may show a small area of defect. 18 In a study by Sharkey et al, 14 magnetic resonance imaging showed diffuse wall motion abnormalities of the ventricle that could not be explained by spasm of any single coronary artery. In addition, the scarring normally associated with AMI was not present, and no Cerebrovascular accident, witnessing a family member have a cerebrovascular accident 1,7 Epilepsy, grand mal seizure 1,14 Acute dyspnea, asthma, pneumothorax 14,15,18,19 Acute abdomen, acute cholecystitis 1,29 Sepsis and hypoxemia with respiratory failure 29 Hip fracture, hip surgery 14,30 Severe pain 18 Severe hypoglycemia 31 Noncardiac surgical procedures 1,15,19 Fear of impending procedure 16 Receiving news of serious diagnosis 28 delayed enhancement with gadolinium contrast medium was apparent, indicating that the myocardial injury was reversible. Clinical Features and Findings Consensus criteria for diagnosing apical ballooning do not yet exist. Table 3 Clinical features of apical ballooning Table 3 provides a summary of clinical features consistent with this abnormality. Patients most often have chest pain mimicking that of AMI. They may also have dyspnea. The pain characteristics are not well delineated. Other reported signs and symptoms include syncope or near syncope, 8 fatigue, malaise, and palpitations. 18 A subset of patients may also have marked hypotension, pulmonary edema, cardiogenic shock, and/or lethal ventricular arrhythmias. These patients require shortterm vasopressors, temporary pacemakers, and intra-aortic balloon pump support while the left ventricle recovers. 13,14,16,22 Electrocardiographic (ECG) findings are variable and cannot be used to diagnose apical ballooning. ECGs show ST-segment elevation or depression, usually in the precordial leads, particularly V 2 to V Reciprocal changes in the inferior leads may not occur, and in most patients, Q waves do not develop. 22 Deeply inverted T waves are common during the recovery phase. Many patients have a markedly prolonged QT interval (normal, 440 milliseconds). 16,22,31,35,36 Compared with findings in AMI, the cardiac biomarkers troponin, creatine kinase, and creatine kinase Onset of signs and symptoms often preceded by emotional/physical stressor Most common in postmenopausal women ST-segment abnormalities that mimic those of acute myocardial infarction Signs and symptoms similar to those of acute myocardial infarction Mild to moderate increase in levels of cardiac enzyme compared with the increases in acute myocardial infarction No significant epicardial coronary artery disease to account for the left ventricular dysfunction Left ventricular ballooning wall motion at the apex with hypercontractility at the base Transient and reversible left ventricular changes with favorable prognosis 22 CRITICALCARENURSE Vol 27, No. 6, DECEMBER

4 stressor, apical ballooning should be considered. Early echocardiography or coronary angiography showing ballooning of the ventricle will be most helpful in differentiating this abnormality from AMI. Prompt recognition of apical ballooning prevents the unnecessary administration of fibrinolytic agents to patients with apical ballooning who have ST-segment elevation. converting enzyme inhibitors, vasopressors, and intra-aortic balloon counterpulsation for hypotension and left-sided heart failure. Shortterm anticoagulation to prevent left ventricular thrombus until the left ventricular function normalizes may be considered. 37 Optimal treatment of transient left ventricular apical ballooning currently is not known and remains to be determined. Early echocardiography or coronary angiography showing ballooning of the ventricle will be most helpful in differentiating this abnormality from AMI. MB are only moderately elevated in apical ballooning, and they do not follow the same rise-and-fall patterns associated with AMI. 22 The reason for this difference is unclear. The characteristic systolic ballooning of the ventricle is clearly evident on echocardiograms and in cardiac catheterization. Ejection fraction may be markedly decreased in the acute phase of the ballooning. Ejection fractions as low as 15% to 40% have been reported. 6,13,14,16,18 Coronary angiography reveals no significant epicardial coronary artery disease to account for the marked left ventricular dysfunction. 12,18 Table 4 gives associated diagnostic findings. Management When a patient s onset of signs and symptoms, especially in a postmenopausal woman, coincides with a significant psychosocial or physical Table 4 Diagnostic findings common in apical ballooning Laboratory tests: Elevated serum/plasma levels of creatine kinase, creatine kinase MB, troponin, norepinephrine, brain natriuretic peptide, dopamine Electrocardiography: ST-segment elevation or depression, T-wave inversion, and/or prolonged QT interval Nuclear stress testing: Evidence of reversible myocardial injury Echocardiography: Marked apical ballooning with systolic dysfunction; akinetic or dyskinetic left ventricle Left ventriculography: Marked apical ballooning with systolic dysfunction; akinetic or dyskinetic left ventricle Coronary angiography: No significant coronary artery disease Cardiac magnetic resonance imaging: Diffuse wall motion abnormalities Complications and Prognosis The most commonly reported complication of apical ballooning is left ventricular failure. 22 Arrhythmias have been reported, including sinus bradycardia, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation. 14,22 Heart block requiring temporary and permanent pacing has been described. 9 Hypotension, pulmonary edema, cardiogenic shock, mitral regurgitation, mural thrombus, left ventricular free-wall rupture, and death have also been reported. 1,19,37,38 Apical ballooning occurs most often in postmenopausal women who have experienced a physical or psychosocial stressor. Left ventricular function improves rapidly, often within 7 to 30 days of the onset of signs and symptoms. 9 The ECG changes may be slower to resolve. 36 The prognosis is generally favorable; a mortality of 0% to 8% has been reported. 14,22 Implications for Nursing Care Patients with apical ballooning typically have the same signs and symptoms as patients with AMI and are admitted to a critical care unit. Goals of care are similar to those for patients with AMI: alleviating pain, reducing anxiety, maintaining contractility, and preventing and Management of apical ballooning is largely empirical; specific guidelines do not exist. In most reported cases, patients are managed according to widely accepted guidelines for non ST-segment myocardial infarction and ST-segment elevation myocardial infarction. Supportive treatment is used for acute complications, such as antiarrhythmic drugs for ventricular arrhythmias; diuretics for pulmonary congestion; and β-blockers, vasodilators, angiotensinhttp://ccn.aacnjournals.org CRITICALCARENURSE Vol 27, No. 6, DECEMBER

5 treating complications, such as arrhythmias, heart failure, and cardiogenic shock Because ST-segment changes, prolonged QT intervals, heart block, and lethal ventricular arrhythmias have been reported, continuous cardiac monitoring is essential. Many patients also have shortness of breath and pulmonary congestion that requires frequent assessment of heart and lung sounds to monitor fluid status. Diuretic therapy is often indicated and can lead to alterations in fluid and electrolyte balance, so regular monitoring of laboratory values and electrolyte replacement is essential. During the acute phase, contractility is affected by the severe dysfunction of the left ventricle, resulting in decreases in ejection fraction, cardiac output, and cardiac index. For some patients, inotropic support with low-dose dopamine or dobutamine may be required to improve cardiac output and cardiac index. A pulmonary artery and/or an arterial catheter may be placed for monitoring hemodynamic parameters and titrating vasoactive agents during the acute phase of the illness. On a short-term basis, intra-aortic balloon counterpulsation may be indicated to decrease left ventricular workload, decrease afterload, improve contractility, and increase stroke volume. Case 1 A 66-year-old woman came to the emergency department of a small hospital because of the sudden onset of severe substernal nonradiating chest pain and shortness of breath. An ECG showed marked T-wave inversion in leads V 3 to V 6. The QT interval was prolonged at 604 milliseconds (Figure 2). The patient s serum troponin level was elevated at 3.35 ng/ml (normal, ng/ml). She had a history of hypothyroidism and no major risk factors for coronary disease. She was the primary caregiver for her husband, who had advanced, rapidly progressing Alzheimer s disease. The diagnosis was non ST-segment elevation myocardial infarction. She was given a weightbased bolus of eptifibatide, and a continuous infusion of the drug at a rate of 2.0 μg/kg per minute was started. She was transferred to a tertiary care facility for urgent cardiac catheterization and treatment. Coronary angiography showed no obstructive lesions (Figures 3 and 4). Testing with methylergonovine (Methergine) ruled out coronary artery spasm. Findings on the left ventriculogram (Figure 5) were markedly abnormal, with apical ballooning and a decreased ejection fraction of 45% (normal, 55%-70%). The left ventricular enddiastolic pressure was 29 mm Hg (normal, 5-12 mm Hg). Because angiograms showed no evidence of ischemic coronary disease, the eptifibatide was discontinued. The patient s hospital course remained uneventful, and she was discharged home on day 4. The final diagnosis was takotsubo cardiomyopathy, or apical ballooning. Discharge medications included enoxaparin 80 mg subcutaneously twice daily for 5 days, warfarin 5 mg/d, hydro - chloro thiazide 50 mg/d, and levo - thyroxine mg/d. Case 2 A 58-year-old woman went to an outlying hospital because she had V3 Figure 2 T-wave inversion and prolonged QT interval in lead V 3 of electrocardiogram of patient in case 1. Figure 3 Left coronary angiogram of patient in case 1. Figure 4 Right coronary angiogram of patient in case 1. Figure 5 Apical ballooning of left ventricle in systole of patient in case CRITICALCARENURSE Vol 27, No. 6, DECEMBER

6 experienced intense chest pain when she found the body of her husband, who had committed suicide. She had a history of hypertension and smoking. The initial ECG showed nonspecific ST-T wave changes. The QTc interval was prolonged at 517 milliseconds, and the troponin level was elevated at 1.3 ng/ml. She was admitted to the intensive care unit for observation. Several hours after admission, severe crushing substernal chest pain developed; she described the intensity as 8 on a scale of 1 to 10. ECGs showed new T-wave inversion in leads V 2 to V 6 (Figure 6). Systolic blood pressure was 80 mm Hg. Transthoracic echocardiography indicated severe akinesis of the anterior wall of the heart and an ejection fraction of 20%. She was transferred to another facility for emergent cardiac catheterization with coronary angiography. The examinations revealed no significant coronary artery disease. She had a markedly elevated left ventricular enddiastolic pressure of 35 mm Hg and severe akinesis and ballooning of the midanterior wall and midinferior wall with relative sparing of the proximal anterior and posterobasal and apical walls of the left ventricle. The diagnosis was takotsubo cardiomyopathy, or apical ballooning. She was transferred to the cardiac intensive care unit for continued monitoring and nursing care. Her remaining hospitalization was uneventful, and she was discharged home on day 4. Discharge medications included amlodipine 5 mg/d, ramipril 5 mg/d, aspirin 325 mg/d, rosuvastatin 10 mg/d, and carvedilol mg twice daily. Case 3 A 50-year-old woman went to an outlying rural hospital because she I II III VI V1 V5 Figure 6 T-wave inversion and prolonged QT interval on electrocardiogram of patient in case 2. had shortness of breath and chest pain after intensely arguing with a family member about her (the patient s) alcoholism. She had a history of type 1 diabetes mellitus and chronic obstructive pulmonary disease, and she was a 35-pack-year smoker. The ECG findings were markedly abnormal, with sinus tachycardia and ST-segment elevation in leads V 2 to V 5 (Figure 7). The QT interval was normal. The troponin level was elevated at 5.28 ng/ml. The patient was hypotensive and had bilateral crackles. Her clinical condition was stabilized in the emergency I II III II avr V 1 avl avf V 2 avr V 1 avl avf V 4 V 5 V 3 V 6 department. She was given 325 mg of chewable aspirin, and treatment with dopamine was started at a rate of 6 μg/kg per minute. She was transferred emergently to another facility for cardiac catheterization and possible percutaneous coronary intervention because of her continuing unstable hemodynamic status. Coronary angiography showed no evidence of obstructive coronary artery disease. Findings on left ventricular angiography were markedly abnormal, with a large area of apical akinesis. The ejection fraction was 15%. Left ventricular end-diastolic Figure 7 ST-segment elevation on electrocardiogram of patient in case 3. V 2 V 4 V 5 V 3 V 6 CRITICALCARENURSE Vol 27, No. 6, DECEMBER

7 pressure was 28 mm Hg. The diagnosis was acute AMI due to coronary vasospasm. She was transferred to the cardiac intensive care unit for continued monitoring and nursing care. Her hemodynamic status remained unstable, and intubation was required. A pulmonary artery catheter was inserted at the bedside to assist in managing hemodynamic status and titrating vasoactive agents. Her hospital course continued to be slow and complicated. Brain natriuretic peptide was elevated throughout the hospitalization, indicating continued left ventricular dysfunction. Echocardiography on day 17 showed dramatic improvements in left ventricular ejection fraction: an increase to 40%. Because of this significant change in left ventricular function, the diagnosis was revised from AMI to takotsubo cardiomyopathy, or apical ballooning. The patient continued to slowly progress and was discharged home on day 28. Discharge medications included carvedilol mg twice daily, lisinopril 5 mg/d, aspirin 325 mg/d, nicotine patch, 21 mg/d topically, pantoprazole 40 mg/d, thiamine 100 mg/d, and folic acid 1 mg/d. Conclusion Transient left ventricular apical ballooning, or takotsubo cardio - myopathy, is an uncommon abnormality with signs and symptoms that mimic those of AMI. Making the diagnosis is difficult without early evaluation via echocardiography or cardiac catheterization. Apical ballooning should be considered as a possible diagnosis by emergency department physicians and cardiologists when patients, especially postmenopausal women whose onset of signs and symptoms coincides with some type of psychosocial or physical stressor, have chest pain and ST-segment elevation or depression. Critical care nurses need to be familiar with apical ballooning because some patients with the abnormality have altered hemodynamic parameters and require vasoactive agents and intra-aortic balloon pumping. No significant coronary lesions account for the markedly abnormal left ventricular akinetic and hypokinetic changes that occur. Apical ballooning is reversible; patients have dramatic improvements in left ventricular wall motion and ejection fraction by 30 days after onset of signs and symptoms. Treatment is empirical and supportive. The prognosis is generally favorable, although some deaths have been reported, usually the result of irreversible cardiogenic shock, refractory ventricular arrhythmias, or other catastrophic cardiovascular event. Acknowledgments I acknowledge the assistance of Jane Eymer, RN, BSN, University of California, Davis Medical Center, Sacramento, California; Siobhan Geary, RN, MS, CNS, Thomas Rhodes, RN, BSN, and Julie Chester Wood, RN, MS, CNS, Sutter Medical Center, Sacramento; and Evelyn Reilly, RN, MS, CNS, Sutter Roseville Medical Center, Roseville, California, in the development of this article. Financial Disclosures None reported. References 1. Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol. 2001;38(1): Satoh H, Tatcishi H, Uchida T, et al. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon M, eds. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure [in Japanese]. Tokyo, Japan: Kagakuhyouronsya Publishing Co; 1990: Dote K, Sato H, Tateishi H, Uchida T, Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases [in Japanese]. J Cardiol. 1991;21(2): Kurisu 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(3): Ako J, Sudhir K, Farouque HMO, Honda Y, Fitzgerald PJ. Transient left ventricular dysfunction under severe stress: brain-heart relationship revisited. Am J Med. 2006; 119: 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(5): Auer J, Porodko M, Berent R, et al. Transient left ventricular apical ballooning mimicking acute coronary syndrome in four patients from central Europe. Croat Med J. 2005;46(6): Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J. 2006;27(13): Lipiecki J, Durel V, Decalf V, et al. Transient left ventricular apical ballooning or the tako-tsubo syndrome [in French]. Arch Mal Coeur Vaiss. 2005;98(4): Azzarelli S, Galassi AR, Amico F, et al. Clinical features of transient left ventricular apical ballooning. Am J Cardiol. 2006;98(9): Chandrasegaram MD, Celermajer DS, Wilson, MK. Apical ballooning syndrome complicated by acute severe mitral regurgitation with left ventricular outflow obstruction: case report. J Cardiothorac Surg. 2007;2: Vasconcelos JTP, Martins S, Sousa JF, et al. Takotsubo cardiomyopathy: a rare cause of cardiogenic shock simulating acute myocardial infarction. Arq Bras Cardiol. 2005; 85(2): /abc/v85n2/en_25316.pdf. Accessed September 4, Desmet WJR, Adriaenssens BFM, Dens JAY. Apical ballooning of the left ventricle: first series in white patients. Heart. 2003;89(9): Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005;111(40): Seth PS, Aurigemma GP, Krasnow JM, Tighe DA, Untereker WJ, Meyer TE. A syndrome of transient left ventricular apical wall motion abnormality in the absence of coronary disease: a perspective from the United States. Cardiology. 2003;100(2): Wittstein HS, Theimann DR, Lima JAC, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med. 2005;352(6): ICD-9 code for apical ballooning. National Center for Health Statistics Web site. /ftpicd9/icdidx_addenda07.pdf. Accessed September 13, Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Koike H, Sasaka K. The clinical features of takotsubo cardiomyopathy. Q J Med. 2003;96a(8): CRITICALCARENURSE Vol 27, No. 6, DECEMBER

8 19. Elian D, Osherov A, Matetzky S, et al. Left ventricular apical ballooning: not an uncommon variant of acute myocardial infarction in women. Clin Cardiol. 2006; 29(1): Aurigemma GP, Tighe DA. Echocardiography and reversible left ventricular dysfunction. Am J Med. 2006;119: Assennato P, Alfano R, Novo G, et al. Two cases of tako-tsubo cardiomyopathy in Caucasians. Ital Heart J. 2005;6(7): Bybee KA, 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(11): Suzuki K, Osada N, Akashi Y, et al. An atypical case of takotsubo cardiomyopathy during alcohol withdrawal: abnormality in the transient left ventricular wall motion and a remarkable elevation in the ST segment. Intern Med. 2004;43(4): Virani SS, Nasser Khan A, Mendoza EC, Ferreira AC, de Marchena E. Takotsubo cardiomyopathy, or broken-heart syndrome. Tex Heart Inst J. 2007;34(1): Nwachukwu IA. Left ventricular apical ballooning syndrome: a case report of an unusual syndrome. Cardiol Rev. 2007;24(3): Hayashi M, Yamada H, Agatsuma T, Nomura H, Kitahara O. A case of takotsubo-shaped hypokinesis of the left ventricle caused by a lightening strike. Int Heart J. 2005;46:(5): Watanabe H, Kodama M, Okura Y, et al. Impact of earthquakes on takotsubo cardiomyopathy. JAMA. 2005;294(3): Villareal RP, Achari A, Wilansky S, Wilson J. Anteroapical stunning and left ventricular outflow obstruction. Mayo Clin Proc. 2001;76: Park JH, Kang SJ, Song JK, et al. Left ventricular apical ballooning due to severe physical stress in patients admitted to the medical ICU. Chest. 2005;128(1): Merli E, Sutcliffe S, Gori M, Sutherland GG. Tako-tsubo cardiomyopathy: new insights into the possible underlying pathophysiology. Eur J Echocardiogr. 2006;7(1): Ohwada R, Hotta M, Kimura H, et al. Ampulla cardiomyopathy after hypoglycemia in three young female patients with anorexia nervosa. Intern Med. 2005;44: Ito K, Sugihara H, Katoh S, Azuma A, Nakagawa M. Assessment of takotsubo (ampulla) cardiomyopathy using 99mTc-tetrofosmin myocardial SPECT: comparison with acute coronary syndrome. Ann Nucl Med. 2003; 17(2): Pison L, De Vusser P, Mullens W. Apical ballooning in relatives. Heart. 2004;90:e Ibanez B, Navarro F, Farre J, et al. Takotsubo transient left ventricular apical ballooning is associated with a left anterior descending coronary artery with a long course along the apical diaphragmatic surface of the left ventricle. Rev Esp Cardiol. 2004;57(3): /wdbcgi.exe/cardio/cardioeng.mrevista_ cardio.fulltext?pident= Accessed September 1, Akashi YJ, Musha H, Nakazawa K, Miyake F. Plasma brain natriuretic peptide in takotsubo cardiomyopathy. QJM. 2004;97(9): Ogura R, Hiasa Y, Takahashi T, et al. Specific findings of the standard 12-lead ECG in patients with takotsubo cardiomyopathy: comparison with the findings of acute anterior myocardial infarction. Circ J. 2003; 67(8): Tibrewala AV, Moss BN, Cooper HA. A rare case of tako-tsubo cardiomyopathy complicated by a left ventricular thrombus. South Med J. 2006;99(1): Akashi YJ, Tejima T, Sakurada H, et al. Left ventricular rupture associated with takotsubo cardiomyopathy. Mayo Clin Proc. 2004;79(6): Leeper B. Cardiovascular system. In: Chulay M, Burns SM. AACN Essentials of Critical Care Nursing. New York, NY: McGraw-Hill Co Inc; 2006: Woods SL, Sivarajan Froelicher ES, Underhill Motzer S, Bridges EJ. Cardiac Nursing, 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; Purgason K. Broken hearts: differentiating stress-induced cardiomyopathy from acute myocardial infarction in the patient presenting with acute coronary syndrome. Dimens Crit Care Nurs. 2006;25(6): CRITICALCARENURSE Vol 27, No. 6, DECEMBER

9 CE Test Test ID C076: Transient Left Ventricular Apical Ballooning Learning objectives: 1. Define transient left ventricular apical ballooning and examine triggers of this syndrome 2. Describe the clinical features of apical ballooning 3. Identify diagnostic findings common in apical ballooning 1. What do the signs and symptoms of apical ballooning mimic? a. Sick sinus syndrome b. Acute myocardial infarction c. Mitral valve rupture d. Aortic stenosis 2. Which of the following statements is false? a. The signs and symptoms of transient left ventricular apical ballooning include chest pain, ST-segment changes, and the release of cardiac biomarkers. b. The symptoms of transient left ventricular apical ballooning are caused by ischemic coronary artery disease. c. The abrupt onset of extensive ballooning occurs most often in postmenopausal women after a traumatic stressor. d. Although the onset is sudden and dramatic, apical ballooning is transient and reversible. 3. What is the incidence of apical ballooning in women compared to men? a. 2 to 4 times higher b. 4 to 7 times higher c. 6 to 9 times higher d. 8 to 11 times higher 4. Which of the following mechanisms is thought to initiate apical ballooning? a. Stunning of the myocardium related to excess catecholamines b. Spasm of the arteries related to lack of estrogen in the blood stream c. Stunning of the myocardium related to unknown toxin d. Spasm of the arteries because of plaque rupture 5. Which of the following statements is false? a. Electrocardiographic (ECG) findings of deeply inverted T waves are common in the recovery phase. b. ECG findings are variable and cannot be used to diagnose apical ballooning. c. Many patients have a markedly prolonged QT interval. d. ECG findings commonly show ST-segment elevation in leads V 1 through V Which 2 studies reveal the characteristic systolic ballooning of the ventricle? a. Cardiac biomarkers and ECG b. Echocardiogram and magnetic resonance imaging c. Cardiac catheterization and positron-emission tomography scan d. Echocardiogram and left ventriculography 7. What are the f indings on coronary angiography for patients with apical ballooning? a. Occlusive lesion in left anterior descending coronary artery b. Occlusive lesion in first diagonal c. No significant disease d. First obtuse marginal spasm 8. Which of the following statements is false? a. Management of apical ballooning is largely empirical. b. Fibrinolytic agents are used to treat patients with apical ballooning. c. Antiarrhythmic drugs are administered for ventricular arrhythmias. d. Short-term anticoagulation may be given to prevent ventricular thrombus. 9. What is the most common complication of apical ballooning? a. Left ventricular rupture b. Mural thrombus c. Left ventricular failure d. Heart block 10. What is the general outcome for patients with apical ballooning? a. High mortality rate because of ventricular rupture b. Left ventricular function improves rapidly c. ECG improves rapidly and resolves within 7 days d. Mortality rate of 15% is reported 11. Which of the following medications is never indicated for apical ballooning? a. Eptifibatide b. Dopamine c. Dobutamine d. Enoxaparin 12. What was the common factor in the 3 case studies presented in the article? a. All had an ejection fraction of less than 30% b. All were diagnosed correctly within 48 hours c. All had troponin levels greater than 2.0 ng/ml d. All were postmenopausal women 1. a Test answers: Mark only one box for your answer to each question. You may photocopy this form. 2. a 3. a 4. a 5. a 6. a Test ID: C076 Form expires: December 1, 2009 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75 %) Category: A, Synergy CERP A Test writer: Jane Baron, RN, CS, ACNP Program evaluation Yes No Objective 1 was met Name Address Member # Objective 2 was met Objective 3 was met City State ZIP Content was relevant to my Country Phone For faster processing, take nursing practice this CE test online at My expectations were met This method of CE is effective RN Lic. 1/St RN Lic. 2/St ( CE Articles in this issue ) for this content or mail this entire page to: The level of difficulty of this test was: Payment by: Visa M/C AMEX Discover Check easy medium difficult AACN, 101 Columbia To complete this program, Card # Expiration Date Aliso Viejo, CA it took me hours/minutes. Signature 7. a 8. a 9. a 10. a 11. a The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center s Commission on Accreditation. AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN programming meets the standards for most other states requiring mandatory continuing education credit for relicensure. 12. a

10 Transient Left Ventricular Apical Ballooning Brenda McCulloch Crit Care Nurse 2007; Copyright 2007 by the American Association of Critical-Care Nurses Published online Personal use only. For copyright permission information: Subscription Information Information for authors Submit a manuscript alerts Critical Care Nurse is an official peer-reviewed journal of the American Association of Critical-Care Nurses (AACN) published bimonthly by AACN, 101 Columbia, Aliso Viejo, CA Telephone: (800) , (949) , ext Fax: (949) Copyright 2016 by AACN. All rights reserved.