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An Unusual Suspect in a Case of Left Ventricular Aneurysm
ARTICLE IN PRESS Journal of Cardiothoracic and Vascular Anesthesia 000 (2019) 15
Contents lists available at ScienceDirect
Journal of Cardiothoracic and Vascular Anesthesia journal homepage: www.jcvaonline.com
E-Challenge
An Unusual Suspect in a Case of Left Ventricular Aneurysm 1XD XDanielle E. Babb, D2X XDO*,1, D3X XArnaldo Vera-Arroyo, D4X XMD*,y, D5X XYiliam Rodriquez-Blanco, D6X XMD*, D7X XMichael Fabbro, D8X XII, DO* *
Jackson Memorial Hospital, University of Miami Miller School of Medicine, Miami, FL y Miami Veteran’s Health Administration, Miami, FL
Key Words: echocardiography; apical left ventricular aneurysm; Chagas cardiomyopathy; nonischemic cardiomyopathy
Although the exact incidence is unknown, most left ventricular aneurysms (LVAs) in the United States are related to coronary atherosclerosis, while other common causes include post-cardiac surgical and traumatic causes.1 Once an aneurysm is suspected on echocardiography, the greatest diagnostic dilemma is differentiating between a true LVA and pseudoaneurysms. Certain echocardiography features favor one diagnosis over the other, and management relies on this determination. Aneurysm location is one of those features. Pseudoaneurysms most commonly are located in the posterior and inferior left ventricular wall, whereas only 3% of true aneurysms are located posteriorly.2 Coronary angiography is usually diagnostic and is the next step in management. Combined with echocardiography findings, coronary angiography also helps differentiate true LVA from pseudoaneurysm to guide treatment.2 On coronary angiography, a true aneurysm will reveal coronary arteries that cover the thinned ventricular wall. In contrast, a pseudoaneurysm causes the classic draping pattern, such that the coronary arteries do not drape over the defect.1 Other imaging modalities including computed tomographic angiography and magnetic resonance have been described, but are time-consuming, expensive, and not universally available.2 No widely accepted societal Conflicts of Interest: The authors have no Conflicts of Interest to disclose. 1 Address reprint requests to Danielle Babb, DO, Jackson Memorial Hospital, University of Miami Miller School of Medicine, 1611 NW 12th Ave, Miami, FL 33136. E-mail address: [email protected] (D.E. Babb). DOI of original article: http://dx.doi.org/10.1053/j.jvca.2019.01.014. https://doi.org/10.1053/j.jvca.2019.01.016 1053-0770/Ó 2019 Elsevier Inc. All rights reserved.
guidelines are currently available. In the setting of a normal coronary angiography study, alternate rare diagnoses for LVA must be considered. Clinical Case The patient was D10X XA 45-year-old woman D1X Xemigrated from El Salvador to the United States 18 years prior with a past medical history significant for hypertriglyceridemia. She presented to her outpatient primary care physician with complaints of nonradiating chest pain associated with left arm numbness, dizziness, intermittent dyspnea at rest, and 2pillow orthopnea for 3 months. Transthoracic echocardiography revealed a left ventricle ejection fraction of 30% to 35%, a large left ventricular apical aneurysm, and heart failure of unknown etiology (New York Heart Association class I). She was admitted to the authors’ institution to determine the cause of heart failure and for further management. On admission, transesophageal echocardiography was performed, which again demonstrated a left apical ventricular aneurysm with a reduced ejection fraction (Figs. 1 and 2). Coronary angiography was performed, which demonstrated completely normal coronaries. E-Challenge With an ischemic cause of heart failure less likely, what other causes should be considered to explain the findings in Figs. 1 and 2?
ARTICLE IN PRESS 2
D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15
Fig 1. Two-chamber view demonstrating left ventricle apical aneurysm.
Clinical Course Given that the patient was symptomatic, the decision was made to resect the aneurysm electively. Intraoperative findings revealed a dyskinetic apex with significant enlargement (Fig 3). The patient was placed on cardiopulmonary bypass, and resection was accomplished by plicating the aneurysm with a beating heart (Fig 4). The patient met extubation criteria at the end of surgery, and inotropes were weaned off after several days. To confirm previous exposure, Trypanosoma titers were sent postoperatively and resulted in positive titers. The patient likely acquired the acute infection 20 to 30 years ago that then progressed to Chagas cardiomyopathy (CCM). Most patients at the authors’ institution in Miami, Florida are Latin American immigrants, thus the authors maintain a high level of suspicion for this disease. After surgery, the patient’s heart failure symptoms were managed aggressively and she eventually was discharged. At postoperative day 60, her left ventricle ejection fraction slightly improved to 40% to 45%. Although at postoperative day 90, she continued to report shortness of breath with moderate physical exertion. Discussion Chagas disease acquired its name from the Brazilian doctor Carlos Chagas, who discovered it in 1909.3 Yet it is not a new
disease. Evidence of the disease can be found in Chinchorro mummies in the Chilean desert that date back 9,000 years.3 Chagas disease is caused by the protozoan Trypanosoma cruzi (T cruzi) and is endemic to Latin America; however, with migration Chagas disease is becoming a global burden. In Latin America, an estimated 6 million people are infected with T cruzi; 300,000 of those people now reside in the United States, and 30,000 to 45,000 of these patients have cardiomyopathy. Infected insect vectors, “kissing” bugs, transmit the protozoa to humans through their feces, contaminating the mucous membranes of people typically residing in poor rural housing.4,5 Other forms of transmission have been described. Clinicians need to maintain suspicion for patients with a history of travel to endemic countries, Latin American immigrants, patients with a history of blood transfusions, and patients with a family history, as vertical transmission is possible.6 Once contracted, a brief acute phase characterized by a nonspecific febrile illness lasting a few weeks may occur.4 Rarely, acute myocarditis may occur at this time. After this acute illness, patients typically remain asymptomatic for decades, causing significant diagnostic challenges for clinicians. CCM is the most serious complication of chronic disease, and develops in 20% to 40% of patients.7 It is within this patient group that LVA may manifest.8 Apical aneurysms are found on echocardiography in greater than 50% of symptomatic patients with CCM compared to asymptomatic patients. The first diagnostic
ARTICLE IN PRESS D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15
3
Fig 2. Four-chamber view demonstrating apical aneurysm.
dilemma for echocardiographers in ventricular aneurysm cases is differentiating between true LVA and pseudoaneurysms or congenital diverticulum. This distinction is essential, because pseudoaneurysms can represent urgent clinical scenarios and avoidance of thrombolytics in these patients is prudent. This is crucial because both LVA and pseudoaneurysms are seen most commonly in myocardial ischemia.2 Pseudoaneurysms are caused by true myocardial wall disruptions with blood being retained often by thin adherent pericardial segments. True aneurysms involve saccular dilation of an intact ventricular wall. Pseudoaneurysms tend to occur in a posterior or posterior-lateral position, which only is seen in a small percentage (3%) of all aneurysm cases.2 Additionally, pseudoaneurysms tend to have narrow openings with larger aneurysmal bodies. Some studies have suggested using criteria comparing the neck opening width to the aneurysmal sac width, with small ratios (<0.5) being suggestive of pseudoaneurysm cases.9 Congenital diverticulum is an appendage of tissue most commonly found in the left ventricle wall and normally has a hook-like appearance.10 Congenital diverticulum are recognized easily by their normal synchronous contractile function, because they contain all 3 layers of myocardium.11 Coronary angiography, the next step in management, can provide additional clues because pseudoaneurysms are devoid of any
coronary flow in the sac wall. Once the diagnosis of a true aneurysm is established, consideration for etiologies is important, particularly in cases with normal coronary angiography. In patients with normal coronaries, the differential diagnoses include trauma, Takotsubo cardiomyopathy, hypertrophic cardiomyopathies, focal myocarditis, glycogen storage disease, Chagas disease, sarcoidosis, amyloidosis, and congenital or idiopathic etiologies.1114 Many of these diagnoses may be suspected based on patient history, clinical scenario, or other echocardiographic findings. CCM is unique in that it often is the only manifestation of chronic Chagas. Apical aneurysms in the setting of dilated cardiomyopathy and normal coronaries are correlated strongly with Chagas’ disease, especially in patients with a history of potential exposure. Aneurysms in Chagas’ disease may have some specific echocardiography findings suggestive of the diagnosis.15 Echocardiographic findings consistent with Chagas include regional wall motion abnormalities, particularly inferior wall hypokinesis, in the absence of coronary disease. Aneurysms also may occur uniquely in the inferior wall (up to 20% of the time) as opposed to the apex or anterior wall as seen in true aneurysm secondary to ischemic events. Global left ventricle dilation and diffuse hypokinesis also are seen in advanced disease.15 Further imaging modalities such as left ventriculography, computed tomographic angiography, and cardiac magnetic
ARTICLE IN PRESS 4
D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15
Fig 4. Intraoperative aneurysm resection. Fig 3. Intraoperative images of large left ventricular apical aneurysm.
resonance (CMR) imaging with gadolinium also may be helpful. CMR is particularly useful because it is a low-risk, noninvasive tool that assesses myocardial function and tissue. CMR may favor certain cardiomyopathies based on the delayed gadolinium enhancement pattern.13 Delayed gadolinium enhancement appears subendocardial to transmural for a myocardial infarction, and a mid-myocardial pattern suggests myocarditis pathologies. A minimal delayed gadolinium enhancement pattern alludes to Takotsubo cardiomyopathy, while an epicardial pattern to the left ventricular free wall suggests Chagas disease.13,16 Treatment is aimed at early diagnosis, imaging surveillance, and, once Chagas has progressed to CCM, treatment of heart failure symptoms. Advanced CCM often requires surgical interventions including ablation procedures, automatic implantable cardioverter-defibrillator and pacemaker implantation, aneurysm resection, left ventricular assist devices, bridging extracorporeal membrane oxygenation, and, lastly, heart transplantation.6 In nonendemic countries like the United States, recognition of cardiac involvement by CCM likely is underappreciated and diagnosis remains challenging. With increasing Latin American immigration, physicians need to maintain a high notion for this disease when patients present with new-onset nonischemic cardiomyopathy with or without a left ventricular apical aneurysm.
References 1 Ba’albaki HA, Clements SD. Left ventricular aneurysm: A review. Clin Cardiol 1989;12:5–13. 2 Zoffoli G, Mangino D, Venturini A, et al. Diagnosing left ventricular aneurysm from pseudo-aneurysm: A case report and a review in literature. J Cardiothorac Surg 2009;4:1–5. 3 Aufderheide AC, Salo W, Madden M, et al. A 9,000-year record of Chagas’ disease. Proc Natl Acad Sci U S A 2004;101:2034–9. 4 Bocchi EA, Bestetti RB, Scanavacca MI, et al. Chronic Chagas heart disease management: From etiology to cardiomyopathy treatment. J Am Coll Cardiol 2017;70:1510–24. 5 Sasagawa E, de Aguilar AVG, de Ramırez MAH, et al. Acute chagas disease in El Salvador 2000-2012 - Need for surveillance and control. Mem Inst Oswaldo Cruz 2014;109:256–8. 6 Gascon J, Albajar P, Ca~nas E, et al. Diagnosis, management, and treatment of chronic Chagas’ heart disease in areas where Trypanosoma cruzi infection is not endemic. Rev Espa~nola Cardiol English Ed 2007;60:285–93. 7 Nunes MCP, Badano LP, Marin-Neto JA, et al. Multimodality imaging evaluation of Chagas disease: An expert consensus of Brazilian Cardiovascular Imaging Department (DIC) and the European Association of Cardiovascular Imaging (EACVI). Eur Hear J Cardiovasc Imaging 2018; 19:459–60. 8 Taleb MM. An infrequent cause of apical ventricular aneurysm in the United States. Heart Views 2017;18:54–7. 9 Gatewood RP, Nanda NC. Differentiation of left ventricular pseudoaneurysm from true aneurysm with two dimensional echocardiography. Am J Cardiol 1980;46:869–78. 10 Ohlow MA. Congenital left ventricular aneurysms and diverticula: Definition, pathophysiology, clinical relevance and treatment. Cardiology 2006; 106:63–72.
ARTICLE IN PRESS D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15 11 Yesin M, Kal¸c {k M, Alizade E, et al. Multimodality imaging of a left ventricular aneurysm in a patient with normal coronary arteries: Unusual localization. Echocardiography 2017;34:1110–1. 12 Leucker TM, Agrawal V, Rahim H, et al. Idiopathic “true” left ventricular aneurysm. J Cardiol Cases 2015;12:202–4. 13 Yal¸c inkaya E, Celik ¸ M, Bugan B. Aneurysm associated with normal coronary arteries: A diagnostic dilemma. Int J Cardiol 2013;168:5096.
5
14 Chowdhury UK, Seth S, Sheil A, et al. Successful aneurysmectomy of a congenital apical left ventricular aneurysm. Texas Heart Inst J 2009; 36:331–3. 15 Acquatella H. Echocardiography in Chagas heart disease. Circulation 2007;115:1124–31. 16 Sechtem U, Mahrholdt H, Vogelsberg H. Cardiac magnetic resonance in myocardial disease. Heart 2007;93:1520–7.
Contents lists available at ScienceDirect
Journal of Cardiothoracic and Vascular Anesthesia journal homepage: www.jcvaonline.com
E-Challenge
An Unusual Suspect in a Case of Left Ventricular Aneurysm 1XD XDanielle E. Babb, D2X XDO*,1, D3X XArnaldo Vera-Arroyo, D4X XMD*,y, D5X XYiliam Rodriquez-Blanco, D6X XMD*, D7X XMichael Fabbro, D8X XII, DO* *
Jackson Memorial Hospital, University of Miami Miller School of Medicine, Miami, FL y Miami Veteran’s Health Administration, Miami, FL
Key Words: echocardiography; apical left ventricular aneurysm; Chagas cardiomyopathy; nonischemic cardiomyopathy
Although the exact incidence is unknown, most left ventricular aneurysms (LVAs) in the United States are related to coronary atherosclerosis, while other common causes include post-cardiac surgical and traumatic causes.1 Once an aneurysm is suspected on echocardiography, the greatest diagnostic dilemma is differentiating between a true LVA and pseudoaneurysms. Certain echocardiography features favor one diagnosis over the other, and management relies on this determination. Aneurysm location is one of those features. Pseudoaneurysms most commonly are located in the posterior and inferior left ventricular wall, whereas only 3% of true aneurysms are located posteriorly.2 Coronary angiography is usually diagnostic and is the next step in management. Combined with echocardiography findings, coronary angiography also helps differentiate true LVA from pseudoaneurysm to guide treatment.2 On coronary angiography, a true aneurysm will reveal coronary arteries that cover the thinned ventricular wall. In contrast, a pseudoaneurysm causes the classic draping pattern, such that the coronary arteries do not drape over the defect.1 Other imaging modalities including computed tomographic angiography and magnetic resonance have been described, but are time-consuming, expensive, and not universally available.2 No widely accepted societal Conflicts of Interest: The authors have no Conflicts of Interest to disclose. 1 Address reprint requests to Danielle Babb, DO, Jackson Memorial Hospital, University of Miami Miller School of Medicine, 1611 NW 12th Ave, Miami, FL 33136. E-mail address: [email protected] (D.E. Babb). DOI of original article: http://dx.doi.org/10.1053/j.jvca.2019.01.014. https://doi.org/10.1053/j.jvca.2019.01.016 1053-0770/Ó 2019 Elsevier Inc. All rights reserved.
guidelines are currently available. In the setting of a normal coronary angiography study, alternate rare diagnoses for LVA must be considered. Clinical Case The patient was D10X XA 45-year-old woman D1X Xemigrated from El Salvador to the United States 18 years prior with a past medical history significant for hypertriglyceridemia. She presented to her outpatient primary care physician with complaints of nonradiating chest pain associated with left arm numbness, dizziness, intermittent dyspnea at rest, and 2pillow orthopnea for 3 months. Transthoracic echocardiography revealed a left ventricle ejection fraction of 30% to 35%, a large left ventricular apical aneurysm, and heart failure of unknown etiology (New York Heart Association class I). She was admitted to the authors’ institution to determine the cause of heart failure and for further management. On admission, transesophageal echocardiography was performed, which again demonstrated a left apical ventricular aneurysm with a reduced ejection fraction (Figs. 1 and 2). Coronary angiography was performed, which demonstrated completely normal coronaries. E-Challenge With an ischemic cause of heart failure less likely, what other causes should be considered to explain the findings in Figs. 1 and 2?
ARTICLE IN PRESS 2
D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15
Fig 1. Two-chamber view demonstrating left ventricle apical aneurysm.
Clinical Course Given that the patient was symptomatic, the decision was made to resect the aneurysm electively. Intraoperative findings revealed a dyskinetic apex with significant enlargement (Fig 3). The patient was placed on cardiopulmonary bypass, and resection was accomplished by plicating the aneurysm with a beating heart (Fig 4). The patient met extubation criteria at the end of surgery, and inotropes were weaned off after several days. To confirm previous exposure, Trypanosoma titers were sent postoperatively and resulted in positive titers. The patient likely acquired the acute infection 20 to 30 years ago that then progressed to Chagas cardiomyopathy (CCM). Most patients at the authors’ institution in Miami, Florida are Latin American immigrants, thus the authors maintain a high level of suspicion for this disease. After surgery, the patient’s heart failure symptoms were managed aggressively and she eventually was discharged. At postoperative day 60, her left ventricle ejection fraction slightly improved to 40% to 45%. Although at postoperative day 90, she continued to report shortness of breath with moderate physical exertion. Discussion Chagas disease acquired its name from the Brazilian doctor Carlos Chagas, who discovered it in 1909.3 Yet it is not a new
disease. Evidence of the disease can be found in Chinchorro mummies in the Chilean desert that date back 9,000 years.3 Chagas disease is caused by the protozoan Trypanosoma cruzi (T cruzi) and is endemic to Latin America; however, with migration Chagas disease is becoming a global burden. In Latin America, an estimated 6 million people are infected with T cruzi; 300,000 of those people now reside in the United States, and 30,000 to 45,000 of these patients have cardiomyopathy. Infected insect vectors, “kissing” bugs, transmit the protozoa to humans through their feces, contaminating the mucous membranes of people typically residing in poor rural housing.4,5 Other forms of transmission have been described. Clinicians need to maintain suspicion for patients with a history of travel to endemic countries, Latin American immigrants, patients with a history of blood transfusions, and patients with a family history, as vertical transmission is possible.6 Once contracted, a brief acute phase characterized by a nonspecific febrile illness lasting a few weeks may occur.4 Rarely, acute myocarditis may occur at this time. After this acute illness, patients typically remain asymptomatic for decades, causing significant diagnostic challenges for clinicians. CCM is the most serious complication of chronic disease, and develops in 20% to 40% of patients.7 It is within this patient group that LVA may manifest.8 Apical aneurysms are found on echocardiography in greater than 50% of symptomatic patients with CCM compared to asymptomatic patients. The first diagnostic
ARTICLE IN PRESS D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15
3
Fig 2. Four-chamber view demonstrating apical aneurysm.
dilemma for echocardiographers in ventricular aneurysm cases is differentiating between true LVA and pseudoaneurysms or congenital diverticulum. This distinction is essential, because pseudoaneurysms can represent urgent clinical scenarios and avoidance of thrombolytics in these patients is prudent. This is crucial because both LVA and pseudoaneurysms are seen most commonly in myocardial ischemia.2 Pseudoaneurysms are caused by true myocardial wall disruptions with blood being retained often by thin adherent pericardial segments. True aneurysms involve saccular dilation of an intact ventricular wall. Pseudoaneurysms tend to occur in a posterior or posterior-lateral position, which only is seen in a small percentage (3%) of all aneurysm cases.2 Additionally, pseudoaneurysms tend to have narrow openings with larger aneurysmal bodies. Some studies have suggested using criteria comparing the neck opening width to the aneurysmal sac width, with small ratios (<0.5) being suggestive of pseudoaneurysm cases.9 Congenital diverticulum is an appendage of tissue most commonly found in the left ventricle wall and normally has a hook-like appearance.10 Congenital diverticulum are recognized easily by their normal synchronous contractile function, because they contain all 3 layers of myocardium.11 Coronary angiography, the next step in management, can provide additional clues because pseudoaneurysms are devoid of any
coronary flow in the sac wall. Once the diagnosis of a true aneurysm is established, consideration for etiologies is important, particularly in cases with normal coronary angiography. In patients with normal coronaries, the differential diagnoses include trauma, Takotsubo cardiomyopathy, hypertrophic cardiomyopathies, focal myocarditis, glycogen storage disease, Chagas disease, sarcoidosis, amyloidosis, and congenital or idiopathic etiologies.1114 Many of these diagnoses may be suspected based on patient history, clinical scenario, or other echocardiographic findings. CCM is unique in that it often is the only manifestation of chronic Chagas. Apical aneurysms in the setting of dilated cardiomyopathy and normal coronaries are correlated strongly with Chagas’ disease, especially in patients with a history of potential exposure. Aneurysms in Chagas’ disease may have some specific echocardiography findings suggestive of the diagnosis.15 Echocardiographic findings consistent with Chagas include regional wall motion abnormalities, particularly inferior wall hypokinesis, in the absence of coronary disease. Aneurysms also may occur uniquely in the inferior wall (up to 20% of the time) as opposed to the apex or anterior wall as seen in true aneurysm secondary to ischemic events. Global left ventricle dilation and diffuse hypokinesis also are seen in advanced disease.15 Further imaging modalities such as left ventriculography, computed tomographic angiography, and cardiac magnetic
ARTICLE IN PRESS 4
D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15
Fig 4. Intraoperative aneurysm resection. Fig 3. Intraoperative images of large left ventricular apical aneurysm.
resonance (CMR) imaging with gadolinium also may be helpful. CMR is particularly useful because it is a low-risk, noninvasive tool that assesses myocardial function and tissue. CMR may favor certain cardiomyopathies based on the delayed gadolinium enhancement pattern.13 Delayed gadolinium enhancement appears subendocardial to transmural for a myocardial infarction, and a mid-myocardial pattern suggests myocarditis pathologies. A minimal delayed gadolinium enhancement pattern alludes to Takotsubo cardiomyopathy, while an epicardial pattern to the left ventricular free wall suggests Chagas disease.13,16 Treatment is aimed at early diagnosis, imaging surveillance, and, once Chagas has progressed to CCM, treatment of heart failure symptoms. Advanced CCM often requires surgical interventions including ablation procedures, automatic implantable cardioverter-defibrillator and pacemaker implantation, aneurysm resection, left ventricular assist devices, bridging extracorporeal membrane oxygenation, and, lastly, heart transplantation.6 In nonendemic countries like the United States, recognition of cardiac involvement by CCM likely is underappreciated and diagnosis remains challenging. With increasing Latin American immigration, physicians need to maintain a high notion for this disease when patients present with new-onset nonischemic cardiomyopathy with or without a left ventricular apical aneurysm.
References 1 Ba’albaki HA, Clements SD. Left ventricular aneurysm: A review. Clin Cardiol 1989;12:5–13. 2 Zoffoli G, Mangino D, Venturini A, et al. Diagnosing left ventricular aneurysm from pseudo-aneurysm: A case report and a review in literature. J Cardiothorac Surg 2009;4:1–5. 3 Aufderheide AC, Salo W, Madden M, et al. A 9,000-year record of Chagas’ disease. Proc Natl Acad Sci U S A 2004;101:2034–9. 4 Bocchi EA, Bestetti RB, Scanavacca MI, et al. Chronic Chagas heart disease management: From etiology to cardiomyopathy treatment. J Am Coll Cardiol 2017;70:1510–24. 5 Sasagawa E, de Aguilar AVG, de Ramırez MAH, et al. Acute chagas disease in El Salvador 2000-2012 - Need for surveillance and control. Mem Inst Oswaldo Cruz 2014;109:256–8. 6 Gascon J, Albajar P, Ca~nas E, et al. Diagnosis, management, and treatment of chronic Chagas’ heart disease in areas where Trypanosoma cruzi infection is not endemic. Rev Espa~nola Cardiol English Ed 2007;60:285–93. 7 Nunes MCP, Badano LP, Marin-Neto JA, et al. Multimodality imaging evaluation of Chagas disease: An expert consensus of Brazilian Cardiovascular Imaging Department (DIC) and the European Association of Cardiovascular Imaging (EACVI). Eur Hear J Cardiovasc Imaging 2018; 19:459–60. 8 Taleb MM. An infrequent cause of apical ventricular aneurysm in the United States. Heart Views 2017;18:54–7. 9 Gatewood RP, Nanda NC. Differentiation of left ventricular pseudoaneurysm from true aneurysm with two dimensional echocardiography. Am J Cardiol 1980;46:869–78. 10 Ohlow MA. Congenital left ventricular aneurysms and diverticula: Definition, pathophysiology, clinical relevance and treatment. Cardiology 2006; 106:63–72.
ARTICLE IN PRESS D.E. Babb et al. / Journal of Cardiothoracic and Vascular Anesthesia 00 (2019) 15 11 Yesin M, Kal¸c {k M, Alizade E, et al. Multimodality imaging of a left ventricular aneurysm in a patient with normal coronary arteries: Unusual localization. Echocardiography 2017;34:1110–1. 12 Leucker TM, Agrawal V, Rahim H, et al. Idiopathic “true” left ventricular aneurysm. J Cardiol Cases 2015;12:202–4. 13 Yal¸c inkaya E, Celik ¸ M, Bugan B. Aneurysm associated with normal coronary arteries: A diagnostic dilemma. Int J Cardiol 2013;168:5096.
5
14 Chowdhury UK, Seth S, Sheil A, et al. Successful aneurysmectomy of a congenital apical left ventricular aneurysm. Texas Heart Inst J 2009; 36:331–3. 15 Acquatella H. Echocardiography in Chagas heart disease. Circulation 2007;115:1124–31. 16 Sechtem U, Mahrholdt H, Vogelsberg H. Cardiac magnetic resonance in myocardial disease. Heart 2007;93:1520–7.