Left Ventricular Free Wall Rupture Research Articles

Left ventricular free wall rupture caused by myocardial ischemia without treatable atherosclerotic coronary disease: a case series

BackgroundThe clinical presentation of left ventricular free wall rupture (LVFWR) varies ranging from uneventful condition to congestive heart failure.Case summaryHere we report two cases of LVFWR with different clinical presentation and notable outcome. A 53-year-old male presenting emergently with signs of myocardial infarction received immediate coronary angiography and thoracic CT-scan showing occlusion of the first marginal coronary branch without possibility of revascularization and minimal pericardial extravasation. Under ICU surveillance, LVFWR occurred 24 h later and was treated by pericardiocentesis and ECMO support followed by immediate uncomplicated surgical repair. Postoperative therapy-refractory vasoplegia and electromechanical dissociation caused fulminant deterioration and the early death of the patient. The second case is a 76-year old male brought to the emergency room after sudden syncope, clinical sings of pericardial tamponade and suspicion of a type A acute aortic dissection. Immediate CT-angiography excluded aortic dissection and revealed massive pericardial effusion and a hypoperfused myocardial area on the territory of the first marginal branch. Immediate sternotomy under mechanical resuscitation enabled removal of the massive intrapericardial clot and revealed LVFWR. After an uncomplicated surgical repair, an uneventful postoperative course, the patient was discharged with sinus rhythm and good biventricular function. One year after the operation, he is living at home, symptom free.DiscussionWhereas the younger patient, who was clinically stable at hospital admission received delayed surgery and did not survive treatment, the older patient, clinically unstable at presentation, went into immediate surgery and had a flawless postoperative course. Thus, early surgical repair of LVFWR leads to best outcome and treating LVFWR as a high emergency regardless of the symptoms improve survival.

Left Ventricular Free Wall Rupture Following Acute Myocardial Infarction: A Case Report and Discussion

We report a case of left ventricular free wall rupture (LVFWR) in a 57-year-old female who developed an abrupt myocardial infarction. The diagnosis was confirmed using echocardiography. The patient underwent a successful surgical repair involving suturing, patch insertion, and coronary artery bypass grafting (CABG). The present case demonstrates that, while LVFWR is generally deadly, it can be adequately controlled with timely diagnosis and surgical intervention. Keywords: left ventricular free wall rupture (LVFWR), Acute myocardial infarction (AMI), coronary artery bypass grafting (CABG).

Conservative treatment of post-infarction left ventricular free-wall rupture: case report

Conservative treatment of post-infarction left ventricular free-wall rupture: case report

Successful sutureless repair of multiple left ventricular free wall ruptures due to Takotsubo cardiomyopathy: a case report

BackgroundTakotsubo cardiomyopathy (TCM) is a temporary and reversible systolic abnormality of the left ventricular apical area resembling a myocardial infarction. Cardiac rupture due to TCM is a rare but fatal complication. Without cardiac surgery, 94% of patients with left ventricular free wall rupture (LVFWR) due to TCM die. Furthermore, successful surgical cases are rare. We report herein the successful treatment of multiple LVFWRs due to TCM using a sutureless repair.Case presentationAn 80-year-old man quarreled with his daughter and had a sudden onset of chest pain. He was transferred to our hospital in shock. Electrocardiography showed ST elevation and contrast-enhanced computed tomography revealed a bloody pericardial effusion. Emergent coronary angiography showed no significant stenosis. Cardiac arrest ensued because of cardiac tamponade. Emergent surgery was undertaken and three oozing lacerations on the lateral and inferior walls were noted. A sutureless repair was performed using TachoSil® patches. We also applied Surgicel Nu-Knit® absorbable hemostat with Hydrofit® where TachoSil® failed to completely adhere because of hematoma formation and achieved complete hemostasis. We diagnosed the ruptures due to TCM according to the Mayo criteria. The patient was discharged on postoperative day 71.ConclusionsA sutureless repair using TachoSil® patches and Surgicel® with Hydrofit® is a minimally invasive and effective method for the treatment of multiple LVFWRs due to TCM.

Successful surgical management of ventricular septal perforation following left ventricular free wall rupture due to acute myocardial infarction: a case report

BackgroundThe mechanical complications associated with acute myocardial infarction can be fatal. We report a life-saving case of a very elderly patient with consecutive mechanical complications of acute myocardial infarction.Case presentationA 90-year-old woman was transferred to our hospital for emergency care due to chest pain. She underwent emergency percutaneous coronary intervention of the left anterior descending branch and was diagnosed with acute myocardial infarction and intra-aortic balloon pumping insertion was performed. After returning to the intensive care unit, she experienced chest pain and went into shock. Echocardiography showed left ventricular free wall rupture, and percutaneous cardiopulmonary support was established. Emergency left ventriculoplasty was performed for the left ventricular free wall rupture. A ventricular septal perforation was observed on postoperative day 9, and its closure through right ventriculotomy was performed on postoperative day 10. On the 128th postoperative day, the patient was transferred to the hospital for rehabilitation.ConclusionsA 90-year-old patient with consecutive left ventricular free wall rupture and ventricular septal perforation after acute myocardial infarction was successfully managed with two surgeries.

Surgical Outcome of Postinfarction Left Ventricular Free Wall Rupture.

Left ventricular free wall rupture (LVFWR) is a rare and fatal complication after acute myocardial infarction. Early recognition and aggressive treatment are recommended. Between August 1999 and February 2023, 11 patients aged between 64 and 79 years developed LVFWR after acute myocardial infarction (mean interval, 3.5 days). Three patients had active bleeding (blowout-type LVFWR), and the other 8 patients experienced the oozing or sealed state. Eight patients were treated using a sutureless technique with Teflon felt and glue, 2 patients were treated using the primary suture closure technique, and 1 was treated using both the primary suture and the sutureless technique with Teflon felt and glue. One patient died in the operating room as a result of bleeding. Cardiovascular stability and hemostasis were achieved in the other 10 patients. There were 3 early deaths (all 3 cases as a result of area bleeding; 1 was treated with primary suture, 2 with sutureless glue). Three patients received percutaneous coronary intervention before discharge. All 8 remaining patients survived and were discharged. Three patients were lost to follow-up. The follow-up period ranged from 2 to 97 months, with 4 patients exhibiting New York Heart Association class I symptoms and 1 exhibiting New York Heart Association class II symptoms. Optimal surgical treatment for postinfarction LVFWR remains controversial. The sutureless technique may be a promising strategy for treating postinfarction LVFWR.

Surgical repair of left ventricular free-wall rupture complicating acute myocardial infarction: a single-center 30 years of experience.

Left ventricular free-wall rupture (LVFWR) is a catastrophic complication of acute myocardial infarction (AMI). Historically, cardiac surgery is considered the treatment of choice. However, because of the rarity of this entity, little is known regarding the efficacy and safety of surgical treatment for post-infarction LVFWR. The aim of this study was to report a single-center experience in this field over a period of 30 years. Patients who developed LVFWR following AMI and underwent surgical repair at our Institution from January 1990 to December 2019 were considered. The primary end-point was in-hospital morality rate; secondary outcomes were long-term survival and postoperative complications. Multivariate analysis was carried out by constructing a logistic regression model to identify risk factors for early mortality. A total of 35 patients were enrolled in this study. The mean age was 68.9 years; 65.7% were male. The oozing type of LVFWR was encountered in 29 individuals, and the blowout type in 6 subjects. Sutured repair was used in 77.1% of patients, and sutureless repair in the remaining cases. The in-hospital mortality rate was 28.6%. Low cardiac output syndrome was the main cause of postoperative death. Multivariable analysis identified age >75 years at operation, preoperative cardiac arrest, concurrent ventricular septal rupture (VSR) as independent predictors of in-hospital death. Follow-up was complete in 100% of patients who survived surgery (mean follow-up: 9.3 ± 7.8 years); among the survivors, 16 patients died during the follow-up with a 3-year and 12-year overall survival rate of 82.5% and 55.2%, respectively. Surgical treatment of LVFWR following AMI is possible with acceptable in-hospital mortality and excellent long-term results. Advanced age, concurrent VSR and cardiac arrest at presentation are independent risk factors of poor early outcome.

CASE-TB-01 - A Rare Case of Spontaneous Closure of Left Ventricular Free-wall Rupture After Acute Myocardial Infarction

CASE-TB-01 - A Rare Case of Spontaneous Closure of Left Ventricular Free-wall Rupture After Acute Myocardial Infarction

Abstract 15948: Highly Suspicious Yet Diagnostically Unrevealing Left Ventricular Free-Wall Rupture Following STEMI

Introduction: Left ventricular wall rupture is a rare but lethal complication following a ST elevation myocardial infarction (STEMI). We present a case of left ventricular free-wall rupture not identified on echocardiography and CT angiography (CTA) despite high suspicion who underwent emergent lifesaving mediastinal exploration and repair. Case: A 52-year-old male with past medical history of hypertension presented with typical chest pain. He was found to have STEMI with 100% left anterior descending (LAD) artery occlusion and underwent percutaneous coronary intervention to mid LAD. Post procedure, he developed atrial fibrillation with rapid ventricular rate, pericarditis, increasing pericardial effusion (Figure 1), and cardiogenic shock. He underwent intra-aortic balloon pump placement with no improvement in hemodynamics and subsequently an Impella 5.5 was placed. On post MI Day 3, he underwent pericardial window in the setting of shock and increasing pericardial effusion. Intraoperative TEE showed signs of tamponade physiology (Figure 2). Repeat echocardiograms and CTA was unrevealing of a rupture. Post MI day 6, he had increasing output from the drains and increasing pericardial effusion with complete right ventricular collapse on bedside echocardiogram. Emergent mediastinal exploration revealed left ventricular (LV) free-wall rupture which was repaired with a bovine patch. Hemodynamics improved and goal directed medical therapy was started. Discussion: Free wall rupture is a rare complication post MI and is reported in only 0.01% of STEMI. It usually occurs within 1 week, majority occurring within 24 h of MI. Small LV wall rupture can be challenging to diagnose on cardiac imaging. This case emphasizes the importance of having a high index of suspicion for diagnosing free wall rupture in patients presenting with hemodynamically unstable pericardial effusion post STEMI. Prompt pericardiocentesis and surgical intervention lead to a good outcome.

Successful conservative treatment for left ventricular free wall rupture after acute myocardial infarction

Left ventricular free wall rupture (LVFWR) is a rare but fatal complication of acute myocardial infarction (AMI). An 81-year-old female patient with several cardiovascular risk factors presented to the emergency department with symptoms of developing a chronic stomachache and cold sweat. An echocardiograph showed wall motion abnormalities from the lateral to posterior wall, as well as pericardial effusion containing clots of up to 17 mm in the posterior wall that indicated LVFWR after AMI. Although she was conscious after being brought to the initial care unit, she suddenly lost consciousness and fell into electromechanical dissociation (EMD). Endotracheal intubation was immediately initiated and her pericardial drainage and intra aortic balloon pump (IABP) placement, and hemodynamics recovered. Although she had 100% obstruction in the left circumflex artery (LCX) #12 on coronary angiography (CAG), she was discharged to the Intensive Care Unit (ICU) without percutaneous coronary intervention (PCI). Conservative treatment such as intubation, sedation, pericardiocentesis and strict blood pressure management as well as treatment by IABP long-term support led to the patient being uneventfully discharged after 60 days.

Alternative Method of Surgical Treatment of Post-Infarction Left Ventricular Free Wall Rupture. Case Report

Acute myocardial infarction (AMI) is one of the causes of death in developed countries, despite the latest medical technologies. AMI is usually accompanied by numerous fatal complications. One of these complications is left ventricular free wall rupture (LVFWR). Myocardial rupture after AMI can occur from 1 day to 3 weeks after the infarction. Most ruptures occur 3-5 days after a heart attack. Left ventricular free wall rupture requires only emergency surgical intervention, which in most cases consists in applying U-shaped sutures or wrapping sutures using Teflon patch.
 The aim. To demonstrate an example of alternative surgical tactics and intraoperative management of a patient with myocardial infarction complicated by rupture of the free wall of the heart with the transition to cardiogenic shock.
 Case report. We presented the clinical case of patient V., 72 years old, who was delivered by ambulance on January 10, 2023 to the intensive care department of the National Amosov Institute of Cardiovascular Surgery (Kyiv, Ukraine). Main diagnosis: ischemic heart disease, acute coronary syndrome with ST-elevation myocardial infarction, cardiogenic shock.
 Conclusion. The only effective method of treatment of rupture of the free wall of the heart is surgical intervention. Using a sandwich patch with resection of necrotic areas of the myocardium and U-shaped sutures with Teflon patch passed from the side of the left ventricular cavity through the myocardium in the peri-infarct zone and through a patch from a vascular prosthesis allows hermetically sew up the LVFWR.

Cardiac wall rupture in systemic lupus erythematosus: a case report and review of the literature.

Cardiac wall rupture (CWR) is a serious and often fatal complication of myocardial infarction (MI). Despite an increase in the incidence of MI in patients with systemic lupus erythematosus (SLE), cases of CWR in these patients have been reported rarely. This study reports an SLE patient with CWR and pseudoaneurysm formation and reviews previously reported cases of CWR in SLE patients. An English language literature review of from the PubMed, EMBASE, and Scopus databases on published cases of CWR in SLE, up until January 2023, was performed and analyzed. The search identified 4 patients, including the present one, 5 cases altogether. All of them were female aged 27-40years, and 3 of them had had SLE for 10years or more. Chest pain and dyspnea were the common presentations. All had left ventricular (LV) wall rupture. Three patients had LV wall rupture with pseudoaneurysm formation (one had MI with normal coronary artery, one myocardial necrosis secondary from small coronary artery vasculitis and one MI from uncertain cause). The other 2 patients had LV free wall rupture (one had MI with extensive coronary atherosclerosis with coronary arteritis, and the other septic myocarditis with septic coronary arteritis) and these 2 patients died before the diagnosis was made. Three patients with pseudoaneurysm received surgical correction with good clinical outcomes in all. Cardiac wall rupture is a serious and often fatal cardiac complication. Emergency diagnosis and appropriate management with an experienced cardiology team is crucial. Surgical correction is the treatment of choice. Key Points • Cardiac wall rupture, a serious and often fatal cardiac complication, has rarely been described in SLE patients. • Emergency diagnosis and appropriate management with an experienced cardiology team is crucial. Surgical correction is the treatment of choice.

[Surgical treatment for obstructive hypertrophic cardiomyopathy: a five-year single-center experience of 421 cases].

Objectives: To examine the short-term and mid-term effects of surgical treatment of obstructive hypertrophic cardiomyopathy (HCM) in one center. Methods: The perioperative data and short-term follow-up outcomes of 421 patients with obstructive HCM who received surgical treatment at Department of Cardiac Surgery, Zhongshan Hospital, Fudan University from January 2017 to December 2021 were analyzed retrospectively. There were 207 males and 214 females, aged (56.5±11.7) years (range: 19 to 78 years). Preoperative New York Heart Association (NYHA) classification included 45 cases of class Ⅱ, 328 cases in class Ⅲ, and 48 cases in class Ⅳ. Fifty-eight patients were diagnosed with latent obstructive HCM and 257 patients had moderate or more mitral regurgitation with 56 patients suffering from intrinsic mitral valve diseases. All procedures were completed by a multidisciplinary team, including professional echocardiologists involving in preoperative planning for proper mitral valve management strategies and intraoperative monitoring. A total of 338 patients underwent septal myectomy alone, and 59 patients underwent mitral valve surgery along with myectomy. A single transaortic approach was used in 355 patients, and a right atrial-atrial septal/atrial sulcus approach was used in 51 other patients. Long-handled minimally invasive surgical instruments were used for the procedures. Student t test, Wilcoxon rank sum test, χ2 test or Fisher exact test were used to compare the data before and after surgery. Results: The aortic cross-clamping time of septal myectomy alone was (34.3±8.5) minutes (range: 21 to 94 minutes). Eighteen patients had intraoperative adverse events and underwent immediate reoperation, including residual obstruction (10 patients), left ventricular free wall rupture (4 patients), ventricular septal perforation (3 patients), and aortic valve perforation (1 patient). Four patients died during hospitalization, and 11 patients developed complete atrioventricular block requiring permanent pacemaker implantation. After discharge, 384 (92.1%) patients received a follow-up visit with a median duration of 9 months. All follow-up patients survived with significantly improved NYHA classifications: 216 patients in class Ⅰ and 168 patients in class Ⅱ (χ2=662.73, P<0.01 as compared to baseline). At 6 months after surgery, follow-up echocardiography showed that the thickness of the ventricular septum ((13.6±2.5) mm vs. (18.2±3.0) mm, t=23.51, P<0.01) and the peak left ventricular outflow tract gradient ((12.0±6.3) mmHg vs. (93.4±19.8) mmHg, 1 mmHg=0.133 kPa, t=78.29, P<0.01) were both significantly lower than baseline values. Conclusion: The construction of the surgical team (including echocardiography experts), proper mitral valve management strategies, identification and management of sub-mitral-valve abnormalities, and application of long-handled minimally invasive surgical instruments are important for the successful implementation of septal myectomy with satisfactory short-and medium-term outcomes.

Cardiac Myocyte-Specific Overexpression of FASTKD1 Prevents Ventricular Rupture After Myocardial Infarction.

Background The mitochondrial mRNA-binding protein FASTKD1 (Fas-activatedserine/threonine[FAST] kinase domain-containing protein 1) protects myocytes from oxidative stress in vitro. However, the role of FASTKD1 in the myocardium in vivo is unknown. Therefore, we developed cardiac-specific FASTKD1 transgenic mice to test the effects of this protein on experimental myocardial infarction (MI). Methods and Results Transgenic mouse lines with cardiac myocyte-specific overexpression of FASTKD1 to varying degrees were generated. These mice displayed normal cardiac morphological features and function at the gross and microscopic levels. Isolated cardiac mitochondria from all transgenic mouse lines showed normal mitochondrial function, ATP levels, and permeability transition pore activity. Male nontransgenic and transgenic mice from the highest-expressing line were subjected to 8 weeks of permanent coronary ligation. Of nontransgenic mice, 40% underwent left ventricular free wall rupture within 7 days of MI compared with 0% of FASTKD1-overexpressing mice. At 3 days after MI, FASTKD1 overexpression did not alter infarct size. However, increased FASTKD1 resulted in decreased neutrophil and increased macrophage infiltration, elevated levels of the extracellular matrix component periostin, and enhanced antioxidant capacity compared with control mice. In contrast, markers of mitochondrial fusion/fission and apoptosis remained unaltered. Instead, transcriptomic analyses indicated activation of the integrated stress response in the FASTKD1 transgenic hearts. Conclusions Cardiac-specific overexpression of FASTKD1 results in viable mice displaying normal cardiac morphological features and function. However, these mice are resistant to MI-induced cardiac rupture and display altered inflammatory, extracellular matrix, and antioxidant responses following MI. Moreover, these protective effects were associated with enhanced activation of the integrated stress response.

A Case of Post-Myocardial Infarction Ventricular Septal Rupture and Intramyocardial Dissection

Ventricular septal rupture (VSR), albeit rare, is a deadly consequence of ST elevation myocardial infarction (STEMI). Our patient described here presented with both post-infarction VSR and intramyocardial dissection (IMD) of the right ventricle (RV), a subtype of left ventricular free wall rupture (LVFWR). This case highlights the importance of prompt diagnosis of these post-myocardial infarction (MI) complications and the current limitations of surgical and percutaneous repair.

Left Ventricular Free Wall Rupture Immediately following Successful Coronary Reperfusion Complicating ST Elevation Myocardial Infarction.

Left Ventricular Free Wall Rupture Immediately following Successful Coronary Reperfusion Complicating ST Elevation Myocardial Infarction.

Left Ventricular Free Wall Rupture Complicated by Post-Transfusion Purpura: A therapeutic challenge

Left Ventricular Free Wall Rupture Complicated by Post-Transfusion Purpura: A therapeutic challenge

Abstract 10604: Critical Role of Cardiac Imaging of Mechanical Complication in ST Elevation Myocardial Infarction: Left Ventricular Free Wall Rupture Diagnosed With CTA and Echocardiography

Case Presentation: An 81-year-old male with a thymoma (treated with surgery including partial pericardiectomy 25 years prior) presented to his local ER with chest pain radiating to his back. Vital signs were stable. EKG showed ST elevations in the lateral leads with Q waves. Troponin was positive. Diagnosis included STEMI as well as possible aortic dissection. CT angiography (CTA) did not show dissection; however, contrast extravasation and left ventricular (LV) free wall rupture was noted. Patient was not given thrombolysis and transferred for tertiary care. On arrival, the patient was pain free, hemodynamically stable, and an echo was obtained. Color Doppler and echo contrast confirmed a LV outpouching along the lateral wall with a “narrow neck” consistent with a pseudoaneurysm (PsA, figure 1). CT surgery declined an emergent operation due to the high risk of mortality with early operative intervention and recommended initial conservative management. After 48 hours, a repeat CTA showed increased size of the PsA (figure 2). The patient chose to be managed medically and eventually passed away 8 days after presentation. Discussion: This patient had a contained LV rupture as a STEMI complication. The CTA showed LV rupture and thrombolysis was avoided. Echo confirmed the diagnosis. This case highlights 1) the utility of imaging in in the diagnosis of LV rupture as it is usually limited by early mortality, and 2) its role in differentiating PsA from true aneurysm, which is characterized by a contained wall rupture while true aneurysms develop due to a weakened, but intact, wall.

The Moment of Left Ventricular Free-wall Rupture.

The Moment of Left Ventricular Free-wall Rupture.

Left Ventricular Pseudoaneurysm: A Rare Cause of Chest Pain to Keep in Mind

A man in his 80s presented with sharp central chest pain, diaphoresis, and dyspnea. He had a remote history of coronary artery bypass graft. Results of the physical examination were unremarkable, and initial vital signs were stable. Electrocardiogram was unrevealing. Troponins were elevated and flat. He was initiated on intravenous nitroglycerin, after which his symptoms resolved. However, his blood pressure decreased to a minimal systolic of 76 and diastolic of 50 mm Hg. Because of the resolution of his symptoms, immediate angiography was deferred, and the patient was admitted to the cardiac intensive care unit. Transthoracic echocardiography (TTE) showed a loculated pericardial fluid collection adjacent to the anterolateral left ventricular (LV) wall (Figure; Video 1, available online at http://www.mayoclinicproceedings.org). Contrast TTE showed extension of the contrast from the main LV cavity to the adjacent pericardial cavity, consistent with pseudoaneurysm (Figure; Video 2, available online at http://www.mayoclinicproceedings.org). Computed tomography angiography of the thoracic aorta confirmed LV myocardial rupture along the anterolateral wall with active extravasation of contrast (Supplemental Figure 1A-D, available online at http://www.mayoclinicproceedings.org). The patient’s hospital stay was complicated by acute kidney injury. In the setting of increased risk for dialysis, he opted for conservative management. He remained hemodynamically stable, and pericardiocentesis was not indicated. He was discharged 1 week later. Predismissal TTE redemonstrated the contained LV anterolateral wall rupture with systolic and end-diastolic flow through the myocardial defect (Supplemental Figure 2; Video 3, available online at http://www.mayoclinicproceedings.org). He did well after discharge and died 4 years later of metastatic bladder cancer. Left ventricular pseudoaneurysms develop when LV free-wall rupture is contained by adherent pericardium or scar tissue and is most commonly secondary to myocardial infarction.1Frances C. Romero A. Grady D. Left ventricular pseudoaneurysm.J Am Coll Cardiol. 1998; 32: 557-561https://doi.org/10.1016/s0735-1097(98)00290-3Crossref PubMed Scopus (0) Google Scholar Mortality rate is high both with surgically (23%) and medically (48%) managed patients. Our patient’s previous cardiac surgery was thought to provide him with protection against complete rupture owing to scar tissue formation along the pericardium. The authors have no competing interests. eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiIxNTQxZDIwOGFjOGU1NzExNTdlMjNhZjAyYmQzOWFjZiIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjcyMjg1NzkzfQ.bVK6mgeslM0bvj2ghgDzATVaMK2nN-hvkaaOINrhzerjUTY0BhHMM0RiEzxLzEbBfhrwaelJakGbXXQRNll3c1A4XIQPAMOuOb2WwBwZngrk3sZqt9PQ4-QR1521dLqyo87FedzewHEVHQp1u1-hU63njZ80S64gIww7AGwvm1GYVyG_PUqN2dsULzDkhx0u4N5mSlj1ic-GJziWbDQxyp_vNNXowt-C79lK4_irrwGt4gwiXrVTBjmVW7EKxw5UnOPiqxuUal_anvunu52uzNW3lrhjfMSIvZiK_HwBXn1MpYIpEXuY1maXiO04cZRMuJsbkyi_csiLCsenlZMhWQ Download .mp4 (0.63 MB) Help with .mp4 files Supplemental Video 1eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiJmNmU1ZDFjYzFjN2ZjM2EwMWM5NDQwZTRiMmVjZTQwMyIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjcyMjg1NzkzfQ.Llq0S-_MHJRqyeGeS8Jl1MGMOD3jHXaMnSq2_kq2VhClHCQx7UQu2w1bavnJDzW-urKRKWcnlXxIP6c8ScTvUdDnqtsubhEVrzHW2JY3Z0uOy9wcg6B_njlmvDJ7DjHkNV_Wg1UShZnAe4D0BMcCn1xyOhNhnmdAmi6V4c4-scHYs1f39hzgdjf9w5F7dKcuSbIKlkrjtEY_qTeY2cR1xdts7_cPrryda-lMKtQI_u3_dJVyf6V98uOfmi83dlBu4IKiMAQTQqVhegEmZZMM2zW5oeMHuoJNa_Aucg2BGVfu0eSp_755fOFZplx8a3eJo6XSzsB117uy6si2bN1Rig Download .mp4 (1.19 MB) Help with .mp4 files Supplemental Video 2Supplemental Figure 2Predismissal transthoracic echocardiography demonstrating contained left ventricular anterolateral wall rupture with systolic flow through the myocardial defect (green arrow).View Large Image Figure ViewerDownload Hi-res image Download (PPT)eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiI0ZmEyNTIzYzc5NzdlNjg0NTUzNmI2MDcxMDM2ZTcxNSIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjcyMjg1NzkzfQ.CLfwOf7c_tQ5ApbvTOhJiynY9JIChxJ0Ho88bUeccmwEp0wB49X9Fp6UwMS-Qib5WLnv2_nCIlFxES7Q4iG6BIz_EeZA793g_oji_oHVeYoGnFheqPblch42qUSdCpa-xMBwZcZ8c-gzQhvpS3I5zNtDduAhHgYApS4ZAabBZ_mf8tP7br0YwC9bwnbMsA_bSc96LWkKylKVzz_u0U1GrNP9PsBT48qp0Gx1eVFZH__eZ7YuQ8oU67aqRZrGIWmPiVzth5eA72Hj4DjTmNP5QgIm_xzs2b015kbpEQSmn5UIU2iD4DPfCHR1S9woNUB6-DHnncT-Dl6Z2dLsB5WWeA Download .mp4 (0.57 MB) Help with .mp4 files Supplemental Video 3