Continuing Education Activity

Left ventricular (LV) rupture is a catastrophic but a common occurrence with acute myocardial infarction patients. The incidence of LV free-wall rupture post-acute myocardial infarction is less than 1%, but mortality is extremely high without prompt surgical intervention. It can also occur in trauma, infections, and malignancies. This activity reviews the evaluation and treatment of rupture and highlights the role of the interprofessional team in evaluating and treating the condition.

Objectives:

• Identify the etiology of left ventricular rupture emergencies.
• Review the appropriate evaluation of left ventricular rupture.
• Outline the management options available for left ventricular rupture.
• Explain the importance of interprofessional team collaboration and communication to improve patient outcomes in patients with left ventricular rupture.

Introduction

Left ventricular (LV) rupture is a catastrophic but a common occurrence with acute myocardial infarction patients. Incidence of LV free-wall rupture post-acute myocardial infarction (AMI) is less than 1%, but mortality is extremely high.[1] It can also occur in blunt or penetrating cardiac trauma, cardiac infection, aortic dissection, primary or secondary cardiac tumors, and infiltrative diseases of the heart. Iatrogenic causes are penetration during percutaneous or surgical cardiac procedures. Also, patients with Takotsubo cardiomyopathy have been reported to have a myocardial rupture.[2] Early diagnosis and immediate surgical intervention are critical as the mortality is extremely high without intervention. Nevertheless, patients can make an outstanding improvement with proper care. Recently, sutureless procedures showed reasonably high success rates, preventing cardiopulmonary bypass.[3]

Etiology

The most common cause of left ventricular rupture is post-AMI. Risk factors associated with left ventricular free wall rupture are no prior history of angina or myocardial infarction, ST elevation in the initial EKG, peak CK-MB above 150 IU/L, female sex, age more than 70 years, anterior location, transmural infarction, and first infarction.[4][5][6] Pericardial effusion of 10 mm or more is correlated with an increased risk of free wall rupture.[7] On the other hand, LV hypertrophy, congestive heart failure (CHF), history of previous infarcts, chronic ischemic heart disease, early use of beta-blockers post-AMI, and timely intervention have protective action.[8] 

Iatrogenic causes include penetrating or blunt trauma from diagnostic catheterization, transcatheter aortic valve replacement (especially transapical approach), placement of temporary or permanent pacing catheters, balloon valvuloplasty, cardiac surgeries such as mitral valve replacement, and pericardiocentesis.[9] Myocardial abscess rupture may occur in infective endocarditis, whereas the rupture may also occur in infections like tuberculosis and echinococcal cysts. Myocardial tumors, including lymphoma and acute myeloblastic leukemia, can cause the rupture of the myocardium of any chamber. Another rare cause is sarcoidosis through transmural noncaseating granulomas.

Epidemiology

Two to four percent of AMIs have the complication of myocardial rupture.[10] Advanced age and leukocytosis have shown to have an increased incidence of myocardial rupture post-AMI.[11] It is also reported to have more occurrence in women than men (1.4:1).[12] Cardiac trauma is seen in less than 10% of traumatic injuries.[13] Motor vehicle accidents also have a common occurrence, and traumatic rupture incidence is high in males. This is more commonly seen in the age group of 15 to 63. A study showed a progressive decrease in incidence and mortality over the years. The incidence decreased from 3.3% to 2.8% to 1.7% in the three groups characterized by three decades. Additionally, mortality also reduced from 96% to 56% and 50%.[14] This can be attributed to the increasing quality of care and early intervention.

Pathophysiology

The right ventricle (RV), LV, right atrium (RA), and left atrium (LA), in the decreasing order of frequency, are the cardiac chambers involved. In the most common cause of the LV rupture (AMI), hemodynamic factors such as increased intracavitary pressure and structural weakness of the myocardium as demonstrated by the necrosis of myocytes, collagen matrix resolution and intense inflammation play important roles in leading to the rupture. It is most commonly observed within 3 to 5 days post-AMI. In the LV, rupture most commonly occurs in the anterior or the lateral wall at the mid-papillary level. Patients can rarely experience ventricular septal and papillary muscle rupture along with the LV free wall rupture. Other consequences are ventricular septal defect (VSD), acute mitral regurgitation (MR), pericardial tamponade, and formation of a pseudoaneurysm. The rupture is sealed by the epicardium or by a hematoma on the surface of the heart of certain patients who survive LV free wall rupture post-AMI. This is identified as LV diverticulum and indicates a subacute pathological state involving free rupture through the pericardial cavity and pseudoaneurysm development.[15] A pseudoaneurysm is created if the rupture region is locally contained by the parietal pericardium and demonstrates the chronic stage of free-wall rupture.[16] 

AMI is the most common cause of LV pseudoaneurysm development. It can also develop following surgical operations, in particular following the mitral valve replacement. As a consequence of cardiac compression between the sternum and the spine, direct impact on the heart (sternal trauma), or deceleration in the setting of an automobile collision, myocardial rupture can occur. This may cause a rupture of the free-wall, interventricular septum, and the papillary muscles. The myocardial injury occurs more often as a consequence of stabbing or gunshot wounds. In the setting of blunt trauma, the ventricular free-wall rupture will result in either pericardial tamponade (when the pericardial wound is obliterated) or intrathoracic hemorrhage which is common in stab wounds and gunshot wounds respectively.[17] Myocardial abscesses in infective endocarditis that rupture transmurally, result in VSD or pericardial tamponade. These abscesses are most commonly observed in the prosthetic aortic valve Staphylococcus aureus endocarditis.

Histopathology

Myocardial rupture is typical during the period of collagen degradation and the formation of new fibrous tissue. Findings that favor the rupture post-AMI are intense inflammatory response, presence of matrix metalloproteinases, and intramyocardial hemorrhage.[18] Myocytes show cytoplasmic hypereosinophilia and nuclear pyknosis after AMI and acquire a distinctive wavy appearance. Interstitial edema and neutrophilic infiltration can be detected around 8 hours after infarction. Cross-striations are lost within 24 hours, and focal hyalinization develops. Within 96 hours of AMI, the degradation and removal of necrotic fibers begin. A spike in collagenase activity occurs on day two and increases on day 7, contributing to the breakdown of collagen. New collagen fibers are noticeable by day 14. Removal of necrotic myocardium is complete after 4 to 6 weeks, and scar tissue replaces the damaged myocardial tissue.

History and Physical

The most common cause of shock post-AMI within one day to three weeks is the myocardial rupture, out of which most occur in the first 3 to 5 days. They usually present as circulatory collapse or cardiogenic shock post- uncomplicated, small, first AMIs. Patients with systemic hypertension, older women, and patients with recurrent post-infarction angina are more prone to the myocardial rupture post-AMI.[19] LV rupture may cause sudden death, which might be the first manifestation in a small number of patients. Hypotension associated with free wall rupture is a cardinal manifestation. Traumatic myocardial rupture presents shortly after an injury, and there can be a simultaneous rupture of the ventricular septum, papillary muscle, pericardium, and the diaphragm.

Cardiogenic shock or hypovolemic shock is the presentation in traumatic myocardial rupture patients. Symptoms include dyspnea, chest pain, hypotension, cold extremities, and occasionally mental status changes. Some patients may manifest cerebral or systemic embolic events from pseudoaneurysms. As a consequence, ventriculopulmonary fistulas formation occurs, presenting as hemoptysis. Some patients present with pericarditis symptoms before the LV rupture post-AMI, such as pleuritic chest pain and friction rub. Tamponade presents with sudden onset bradycardia, clear lung fields, and distended neck veins. Kussmaul sign, muffled heart sounds, and pulsus paradoxus can be observed on physical examination. Hypovolemic shock may occur and manifests as hypotension, tachycardia, cool extremities, and pallor. Friction rubs may be heard in pseudoaneurysms.

Evaluation

Physicians should have a low threshold in suspicion of myocardial rupture post-AMI. Early diagnosis and emergent surgical intervention can increase the survival rate of up to 75%. Cardiac injuries need to be considered in all high-velocity deceleration blunt traumas. A bedside transthoracic echocardiography (TTE) is the diagnostic modality of choice. LV wall motion abnormality or myocardial injury is often apparent. Tamponade is seen as pericardial effusion, diastolic RV collapse, atrial collapse, and inspiratory decrease in Doppler flow velocities across the mitral valve. Associated papillary muscle rupture may be seen as a tear in the muscle head or may appear as a mobile echo density that prolapses into the LA in systole. Focused Assessment with Sonography in Trauma (FAST) can best accomplish the diagnosis promptly in the event of blunt thoracic trauma.[20][21] 

Pseudoaneurysm is seen as an echo-free space enlarging in systole and communicating with LV by a narrow neck. Chest X-ray (CXR) may show cardiomegaly with clear lung fields in LV rupture and pseudoaneurysm. Hemothorax may be observed with an associated tear of the pericardium. Mediastinal widening may also be seen in the event of aortic dissection. Computed tomography (CT) and magnetic resonance imaging (MRI) can be useful when TTE provides suboptimal images in stable patients such as pseudoaneurysm. Electrocardiography (ECG) showing persistent ST-segment elevation post-AMI is correlated with a high incidence of myocardial rupture.[22] LV free wall rupture often presents as pulseless electrical activity and sudden bradycardia on ECG. Cardiac catheterization, coronary angiography, and ventriculography may be required in stable AMI patients before the surgical intervention to assess the severity and distribution of ischemia.

Treatment / Management

Surgical intervention is crucial in the treatment of LV rupture, while medical therapy can play a supporting role [23]. Prompt consultation with a cardiothoracic surgeon is indicated. Patients need to be transferred to the operating room immediately. Surgical drainage of hemopericardium may be required.[24] Intra-aortic balloon pumps are advocated by some doctors for the LV free wall rupture. Pericardiocentesis is relatively contraindicated because of the potential risk of aggravating the rupture. Patients need to be placed on complete bed rest and nothing by mouth (nil per os; NPO). Medical therapy stabilizes patients in the time of preparation for surgery. Rapid fluid administration increased preload and improves cardiac output. Inotropes may also be required.

LV free wall rupture is managed by resection of the infarcted area and closure of the area with polytetrafluoroethylene or polyester patches or by biologic glues. Surgical repair is recommended for pseudoaneurysms even if asymptomatic as they carry a high risk of rupture. Associated VSDs are closed by patch depending on the size. If there is associated papillary muscle rupture, it is treated with mitral valve replacement. Coronary artery bypass surgery (CABG) is likely needed in most cases while treating mechanical complications post-AMI. 

Differential Diagnosis

• RV infarction: Right ventricular infarction can cause heart failure, and patients present with hypotension, distended neck veins, and clear lung fields. 
• Cardiogenic shock: Patients present with hypotension, absence of hypovolemia, and clinical signs of poor perfusion.
• Hemorrhagic shock: Patients present with hemodynamic instability such as hypotension, tachycardia, and also decreased urine output, and altered mental status. 
• Cardiogenic pulmonary edema: It can present post-papillary rupture, or VSD can be seen on CXR. A high index of suspicion of papillary muscle rupture is needed in patients with pulmonary edema, even in asymptomatic patients. 
• MR: MR can occur from papillary muscle rupture and can present with acute pulmonary edema with manifestations of tachycardia, tachypnea, respiratory distress, diffuse pulmonary rales, and hypotension along with MR signs.
• Cardiac tamponade: It can be a consequence of LV rupture. It is more common with stab wounds. Patients present with dyspnea, tachycardia, and elevated jugular venous pressure (JVP).

Prognosis

Etiology, size, and hemodynamic factors affect the prognosis of the condition. Hence, early diagnosis and immediate surgical intervention is the key.[25] A fair amount of in-hospital mortality in patients post-AMI attribute to myocardial rupture. Mortality comes down from the first few days to the two weeks post-AMI. Mortality in rupture due to blunt trauma also decreases if early intervention is made available at the hospital.[26] Type and size of the injury, rapidity of transfer to the hospital, patient's hemodynamic stability, and the time till intervention play an important role in in-hospital mortality. Expectedly, LV rupture has high mortality than RV rupture. Hemothorax, cardiac tamponade, and sudden death are fatal consequences of the LV rupture.

Complications

Cardiac tamponade and hemothorax are the two significant complications of the LV rupture.[27] Tamponade is a medical emergency occurring after the accumulation of free blood in the pericardial space reducing the ventricular filling and later causes hemodynamic compromise. It can cause pulmonary edema, shock, and death. Similarly, hemothorax occurs due to the accumulation of free blood in the pleural space. Tube thoracostomy or a video-assisted thoracoscopic surgery (VATS) is required in management. However, thoracotomy is required in massive hemothorax or when the bleeding is persistent. Sudden death may be the first manifestation in some patients of LV rupture.

Postoperative and Rehabilitation Care

Postoperative management includes bed rest, blood pressure control, heart rate control, inotropic support, and avoidance of agitation.[24] Bed rest prevents the development of hypertension, and avoidance of agitation supports it. Heart rate control reduces myocardial oxygen demand promoting heart recovery. Inotropic support is required to prevent tissue hypo-perfusion. Intra-aortic balloon pump, when present, increases coronary blood flow and prevents post-cardiotomy low-cardiac output syndrome. 

Deterrence and Patient Education

To establish and introduce successful postoperative educational strategies, awareness of the effects of the specific approach, mode of delivery, and dose of educational interventions is important. It is essential to understand the relationships of patient characteristics to outcomes. Physicians and nurses play a vital role in patient education. Content individualization, the usage of interactive media for delivery, one-on-one education provision, and the enhancement in educational and health outcomes in various sessions have shown good results.[28] Patients need to be educated regarding the wound dressing and watching for signs of infection. They should also be educated regarding the warning signs if the doctor or nurse needs to be informed. Other instructions regarding the diet, medications, and physical activity need to be explained to the patient to improve cooperation and outcomes.

Enhancing Healthcare Team Outcomes

An interprofessional team that uses a comprehensive and structured postoperative care strategy will help achieve the best possible outcomes. The role of nursing care cannot be undermined, especially in the event of surgical wound infections. Consultation with a social worker and community nurses might be necessary if the patient needs to be discharged home with a drain. A physical therapist might be needed in the event of deep vein thrombosis with long term immobility in the hospital. Communication, joint decision making, and cooperation remain the keys to positive outcomes. Early detection of symptoms and signs is the key to decreasing mortality, especially in this acute critical condition of myocardial rupture. Hence, interprofessional treatment should include an organized care framework paired with an evidence-based approach to coordinating and reviewing all collaborative operations.[Level III]

To improve outcomes and decrease the high mortality in LV rupture, prompt consultation with an interprofessional group of specialists is recommended. While cardiothoracic surgeons and anesthesiologists play primary roles during surgical intervention, cardiologists and intensive care specialists play a predominant role in pre/post-surgical management. Nurses play an important role as they monitor the vital signs, pre and postoperative management, and patient education. The pharmacist must ensure that the patient is on the right analgesics, antiemetics, and antibiotics in the event of wound infection. 

Postoperative management of the patients required interprofessional integrated work to improve outcomes. Bed rest is essential as it prevents arterial hypertension or hypertensive crisis and is to be carefully checked by nurses. Heart rate control, optimum inotropic support, and avoiding agitation are best achieved by cooperation between the physicians, pharmacists, and nurses. Inotropic support postoperatively prevents tissue hypoperfusion. 

In conclusion, left ventricular free-wall rupture is a potentially life-threatening mechanical complication of acute myocardial infarction. It mostly occurs in patients with ST-elevation MI. Other causes, such as infections and trauma, are also responsible. Diagnosis is markedly facilitated by a high index of suspicion and transthoracic echocardiography. Surgical intervention (Oxford CEBM level of evidence III) is the definitive treatment, and medical treatment includes fluids, inotropes, and vasopressors. American College of Cardiology highlights that making the diagnosis early is important, and the threshold for suspicion needs to be low. Emergent surgical intervention and stabilization of the patients improve survival.