Left Ventricular Rupture

Etiology

LV rupture most commonly occurs following acute MI. Risk factors linked to LV free wall rupture include no prior history of angina or MI, initial electrocardiogram (EKG) showing ST elevation, peak creatine kinase-MB (CK-MB) levels exceeding 150 IU/L, female sex, age over 70, anterior infarct location, transmural MI, and first-time infarction.[5][6][7] A 10 mm or greater pericardial effusion is also associated with an elevated risk of rupture.[8] Conversely, protective factors include LV hypertrophy, congestive heart failure (CHF), history of previous MIs, chronic ischemic heart disease, early administration of beta-blockers after an acute MI, and prompt intervention.[9] 

Iatrogenic causes of LV rupture include trauma from diagnostic catheterizations, transcatheter aortic valve replacements (mainly via the transapical approach), placement of pacing catheters (temporary or permanent), balloon valvuloplasty, and cardiac surgeries such as mitral valve replacement, and pericardiocentesis.[10] Rupture may also occur in the setting of myocardial abscesses related to infective endocarditis and infections such as tuberculosis and echinococcal cysts. Myocardial tumors, including lymphoma and acute myeloblastic leukemia, can also lead to myocardial rupture, as can rare conditions like sarcoidosis with transmural noncaseating granulomas.

Epidemiology

Myocardial rupture complicates 2% to 4% of acute MIs.[11] Advanced age and leukocytosis are associated with increased incidence after an acute MI.[12] Women experience myocardial rupture more frequently than men, with a ratio of 1.4 to 1.[13] Cardiac trauma occurs in less than 10% of traumatic injuries, notably in sharp-force injuries (stabbings and gunshot wounds) and in motor vehicle accidents, with a higher incidence among men between 15 and 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 3 groups characterized by 3 decades. Mortality also reduced from 96% to 56% and 50%.[14] This reduction 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) are the cardiac chambers affected, in decreasing order of frequency. An acute MI is the most common cause of LV rupture. In this condition, factors like high pressure inside the heart chamber and structural weakness of the heart muscle are due to necrosis of heart cells, breakdown of the collagen matrix, and intense inflammation, which contribute to the rupture. This process usually happens within 3 to 5 days after an acute MI.

In the LV, rupture typically occurs in the anterior or lateral wall at the midpapillary level. Rarely, patients may experience ventricular septal and papillary muscle rupture and LV free wall rupture. Other complications include ventricular septal defect (VSD), acute mitral regurgitation (MR), pericardial tamponade, and pseudoaneurysm formation. Some patients who survive LV free wall rupture after an acute MI may develop a condition where the rupture is sealed by the epicardium or by a hematoma on the heart's surface, known as LV diverticulum, which indicates a subacute pathological state involving rupture through the pericardial cavity and pseudoaneurysm development.[15] A pseudoaneurysm is created if the parietal pericardium locally contains the rupture region and demonstrates the chronic stage of free-wall rupture.[16]  

Acute MI is the most common cause of LV pseudoaneurysm. Pseudoaneurysms can also develop after surgeries, especially mitral valve replacement. Myocardial rupture can occur due to direct trauma to the heart, such as from a car accident or impact between the sternum and spine, causing a rupture in the heart's free wall, interventricular septum, or 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] In infective endocarditis, ruptured myocardial abscesses can cause VSD or pericardial tamponade, especially in cases of Staphylococcus aureus infection in a prosthetic aortic valve.

Histopathology

Myocardial rupture often occurs during the breakdown of collagen and the formation of new fibrous tissue. Factors that increase the risk of rupture after an acute MI include a strong inflammatory response, the presence of matrix metalloproteinases, and intramyocardial hemorrhage.[18] After an acute MI, myocytes show changes like cytoplasmic hypereosinophilia and nuclear pyknosis, giving them a distinctive wavy appearance. About 8 hours after the infarction, interstitial edema and neutrophilic infiltration appear. Within 24 hours, the myocytes lose their cross-striations, and focal hyalinization occurs. By 96 hours, the process of degrading and removing necrotic fibers begins. Collagenase activity spikes on day 2 and peaks by day 7, leading to collagen breakdown. New collagen fibers start forming by day 14. After 4 to 6 weeks, the necrotic myocardium is completely removed and replaced by scar tissue.

History and Physical

The most common cause of shock after an acute MI within 1 day to 3 weeks is myocardial rupture, out of which most occur in the first 3 to 5 days. They usually present as circulatory collapse or cardiogenic shock after initial, small, and uncomplicated acute MIs. Patients with systemic hypertension, older women, and patients with recurrent postinfarction angina are more prone to myocardial rupture after an acute MI.[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 diaphragm.

Traumatic myocardial rupture presents with symptoms like cardiogenic or hypovolemic shock, including difficulty breathing, chest pain, low blood pressure, cold extremities, and sometimes changes in mental status. Some patients may experience cerebral or systemic embolic events from pseudoaneurysms, leading to ventriculopulmonary fistula formation, which causes hemoptysis. Before LV rupture after an acute MI, some patients may have pericarditis symptoms such as pleuritic chest pain and a friction rub. Tamponade, a serious condition, presents with a sudden slow heart rate, clear lung sounds, and swollen neck veins. Physical examination may show Kussmaul sign, muffled heart sounds, and pulsus paradoxus. Further, hypovolemic shock may present as low blood pressure, rapid heartbeat, cold extremities, and pale skin; friction rubs may be heard in pseudoaneurysms.

Evaluation

Physicians should have a low threshold in suspicion of myocardial rupture after an acute MI. Early diagnosis and emergent surgical intervention can increase the survival rate by 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. A focused assessment with sonography in trauma (FAST) exam can best accomplish the diagnosis promptly in the event of blunt thoracic trauma.[20][21] 

Pseudoaneurysm is an echo-free space enlarging in systole and communicating with LV by a narrow neck. Chest radiographs 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 helpful when TTE provides suboptimal images in stable patients such as pseudoaneurysm. EKG showing persistent ST-segment elevation after an acute MI is correlated with a high incidence of myocardial rupture.[22] LV free wall rupture often presents as pulseless electrical activity and sudden bradycardia on EKG. Cardiac catheterization, coronary angiography, and ventriculography may be required in patients with stable acute MI before the surgical intervention to assess the severity and distribution of ischemia.

Treatment / Management

Surgical intervention is crucial in treating 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] Some clinicians advocate intraaortic balloon pumps for LV-free wall rupture. Pericardiocentesis is relatively contraindicated because of the potential risk of aggravating the rupture. Patients must be placed on complete bed rest and have nothing by mouth. Medical therapy stabilizes patients in the time of preparation for surgery, and rapid fluid administration increases preload and improves cardiac output; inotropes may also be required.(B3)

LV-free wall rupture is managed by resectioning the infarcted area and closure of the region with polytetrafluoroethylene or polyester patches or biological glues. Surgical repair is recommended for pseudoaneurysms, even if asymptomatic, as they carry a high risk of rupture. Associated ventricular septum defects are closed by patch, depending on their size. If there is associated papillary muscle rupture, it is treated with mitral valve replacement. Coronary artery bypass surgery is likely needed in most cases while treating mechanical complications after an acute MI.[25]

Differential Diagnosis

When considering LV rupture, the following conditions are included in the differential diagnosis:

• RV infarction: RV 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, decreased urine output, and altered mental status. 
• Cardiogenic pulmonary edema: This life-threatening condition occurs when fluid builds up in the lungs due to a heart problem, such as papillary rupture or VSD. This can be seen on chest x-rays, ultrasound, and CT. Even in those who are asymptomatic, a high index of suspicion of papillary muscle rupture is needed in patients with pulmonary edema. 
• MR: MR can present with acute pulmonary edema, with manifestations of tachycardia, tachypnea, respiratory distress, diffuse pulmonary rales, and hypotension.
• Cardiac tamponade: Patients present with dyspnea, tachycardia, and elevated jugular venous pressure; this can be a consequence of LV rupture and is more common with stab wounds.

Prognosis

Etiology, size, and hemodynamic factors affect the prognosis of the condition. Therefore, early diagnosis and immediate surgery are crucial.[26] A significant amount of in-hospital deaths in patients after an acute MI is due to myocardial rupture. The mortality rate decreases from the first few days to 2 weeks postacute MI. Mortality from rupture due to blunt trauma decreases with early hospital intervention.[27] The type and size of the injury, rapid transfer to the hospital, the patient's hemodynamic stability, and the time to intervention play an essential role in in-hospital mortality. Expectedly, LV rupture has a higher mortality than RV rupture. Hemothorax, cardiac tamponade, and sudden death are fatal consequences of LV rupture.[28]

Complications

Cardiac tamponade and hemothorax are the 2 significant complications of LV rupture.[29] Tamponade is a medical emergency that occurs after the accumulation of free blood in the pericardial space, which reduces the ventricular filling and later causes hemodynamic compromise, causing pulmonary edema, shock, and death. Similarly, hemothorax occurs due to the accumulation of free blood in the pleural space. Tube thoracostomy or video-assisted thoracoscopic surgery is required in management. However, thoracotomy is needed in massive hemothorax or when the bleeding is persistent. Sudden death may be the first manifestation in some patients of LV rupture.