AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

Section 2 of 11  

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Background

Myocardial rupture occurs in the setting of acute myocardial infarction (AMI), blunt and penetrating cardiac trauma, primary cardiac infection, primary and secondary cardiac tumors, infiltrative diseases of the heart, and aortic dissection. The clinical presentation of myocardial rupture depends on the mechanism and site of injury and the hemodynamic effects of the rupture. Mortality rates are extremely high unless early diagnosis and surgical intervention are provided rapidly.

Pathophysiology

AMI is the most common etiology of myocardial rupture. Ischemic myocardial rupture may involve the left ventricular (LV) and right ventricular (RV) free walls, ventricular septum, and LV papillary muscle, in decreasing order of frequency. Myocardial rupture rarely involves the left or right atrial walls.

The consequences of myocardial rupture in the setting of AMI can include pericardial tamponade, ventricular septal defect (VSD) with left-to-right shunt, acute mitral regurgitation (MR), or formation of a pseudoaneurysm. In most instances, the catastrophic clinical presentation occurs within 3-5 days of a rather small AMI. Both hemodynamic factors (increased intracavitary pressure) and regional myocardial structural weakness (myocyte necrosis, collagen matrix resolution, intense inflammation) are important contributory factors to myocardial rupture in the setting of AMI.

In rare instances, patients have been reported to simultaneously experience LV free wall rupture and ventricular septal or papillary muscle rupture (double rupture) following AMI. In the case of a papillary muscle rupture, the posteromedial papillary muscle is twice as likely to rupture as is the anterolateral papillary muscle. This likelihood is because the anteromedial papillary muscle is more often supplied by 2 arterial systems (left anterior descending and left circumflex coronary arteries), whereas the posteromedial papillary muscle is frequently supplied by only one coronary artery (usually the right) system. Rupture of both papillary muscles following AMI has been reported.

In some patients who survive LV free wall rupture following AMI, the rupture can be sealed by the epicardium (visceral pericardium) or by a hematoma on the epicardial surface of the heart. This entity has been referred to as LV diverticulum or contained myocardial rupture and represents a subacute pathologic condition between free rupture into the pericardial cavity and formation of a pseudoaneurysm. A pseudoaneurysm is formed if the area of rupture is contained locally by the adjacent parietal pericardium and represents the chronic stage of LV free wall rupture. The most common etiology of LV pseudoaneurysm is AMI. (LV pseudoaneurysm is twice as common with inferior, rather than anterior, AMI.) LV pseudoaneurysms may develop following surgery, especially following mitral valve replacement.

Blunt cardiac trauma, most commonly in the setting of an automobile accident, may cause myocardial rupture as a result of cardiac compression between the sternum and the spine, direct impact (sternal trauma), or from deceleration injury. It may result in rupture of the papillary muscles, cardiac free wall, or the ventricular septum. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium.

However, among those who reach the hospital alive, the right atrium is the most commonly involved chamber. In up to 30% of cases, the rupture involves more than one chamber. Delayed myocardial rupture has been reported as a result of cardiac contusion. Acute mitral or tricuspid regurgitation, VSD, or pericardial tamponade may result from myocardial rupture secondary to blunt cardiac trauma.

Penetrating myocardial injury occurs most commonly as a result of stab or gunshot wounds. Unlike blunt trauma, penetrating cardiac injury always involves the pericardium. Consequently, ventricular free-wall rupture in this setting may result in either pericardial tamponade (if the pericardial wound is obliterated) or intrathoracic hemorrhage. While pericardial tamponade is more common with stab wounds, gunshot wounds more frequently are associated with hypovolemic shock. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium.

Myocardial abscesses accompanying infective endocarditis may rupture transmurally, resulting in VSD or pericardial tamponade (pyohemopericardium). Such abscesses are observed most commonly in the setting of Staphylococcus aureus endocarditis involving prosthetic valves in the aortic position. Rarely, myocardial necrosis due to acute myocarditis, tuberculosis, or sarcoidosis may result in myocardial rupture.

Myocardial rupture is rarely caused by primary (hemangiopericytoma, angiosarcoma, lymphoma) or secondary (metastatic) cardiac tumors. Lymphomas and acute myeloblastic leukemia also have been associated with myocardial rupture.

Frequency

United States

Myocardial rupture complicates up to 10% of AMIs. Approximately 6-10% of penetrating chest wounds and 15-75% of blunt chest traumas are associated with cardiac injury. Myocardial rupture occurs in 10-15% of fatal motor vehicle accidents. Incidence of cardiac rupture following blunt trauma is 0.5-2% among hospital trauma admissions.

Mortality/Morbidity

• Myocardial rupture is responsible for nearly 15% of all in-hospital deaths among patients with AMI. It is the second most common cause, after pump failure, of in-hospital mortality among patients with AMI.
• The overall mortality rate from myocardial rupture following blunt trauma is 76-93%. However, among those who reach the hospital alive, the mortality rate is 29-50%. Mortality from myocardial rupture resulting from penetrating trauma ranges from 62-89% in the field to 2-83% after reaching a hospital. The latter largely depends on the type of injury, rapidity of the transfer to a hospital, and patients' vital signs and condition upon arrival.
• Following myocardial rupture as a result of penetrating cardiac trauma, hospital mortality is higher in those presenting with hypovolemia rather than pericardial tamponade (22% vs 8%). In-hospital mortality is lowest for patients with RV rupture.

Sex

• Myocardial rupture after AMI is reported more commonly in women than in men (1.4:1).
• Traumatic myocardial rupture is more common in males (up to 85% in some series) than in females.

Age

• Myocardial rupture after AMI is more common in patients aged 60 years or older.
• Traumatic myocardial rupture is observed more commonly in those aged 15-63 years (mean, 34 y).

CLINICAL

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History

• Myocardial rupture after AMI may occur from 1 day to 3 weeks after infarction. Most ruptures occur 3-5 days after infarction.
• • In most patients, myocardial rupture manifests as a catastrophic event (acute pulmonary edema, cardiogenic shock, or circulatory collapse) within days of a first, small, uncomplicated AMI.
  • Older women, especially those with recurrent postinfarction angina, and patients with systemic hypertension more commonly experience myocardial rupture following AMI.
  • Acute onset of shortness of breath, chest pain, shock, diaphoresis, unexplained emesis, cool and clammy skin, and syncope may herald the onset of ventricular septal rupture following AMI.
  • Sudden death due to LV free-wall rupture may be the first manifestation of coronary artery disease in a small percentage of patients with AMI.
• Immediate, early, or delayed acute pulmonary edema (papillary muscle rupture), congestive heart failure (ventricular septal rupture), and hypotension (free-wall rupture) are the cardinal manifestations of myocardial rupture following blunt chest trauma. Concomitant rupture of the myocardium, pericardium, and diaphragm may result in the accumulation of blood in the abdominal cavity.
• In patients with traumatic myocardial rupture, manifestations depend on the site, mode, and extent of cardiac injury.
• • Sudden death occurs shortly after the injury in most patients with traumatic myocardial rupture and is due to pericardial tamponade or exsanguination.
  • Cardiogenic or hypovolemic shock is the predominant manifestation of traumatic myocardial rupture in patients who reach a hospital.
  • Patients with pericardial tamponade may present with dyspnea, chest pain, hypotension, cold peripheries, and mental status changes.
• A small percentage of patients with significant penetrating cardiac trauma have few or no symptoms upon presentation to a hospital.
• Pseudoaneurysms may manifest as cerebral or systemic embolic events or sudden death (rupture). Hemoptysis may occur due to the formation of ventriculopulmonary fistulas. Approximately 10% of patients with pseudoaneurysm are asymptomatic.

Physical

• Of those who sustain cardiac trauma from stab wounds, 18-35% remain without clinical signs of myocardial injury.
• Papillary muscle rupture (partial or complete)
• • Acute pulmonary edema manifests as tachypnea, tachycardia, hypotension, respiratory distress, diffuse pulmonary rales, and signs of MR.
  • The MR murmur may be absent or atypical (soft and not holosystolic) due to rapid equalization of pressures between the left ventricle and left atrium. This equalization is due to the noncompliance of the acutely volume-overloaded left atrium (ie, the left atrial pressure increases sharply in response to sudden rise in volume).
  • Sudden unexplained hypotension and/or pulmonary edema in patients experiencing their first inferior AMI should raise the possibility of papillary muscle rupture, even in the absence of a murmur.
• Left ventricle free-wall rupture
• • Post-AMI pericarditis manifested as pleuritic chest pain and friction rub may be present in some patients prior to onset of rupture and generally indicates transmural extension of the infarct. Cardiogenic shock due to pericardial tamponade manifests as sudden onset of bradycardia, clear lung fields, distended neck veins, Kussmaul sign (ie, paradoxical inspiratory increase in jugular venous pressure), muffled heart sounds, and pulsus paradoxus (ie, an inspiratory drop in systolic blood pressure of >10 mm Hg).
  • Hypovolemic shock may occur due to direct communication with the thoracic or abdominal cavity through a pericardial tear. This manifests as hypotension, tachycardia, cool and clammy extremities, pallor, and diaphoresis.
• Ventricular septal rupture
• • Hypotension may be present.
  • Patients may have acute pulmonary edema.
  • A loud holosystolic murmur may be heard at the lower left sternal border or diffusely over the precordium and is often associated with a thrill.
  • Ventricular arrhythmias may be present.
• Pseudoaneurysm
• • A friction rub may be heard.
  • Pseudoaneurysms frequently rupture, resulting in cardiogenic or hypovolemic shock.
  • Some patients may have a systolic murmur due to the turbulent flow across the narrow neck of the pseudoaneurysm.
  • Systemic embolism that originates from the pseudoaneurysm may result in various cerebrovascular or systemic ischemic symptoms.
  • Arrhythmia may be present, especially ventricular tachycardia and fibrillation.

Causes

• Acute myocardial infarction
• • Risk factors for myocardial rupture following AMI include a relatively small first AMI, female sex, age older than 60 years, hypertension, use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids during the acute phase of AMI (interference with the healing process), late thrombolysis (>11 h), postinfarct angina and elevated peak serum C-reactive protein.
  • Protective factors include LV hypertrophy, history of previous infarcts, congestive heart failure, history of chronic ischemic heart disease, early use of beta-blockers after AMI, and successful (and timely) primary percutaneous coronary intervention.
• Trauma
• • Trauma may be blunt or penetrating.
  • Trauma also may be iatrogenic in nature, resulting from (1) diagnostic catheterization, including transseptal puncture and endomyocardial biopsy; (2) balloon valvuloplasty; (3) pericardiocentesis; (4) placement of temporary or permanent pacing catheters; and (5) cardiac surgery, especially mitral valve replacement.
• Infection
• • Rupture of a myocardial abscess or AMI secondary to coronary embolism of the vegetative material may occur in patients with infective endocarditis.
  • Other infections may include tuberculosis, echinococcal cysts, and myocarditis.
• Aortic dissection
• Malignancy
• • Primary cardiac tumors may be present.
  • Patients may have secondary or metastatic tumors of the heart.
  • Patients may have lymphoma or acute myeloblastic leukemia.
• Sarcoidosis

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

True ventricular aneurysm
Cardiac contusion

WORKUP

Section 5 of 11  

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Lab Studies

• Cardiac enzymes
• • Both peak creatine kinase and its cardiac isoenzyme (MB fraction) are elevated in most patients with significant myocardial damage. However, normal levels of these enzymes may be present in patients with traumatic myocardial injury.
  • Troponin I and T levels may provide a more accurate means of detecting myocardial injury under these circumstances.

Imaging Studies

• Chest radiographs
• • Chest radiographs may show cardiomegaly with clear lung fields in patients with free-wall rupture or pseudoaneurysm
  • Pulmonary edema with a normal cardiothoracic ratio may be present following papillary muscle or ventricular septal rupture.
  • Mediastinal widening with or without pleural effusion (hemothorax) may be present in those with aortic dissection.
  • Hemothorax also may be observed in patients with free-wall rupture with an associated pericardial tear.
• Emergency bedside transthoracic echocardiogram (TTE) is the diagnostic modality of choice in all types of myocardial rupture. It may show the following:
• • A regional LV or RV wall motion abnormality due to AMI or traumatic myocardial injury may be revealed.
  • Evidence of cardiac tamponade manifests as diffuse or loculated pericardial effusion, atrial collapse, diastolic RV collapse, and marked inspiratory decrease in transmitral Doppler flow velocities.
  • Sampling pulmonary venous and hepatic blood flow with pulse-wave Doppler may help reveal the hemodynamic significance of pericardial effusion.
  • Ruptured papillary muscle may appear as a mobile echo density prolapsing into the left atrium during systole or as a flail mitral leaflet. Occasionally, a tear may be evident in one of the papillary muscle heads. Color-flow Doppler can determine the severity and mechanism of MR and differentiate papillary muscle rupture from VSD. Acute severe MR may be difficult to identify with color Doppler because of the patient's general condition (acute pulmonary edema that results in tachypnea and tachycardia) and a low pressure difference between left ventricle and atrium during systole.
  • The size, location, and type of VSD are demonstrated in more than two thirds of patients. Color-flow Doppler is especially useful for detection of the high-velocity turbulent flow through the defect in almost all patients. Color Doppler can be used to estimate the severity of the shunt. Continuous-wave Doppler can be used to estimate the RV systolic pressure with the use of the Bernoulli equation and systemic systolic blood pressure.
  • Pseudoaneurysm appears as an echo-free space that enlarges during systole and communicates with the ventricular cavity by a narrow neck. It may be partially or completely filled with thrombus. Doppler studies may show flow through the narrow neck.
  • No abnormalities are observed in up to 20% of those with penetrating and blunt cardiac injury.
  • Transesophageal echocardiogram (TEE) is valuable in unstable intubated patients if TTE findings are suboptimal or negative despite a high index of suspicion for aortic dissection or papillary muscle rupture.
• CT scan and MRI are useful imaging techniques when echocardiography produces suboptimal images in stable patients, such as those with pseudoaneurysm.

Other Tests

• Electrocardiogram
• • Evidence for transmural (ST elevation) AMI is present in most patients with ischemic myocardial rupture prior to the event. Persistent ST segment elevation following AMI is associated with higher incidence of myocardial rupture. In the setting of an anterior AMI, ST elevation or development of Q waves in inferior leads (as a result of occlusion of a large, wrap-around left anterior descending coronary artery) is associated with an increased risk of VSD.
  • Following traumatic cardiac injury, ECG changes usually are nonspecific.
  • Free wall rupture is often associated with a sudden onset of bradycardia and electromechanical dissociation (pulseless electrical activity).
  • In pericardial tamponade, the ECG may show low-voltage QRS complexes, especially in the precordial leads. Electrical alternans, commonly seen with large, slowly accumulating effusions, is often absent in the setting of acute hemorrhagic pericardial tamponade.
  • Right bundle branch block is frequently observed in patients with VSD. Less frequently, patients may have complete heart block.
  • Patients with pseudoaneurysm may demonstrate ST-segment elevation, nonspecific ST changes, or pathologic Q waves on ECG.
  • All patients with significant thoracic blunt trauma should have ECG and cardiac monitoring. The ECG may show ST elevation or nonspecific ST-T changes. Normal ECG findings do not exclude myocardial injury following blunt trauma.

Procedures

• Cardiac catheterization
• • In patients with AMI complicated by myocardial rupture, emergency cardiac catheterization, coronary angiography, and ventriculography may be necessary in a relatively stable patient prior to surgical intervention. The aim of the study under these circumstances is to assess the distribution and severity of coronary artery disease. Timely surgical intervention, however, is essential in the treatment of these patients and should not be delayed.
  • Coronary and LV angiography may be also useful for diagnosis of pseudoaneurysm, MR, and VSD, in rare instances.
• Intraaortic balloon counterpulsation can be used to temporarily stabilize patients with VSD or papillary muscle rupture. Although advocated by some, intraaortic balloon pumps are not generally used in the treatment of patients with LV free wall rupture.
• Swan-Ganz catheterization
• • Presence of large V waves upon pulmonary artery wedge tracing can help diagnose acute MR. However, a large acute VSD may also produce large V waves.
  • Swan-Ganz catheterization can be useful for hemodynamic monitoring and guiding initial medical management of a VSD. Oxygen saturation step-up from the right atrium to the right ventricle of greater than 10% is highly suggestive of the presence of a large VSD.
  • In case of pericardial effusion, the elevation (generally >15 mm Hg) and equalization (within 5 mm Hg) of diastolic pressures (LV, pulmonary capillary wedge, RV and right atrial) indicates tamponade.
• Pericardiocentesis and surgical drainage of hemopericardium may be indicated.

Histologic Findings

Following AMI, myocytes exhibit cytoplasmic hypereosinophilia and nuclear pyknosis, and they develop a typical wavy appearance. Approximately 8 hours after AMI, interstitial edema and neutrophilic infiltration can be observed. After 24 hours, cross-striations are lost and focal hyalinization appears. Removal of necrotic fibers starts within 96 hours of AMI. An increase in collagenase activity appears by day 2 and peaks at day 7, leading to collagen degradation. New collagen fibers (type III early and type I later) are evident by day 14. After 4-6 weeks, removal of necrotic myocardium is complete, and it is replaced by scar tissue.

Ischemic myocardial rupture commonly occurs between the time of collagen degradation and the laying down of new fibrous tissue (days 2-14 postinfarction). Intense inflammatory response (evidenced by the number of leukocytes), expression of matrix metalloproteinases (collagenases), and presence of intramyocardial hemorrhage (often intensified by thrombolysis, especially if administered late) are pathologic findings that favor myocardial rupture following AMI.

TREATMENT

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Medical Care

• Early surgical intervention is essential for the treatment of myocardial rupture. Medical therapy may be used in some cases to stabilize the patient during the time needed to assemble the surgical team.
• • In less severe cases of papillary muscle rupture, vasodilators should be started to decrease afterload in an attempt to stabilize patients before surgery. This is often accomplished with intravenous nitroprusside. In severe cases, insertion of an intraaortic balloon pump may be necessary.
  • In VSD, intravenous inotropic agents, vasodilators, and diuretics can be used to increase cardiac output and decrease afterload. Insertion of an intraaortic balloon pump is helpful.
  • Rapid fluid administration to increase preload and inotropic drugs to improve cardiac output can be useful in case of free-wall rupture while patient is being transferred to the operating room.

Surgical Care

• In most patients, immediate surgery is necessary and should not be delayed by attempts to stabilize the patient medically.
• • Mitral valve replacement generally is necessary for papillary muscle rupture.
  • Surgical therapy for free-wall rupture includes resection of the infarcted area and closure of the rupture zone with Teflon or Dacron patches or with the use of biological glues. Successful off-pump surgery (without the use of cardiopulmonary bypass) has been reported.
  • VSDs can be closed directly or by placement of a patch, depending on the size of the defect and the timing of the surgery.
  • Pseudoaneurysms carry a high risk of rupture, even though long-term survivors have been reported. Therefore, surgical repair is recommended, even in asymptomatic patients. Surgical repair is similar to ventricular rupture.
  • Coronary artery bypass surgery is often needed as part of the treatment of patients with mechanical complications of AMI undergoing surgical correction. This is especially true for patients with VSD.
  • A recent report of the Society of Thoracic Surgery National Cardiac Database has indicated that patients undergoing coronary artery bypass surgery for cardiogenic shock following acute myocardial infarction have a 19% operative mortality. This increases to 31% for those also requiring mitral valve replacement and to 58% if repair of a ruptured ventricular septum is required.¹

Consultations

• Immediate consultation with a cardiothoracic surgeon is indicated in all cases of myocardial rupture.

Diet

• Nothing by mouth (NPO)

Activity

• Complete bed rest

MEDICATION

Section 7 of 11  

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Medications are useful to help stabilize patients who are waiting for emergency surgery.

Drug Category: Inotropic agents

Used in patients with VSD and free-wall rupture to increase myocardial contractility and cardiac output in the state of hypotension.

Drug Category: Vasodilators

May be used in VSD and MR to decrease afterload and, subsequently, severity of shunt.

Drug Category: Diuretics

Can be used in pulmonary edema caused by VSD or MR.

FOLLOW-UP

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Further Inpatient Care

All patients with cardiac rupture should be transferred to the operating room immediately and admitted to the medical ICU or surgical ICU after surgery.

Transfer

Transfer should be considered only for patients who are in a center without a cardiothoracic surgery unit. The outcome in this setting is quite poor.

Deterrence/Prevention

• Coronary risk factor modification decreases risk of AMI.
• Avoid NSAIDs or corticosteroids in the early phase of AMI.
• Control hypertension and use beta-blockers early in patients with AMI.
• Early successful percutaneous coronary intervention (balloon angioplasty and placement of stent) reduces the risk of myocardial rupture following AMI.
• Using seat belts can significantly reduce the rate of blunt thoracic trauma resulting from high-speed accidents.

Complications

• Tamponade
• Hemothorax
• Sudden death

Prognosis

• Prognosis depends on the type, size, hemodynamic effects, and cause of myocardial rupture.
• Making a quick diagnosis and initiating surgical intervention is crucial. Approximately 50% of patients with cardiac rupture following AMI die within 5 days, and 82% die within 2 weeks of the index infarction. Aggressive early diagnosis and surgery may confer a survival rate as high as 75%.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Physicians should have a high index of suspicion for myocardial rupture following AMI. Especially during the first week, make the diagnosis and perform emergency life-saving interventions. Failure to diagnose or act quickly could expose physicians to legal liability.
• The possibility of cardiac injury should be considered in all patients with high-velocity deceleration blunt injuries. Failure to diagnose myocardial rupture or early discharge of stable patients from the emergency department could result in serious legal consequences.

MULTIMEDIA

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Media file 1:  Magnified photograph of a transverse section of the mid left ventricle (LV) showing a transmural lateral free-wall rupture (R).
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Media type:  Photo

Media file 2:  Photograph of the heart of a 43-year-old man demonstrating the site of a stab wound over the left ventricular lateral free wall (shown as a vertical tear).
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Media type:  Photo

Media file 3:  Photograph of the mitral valve and subvalvular apparatus showing the site of an ischemic papillary muscle (PM) rupture (R).
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Media type:  Photo

Media file 4:  Chest radiograph in posteroanterior projection showing a large pseudoaneurysm manifesting as a bulge in the left cardiac border.
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Media type:  X-RAY

Media file 5:  Photograph of a heart sectioned transversely at the mid left ventricular level showing a posterior ventricular septal defect at the site of a recent acute myocardial infarction.
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Media type:  Photo

REFERENCES

Section 11 of 11

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Article Last Updated: May 1, 2008