Myocardial Rupture Workup

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.

Chest radiographs

Chest radiographs may show cardiomegaly with clear lung fields in patients with free-wall rupture or pseudoaneurysm (see following image).

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.

Transthoracic echocardiogram (TTE)

Emergency bedside 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)

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 and MRI

CT scan and MRI are useful imaging techniques when echocardiography produces suboptimal images in stable patients, such as those with pseudoaneurysm.

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.

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

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

Pericardiocentesis and surgical drainage of hemopericardium may be indicated.

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.