Myocardial Infarction Complicated by Left Ventricular Free Wall Rupture
By: Michael Tamberella III, MD
Introduction:
The most common mechanical complication following myocardial infarctions (MIs) include acute ventricular septal defect (VSD), papillary muscle rupture and free wall rupture. We describe here a case of sudden hemodynamic collapse caused by cardiac tamponade resulting from a free wall rupture.
Case History:
The patient is a 71 year old female who presented to a local hospital in Cleveland on 6/13 with complaint of stuttering chest pain and shortness of breath for 3 days. The patient denied any nausea, vomiting, diaphoresis or syncopal symptoms. The pain awoke the patient from sleep approximately 24 hours prior to her seeking medical attention. She tried several over-the-counter pain medications prior to arriving at the emergency room with little relief.
ECG revealed normal sinus rhythm with R>S in V1 and V2 and nonspecific ST changes (See Figure 1). Initial enzymes were positive with a CK 282 CKMB 14.8 and Troponin I 3.1. She became asymptomatic after initiation of therapy with heparin, nitroglycerin IV, metoprolol and aspirin. Approximately 36 hours after presentation she became acutely hypotensive, tachycardic, tachypneic, and diaphoretic. ECG revealed an acute injury pattern in the infero-posterior leads (see Figure 2). The patient was emergently intubated and started on high dose dopamine and dobutamine then transferred to The Cleveland Clinic for further management. Upon arrival the patient’s exam was significant for a blood pressure of 60/20, regular tachycardia at 120 bpm, jugular venous distention to the angle of the mandible, soft distant S1 and S2 and no appreciable murmurs. Lung exam was significant for marked rales throughout both lung fields.
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Figure 1 - ECG at presentation
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Figure 2 - ECG at time of transfer
The patient first underwent urgent intra-aortic balloon pump insertion that resulted in very little change in hemodynamics. Right heart catheterization was performed revealing a pulmonary artery pressure of 40/24 central venous pressure 20 and wedge pressure 22. Intravenous fluids were administered and a transthoracic echocardiogram was performed (See Figure 3, Videos 1 and 2).
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Figure 3 - Hepatic Vein Flow showing diastolic flow reversal
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Click here for Video 2 *- IVC plethora
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Since the patient remained hemodynamically unchanged for approximately one hour the decision was made to take the patient to the cath lab were she was found to have single vessel CAD involving the lateral circumflex artery. In addition no pericardial staining could be seen by ventriculography. The patient was transferred to the OR for open drainage of the pericardial effusion. There she was found to have and large hematoma involving the anterior pericardial space as well as a pinpoint rupture within the area of infarcted tissue of the posterior wall. The patient underwent a pericardial patch and single vessel CABG and tolerated the procedure well. She was eventually discharged to home after 7 days.
Discussion:
Although cardiac rupture complicates less than 1% of all MI’s, it accounts for approximately 7.3% of post MI in-hospital mortality 1. Risk factors for cardiac rupture includes first MI, small transmural MI, female sex, preserved LV function, hypertension, older age and poor collaterals 2, 3.
The diagnosis of cardiac rupture should be suspected based on clinical grounds. The most common findings include hypotension, syncope, and EMD. ECG findings are non-specific and include ST segment elevation, low QRS amplitude, T-wave inversion, and intraventricular conduction delays 4. Echocardiographic findings include pericardial effusion, often with tamponade physiology, and occasionally identification of the myocardial tear 4. Angiographically the infarct related vessel is usually the LAD or circumflex. The RCA is rarely the culprit vessel 3.
It is believed that rupture is the result of thinning and dilation of the infarcted tissue that then has elevated wall stress leading to disruption. Three distinct clinical and pathologic forms of free wall rupture have been described. These include: 1) sudden massive hemorrhage with sudden death (most common) occurring within 24 hours of infarct, 2) rupture through a necrotic area of myocardium with thrombus formation, and 3) hemorrhage into the pericardial space which is slow and repetitive usually through a pre-existing aneurysm with survival for several days. 4
Early fibrinolytic trials reported an early increase in the rate of free wall rupture in patients who were randomized to fibrinolytic therapy compared to those randomized to placebo. However, fibrinolytic therapy has been associated with improved overall survival. In addition the rate of aneurysm formation and subsequent late myocardial rupture is reduced with the use of fibrinolytic therapy.
Although surgical intervention can be undertaken in selected cases of subacute rupture, most events are rapidly fatal. Once the diagnosis is made, the patient should be taken urgently to the OR for open pericardial drainage and repair of the rupture. Patients with suspected free wall rupture should not undergo elective pericardiocentesis, which may dislodge thrombus that is keeping the patient from hemorrhaging further into the pericardial space. If however the patient deteriorates into EMD then pericardiocentesis should be performed as a bridge to definitive therapy.
Comments from Dr. Eric Topol:
This is a classic case of free wall contained rupture after a circumflex MI in a patient not presenting early for reperfusion therapy. The posterior MI ECG pattern (which later extended) along with acute decompensation tipped off the team for the diagnosis. The tamponade physiology on the right heart catheterization provided confirmation of the clinical and echocardiographic findings and set up immediate surgical intervention---the treatment of choice. All too often the diagnosis is not made promptly, and that is why one should always think of contained rupture as a cause of sudden decompensation after an acute MI.
References
- Becker et al. A Composite View of Cardiac Rupture in the United States National Registry of Myocardial Infarction. JACC May 1996 27:1321-26.
- Schuster EH. and Bulkley, BH. Expansion of Transmural Myocardial Infarction: A Pathophysiologic Factor in Cardiac Rupture. Circulation 1979 60 (7) 1532-38.
- Slater et al. Cardiogenic Shock due to Cardiac Free-wall Rupture or Tamponade After Acute Myocardial Infarction: A Report from the SHOCK Trial Registry. JACC September 2000 36A:1117-22.
- Lopez-Sendon et al. Diagnosis of Subacute Ventricular Wall Rupture After Acute Myocardial Infarction: Sensitivity and Specificity of Clinical, Hemodynamic and Echocardiographic Criteria. JACC May 1992 19:1145-53.
