Left ventricular free-wall rupture (LVFWR) is a life-threatening sequela of acute myocardial infarction. Contrast-enhanced echocardiography can be used urgently at the bedside to identify LVFWR. Early recognition is paramount, because emergency surgical correction is the only treatment. We describe the use of contrast-enhanced echocardiography in a patient who sustained pulseless electrical activity 5 days after a myocardial infarction (MI). Direct views of a tear in the myocardium enabled rapid confirmation of the diagnosis and expeditious surgical treatment.

Case Report

In January 2013, a 59-year-old woman with hypertension and hypercholesterolemia presented at another hospital with a 2-day history of chest pain. She was treated for non-ST-segment-elevation MI. Her initial serum troponin T level was 0.96 ng/mL (normal, <0.01 ng/mL). An electrocardiogram revealed ST-segment elevation in lead aVL, borderline but nondiagnostic ST-segment elevation in adjacent lead I, rsR′ in lead V₂, and ST-segment depression in the anterolateral and inferior leads (Fig. 1). The patient was admitted to the intensive care unit and was given aspirin, low-molecular-weight heparin, a glycoprotein IIb/IIIa inhibitor, and a nitroglycerin infusion. Her serum troponin T level peaked at 3.79 ng/mL.

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The patient was transferred to our hospital the next day for elective cardiac catheterization. An electrocardiogram revealed a recent posterolateral infarction (Fig. 2). Coronary angiograms showed an occluded left circumflex coronary artery; faint collateral vessels from a patent, dominant right coronary artery; a 70% stenosis of the first diagonal branch; and a 90% stenosis of the right posterior descending artery (RPDA). Left ventriculograms revealed severe hypokinesis of the inferolateral wall and overall mild left ventricular (LV) dysfunction. No intervention was performed, because the patient was no longer symptomatic and was well beyond 24 hours from symptom onset and presentation.

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On hospital day 3, the patient sustained a retroperitoneal hemorrhage and was transfused with 2 units of packed red blood cells. On hospital day 5, she became acutely unresponsive and pulseless while conversing with her family. Advanced cardiac life support was initiated immediately. She remained hemodynamically unstable and needed intravenous fluids and vasopressors. A bedside transthoracic echocardiogram (TTE) revealed a moderate-sized, heterogeneous-appearing pericardial effusion with cardiac tamponade. After emergency pericardiocentesis yielded 500 mL of bloody fluid, the patient's pulse rate and blood pressure immediately became normal.

Repeat TTE after the pericardiocentesis revealed the known akinesis of the inferolateral and anterolateral walls. We suspected LVFWR as the cause of the patient's sudden hemodynamic collapse. An equivocal echolucency in the inferolateral wall suggested LVFWR; however, suboptimal endocardial definition precluded definitive diagnosis (Fig. 3). The ultrasonographic contrast agent Optison^™ (GE Healthcare; Princeton, NJ)—injected intravenously to improve endocardial border definition—indisputably revealed systolic extrusion of the contrast medium into an echolucent slit in the inferolateral wall, consistent with the now-contained LVFWR (Fig. 4). In the operating room, the diagnosis of LVFWR was confirmed (Fig. 5). The grossly necrotic myocardial tissue immediately around the hole necessitated débridement and repair with use of a bovine pericardial patch. A large blood clot was evacuated from the pericardium, and the patient underwent concurrent 2-vessel coronary artery bypass grafting, consisting of reverse saphenous vein grafts to the diagonal branch and to the RPDA. Postoperatively, the patient remained critically ill: acute renal and liver failure mandated continuous venovenous hemodialysis and the subsequent use of a molecular adsorption recirculation system. Her postoperative course was further complicated by intracranial hemorrhage and multiple arterial and venous embolisms associated with heparin-induced thrombocytopenia. On hospital day 26, the patient's family withdrew care, and she died.

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Discussion

Mechanical complications of MI include LVFWR, ventricular septal rupture, right ventricular failure, and papillary muscle rupture with acute mitral regurgitation. In 1647, William Harvey described the first case of LVFWR in a postmortem specimen as “having a rent in it of size sufficient to admit any of my fingers.”¹ Typically, LVFWR occurs within 5 days of the onset of MI, with the highest incidence on the first day.² The incidence of LVFWR during the fibrinolytic period in ST-elevation MI (STEMI) has been lower than during pre-fibrinolytic years, and is estimated to be 0.85%.³ Paradoxically, despite conferring an overall mortality-rate benefit, fibrinolytic agents have been implicated in the accelerated occurrence of LVFWR within the first 24 to 48 hours after MI.⁴

The incidence of LVFWR, along with other mechanical sequelae, has decreased consequent to successful PCI in the infarct-related artery and supportive medical therapy for STEMI.⁵ In a large contemporary study of primary PCI in STEMI, the incidence of LVFWR was 0.52%, and the 90-day survival rate was 37%.⁶ Risk factors associated with LVFWR include advanced age, female sex, first-time MI, anterior-wall MI, ST-segment elevation or Q-wave development on the initial ECG, large infarct size, and late or failed PCI.^7–9 A large transmural MI in a patient without a history of angina or prior MI confers the highest risk of rupture, possibly because of absent collateral circulation that would be essential to minimize the development of substantial necrotic and vulnerable myocardial tissue. Other potential mechanisms are hampered fibrotic healing, abnormal cardiac inflammation and remodeling, and damage to extracellular matrix proteins.⁹

Patients with LVFWR often present with cardiac tamponade, acute cardiogenic shock, heart failure, or sudden death. However, some patients with contained and subacute rupture might experience a more indolent course; nonspecific symptoms such as pleuritic chest pain, repetitive and unprovoked emesis, restlessness, and agitation might engender a low degree of clinical suspicion.¹⁰ Acute nonsurgical treatment of LVFWR consists of aggressive volume resuscitation with inotropic and vasopressor support, pericardiocentesis, and percutaneous circulatory support, such as intra-aortic balloon counterpulsation and extracorporeal membrane oxygenation.^11,12 Surgical repair involving infarctectomy and patching is the only definitive treatment, yet even successful surgery carries a high mortality rate.¹³

Echocardiography is crucial in the prompt diagnosis of LVFWR and is often the only readily accessible diagnostic method in the presence of an acutely deteriorating patient. Pericardial effusion is the most frequent echocardiographic finding, with a sensitivity as high as 100%; however, the specificity might be lower, because the causes of pericardial effusion after MI include pericarditis, hemorrhage from postinfarcted myocardium, coronary perforation, and myocardial rupture. Conversely, the absence of effusion does not exclude the diagnosis of LVFWR.^13,14 Further supporting the diagnosis are echogenic layering in the pericardium that suggests pericardial thrombus, regional myocardial dilation, and an abnormally thin and akinetic myocardium. During color-flow Doppler echocardiographic evaluation, a color-flow jet through a visible wall defect is diagnostic of LVFWR. However, a color-flow jet might be absent when pericardial thrombus plugs the rupture site. Interruption of the endocardium, in itself, is not specific for LVFWR: myocardial diverticula, pseudoaneurysms, subepicardial aneurysms (“pseudo-pseudoaneurysms”), and aneurysms can have a similar echocardiographic appearance. Congenital myocardial diverticula are often asymptomatic and can be distinguished from acquired myocardial defects caused by MI or trauma. Acquired causes typically feature a wide neck, no myocardium on histologic evaluation, and a layer of fibrous tissue, and they exhibit akinetic or dyskinetic contractile function of the LV wall during systole.¹⁵ Pseudoaneurysms, a contained form of LVFWR, consist of an outpouching from the ventricular wall with organized hematoma and pericardium. They are associated with a 35%-to-40% risk of subsequent progression.¹⁶

Subepicardial aneurysm is an incomplete myocardial tear that involves all but the epicardial layer of the myocardium. This rare disease entity is thought to be a pre-rupture state.¹⁷ Cardiac computed tomographic and magnetic resonance imaging can be considered in equivocal and stable cases. Left ventriculography is generally insensitive and impractical in a suspected case of frank myocardial rupture.¹⁸

Left ventricular opacification with use of ultrasonographic contrast agents improves endocardial border definition in the face of technically suboptimal image quality. This imaging technique also substantially improves the evaluation of LV wall motion, wall thickness, and volume, and facilitates the recognition of intracardiac masses such as tumors and thrombi. Three such contrast agents are approved for clinical use in Europe: SonoVue^™ (Bracco Diagnostics S.p.A.; Milan, Italy), Optison, and Luminity^™ (Lantheus Medical Imaging; North Billerica, Mass); however, only the last two are approved by the U.S. Food and Drug Administration (FDA) (Luminity is marketed as Definity^™ in the U.S.). These agents are generally safe and well tolerated, even in a critically ill patient.^19,20 Contraindications to their use include right-to-left, bidirectional, or transient right-to-left intracardiac shunts; and hypersensitivity to perflutren, blood products, or albumin (for Optison only). When patients have pulmonary hypertension or unstable cardiopulmonary conditions, the FDA recommends close monitoring of vital signs and oxygen saturation during and for 30 minutes after administering the agents.²¹

For the use of contrast agents for LV opacification and endocardial border definition, the ultrasound machine's setting needs to be adjusted to optimize real-time image acquisition. Of most importance, the mechanical index needs to be low (ideally between 0.15 and 0.3), to avoid the destruction of microbubbles by emitted ultrasonographic waves.²¹ Our patient's clinical deterioration occurred when cardiac sonographers were not immediately available, thus illustrating the importance of the treating cardiologist's proficiency in performing bedside TTE and understanding of the adjustments necessary for ultrasonographic contrast use.

The usefulness of contrast-enhanced echocardiography has been reported in the management of impending LVFWR.^22–25 In our patient with acute LVFWR, rapid confirmation of the diagnosis was aided by the use of bedside contrast-enhanced echocardiography, and by our cardiologists' familiarity with this diagnostic method in the care of a critically ill patient. Furthermore, this case highlights the acute nature of mechanical sequelae of MI, particularly because reperfusion therapy was not administered. Clinical suspicion for LVFWR combined with expeditious recognition is paramount in treating acute hemodynamic collapse in the post-MI patient. Bedside TTE aided by the intravenous administration of an ultrasonographic contrast agent serves a crucial role in the prompt diagnosis of this often fatal complication of acute MI.