Left Ventricular Free Wall Rupture in Acute Myocardial Infarction

Abstract

We describe a case of subacute left ventricular free wall rupture during acute myocardial infarction in a 68-year-old man. The diagnosis was confirmed by echocardiography. The patient was supported by an intra-aortic balloon pump until the ruptured wall could be successfully repaired by suturing and gluing a pericardial patch over the defect and bypassing the left anterior descending coronary artery with a vein graft. This case demonstrates that left ventricular free wall rupture is not always fatal and that early diagnosis and institution of intra-aortic balloon pump support in such patients can allow successful bridging to definitive emergency surgical therapy.

Left ventricular free wall rupture (LVFWR) is a rare complication of acute myocardial infarction (AMI), occurring in approximately 2% of cases¹ but even less frequently when primary percutaneous intervention can be performed.² This complication is often fatal. We describe the presentation and successful treatment of a subacute LVFWR during an AMI in an elderly man.

Case Report

A 68-year-old man was seen in a local emergency room for severe retrosternal chest pain accompanied by dyspnea and sweating. A presumed diagnosis of anterior-wall acute myocardial infarction (AMI) with S-T segment elevation was made. Treatment with reteplase was started. The patient continued to have chest pain, however, and the S-T segment elevations did not resolve. Consequently, the patient was transferred to a tertiary care center, where he underwent percutaneous coronary intervention to deploy a stent in the proximal left descending coronary artery. Abciximab and clopidogrel were administered during this procedure. The rest of the epicardial coronary arteries were found to be normal. The patient's postoperative course over the next 24 hours was uneventful, with no arrhythmia or symptoms of heart failure, until his blood pressure suddenly dropped and he became confused. Dopamine was started, and the patient was transferred to our hospital.

On arrival, the patient was in a state of hemodynamic collapse. He was sweating and lethargic. His blood pressure was 60/45 mmHg, his heart rate was 110 beats/min, and an electrocardiogram showed sinus tachycardia. Auscultation revealed no audible rub or S₃ gallop and no new murmurs. Signs of systemic hypoperfusion and cardiogenic shock were noted, and intra-aortic balloon pump (IABP) support was begun immediately. Further electrocardiography revealed sinus tachycardia, low-voltage QRS complexes with diffuse S-T segment elevations, and no electrical alternans. Right heart catheterization showed equalization of diastolic pressures. Echocardiography revealed a large pericardial effusion and manifestations of cardiac tamponade but no signs of myocardial tear, mitral regurgitation, or ventricular septal defect. Once IABP support had sufficiently improved the patient's hemodynamic status, the patient was transported to the operating room. The heart was approached through a sternotomy; then 500 mL of bloody fluid was drained from the pericardium. A pericardial patch was sutured and glued in place over the apical tear, and a vein graft was sutured to the left anterior descending coronary artery. The patient recovered quickly from surgery. After several weeks, he was fully ambulatory and was discharged from the hospital.

At the 3-month follow-up visit, the patient was taking statins, diuretics, β-blockers, angiotensin-converting enzyme inhibitors, and warfarin. Follow-up echocardiography revealed a left ventricular systolic function of 25% to 30%, mild enlargement of the left ventricle in the presence of a moderately large apical aneurysm, and no pericardial effusion.

Discussion

Myocardial rupture is a complication of AMI that directly causes death in 8% of patients.³ A rare but catastrophic form of this complication is LVFWR, the incidence of which is lowered when primary percutaneous intervention can be performed.² The traditional risk factors of LVFWR are older age, female sex, previous hypertension, and a 1st lateral or anterior-wall AMI.^2–7 Contrary to several reports, steroid use and late thrombolysis do not appear to increase the risk of LVFWR.^8,9

Classic LVFWR usually produces symptoms within the first 24 hours after an AMI and almost always by the end of the 1st week.¹⁰ Clinical manifestations depend on the amount and rate of pericardial bleeding. In most cases, sudden hemodynamic collapse is followed quickly by electromechanical dissociation and death. In some cases, a blood clot will seal pericardial leaks and form a left ventricular pseudoaneurysm.¹¹ A subacute variant of LVFWR, marked by slow repetitive bleeding, occurs in approximately one third of cases.^6,12 Unlike patients with classic LVFWR, patients with the subacute variant may survive until emergency surgery can be performed.

Several studies have tried to identify the premonitory signs and symptoms of fatal LVFWR.5,6,12,13 Prodromal manifestations reported so far include persistent chest pain (often erroneously attributed to ischemia), intractable vomiting, restlessness, persistent S-T segment elevation, and positive T wave deflection that persists for 72 hours after the onset of chest pain.^6,13 Other classic signs of cardiac tamponade, including pulsus paradoxus and diastolic pressure equalization, are usually absent.¹² Electromechanical dissociation may occur but has limited diagnostic value.⁵

Echocardiography is the considered the best choice for definitive diagnosis of LVFWR. The main echocardiographic findings in patients with LVFWR are pericardial effusion and intrapericardial echoes; occasionally, right-heart collapse or the actual tear itself can be seen. Echocardiography has a diagnostic sensitivity of 100% and a specificity of 93%.^12,14 Although hemopericardium may result from thrombolytic and glycoprotein IIb/IIIa inhibitor therapy, LVFWR should always be considered the leading diagnosis in a patient with AMI who is hypotensive and has pericardial effusion.

The definitive treatment for LVFWR is emergency surgical repair; most often, pericardial patch placement is performed with either biological glue or epicardial sutures.^15,16 Other surgical techniques include infarctectomy with patch placement and ventricular wall reconstruction.^15,17 Temporary therapeutic measures include rapid fluid infusion, administration of positive inotropic agents, and pericardiocentesis.¹⁷

Intra-aortic balloon pump support is a widely accepted treatment for ventricular septal rupture complicating AMI.¹⁸ However, its role in patients with LVFWR is less clear. Although Pifarre and colleagues suggested long ago that IABP support is a necessary step in achieving postsurgical survival,¹⁹ IABP support is not included in current treatment protocols and is used infrequently in patients with LVFWR.^10,20 In our opinion, IABP support should be a routine part of initial hemodynamic stabilization. In the present case, we believe that reducing both afterload and wall tension through the use of IABP support significantly improved our patient's chances of survival until surgical treatment could be performed (Fig. 1).

Fig. 1 Algorithm for clinical management of left ventricular free wall rupture in acute myocardial infarction.

EMD = electromechanical dissociation; IABP = intra-aortic balloon pump; IV = intravenous; LVFWR = left ventricular free wall rupture

Some authors have suggested that medical therapy might be appropriate in patients with LVFWR and pseudoaneurysm formation²¹ or in patients whose hemodynamic recovery is rapid.²⁰ Although off-pump repair has been described,²² the combination of surgical repair with coronary artery bypass grafting is most often advocated. This approach is very practical, because 80% of patients who experience LVFWR have multivessel coronary artery disease.¹⁷

In the case reported here, the patient presented with symptoms that suggested subacute LVFWR. Although the slow leakage of blood did cause hemodynamic instability, the leakage was not severe enough to cause complete hemodynamic collapse and massive hemopericardium. Because the patient was receiving IABP support during the period of slow deterioration, we were able to proceed quickly and successfully with combination surgical repair and coronary artery bypass grafting. Moreover, since the patient had very recently undergone coronary catheterization, we were not faced with the dilemma of whether to perform emergency coronary angiography preoperatively in order to determine which coronary arteries to bypass, or whether to proceed directly to surgery and perform empirically based bypassing of all of the major epicardial coronary arteries.⁷

In summary, the present case demonstrates that left ventricular free wall rupture is not always fatal and that early diagnosis and the institution of IABP support in patients with subacute left ventricular free wall rupture can allow successful bridging to definitive emergency surgical therapy.