Survival of an Octogenarian after Rupture of the Left Ventricular Free Wall Caused by Myocardial Infarction

Abstract

Left ventricular free wall rupture is an uncommon complication after a myocardial infarction that is associated with a high mortality rate from pericardial tamponade, especially in the elderly. Early recognition and management of this clinical entity affects the outcome; therefore, a high index of suspicion is imperative. We present a case of an 80-year-old man admitted with myocardial infarction, who had subsequent findings of left ventricular free wall rupture complicated by pericardial tamponade. Emergent surgical repair led to successful recovery. A brief overview of the clinical presentation, diagnosis, and management of this challenging and potentially fatal complication is presented.

Ventricular free wall rupture is the 2nd-most-common cause of death in patients with acute myocardial infarction.¹ Since the time in which coronary care units came into widespread use, there appears to have been a rise in the frequency of ventricular free wall rupture in association with acute myocardial infarction.² The diagnosis of free wall rupture is seldom made before death, and death is inevitable if intervention is not prompt. Advanced age is one of the risk factors for the development of this complication.³ Early detection with appropriate diagnostic techniques can lead to successful treatment of ventricular free wall rupture. We report the case of an elderly man with acute myocardial infarction who developed rupture of the left ventricular free wall after his admission to the hospital. Timely detection and surgery led to a favorable outcome.

Case Report

An 80-year-old man presented at the emergency department of York Hospital (York, Pa) with chest and abdominal discomfort that had begun 3 days earlier. His medical and family history was noncontributory. He had a remote history of smoking (40 pack-years). On physical examination, the patient was in no apparent distress. His pulse rate was 82/min in regular rhythm, his blood pressure was 112/80 mmHg, and his respiratory rate was 22/min. He was afebrile. He had a jugular venous distention up to 7 cm. Heart sounds were regular, with an S₄ gallop and no obvious murmur or rub. The respiratory examination was notable due to diminished breath sounds at both lung bases. The gross examinations of the abdomen and nervous system were unremarkable. Laboratory investigation revealed abnormal cardiac markers: creatine kinase elevated to 327 U/L, MB fraction of 10.4 ng/mL, and cardiac troponin I of 10 ng/mL. An initial electrocardiogram showed sinus rhythm at 98 beats/min with frequent premature atrial complexes, ST segment elevation up to 1 mm in leads V₅ and V₆, and flattened T waves in leads II, III, and aVF. The patient was admitted to the coronary care unit with a diagnosis of myocardial infarction. Six hours after presentation, the patient developed an acute episode of chest discomfort, shortness of breath, and diaphoresis. An electrocardiogram performed at this time revealed ST segment elevation up to 3 mm in leads II, III, aVF, V₅, and V₆ consistent with a large acute myocardial infarction of the inferior and lateral walls. As a consequence of the above findings, thrombolytic therapy was initiated in the form of double-bolus reteplase, and acute symptoms subsequently resolved.

Due to persistent hypotension (systolic blood pressure of 90 mmHg), an echocardiogram was performed to look for mechanical complications of acute myocardial infarction. The test disclosed severe hypokinesis of the inferior, posterior, and lateral walls. There was a 1- to 2-mm diameter echo-dense structure within the pericardial space, which was most likely consistent with thrombus or hematoma. The patient underwent urgent cardiac catheterization. Right heart catheterization, performed initially, revealed near equalization of pressures in all 4 cardiac chambers. The mean right atrial pressure was 18 mmHg, right ventricular pressure was 35/16 mmHg, pulmonary artery pressure was 40/18 mmHg (mean, 27 mmHg), and mean pulmonary capillary wedge pressure was 20 mmHg. These findings were consistent with pericardial tamponade. A left ventriculogram revealed extrusion of dye from the posterior lateral wall into the pericardial space, which was consistent with contained left ventricular free wall rupture (Fig. 1). The patient underwent emergent cardiac surgery with successful repair of the defect in the left ventricular free wall. He tolerated the surgery well, had no complications during the rest of his hospital stay, and left the hospital after successful rehabilitation therapy.

Fig. 1 Left ventriculogram A) in early systole shows extrusion of contrast dye in pericardial space (arrow); and B) in late systole shows persistence of contrast dye (arrow).

Discussion

Left ventricular rupture is the 2nd leading cause of in-hospital death among patients with acute myocardial infarction. It has been noted that there has been an increase in the frequency of left ventricular free wall rupture during myocardial infarction since the use of coronary care units became widespread.² The complication is almost universally fatal, and the diagnosis is seldom made before death; therefore, a high index of suspicion is required to detect this potentially devastating complication. Certain patient characteristics increase the risk of developing left ventricular rupture secondary to myocardial infarction: they include age >55 years, 1st transmural infarction, Killip class I or II, persistent ST segment elevation, persistent or recurrent chest pain, sudden or progressive hypotension, and sudden electromechanical dissociation.^3,4

Eighty-five percent of ventricular wall ruptures occur within the 1st week and 40% within the first 24 hours after myocardial infarction.² The rupture is frequently caused by an increase in wall tension in the zone where necrosis and ischemia have created dilatation and thinning of the myocardium.⁵ The common initial clinical symptom is substernal chest pain, and the duration can range from 30 minutes to 6 hours.⁴ The important clinical signs include hypotension, bradycardia, increased venous pressure, quiet heart sounds, pulsus paradoxus, and cardiogenic shock (out of proportion to the myocardial damage that is implied by the electrocardiogram).⁶ Continuous electrocardiographic monitoring often shows electromechanical dissociation after free wall rupture. In patients who experienced a 1st myocardial infarction and were not in heart failure, electromechanical dissociation was found to have a very high sensitivity and specificity as a sign of left ventricular free wall rupture.⁷

The quickest and most sensitive imaging test to confirm cardiac rupture is a transthoracic echocardiogram; fluid in the pericardial sac is the most consistent finding.⁸ Other echocardiographic findings compatible with rupture are visible wall defects and echogenic masses in the effusion.⁸ Right cardiac catheterization may show equal pressure in the right cardiac chambers.⁹ The initial objective of management is resuscitation of the patient to achieve hemodynamic competence and urine output. This is best done by rapid infusion of fluids, together with inotropic support.¹⁰ Pericardiocentesis should be carried out if the patient remains hypotensive with signs of peripheral hypoperfusion. A small quantity of pericardial fluid is withdrawn in order to achieve hemodynamic stability. Prompt surgical repair is the definitive treatment for cardiac rupture. However, operative mortality rates are high. Lopez-Sendon and colleagues¹¹ reported an immediate operative mortality rate of 24% and a hospital mortality rate of 52%. Long-term survival with partial or complete recovery is reported with increasing frequency, and this may become more common with greater awareness of the complication and the availability of echocardiography, both of which enable earlier attempts at surgical repair.¹²

In conclusion, our case illustrates the importance of early recognition of left ventricular free wall rupture as a mechanical complication of acute myocardial infarction. In this patient, early clinical suspicion of this highly lethal complication—which prompted urgent echocardiography and cardiac catheterization followed by emergent cardiac surgery—probably played a crucial role in survival. Clinical suspicion of ventricular wall rupture should be high in patients who exhibit persistent hypotension or shock after myocardial infarction. High clinical suspicion, prompt diagnosis, and emergent surgical treatment can result in a successful outcome, provided that the rupture is still contained at the time of cardiac surgery.