Acute myocardial infarction complicated by LV free wall rupture: the benefits of echocardiography
1 Westmead Private Cardiology, Corner Darcy and Mons Road, Westmead, NSW 2145, Australia
2 Westmead Private Hospital, Corner Darcy and Mons Road, Westmead, NSW 2145, Australia
3 Suite 7, Level 1, Children's Hospital Medical Centre, 2 Hainsworth Street, Westmead, NSW 2145, Australia
Received 12 July 2007; accepted after revision 5 August 2007; online publish-ahead-of-print 4 October 2007.
* Corresponding author. Westmead Private Cardiology, Corner Darcy and Mons Road, Westmead, NSW 2145, Australia. Tel: +61 02 9687 0866. E-mail address: stoodley{at}tpg.com.au
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Abstract |
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The recent increase in the number of cases of left ventricular free wall rupture being diagnosed before death and in the number of surgical repairs attempted is largely due to echocardiography. We report a case that highlights the value of echocardiography in the diagnosis and treatment of left ventricular free wall rupture following acute myocardial infarction.
Keywords: LV free wall rupture; Myocardial infarction; Echocardiography
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Case study |
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A 48-year-old hypertensive male smoker was admitted to hospital with chest pain and dyspnoea. He had an acute inferior myocardial infarction and biventricular failure. At angiography 2 weeks later, there was graftable triple vessel coronary artery disease. Gated heart pool scan demonstrated a significantly reduced left ventricular (LV) ejection fraction of 25%.
Transthoracic echocardiography (TTE) confirmed the poor LV function, and identified inferior, inferoseptal and inferolateral akinesia (Figure 1). A localized pericardial effusion with loculations, adjacent to the akinetic segments was noted. The localized pericardial effusion had echogenic specks within, suggestive of an exudative effusion. Additionally, fibrinous strands were present within the loculated area around the inferolateral LV wall (Figure 2 and supplemental avi images). In view of these findings, it was noted that a contained LV rupture could not be ruled out and the cardiothoracic surgeons were notified of this possibility prior to coronary artery bypass grafting (CABG).
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One week following the TTE the patient underwent CABG. The operative findings demonstrated a large haemorrhagic pericardial effusion; the entire heart was covered in a thick fibrinous peel. There were adhesions over the left lateral aspect of the heart. The obtuse margin of the heart was haemorrhagic consistent with a contained or limited full thickness ventricular rupture. As a prior diagnosis of possible ventricular rupture had been made, the cardiothoracic surgeons were careful in the assessment of the inferolateral region.
While the haemorrhagic effusion and subsequent fibrinous exudates made identification of the coronaries difficult, coronary artery bypass grafting of 2 vessels proceeded without major complication and specific repair to the previous rupture was not required.
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Discussion |
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Cardiac rupture during the course of myocardial infarction can occur at different sites of the heart based on the site of infarction. The left ventricular free wall (LVFW), ventricular septum and papillary muscle are common sites. Of these, LVFW rupture is the most common and after cardiogenic shock, is the leading cause of death following acute myocardial infarction.1–3
Four morphological patterns of myocardial rupture have been described. Type 1 involves a direct trajectory of rupture with little dissection or bloody infiltration of the myocardium. Type 2 involves multicanalicular trajectories with extensive myocardial dissection and bloody infiltration of the adjacent myocardium. Types 1 and 2 are associated with the poorest survival, even if identified early.4
When patients do survive the acute period, the majority present with a type 3 or 4 rupture. A type 3 rupture is described as one protected either by thrombus formation on the endocardial side of the rupture or by a pericardial symphysis on the epicardial side. In a type 4 rupture, into which category our case study falls, the ventricular wall is typically thinned and dilated but the rupture does not extend through all layers of the myocardium.4
Some patients with cardiac rupture succumb almost immediately. However, rupture may be delayed and only occur later in the first week in the setting of myocardial necrosis. In such cases, early recognition enables potentially life-saving interventions, of which surgery is often the treatment of choice, to be implemented promptly.5
Recognizing at risk patients (patients older than 60 years, of female gender, those with pre-existing hypertension and those with no previous myocardial infarction) is of importance, as early intervention needs to be planned in these cases. Understanding the typical clinical presentation, which includes positional pleuritic chest pain, repetitive and unprovoked emesis and restlessness and agitation, also helps with early recognition. Further, prior knowledge for surgeons can help in terms of discussing perioperative risk with the patient and family and also the need to evaluate possible ventricular repair.
However, the sub-acute form of LVFW rupture presents differently. Typical symptoms include acute onset or progressive hypotension associated with pericardial tamponade but without cardiac arrest. The sub-acute form may be repaired surgically, to prevent overt rupture.2
In all cases, the recent significant increase in the number diagnosed before death and the number of surgical repairs attempted is largely due to the widespread availability and use of cardiac imaging, particularly echocardiography.1 That is, echocardiography provides invaluable diagnostic information as well as an indication regarding the possible extent and location of the rupture prior to surgery.
The most frequent echocardiographic finding in the case of LVFW rupture is a localized pericardial effusion overlying the infarcted akinetic area. Other signs include echogenic ‘specks’ within the effusion and visible wall defects.3 In our case, each of the frequent findings were observed, and meant that the surgeon anticipated myocardial rupture and made a careful examination of the inferior, inferoseptal and inferolateral segments.
Our case study further highlights the value of echocardiography following acute myocardial infarction. Echocardiography aids in early recognition of cardiac rupture, whether presentation is in the acute or sub-acute phase. Echocardiography also helps to define the possible site of rupture and enables potentially life-saving interventions, which often involve surgery, to be planned and implemented promptly in such patients who are often critically unwell.
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Supplementary material |
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Supplementary material associated with this article can be found in the online version.
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References |
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- Reardon MJ, Carr CL, Diamond A, Letsou GV, Safi HJ, Espada R, et al. Ischaemic left ventricular free wall rupture: prediction, diagnosis and treatment. Ann Thorac Surg (1997) 64:1509–13.
[Abstract/Free Full Text] - Figueras J, Cortadellas J, Evangelista A, Soler-Soler J. Medical management of selected patients with left ventricular free wall rupture during acute myocardial infarction. J Am Coll Cardiol (1997) 29:512–8.[Abstract]
- Wehrens XHT, Doevendans PA. Cardiac rupture complicating myocardial infarction. Int J Cardiol (2004) 95:285–92.[CrossRef][Web of Science][Medline]
- Helmy TA, Nicholson WJ, Lick S, Uretsky BF. Contained myocardial rupture: a variant linking complete and incomplete rupture. Heart (2005) 91.
- Dencker M, Tasevska G, Grubb D, Stagmo M, Gustafsson R. Unexpected rupture of the left ventricular free wall in the echo-lab. Eur J Echocardiogr (2007) doi:10.1016/j.euje.2007.02.009.
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