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Ann Thorac Surg 1997;64:1509-1513
© 1997 The Society of Thoracic Surgeons

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Current Reviews

Ischemic Left Ventricular Free Wall Rupture: Prediction, Diagnosis, and Treatment

Department of Surgery, Section of Cardiothoracic Surgery, Baylor College of Medicine, Houston, Texas

	Abstract

Top Footnotes Abstract Introduction Case Presentation Comment References

 
Left ventricular free wall rupture is the third leading complication and the second most common cause of death after myocardial infarction. Its occurrence has been considered an unpredictable event usually leading to death. An increased appreciation for the clinical presentation of this syndrome and the nearly ubiquitous use of echocardiography have fostered a rise in the antemortem diagnosis of left ventricular free wall rupture, allowing the possibility of operative repair. Despite the increased reporting of left ventricular free wall rupture, the experience of any one surgeon or surgical group tends to be quite small. We review the current status of rupture prediction, clinical presentation, diagnosis, and treatment options. A recent case of left ventricular free wall rupture referred to the Baylor Cardiothoracic Surgery Group with the misdiagnosis of ruptured dissection of the ascending thoracic aorta is presented to illustrate our approach to this clinical situation.

	Introduction

Top Footnotes Abstract Introduction Case Presentation Comment References

 
Approximately 500,000 people per year in the United States experience an acute myocardial infarction. Left ventricular free wall rupture is a well-recognized complication of myocardial infarction and a frequent cause of death. The first clinical report of cardiac rupture is probably the reference by William Harvey in 1649, describing the autopsy of a knight who suffered severe chest pain and was found to have a free wall rupture at autopsy. The association with coronary artery obstruction was first suggested in 1850 by the English surgeon Joseph Hodgron. Survival without operative intervention has been described but appears to be an uncommon event. The first reports of successful surgical repairs appeared in 1972. The widespread availability and use of cardiac imaging, particularly echocardiography, have increased the number of cases diagnosed before death and the number of surgical repairs attempted. Despite this, the total number of surgical repairs reported in the English-language literature is small, and the experience of any one surgeon or surgical group continues to be very small.

We recently treated a patient transferred from another institution with the presumed transfer diagnosis of ruptured dissection of an ascending thoracic aortic aneurysm, which proved to be a left ventricular free wall rupture on emergency exploration. This precipitated our current review of the status of prediction of left ventricular free wall rupture, modes of clinical presentation, appropriate diagnostic tests, and treatment strategies.

	Case Presentation

Top Footnotes Abstract Introduction Case Presentation Comment References

 
The patient is a 46-year-old man with a history of hypertension who collapsed while at work. He had no other positive medical history. He was taken to an area hospital, where he was found to be hypotensive and diaphoretic and complained of chest pain. Electrocardiogram (ECG) results suggested ischemia of the lateral wall, and a computed tomographic scan of the chest showed a large amount of blood around the pericardium (Fig 1). The patient was diagnosed with rupture of an ascending aortic aneurysm and was transferred to our institution by helicopter.

View larger version (146K): [in this window] [in a new window]   Fig 1. . Computed tomographic scan of the chest showing hemopericardium.

At operation, the patient underwent immediate median sternotomy and pericardiotomy for relief of tamponade. His hemodynamic indices improved immediately, and he was found to have a normal ascending aorta but a large myocardial infarction in the distribution of the second obtuse marginal coronary artery, with necrosis and free wall bleeding from this area of the heart. The patient was placed rapidly on cardiopulmonary bypass with arterial cannulation in the distal ascending aorta and dual stage venous cannulation through the right atrial appendage. A retrograde cardioplegic cannula was placed in the coronary sinus, an antegrade cardioplegic needle was placed in the ascending aorta, and a pulmonary artery sump was placed after the institution of cardiopulmonary bypass. The heart was inspected thoroughly and was confirmed to have extensive necrosis in the obtuse marginal distribution with free bleeding from the site. Coronary plaque could be palpated easily in the proximal left anterior descending coronary artery. The right coronary artery was normal to palpation. The ascending aorta was cross-clamped, cardioplegic arrest was induced with antegrade and retrograde cold blood potassium cardioplegia, and iced saline solution was placed on the heart. Reversed autogenous saphenous vein bypass was performed from the ascending aorta to the distal left anterior descending coronary artery. The area of necrosis was inspected and was found to be extremely friable, with debridement performed easily with the use of forceps only. Infarctectomy of this area was carried out; the myocardium was debrided with forceps back to healthy tissue that would no longer debride. A Dacron patch was fashioned to fit this space and was sutured with pledgeted interrupted 2-0 Ticron sutures; the edge of the patch was oversewn to the myocardium with a running 2-0 Prolene (Ethicon, Somerville, NJ) suture (Fig 2). An intraaortic balloon pump was placed, and the patient was weaned from cardiopulmonary bypass with dopamine and dobutamine support. Lifting the heart after discontinuation of cardiopulmonary bypass was strictly avoided to prevent tearing of the patch area. The patient improved hemodynamically, allowing removal of the intraaortic balloon pump on postoperative day 2 and discontinuation of inotropic support on postoperative day 4. An inferior vena caval filter was placed on postoperative day 10 because of deep venous thrombosis and suspected pulmonary emboli. He was given heparin and transitioned to warfarin treatment and discharged on postoperative day 17. At 2-month follow-up, he had returned to his job as a computer programmer and had resumed daily activities without limitations.

View larger version (55K): [in this window] [in a new window]   Fig 2. . (A) Infarction and area of rupture; infarctectomy to good tissue. (B) Technique of patch repair.

	Comment

Top Footnotes Abstract Introduction Case Presentation Comment References

Certain patients have an increased risk for free wall rupture after myocardial infarction. Patient characteristics of those with increased risk include age greater than 60 years, female sex, preexisting hypertension, and no history of myocardial infarctions [4, 13]. Other potential risk factors include lack of left ventricular hypertrophy, no mural thrombus, and an acute transmural infarction [6]. Although these characteristics are well known, they are not specific enough to predict which patients are at risk of rupture. Several studies have been done to determine clinical symptoms or laboratory tests that might help predict free wall rupture after myocardial infarction. Oliva and colleagues [13] studied 70 consecutive patients with left ventricular rupture. The data were collected retrospectively in 64 patients and prospectively in 6 patients [13]. They reviewed clinical records and ECGs of all patients and found clinical symptoms and an ECG change common only to those patients who eventually had rupture. The symptoms included positional pleuritic chest pain, repetitive and unprovoked emesis, and restlessness and agitation. Oliva and colleagues [13] calculated these clinical symptoms to have sensitivities of 86%, 84%, and 55%, respectively, and specificities of 72%, 95%, and 95%. They also found that 84% of the patients with rupture had two of the three symptoms, as compared with 3% of those patients who did not have rupture. Twenty-one percent of the patients with rupture had all three symptoms [13]. The common ECG change was a persistent or progressive ST segment elevation 24 to 72 hours postinfarction in the absence of reinfarction, pericarditis, or ventricular aneurysm formation. This occurred in 64% of those patients who had rupture and in only 22% of those who did not [13]. Oliva and colleagues [13] concluded that one could obtain a good predictive value for rupture by looking for the persistent ST elevation and the clinical symptoms described.

Serum C-reactive protein (CRP) levels have been studied to determine whether this inflammatory phase protein should be used to identify patients at risk of free wall rupture [11]. The level of CRP was measured in 9 consecutive patients with rupture (7 with free wall and 2 with septal rupture) and in 28 consecutive patients who did not have rupture. It was found that in those patients who eventually had rupture, CRP levels increased rapidly by day 2 after the myocardial infarction and remained elevated (>20 mg/dL). In contrast, patients who did not have rupture did not have a rapid rise in their CRP level, and it did not exceed 10 mg/dL [11]. The study group concluded that patients with persistently high levels of CRP, particularly greater than 20 mg/dL, have a high probability of rupture [11].

Rupture of the left ventricular free wall generally occurs between 1 and 7 days after myocardial infarction [6, 10, 12, 14]. The patient often has prolonged severe chest pain followed by hypotension and bradycardia. The patient demonstrates increased venous pressure, quiet heart sounds, pulsus paradoxus, and cardiogenic shock, which occurs late and is out of proportion to the amount of myocardial damage implied by the ECG [4, 6]. Patients having continuous ECG monitoring often show electromechanical dissociation (EMD) [7]. The occurrence of EMD is a very valuable sign of rupture in patients who have had their first myocardial infarction and did not have signs of heart failure before the rupture. In their study on EMD associated with free wall rupture, Figueras and associates [15] found that EMD had a high sensitivity and specificity as a sign of left ventricular free wall rupture when it occurred in patients who had had their first myocardial infarction and were not in heart failure before rupture; however, in patients with heart failure before rupture, the predictive value of EMD was not as good.

The fastest and most sensitive diagnostic test to confirm cardiac rupture is transthoracic echocardiography [6, 7]. The most consistent finding is pericardial effusion. Other echocardiographic signs consistent with rupture are echogenic masses in the effusion fluid and visible wall defects [6, 7]. It is reported that the sensitivities of echogenic masses in the effusion fluid and of wall defect are 97% and 97%, and specificities are 93% and 98%, respectively [7]. These data suggest that transthoracic echocardiography plays a major role in the diagnosis of free wall rupture.

The role of invasive diagnostic testing is unclear. Ventriculography is very insensitive because it requires an ongoing leak through the ventricular wall, which is an unusual occurrence in patients stable enough to undergo this procedure [6]. Cardiac catheterization and coronary angiography were recommended by Pifarré and coworkers [16] in a review of 4 cases in 1983, to delineate coronary anatomy and allow coronary artery bypass if necessary. It should be noted that in 3 of the 4 cases they operated on, the diagnosis of free wall rupture was made at operation and was not suspected preoperatively. Indeed, cardiac catheterization provides no further information than echocardiography for diagnosing free wall rupture [6]. The benefit of doing angiography versus the risk of the patient's dying because of delayed treatment is unknown because only 9 of the reported 87 long-term survivors of free wall rupture had coronary artery bypass grafting as part of their surgical treatment [6]. We agree with the reviewer's comments to the article of Pifarré and coworkers [16] that operation should not be delayed unnecessarily for cardiac catheterization in these critically ill patients.

Four patterns of ruptures on a left ventricle have been described [4]. Type I is a direct tear to the muscle in one direction without dissection or bloody infiltration. Type II is a dissection through the muscle in multiple directions with bloody infiltration. Type III is a rupture that has its opening protected either by a thrombus or by a pericardial symphysis. Type IV is an incomplete rupture, indicating that the tear does not go completely through the muscle. These types of ruptures have been found to occur more commonly on the anterior or lateral wall of the left ventricle, and more specifically, at about the middle of the ventricle along the axis from the base to the apex [3, 4]. Why most ruptures occur here is not fully understood. One theory involves the innate anatomic muscular arrangement of the left ventricle [3]. Another is that it may be associated with the site of papillary muscle insertion. Veinot and associates [3] studied 25 consecutive patients with left ventricular free wall rupture. The hearts were examined grossly and microscopically [3]. They reported that they did not find an association between papillary muscle infarction and the site where the initial endocardial tear occurred. However, they found that 80% of the ruptures occurred between the papillary muscle insertions or within 1 cm of either side of the insertion sites. From this finding, they postulated that the increased stress at the site of muscle insertion due to the different arrangement of muscle fibers at this site may play a role in rupture of the myocardium [3].

Much debate has arisen concerning the association of thrombolytic use with myocardial rupture. In their metaanalysis, Honan and colleagues [17] reported that the odds ratio of cardiac rupture increased with delay in the mean time to thrombolytic treatment. There is microscopic evidence for why late treatment with thrombolytic agents may increase the risk of rupture. Plasmin, an enzyme activated by the use of thrombolytic agents, is known to break down collagen [18, 19]. Thus, plasmin can prevent repair of the infarcted tissue, leaving it fragile. The use of thrombolytic drugs also raises the potential for intramyocardial hemorrhage, which would increase the volume and pressure on the poorly healing heart; this overload can cause the heart to rupture [18]. Although one study reported that cardiac rupture was correlated with time to treatment, other studies have not found this to be true [10]. One particular study on the relation between thrombolysis and rupture is the Late Assessment of Thrombolytic Efficacy (LATE) study by Becker and associates [10]. This study included 5,711 patients who were randomly assigned to receive either recombinant tissue-type plasminogen activator (rt-PA) or a matching placebo. The study demonstrated that the group receiving rt-PA within 6 to 12 hours of symptom onset had the highest number of ruptures, but the data were not statistically significant. Another group receiving rt-PA between 12 and 24 hours from symptom onset had fewer ruptures than the placebo group. Becker and associates [10] concluded that beginning late treatment with rt-PA is not associated with an increased risk for rupture. However, these data may not hold true for other thrombolytic agents that are not as specific as rt-PA.

The first objective of treatment is resuscitation of the patient to achieve hemodynamic stability. This can best be done by rapid infusion of fluids along with inotropic support [20]. The next potential step is pericardiocentesis. If successful, it decreases the threat of tamponade and allows a clinically more stable patient at the time definitive treatment is started. Placement on an intraaortic balloon pump, as suggested by Pifarré and associates [16], should be done early. Although there have been a few reported cases of long-term survival without operation [5], operation is the best choice of treatment in almost all circumstances. Several different approaches have been used successfully with long-term survival of the patient, including the use of biologically glued pericardial patches [21, 22], the use of pledgeted sutures alone for ruptures of the anterior and lateral wall [23], and the use of Dacron prosthesis and infarctectomy [24, 25]. The classic approach is to remove the area of infarction and replace it with a prosthetic patch under cardiopulmonary bypass, as was first described by Daggett and coworkers in 1974 [26] and further refined in their work on postinfarction ventricular septal rupture [25]. In hospitals that do not have the equipment for cardiopulmonary bypass, patients with anterior or lateral rupture may still have a chance for survival because ruptures in these areas can be oversewn with pledgeted sutures without cardiopulmonary bypass. The patient then can be transferred for further treatment. In cases in which a large portion of the left ventricular free wall is infarcted and removal of the area would leave a small left ventricular cavity with compromised output, a Dacron prosthesis should be used [26].

Because cardiac rupture is associated with multivessel disease in 80% of cases [3, 4], it has been advocated that before closing the defect, one should establish cardiopulmonary bypass and bypass all major vessels empirically [4]. This will allow revascularization and prevent the possible occurrence of early postoperative ischemia. There are no conclusive data to support or refute revascularization at the time of repair because few cases have diagnostic coronary arteriograms, the number of reported survivors is small, and there is no substantial long-term follow-up of bypassed and nonbypassed patients. We choose to bypass vessels with clinically apparent disease.

Surgical repair of the rupture site is the definitive treatment for cardiac rupture, although there are few data on operative mortality rates. Lopez-Sendon and colleagues [27] reported an immediate operative mortality rate of 24% and a hospital mortality rate of 52%. Other reports listed the operative mortality rate as 24% to 35% [7] and 35% [28]. These mortality rates are high, but probably underestimate the true mortality because numerous cases of attempted repair resulting in death are likely unreported. Long-term survival has been accomplished with surgical repair, and this may become more common as clinical predicting factors and early diagnosis are better established, allowing earlier attempts at surgical repair.

In conclusion, left ventricular free wall rupture, if unrecognized and untreated, usually leads to a rapid death. Improved identification of patients at risk, understanding of the clinical presentation, and institution of rapid bedside echocardiography will allow diagnosis for prompt resuscitation and surgical salvage of these desperately ill patients.

	Footnotes

Top Footnotes Abstract Introduction Case Presentation Comment References

 
Address reprint requests to Dr Reardon, 6550 Fannin, Suite 2435, Houston, TX 77030 (e-mail: reardonm{at}bcm.tmc.edu).

	References

Top Footnotes Abstract Introduction Case Presentation Comment References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Michael J. Reardon Angela Diamond George V. Letsou Hazim J. Safi Rafael Espada John C. Baldwin Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Reardon, M. J. Articles by Baldwin, J. C. Search for Related Content PubMed PubMed Citation Articles by Reardon, M. J. Articles by Baldwin, J. C.