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Ann Thorac Surg 2000;70:1345-1349
© 2000 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Successful repair of myocardial free wall rupture after thrombolytic therapy for acute infarction

^a Division of Cardiothoracic Surgery and Division of Cardiology, St. Luke’s-Roosevelt Hospital Center, Continuum Health Partners, Columbia University College of Physicians and Surgeons, New York, New York, USA

Address reprint requests to Dr Connery, St. Luke’s-Roosevelt Hospital Center, 1111 Amsterdam Ave, New York, NY 10025

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. Controversy exists regarding the timing of thrombolytic administration and rupture rate.

Methods. Hospital records at St. Luke’s-Roosevelt Hospital of the 4 study patients were reviewed and compared with those of 41 patients from a group of 537 patients concurrently admitted with a diagnosis of myocardial infarction (MI).

Results. Four patients experienced ventricular free wall rupture after having a MI between November 17, 1993, and July 28, 1995. All received tissue plasminogen activator. In 1 patient, pericardial effusion associated with a pseudoaneurysm was discovered in the operating room. The 3 others developed clinical pericardial tamponade before surgery. All 4 patients survived and left the hospital on postoperative days 10, 11, 11, and 82, respectively. During this same time period, 537 patients were admitted with MI, 41 of whom died; the study’s 4 patients were compared with these 41.

Conclusions. These data demonstrate that rupture of the ventricular free wall can occur early after thrombolytic therapy and may have a subacute course. Prompt diagnosis and surgery offer excellent chances of surviving this fatal condition.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Most heart ruptures involve the left ventricular free wall. Left ventricular free wall or cardiac rupture occurs in 1% to 3% of all patients suffering from myocardial infarction (MI) and is involved in 8% to 17% of all infarct deaths, accounting for up to one third of in-hospital deaths post-MI. It is second only to cardiac failure and ahead of arrhythmia as a cause of in-hospital death. Most ruptures occur in the first week of infarction: 40% occur within the first 24 hours and 85% in the first week. Postinfarction rupture causes an estimated 25,000 fatalities per year in the United States [1–3]. The median time to rupture is 6 days. Patients dying of cardiac rupture have smaller infarcts than those dying of cardiogenic shock or arrhythmias [4], which suggests the potential for a favorable prognosis if the rupture can be repaired.

Controversy exists regarding the timing of thrombolytic administration and rupture rate [5, 6]. Unanswered questions include (1) whether earlier ruptures were necessarily fatal (ie, ruptures occurring within 7 days of thrombolytic therapy administered within 6 hours of chest pain onset); and (2) whether early identification and treatment could result in survival.

To investigate the relationship of thrombolysis to cardiac rupture in our institution, we undertook a retrospective chart review of all patients who were admitted for MI to our institution from November 17, 1993, to July 28, 1995, and who died. Cause of death was noted, and these fatalities were further subdivided as to whether or not these patients had received thrombolytic therapy. During this period, 4 patients underwent surgery for such isolated free wall rupture and survived.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
This study is presented in accordance with the guidelines of this hospital’s institutional review board. Hospital records at St. Luke’s-Roosevelt Hospital of the 4 study patients were reviewed for demographic data and cardiac risk factors. Each patient’s hospital course was summarized, and exact time points of chest pain onset, thrombolytic administration, and time of operation; lab values; and procedures were reviewed. For the time period from November 17, 1993, to July 28, 1995, which represents the admission dates of the first and last of the 4 patients presented, all patients (N = 537) admitted with a diagnosis of MI were extracted from the hospital database. From this group of 537 patients, data from the 41 patients who died were compared with data from the 4 patients who are the subjects of this study (Tables 1 and 2).

Patient 2
A 66-year-old man with cardiac risk factors of age and male sex was admitted with severe chest pain and dyspnea. Vital signs were stable, and ECG revealed anterolateral wall MI. Aspirin was given, and tPA was started at 5.75 hours after chest pain onset, along with intravenous nitroglycerin for relief of chest pain. Total CK/CK-MB/CK MB% peaked at 8806/490/4.9%. Echocardiogram on HD 2 showed left ventricular hypertrophy with wall motion defect of the interventricular septum and apex, with ejection fraction of 35% to 40%. On HD 7, the patient underwent cardiac catheterization, which showed a dyskinetic apex and anterolateral wall with ventricular aneurysm and triple-vessel coronary artery disease. Operative revascularization was planned. On HD 8, the patient’s blood pressure was noted to fall to 90 to 100 mm Hg, systolic, and his creatinine had risen to 1.7 from 1.1 mg/dl on admission. He remained symptom-free and stable. On HD 13, in the operative room, 200 mL of blood was evacuated by pericardiotomy. An anterior left ventricular pseudoaneurysm was found with blood leaking through a 2.5-cm rupture. Using extracorporeal circulation, the left ventricle was repaired with a buttressing Dacron patch secured with a running polypropylene suture. A triple coronary artery bypass grafting was performed. The patient recovered uneventfully and was discharged on postoperative day 10, HD 23.

Patient 3
A 57-year-old man with no prior cardiac history was admitted to another institution with substernal chest pain. His vital signs were stable, and ECG revealed anterolateral ischemia. tPA was administered 3 hours after chest pain onset. Aspirin, intravenous nitroglycerin, and heparin were given, and the chest pain abated. Total CK/CK-MB/CK MB% peaked at 10 100/506/5%. Overnight, the patient became anuric, and the following morning he became hypotensive. On arrival at St. Luke’s-Roosevelt Hospital, he was noted to be normotensive on dopamine. Posteroanterior catheterization showed a cardiac index of 1.7 L · min^-1 · m^-2 and pulmonary capillary wedge pressure of 34 mm Hg. Intraaortic balloon pump counterpulsation was initiated. Echocardiogram revealed a small anteroapical effusion. A follow-up echocardiogram the next day showed increased anteroapical effusion with mild right-chamber collapse. Despite this, the patient maintained adequate blood pressure and a cardiac index of 2.0 L · min^-1 · m^-2 with pulmonary capillary wedge pressure of 17 mm Hg with intraaortic balloon pump on 1:2 assist. Pericardiocentesis drained 52 mL of nonclotting blood. Cardiac catheterization revealed critical proximal and midleft anterior descending coronary artery stenoses. The patient remained hemodynamically stable. The following day, echocardiogram revealed an apical pericardial thrombus with worsened tamponade. The patient was taken to the operating room at 109 hours after the onset of chest pain, and a subacute rupture was primarily repaired and buttressed with a Dacron patch with running polypropylene suture in viable myocardium. A single saphenous vein bypass graft to the left anterior descending coronary artery was performed. The patient recovered uneventfully and went home on postoperative day 11.

Patient 4
A 75-year-old woman with cardiac risk factors of hypertension, angina, hypercholesterolemia, age, family history, and being postmenopausal was admitted complaining of chest pain. She had stable vital signs, and ECG showed an anterior wall MI. tPA was given 2 hours after the commencement of chest pain, along with heparin, relieving her chest pain. Cardiac catheterization revealed a severe proximal left anterior descending coronary artery lesion, which was opened with percutaneous transluminal coronary angioplasty. Nine hours after chest pain onset, the patient complained of a new chest pain. ECG revealed no new changes except for frequent premature ventricular contractions. Subsequently, hypotension developed in the patient; the hypotension partially responded to fluid challenge and dopamine. Echocardiogram showed pericardial effusion with tamponade. Pericardiocentesis removed 100 mL of nonclotting blood with immediate but temporary improvement of blood pressure. The patient was taken to the operating room for emergent closure of rupture. En route, the patient went into electromechanical dissociation (EMD). Advanced cardiac life support was administered, and in the operating room she underwent emergent sternotomy and open cardiac massage while emergent cardiopulmonary bypass was initiated. There was active bleeding from an inferoapical infarct from multiple sites with a 1.5-cm rent in the apex. The rupture was plicated with Teflon buttresses (DuPont, Wilmington, DE). The patient was transferred to the open heart recovery room in stable condition. She did not regain consciousness in the hospital and was transferred to a nursing home on HD 82. She subsequently made a partial recovery and currently resides in an assisted living facility and ambulates, with assistance, nearly 5 years later, at age 80.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
Table 2 summarizes the demographic and clinical information of the 4 patients. One patient was comatose after suffering an arrest en route to surgery and was discharged on mechanical ventilation to a nursing home; this patient subsequently made a significant recovery. The remaining 3 patients left the hospital after an average length of stay of 17 days (range, 13 to 23). During this same period, from November 17, 1993, to July 28, 1995, 537 patients were admitted to this institution with the diagnosis of MI. Of the 537 patients, 320 (60%) were men and 217 (40%) were women. Of these, 41 died, for an overall mortality rate of 7.6% (see Table 1). One patient died from cardiac rupture involving the interventricular septum and both ventricles. Five patients had the diagnosis of EMD arrest, and 24 were diagnosed with asystolic arrest. Thrombolytics were administered to 11 of the 41 patients. Median time to death was 3 days, with a range of 1 to 51 days. Of those who received thrombolytics, 2 of 11 (18%) underwent EMD arrest, and 6 of 11 (55%) died from asystolic arrest. Of those who received no lytic therapy, 3 of 30 (10%) underwent EMD arrest, and 18 of 30 (60%) underwent asystolic arrest. By extrapolation, if those who died from EMD arrest are added to the 1 patient who died from rupture, an estimated 6 of 41 patients (15%) probably died from rupture. This is a valid estimation, utilizing the findings of Figueras and colleagues [7], who in an autopsy-controlled study showed that 95% of patients with postinfarction EMD without heart failure had myocardial rupture. This may underestimate the true rupture rate, which could include some of the 24 of 41 patients (59%) who underwent asystolic arrest.

	Comment

Top Abstract Introduction Patients and methods Results Comment References

 
Cardiac rupture has been extensively reviewed. It is more common in older patients [8] and in those with transmural infarction lacking collateral circulation. There is an equal sex distribution. Because MIs occur at more advanced ages in women, proportionally more women rupture than men. Presence of previous MI is seen in only 15% to 24% of patients. Myocardial rupture is caused by necrosis of the transmural myocardial wall, usually with hemorrhagic transformation of the acute infarct. The rupture rate is three times greater in patients having their first MIs [2]. Approximately half of ruptures are serpiginous rather than simple tears. The most common site of rupture is the lateral aspect of the ventricular wall. Ruptures involving the right ventricular wall and interventricular septum are rare. The phenomenon of infarct expansion with recurrent chest pain, wall thinning, and disproportionate cardiac dilatation may cause rupture [9]. Rupture is 9.2 times more likely with no prior history of angina, ECG evidence of transmural MI, and peak CK-MB of 150 IU/L or greater [10].

The advent of the cardiac care unit is believed to have resulted in a relative decrease in death from arrhythmic complications of MI, with a proportionate increase in mortality due to cardiogenic shock and rupture [2]. Bates and colleagues found that of 14 795 patients reported dying from MI from 1928 to 1973, 8% (1185) died from myocardial rupture [11]. From 1977 to 1992, Pollak and colleagues reported a 20% rupture rate among 533 post-MI deaths, but they also noted that the rupture rate remained unchanged with thrombolytic therapy while overall mortality decreased [12].

Thrombolytic therapy and rupture
Rupture occurs when transmural pressures exceed the tensile strength of the heart’s connective tissue substrate. Lyon and colleagues demonstrated tremendous compliance to supraphysiologic pressures in ex vivo lamb hearts. Rupture occurs at the weakest points in the healthy heart: papillary muscle (54%), interventricular septum (30%), and left ventricular free wall (16%) [13]. Rupture in the setting of MI also occurs in the weakest point, the noncompliant infarct zone. Increased outflow resistance, manifested as hypertension or structural impediments such as aortic valve stenosis, may play a significant role in rupture [14]. Intraaortic balloon pump counterpulsation may be an important adjunct in reducing transmural forces in those with impending rupture or stable pseudoaneurysm. Nitrates may decrease rupture by 30% [15]. Benefits of pharmacologic afterload reduction must be weighed against drug effects on the heart’s tissue substrate [16].

Previous data suggested that treatment with thrombolytic agents decreased mortality from all causes even when administered later than the generally used 4- to 6-hour time frame. However, the odds ratio of cardiac rupture (thrombolytic-treated patients vs control) increased significantly as time to treatment was delayed. There was a beneficial effect with a reduction in cardiac rupture rate in patients treated with streptokinase within 5 hours of symptom onset [5]. Afterward, a significantly increased rupture rate developed in those patients who underwent delayed treatment.

The LATE (Late Assessment of Thrombolytic Efficacy) study did not show conclusively that late treatment with tPA increased the incidence of cardiac rupture. However, the time course to rupture was noted to be accelerated, because 18 out of 29 patients ruptured within 1 day, and 28 out of 29 ruptured within 7 days.

The LATE study did demonstrate that thrombolytic administration from 6 to 24 hours after the onset of symptoms reduced the rupture rate but also decreased the time to rupture. Late rupture is caused by infarct expansion, which is reduced by reperfusion [17]. However, early rupture, which has a different pathologic substrate, is increased by reperfusion [18]. Reperfusion may contribute to significant myocardial hemorrhage, which dissects through the infarct zone, thus contributing to early myocardial rupture [6]. These findings point to an important biochemical effect of tPA on the infarcting myocardium that is separate from its ability to trigger clot lysis.

Successful reperfusion with subsequent delivery of tPA and activated plasmin to ischemic tissues may also have detrimental effects on connective tissue. Plasmin activation, as well as infarction per se, activates proteolytic enzymes and causes collagen and elastin breakdown in rats and humans [19, 20]. Plasmin activates matrix metalloproteinases, including collagenases and metalloelastases [21], which may decrease the burst strength of ischemic-reperfused myocardial tissues. The decreased time to rupture suggests an important biochemical effect; differences in rupture rate related to sex or age may reflect differences in biochemical substrate. Actively blocking the action of these plasmin-activated proteolytic enzymes with tissues inhibitors of metalloproteinases [22] or tetracycline (an inhibitor of matrix metalloproteinases) may play a future role in the pharmacotherapy of MI.

Diagnosis and management
Timely diagnosis is the key to survival. The patients in our series survived to be diagnosed. Most of the patients who died succumbed within 3 days of admission. The study patients who demonstrated hypotension before operation manifested it in 9, 24.5, and 97.5 hours. This most likely reflects the rate of blood accumulation in the pericardium and emphasizes that rupture is not necessarily a "blowout" event. Patient 2 had a pseudoaneurysm discovered in the operating room; there was a stable clot without gross hemorrhage. Anagnostopoulos and colleagues described discovering cardiac rupture at the time of anesthesia induction for a bypass grafting procedure[23]. The afforded time for preoperative diagnosis is a function of the rate of leak. We believe that survival depends on identifying the rupture before the "blowout phase."

This study confirms the role of echocardiography in the diagnosis of rupture and reiterates the need for prompt study in a patient who becomes unstable [24], even if the hypotension is transient. Pericardiocentesis may play an important adjunctive role in diagnosis and palliation of tamponade, but it is often misleading and unhelpful, because much of the space is taken up by nonaspirable clot. López-Sendón and colleagues demonstrated that one third of all ruptures were subacute and that the combination of clinical values and echocardiographic findings allow for a high sensitivity and specificity not afforded by any single test or finding [25]. Most patients do not survive after initial rupture, as these patients did, but rather die soon after rupturing. In our study, there were an additional 5 patients in the nonoperative group with suspected ruptures who were missed. Such patients may one day benefit from a protocol that emphasizes early identification of rupture risks, administration of proteinase inhibitors, and emergent thoracotomy for those identified as at risk who undergo EMD arrest.

Principles of repair of left ventricular free wall rupture are to stop the bleeding, anchor the repair on healthy tissue, and minimize distortion of heart geometry. In this series, no single approach prevailed, because the method for each repair was dictated by the nature of the rupture and its surrounding tissues. A Dacron mesh patch with running polypropylene suture repair was used in 3 of 4 patients, whereas 1 of 4 was repaired with primary closure with Teflon strip buttresses. Off-pump repair was used with 1 of the patients. Other techniques, including a periinfarct pursestring technique [26], a sutureless technique with cyanoacrylate glue [27], and creation of a fistula to the right atrium [28], have been also described.

This study confirms that those who rupture early after thrombolysis can be repaired. This study underscores the need for vigilance and a high index of suspicion. Surgical decision making and intervention is crucial in this highly selected subpopulation of patients. Ultimately, therapies directed specifically at prevention of rupture may be the best avenue for preventing deaths.

	References

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This Article Abstract Full Text (PDF) 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): Cliff P. Connery Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Park, W. M. Articles by Anagnostopoulos, C. E. Search for Related Content PubMed PubMed Citation Articles by Park, W. M. Articles by Anagnostopoulos, C. E.