Subacute Left Ventricular Rupture Supported with a Percutaneous Left Ventricular Assist Device

ABSTRACT: Cardiac rupture is a fatal complication of transmural myocardial infarction that is associated with high mortality. We describe the successful management of a case of subacute cardiac rupture and cardiogenic shock supported by a percutaneous left ventricular assist device (LVAD) as a bridge to surgery.

J INVASIVE CARDIOL 2011;23:246–247

Key words: heart failure, ventricular assist device, left ventricular aneurysm

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Cardiac rupture is a fatal complication of transmural myocardial infarction that is associated with high mortality.¹ We describe the successful management of a case of subacute cardiac rupture and cardiogenic shock supported by a percutaneous left ventricular assist device (LVAD) as a bridge to surgery. This report highlights the potential life-saving role of percutaneous ventricular decompression as a method to stabilize and successfully bridge patients to a surgically implanted LVAD in this critically ill population.

Case Report

A 45-year-old male smoker presented with a two-week history of chest discomfort, diaphoresis, and severe dyspnea. The admission electrocardiogram (ECG) showed monomorphic ventricular tachycardia, which was successfully cardioverted to sinus rhythm. Cardiac biomarkers revealed an elevated troponin I of 2.8 ng/ml, but normal creatine phosphokinase (CPK) of 86 U/L. Over 6 hours, respiratory failure ensued, requiring mechanical ventilatory support. Emergent cardiac catheterization revealed an ostial occlusion of the left anterior descending (LAD) artery (Figure 1A). Left ventriculography demonstrated a severely depressed ejection fraction of 10%, an anterior wall aneurysm with adherent thrombus and an elevated left ventricular end-diastolic pressure of 40 mmHg (Figure 1B). A transthoracic echocardiogram confirmed an anterior aneurysm with layering thrombus in the left ventricle (LV), preserved right ventricular function, and a small pericardial effusion. Intra-aortic balloon counterpulsation and inotropic therapy were initiated; however, over the next 24 hours, the patient’s hemodynamics worsened with a pulmonary capillary wedge pressure (PCWP) of 30 mmHg, Fick cardiac index (CI) of 1.37 L/min/m², and a pulmonary artery O₂ saturation (PAO2) of 43%. Due to worsening renal failure and refractory cardiogenic shock, a TandemHeart percutaneous left ventricular assist device (pLVAD; CardiacAssist, Inc., Pittsburgh, Pennsylvania) was implanted as previously described (Figure 1C),² with rapid improvement in hemodynamic parameters (PCWP of 18 mmHg, Fick CI of 3.23 L/min/m², PAO₂ of 76%). At 6,800 rpm, the pLVAD provided 4.5 L/min of flow and transesophageal echocardiography (TEE) documented decompression of the LV cavity with pronounced stasis (Figure 1D).

Over the subsequent 24 hours following pLVAD placement, the patient’s creatinine improved and he was referred for a HeartMate-II LVAD (Thoratec Corporation, Pleasanton, California). Intra-operative examination revealed hemo-pericardium with a subacute rupture of the anterior LV aneurysm, active bleeding and adherent clot to the epicardium (Figure 2A). 

Using standard aortic and bi-caval venous cannulation, cardiopulmonary bypass was initiated. With the heart beating, the TandemHeart pLVAD transeptal cannula was removed, the septal defect was closed primarily, and the triscupid valve repaired with a 28 mm Edwards MC3 annuloplasty ring (Edwards Lifesciences Corporation, Irvine, California). The ventricular apex was then cored. Through this ventriculotomy intracavitary, thrombus was removed, and the aneurysm was isolated using an 8-cm diameter bovine pericardium patch and 4-0 pledgeted Prolene sutures. After isolation of the aneurysmal segment, a HeartMate-II LVAD was successfully implanted using the same ventriculotomy (Figure 2B). Three weeks after successful implantation of the surgical LVAD, the patient developed sepsis and expired.

Discussion

Nearly one-quarter to one-half of patients who present with ST-segment elevation myocardial infarction (STEMI) do not receive reperfusion therapy, primarily due to delayed presentation to medical care.^3,4 Guidelines for the management of STEMI recommend against revascularization for patients presenting beyond 24 hours of their index event.^5,6 For this population, worse long-term outcomes are likely related to adverse ventricular remodeling and mechanical complications after MI.

The development of an LV aneurysm after transmural MI has been well described.^7,8 Following MI, LV myofibril organization in both the infarcted and non-infarcted myocardium becomes distorted and the LV chamber enlarges, converting from an elliptical to spherical structure.^9,10 After an anterior MI, up to 50% of LV cavities undergo either limited or progressive dilatation over the subsequent four weeks.⁷ Ultimately, chamber enlargement outpaces compensatory myocyte hypertrophy, leading to a net increase in LV wall tension and a decline in myocardial performance.¹⁰ As confirmed by echocardiographic and pathologic studies, the degree of infarct expansion correlates directly to the risk of cardiac rupture.^11,12 In a recent review of patients presenting with cardiac rupture, mortality rates for incomplete versus complete rupture were 12% and 36%, respectively.¹ Early diagnosis and therapeutic intervention for patients with cardiac rupture may lead to improved survival.

The role of surgically implanted mechanical support devices for cardiogenic shock has been well characterized in the surgical literature. Mechanical unloading of the LV is associated with reduced wall tension, reduced matrix metalloproteinase expression, improved beta-receptor density, and increased collagen synthesis.¹³ As a result, the primary mechanisms promoting aneurysm formation and cardiac rupture are subtended. However, in many cases of cardiac rupture, patients present with multi-organ failure or hemodynamic instability, precluding the benefits of surgical intervention. In these cases, percutaneous mechanical circulatory support may provide a bridge to operative success.

While percutaneous LV support has been described in ventricular septal rupture,^14,15 their use in subacute cardiac rupture has not been reported. In this case, with active unloading of the LV as evidenced by transesophageal echocardiogram imaging and hemodynamic measurements, pressure and volume overload promoting progressive LV rupture was likely reduced and allowed for successful bridging to definitive surgical repair. Based on this clinical experience, the use of pLVADs may improve the likelihood of successfully bridging patients with subacute cardiac rupture to surgical LVAD implantation by: 1) reducing LV wall tension; 2) promoting molecular mechanisms leading to myocardial fibrosis and stabilization; and 3) improving acute hemodynamics and systemic perfusion.

Acknowledgment. We would like to thank Benjamin M. Kalsmith, MD, for his contribution to this manuscript.

References

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From Tufts Medical Center, Boston, Massachusetts.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted January 4, 2011, provisional acceptance given February 10, 2011, final version accepted February 11, 2011.
Address for correspondence: Navin K. Kapur, MD, Assistant Professor, Division of Cardiology, Assistant Director, Interventional Cardiology, Investigator, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111. Email: nkapur@tuftsmedicalcenter.org
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