Complex Case

High-Risk Coronary Intervention with a Percutaneous Ventricular Assist Device in the Presence of an Unstable Left Ventricular Th

Navin K. Kapur, MD, Chris Pan, BSc, Barath Krishnamurthy, MD
Navin K. Kapur, MD, Chris Pan, BSc, Barath Krishnamurthy, MD

High-Risk Coronary Intervention with a Percutaneous Ventricular Assist Device in the Presence of an Unstable Left Ventricular Thrombus

ABSTRACT: Left ventricular (LV) thrombus is one of the most common complications of myocardial infarction (MI). Contemporary devices for mechanical support during high-risk percutaneous coronary intervention (PCI) include intra-aortic balloon pumps (IABPs) or percutaneous left ventricular assist devices (pVADs). We describe the case of an elderly patient presenting with critical double-vessel disease, severely depressed LV function, and a large LV thrombus in the setting of a mechanical fall causing spinal cord compression. In this report, we describe the use of a TandemHeart pVAD during high-risk PCI in the presence of an unstable LV thrombus.

J INVASIVE CARDIOL 2010;22:E138–E140

Key words: ventricular assist device, thrombus, coronary intervention
Left ventricular (LV) thrombus is one of the most common complications of myocardial infarction (MI). The risk of developing an LV thrombus is highest within the first 2 weeks post MI, yet can develop anytime in association with worsening LV systolic function.1 In most cases, coronary revascularization can be accomplished either percutaneously or surgically despite the presence of an LV thrombus. However, in patients at high risk for complications from surgery due to comorbidities, percutaneous coronary intervention (PCI) may often be a better option. Contemporary mechanical support for high-risk PCI includes intra-aortic balloon pump (IABP) counterpulsation or percutaneous left ventricular assist devices (pVADs) such as the TandemHeart (CardiacAssist, Inc., Pittsburgh, Pennsylvania) or Impella (Abiomed, Danvers, Massachusetts).2 In the presence of LV thrombus, use of an Impella pVAD is prohibited due to required placement of the device in the LV cavity. In this report, we describe the use of a TandemHeart pVAD during high-risk PCI in the presence of an unstable LV thrombus. Case Description. An 80-year-old male with no prior cardiac history presented with a non-ST-segment elevation myocardial infarction as a consequence of a mechanical fall complicated by spinal cord compression at the level of the third cervical vertebra. Transthoracic echocardiography documented an apical left ventricular (LV) aneurysm with mobile LV thrombi (Figure 1), global hypokinesis, an estimated LV ejection fraction of 10% and mild mitral regurgitation. Baseline electrocardiography showed sinus rhythm with a left bundle branch block. Hemodynamics via a pulmonary artery catheter showed moderately elevated right and left heart filling pressures (right atrial pressure: 14 mmHg; pulmonary capillary wedge pressure: 18 mmHg). Coronary angiography revealed heavily calcified coronary arteries and a subtotally occluded mid-left anterior descending (LAD) artery. The distal LAD was diffusely diseased with an occluded apical branch. The left circumflex (LCx) artery had critical sequential stenoses in the first obtuse marginal branch. The right coronary artery (RCA) had moderate ostial disease. A rest myocardial perfusion test showed anterolateral wall viability and a fixed apical defect with severe global hypokinesis. The patient was judged to be at high risk for coronary artery bypass surgery due to a heavily calcified aorta, severe LV dysfunction, remote history of stroke and recent spinal injury. Based on his clinical history, a calculated EuroSCORE of operative risk was 83.55. After extensive discussion regarding the advantages and disadvantages of medical therapy versus coronary intervention, the patient elected to pursue percutaneous revascularization. Due to his severely depressed LV function and mutlivessel coronary disease, a TandemHeart pVAD was used to support the procedure. To avoid mechanical disruption of the LV thrombi, placement of the pVAD left atrial inflow cannula was accomplished by placing a standard 0.35 J-wire into the left superior pulmonary vein with fluoroscopic and intracardiac echocardiographic guidance. The patient underwent bare-metal stenting of the LCx, then the LAD stenoses in anticipation of neurosurgery for spinal cord compression (Figure 2). Post-intervention angiography and intravascular ultrasound interrogation showed widely patent and well-apposed LAD and LCx stents with diffuse distal LAD disease and coronary-cameral fistulae filling the LV apex (Figure 3). The pVAD was removed immediately after coronary intervention using manual compression without complication. Seventy-two hours post intervention, the patient developed transient complete heart block and hemodynamic compromise requiring brief cardiopulmonary resuscitation including chest compressions. Twenty-four hours later, a cold right hand was noted and emergent surgical embolectomy of an organized thrombo-embolus in the right brachial artery was successfully performed (Figure 4). After placement of a dual-chamber pacemaker, the patient was discharged. Spinal surgery was performed within 8 weeks after discharge. At 6-month follow up, the patient remained physically active with no functional limitation secondary to cardiovascular symptoms. Discussion Historically, the incidence of LV thrombus formation after MI has been reported to be 20–60% prior to the era of reperfusion therapy.1 An analysis of the Gruppo Italiano per lo Studio della Sopravvivenza dell’Infarto Miocardico-3 (GISSI-3) database, demonstrated that LV thrombosis occurred in 427 patients (5.1%) of the total 8,326 patients at low-to-medium risk for LV thrombi: 292 of 2,544 patients (11.5%) with anterior acute MI and 135 of 5,782 patients (2.3%) with acute MI in other sites.3 A contemporary analysis of 642 patients with anterior MI also reported similar rates of LV thrombosis (6.2%).4 Furthermore, A case series of 85 patients with LV thrombus after MI showed a 13% embolic event rate compared to 2% in the control group.5 A meta-analysis of 856 patients with anterior MI showed the odds ratio for increased risk of emboli from LV thrombus to be 5.45 (95% CI 3.02–9.83), with an event rate difference of 0.09 (95% CI 0.03–0.14).6 Using current-generation pVADs, high-risk PCI is emerging as a subset of procedures that require careful patient evaluation, device selection and a realistic assessment of technical, procedural and clinical success. A detailed discussion regarding the risks, benefits and alternatives to high-risk PCI is mandatory and should include a realistic assessment of the merits of medical therapy alone. In this case, because of the potential for lifelong disability due to cervical spine injury, we pursued high-risk PCI in the setting of an unstable LV thrombus. The thromboembolic event in this case did not correlate temporally with the use of the pVAD, but rather occurred in the setting of chest compressions 72 hours after successful decannulation of the pVAD. Important considerations during the preprocedural evaluation of patients referred for high-risk PCI with pVAD support in the setting of a known LV thrombus include a baseline assessment of: 1) mitral valve competency; and 2) careful placement of the left atrial inflow cannula for the pVAD without entering the LV. In the setting of severe mitral regurgitation, use of a pVAD may be considered higher risk due to the possibility of dislodging an LV thrombus by negative pressures generated at the tip of the atrial inflow cannula. To avoid mechanical disruption of an existing LV thrombus, placement of a standard J-wire into the left superior vein or coiling an Inoue wire (Toray Industries, Japan) in the left atrium may prevent inadvertent entry into the LV cavity. Acknowledgment. We wish to acknowledge David Denofrio, MD, for his assistance with the preparation of this manuscript.

Editorial Comment

Complex coronary lesions with low LVEF ( — Samin K. Sharma, MD
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From the Tufts Medical Center, Division of Cardiology, Boston, Massachusetts. The authors report no conflicts of interest regarding the content herein. Manuscript submitted November 6, 2009, provisional acceptance given November 16, 2009, final version accepted December 4, 2009. Address for correspondence: Navin K. Kapur, MD, Tufts Medical Center, Division of Cardiology, 800 Washington Street, Box #80, Boston, MA 02111. E-mail: