Percutaneous Ventricular Assist Device Placement during Active Cardiopulmonary Resuscitation for Severe Refractory Cardiogenic Shock after Acute Myocardial Infarction

Abstract

Cardiogenic shock after acute myocardial infarction is associated with a high mortality rate despite modern reperfusion methods and intra-aortic balloon pump support. For myocardial infarction patients in cardiogenic shock that is refractory to intra-aortic ballon pump counterpulsation and pressors (severe refractory cardiogenic shock), there are limited means to rapidly provide additional hemodynamic support.

We present the case of a 49-year-old man who presented with an anterior wall acute myocardial infarction complicated by cardiogenic shock. After resuscitation and stabilization with intra-aortic balloon pump and pressor support, the patient underwent successful emergent percutaneous transluminal coronary angioplasty and stenting of the left anterior descending coronary artery. Forty-eight hours later, the patient again went into severe refractory cardiogenic shock; pulseless electrical activity arrest followed. Cardiopulmonary resuscitation was started, and the patient underwent urgent placement of a TandemHeart® percutaneous ventricular assist device. The device enabled the reversal of terminal hemodynamic collapse during active cardiopulmonary resuscitation, subsequent stabilization of the patient, and discharge of the patient from the hospital after device removal. In this patient, the percutaneous ventricular assist device was successful in the treatment of severe refractory cardiogenic shock after acute myocardial infarction.

Cardiogenic shock as a complication of acute myocardial infarction is associated with significant mortality rates, despite the use of intra-aortic balloon pump (IABP) counterpulsation and modern coronary reperfusion.^1–7 In patients who experience an acute myocardial infarction and go into cardiogenic shock, the prompt reversal of hypoperfusion is essential to support organ function, both during myocardial recovery after treatment and to stabilize the patient for definitive percutaneous or surgical intervention. To date, limited pharmacologic and mechanical means have been available to maintain hemodynamic support in patients with severely depressed left ventricular function and circulatory collapse.

The most commonly used form of mechanical support for patients in cardiogenic shock is IABP counterpulsation. However, IABP support is often inadequate to reverse the persistent hemodynamic compromise in patients who are in severe refractory cardiogenic shock (SRCS) after acute myocardial infarction, and mortality rates range from 52% to 76%.^9–11 Resuscitation has also been attempted with cardiopulmonary bypass support (CPS) and surgically placed left ventricular assist devices (temporary and permanent); these procedures are associated with significant morbidity and mortality rates.^12–14 Moreover, surgical implantation of mechanical assist devices in SRCS patients is often not technically feasible because of the frequent need for chest compression during active cardiopulmonary resuscitation (CPR). Extracorporeal life support (extracorporeal membrane oxygenation [ECMO]) is another method that has been used to resuscitate patients in SRCS; however, the high rates of thromboembolic complications and device-associated deaths have limited the usefulness of ECMO as a means of circulatory support in these patients.^15–22

The TandemHeart® (CardiacAssist, Inc.; Pittsburgh, Pa) is a percutaneously placed continuous-flow left ventricular assist device (pVAD) capable of complete hemodynamic support.²² In light of the high mortality rates in patients who present in cardiogenic shock after acute myocardial infarction, the frequency of IABP-support failure, and the limitations of surgical approaches in such patients, we sought to determine the efficacy of the pVAD in a patient who remained in SRCS after an acute myocardial infarction despite IABP and pressor support, and who required active CPR at the time of pVAD placement.

Case Report

A 49-year-old man presented at the emergency department of St. Luke's Episcopal Hospital in the winter of 2005 with acute onset of crushing substernal chest pain, which had been preceded by several days of unstable angina pectoris. His medical history included coronary artery disease with coronary atherectomy in 1992, hypertension, and medical noncompliance. His blood pressure was 87/60 mmHg; heart rate, 113 beats/min; respiratory rate, 32 breaths/min; and oxygen saturation, 82% on room air. Telemetric monitoring revealed sinus tachycardia with ST depression in leads II and III. The patient was placed on 100% oxygen via a non-rebreather facemask, and his oxygen saturation improved to 94%. He was started on intravenous (IV) heparin and IV eptifibatide, and was given a 600-mg oral dose of clopidogrel. During activation of the cardiac catheterization laboratory, physical examination showed the patient to be in significant distress, with jugular venous pressure to the angle of the mandible, rales throughout the lung fields bilaterally, a left ventricular S₃, and a grade 2/6 holosystolic murmur at the left lower sternal border with radiation to the apex. His distal upper and lower extremities were cold. The electrocardiographic findings were consistent with an acute anterior wall myocardial infarction, and ST depressions in the inferior leads were suggestive of inferior wall ischemia or reciprocal changes.

During the evaluation, the patient rapidly decompensated, and he was immediately intubated. Vasopressin and norepinephrine were started intravenously, and an IABP was placed emergently. After being stabilized and prepared for his transport to the cardiac catheterization laboratory, the patient went into hemodynamically unstable polymorphic ventricular tachycardia. Cardiopulmonary resuscitation was initiated, and the patient underwent successful cardioversion with 1 shock at 360 J and was transferred to the catheterization laboratory. Coronary angiography revealed a 90% occlusion composed of fresh thrombus in the proximal left anterior descending (LAD) artery, a calcified 80% to 85% stenosis of the mid left circumflex (LCx) artery, and proximal chronic total occlusion of the right coronary artery with collateral vessels from the LCx. Intracoronary abciximab was administered, and the LAD was engaged successfully with a guidewire. Percutaneous transluminal coronary angioplasty was performed, and 2 CYPHER® 3.0 × 15-mm stents (Cordis Corporation, a Johnson & Johnson company; Miami Lakes, Fla) were placed in the LAD. Final angiography demonstrated excellent results, with Thrombolysis in Myocardial Infarction (TIMI) 3 flow and a myocardial blush grade of 3. During the procedure, the patient had several episodes of polymorphic ventricular tachycardia and ventricular fibrillation, each successfully treated with cardioversion. The door-to-balloon time was 33 minutes.

Weaning of the patient from pressors was started in the catheterization laboratory, and he was transferred to the cardiac intensive care unit for observation. Approximately 48 hours after intervention, pending extubation and removal of the IABP, the patient began to have progressive onset of hypoxia, hypotension, and anuria. Ventilator oxygen support was increased to 100%, and IV vasopressin, IV norepinephrine, and IV dopamine were started. The patient remained hypotensive, with an invasive arterial blood pressure of 78/43 mmHg despite one-to-one IABP counterpulsation and triple-pressor sup-port. The physical examination results were unchanged relative to admission findings and were again consistent with cardiogenic shock. Bedside echocardiography with a portable hand-held unit revealed an ejection fraction of 0.20, anterolateral and lateral wall akinesis, and mild mitral regurgitation; there were no findings to suggest ventricular rupture, ventricular septal defect, or tamponade. The patient again rapidly decompensated and went into pulseless electrical activity arrest. Cardiac compressions were initiated, and resuscitation was started in accordance with advanced cardiac life support guidelines. The patient was emergently transferred to the cardiac catheterization laboratory for planned pVAD placement and coronary angiography, while receiving cardiac compressions and medical support. The pVAD was placed during active CPR and chest compressions. The patient's invasive arterial blood pressure improved from 60/20 mmHg to 103/61 mmHg at a pVAD flow rate of 4.0 L/min.^24–26 Repeat angiography showed patency of both LAD stents with TIMI 3 flow and a myocardial blush grade of 3. Because the LAD stents were pa-tent, we suspected that a temporary total occlusion of the mid LCx lesions had occurred and then spontaneously resolved. The mid LCx lesion was pre-dilated, and a CYPHER® 3.0 × 21-mm stent was placed in the vessel. Final angiography revealed no residual stenosis, TIMI 3 flow, and a myocardial blush grade of 3. The time from onset of cardiogenic shock to pVAD placement was 39 minutes. The time from onset of cardiogenic shock to LCx angioplasty was 49 minutes.

The patient was weaned from dopamine and norepinephrine and was then transferred from the catheterization laboratory to cardiovascular surgical recovery for continuation of pVAD support. Diuresis began after the administration of 120 mg of IV furosemide. The IABP support was continued in order to maintain pulsatile flow and facilitate weaning from the pVAD. The patient had remained unresponsive after resuscitation; therefore, hypothermia protocol was started upon his arrival to cardiovascular surgical recovery, 66 minutes after cardiac arrest (Fig. 1). After 24 hours of hypothermia, the patient was warmed and found to be neurologically intact. He continued to improve hemodynamically, and the pVAD was removed 48 hours after placement. The patient was extubated, and IABP support was discontinued. He was transferred to a telemetry floor 48 hours later. A transthoracic echocardiogram 5 days later showed an ejection fraction of 0.55, normal wall motion, and trace mitral regurgitation. The rest of the patient's hospital course was unremarkable, and he was discharged on hospital day 15. At the 6-month follow-up, the patient was well, his ejection fraction remained at 0.55 on repeat echocardiography, and he had required no further hospitalization.

Fig. 1 Timeline of hospital course.

CCU = cardiac intensive care unit; CV = cardiovascular; EF = ejection fraction; IABP = intra-aortic balloon pump; LAD = left anterior descending coronary artery; LCx = left circumflex coronary artery; LV = left ventricular; MI = myocardial infarction; MR = mitral regurgitation; PCI = percutaneous coronary intervention; pVAD = percutaneous ventricular assist device; TTE = transthoracic echocardiography

Discussion

As this case demonstrates, IABP and pressor support can be inadequate to reverse the terminal circulatory collapse seen in patients who present in SRCS after acute myocardial infarction. The pVAD, however, can rapidly resuscitate and stabilize patients in SRCS, enabling subsequent percutaneous or surgical intervention. Moreover, the pVAD—as opposed to surgically placed mechanical assist devices—can be placed in SRCS patients as they undergo active chest compressions during CPR.

Few studies have evaluated patients who are in SRCS after acute myocardial infarction, because of the difficulty in studying and randomizing this extremely high-risk group. Studies of emergent placement of permanent and temporary left ventricular assist devices in patients in SRCS have reported mortality rates ranging from 64% to 80%, depending on the extent of multiple-system organ failure.^27,28 Studies of CPS in patients with SRCS have also shown unacceptably high 30-day mortality rates (up to 67%) and prohibitive increases in severe vascular complications; these findings emphasize the limited usefulness of CPS in cases of SRCS.^29,30

In addition to emergent surgical placement of left ventricular assist devices and CPS, ECMO has also been used as a means to resuscitate SRCS patients.^31–33 Like the pVAD, ECMO can be implemented rapidly during cardiac arrest and active resuscitation. However, the mortality rates in SRCS patients receiving ECMO support approach 50%.27,30,33–36 Moreover, unlike pVAD support, ECMO has important limitations, including inadequate left ventricular decompression that necessitates catecholamine therapy to prevent pulmonary hypertension, and increased left ventricular afterload that may prevent myocardial recovery.16–18,29,33–36 Extracorporeal life support has also been associated with an increased rate of device-related mortality (up to 50%) and an increased risk of vascular complications with subsequent limb ischemia (up to 35%).27,30,33–36

In our patient, who was in SRCS after acute myocardial infarction, the pVAD reversed the terminal systemic hypoperfusion, resuscitating the patient during active CPR. In the past, such patients have undergone resuscitation and stabilization with ECMO or surgically implanted devices that were associated with significant morbidity and mortality rates. Now, the pVAD provides an additional means of hemodynamic support in these patients—one that rapidly reverses the terminal circulatory collapse, improves end-organ perfusion, and can be implanted during active CPR. Despite the fact that the pVAD can resuscitate and stabilize patients who are in SRCS and those who cannot be resuscitated with CPR, the use of this device should be reserved for patients with a potentially reversible cause of circulatory collapse or for patients in whom surgical left ventricular assist device placement or orthotopic heart transplantation is planned.

Limited options are available for the resuscitation and stabilization of patients in severe refractory cardiogenic shock who are undergoing active cardiopulmonary resuscitation after ischemic or nonischemic acute left ventricular failure. Therefore, further studies are needed to evaluate the efficacy of the pVAD in such situations.