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Department of Cardiac Transplantation and Heart Failure, Texas Heart Institute at St. Luke's Episcopal Hospital, Houston, Texas
Accepted for publication January 11, 2008.
* Address correspondence to Dr Gregoric, P.O. Box 20345, MC 2-114A, Houston, TX 77225-0345 (Email: epongratz{at}heart.thi.tmc.edu).
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Introduction |
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Traditionally, intraaortic balloon pump (IABP) counterpulsation has been used for mechanical circulatory support in cardiogenic shock patients, but IABP support can only modestly increase cardiac output and coronary blood flow, and it cannot provide total circulatory support in the setting of hemodynamic collapse [4].
Percutaneous left ventricular assist devices (pVADs) can provide superior circulatory support compared with the IABP in patients with cardiogenic shock [5]. They may be used for hemodynamic support of patients undergoing high-risk percutaneous coronary interventions [6]. They have also been used as bridges to recovery in the setting of acute fulminant myocarditis and as short-term bridges to transplantation in patients with acute decompensated heart failure [7].
We describe the case of a patient in cardiogenic shock after myocardial infarction. A pVAD was used to provide immediate active hemodynamic support, and, because the patient's condition necessitated surgical revascularization, pVAD support was continued during off-pump coronary artery bypass.
A 59-year-old man with a history of poorly controlled diabetes mellitus, hypertension, dyslipidemia, and tobacco use was admitted to another hospital for acute-onset chest pain. He had already experienced an ST-segment–elevation myocardial infarction of the anteroseptal region, complicated by acute pulmonary edema. In the cardiac catheterization laboratory, rapid decompensation necessitated intubation and IABP insertion. A coronary angiogram revealed critical 95% stenosis of the distal left main coronary artery and occlusion of the proximal right coronary artery. A left ventriculogram revealed inferior akinesis and severe anterior hypokinesis. Emergency coronary revascularization was considered, but his rapid hemodynamic deterioration resulted in the development of refractory cardiogenic shock.
A TandemHeart pVAD (Cardiac Assist, Pittsburgh, PA) was placed in the standard fashion as a bridge to surgical coronary revascularization. However, because of episodes of ventricular tachycardia/ventricular fibrillation storm, emergency surgical revascularization could not be pursued; instead, he underwent high-risk percutaneous coronary interventions for the distal left main stenosis.
The patient was taken to the critical care unit in critical but stable condition while on pVAD and vasopressor support. Active upper gastrointestinal bleeding complicated his recovery. Gastroscopy failed to identify the bleeding site, but it did reveal diffuse, active mucosal oozing. The bleeding stopped with the discontinuation of heparin. The patient was then transferred to our institution for consideration for heart transplantation. He was still intubated and was receiving pVAD support.
At our institution, an echocardiogram showed severely depressed left ventricular function with a left ventricular ejection fraction of 15%. We opted to perform elective surgical coronary revascularization, but because of his previous upper gastrointestinal bleeding, we were reluctant to use extracorporeal circulation. Because the patient was already receiving active circulatory support with the pVAD, off-pump cardiac revascularization was performed with the aid of the pVAD instead of cardiopulmonary bypass. The patient tolerated the procedure well. During surgery there were no episodes of hypotension, cardiac arrest, or malignant arrhythmias.
During the following week, consecutive echocardiograms showed steady improvement of the left ventricular ejection fraction (30% to 35%). The patient was weaned from vasopressor support. The pVAD was removed 11 days later.
Three weeks after the initial ST-segment–elevation myocardial infarction, the patient was discharged home.
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Because of aggressive medical management and the widespread use of percutaneous coronary interventions for acute myocardial infarction, the incidence of cardiogenic shock seems to be decreasing. However, when cardiogenic shock does occur, it has an unacceptably high (as much as 70%) in-hospital mortality [1]. Despite this high mortality, very few therapeutic advances have been made in the treatment of cardiogenic shock.
The first line of treatment is usually pharmacologic. If hemodynamic measurements fail to respond to medications, then an IABP is inserted. However, neither medical management nor IABP placement has proven effective long term; emergency revascularization has been the only approach shown to improve long-term survival in these patients [2, 3]. To date, there are no published strategies in the medical literature that outline how to improve short-term survival in cardiogenic shock patients.
Percutaneous VADs have been shown to provide support that is superior to that provided by the IABP [5, 7]. Compared with the IABP, pVADs can increase the cardiac power index by > 60% and improve other hemodynamic measurements [5]. In addition, serum lactate levels decrease in pVAD patients, indicating reversal of cardiogenic shock and re-establishment of end-organ perfusion [5]. The Impella Recover 2.5 (ABIOMED, Danvers, MA) is another type of pVAD that may provide superior support to that of the IABP; however, it may not increase the cardiac power index sufficiently to resuscitate patients in refractory cardiogenic shock. The larger Impella 5.0 requires surgical exposure for insertion. Such a time delay may be critical for patients who are in refractory cardiogenic shock or who are undergoing cardiopulmonary resuscitation. Once inserted in a stable patient, the Impella 5.0 may be used for support during off-pump coronary artery bypass [8].
In our patient, surgical revascularization was indicated, but when refractory cardiogenic shock developed, we opted to continue pVAD support in the hope of reversing the cardiogenic shock and stabilizing the patient's condition before surgery. Because of his upper gastrointestinal bleeding, we were reluctant to perform classic coronary revascularization with the aid of cardiopulmonary bypass, which requires full heparinization. Thus, we performed the surgery using the pVAD for circulatory support. The patient tolerated the procedure well, with no episodes of hypotension, cardiac arrest, or malignant rhythm disturbances.
Further prospective randomized trials are warranted to precisely establish the role of these devices for the management of patients in cardiogenic shock; however, we believe that eventually pVADs will replace the IABP as the gold standard of treatment for these patients.
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