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Ann Thorac Surg 2002;73:745-750
© 2002 The Society of Thoracic Surgeons
a Department of Surgery, Columbia University College of Physicians and Surgeons, New York, New York, USA
b Department of Pathology, Columbia University College of Physicians and Surgeons, New York, New York, USA
Accepted for publication October 16, 2001.
* Address reprint requests to Dr Naka, Department of Surgery, Columbia University, College of Physicians and Surgeons, MHB7-435, 177 Fort Washington Ave, New York, NY 10032 USA
e-mail: yn33{at}columbia.edu
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Abstract |
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Methods. We retrospectively analyzed Thoratec Vented Electrical LVAD recipients between June 1996 and September 1999. RVD was defined as inotropic requirement 14 days or more or need for RVAD postoperatively, or both.
Results. Sixty-nine LVAD recipients were analyzed. Twenty-one patients (30.4%) had RVD, with 1 patient requiring RVAD insertion, and there were 48 non-RVD patients. There were no significant differences between both groups for age, sex, etiology of congestive heart failure, days of support, and preoperative hemodynamics. Preoperative right ventricle stroke work index (mm Hg · m-2 · L-1) had a trend toward being lower in the RVD group (4.1 ± 3.2 versus 6.1 ± 3.7, p = 0.06). A higher preoperative total bilirubin (mg/dL) was noticed in the RVD group (4.0 ± 5.2 versus 2.1 ± 1.7). The RVD group had a higher postoperative creatinine (2.2 ± 1.4 mg/dL versus 1.5 ± 0.8 mg/dL), incidence of continuous venovenous hemofiltration dialysis (73% versus 26%), transfusion of packed red blood cells (43.2 ± 28.6 units versus 24.7 ± 18.9 units), platelets (58.6 ± 46.1 units versus 30.2 ± 20.4 units), with longer intensive care unit length of stay (33.6 ± 34.7 days versus 9.1 ± 6.9) and higher mortality (42.8% versus 14.5%). When deaths were excluded, both intensive care unit and postoperative length of stay were significantly longer in the RVD group.
Conclusions. RVD in LVAD recipients remains poorly identified and is associated with a high transfusion rate and end organ failure that results in increased intensive care unit and hospital length of stay, and a high mortality rate. Preoperative identification of risk factors for RVD may select patients who would benefit from a biventricular assist device and prevent the subsequent end organ failure.
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Material and methods |
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TopAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Patients
We conducted a retrospective analysis of 95 Vented-Electrical Heartmate LVADs implanted between June 1996 and September 1999. All other assist devices were excluded to avoid a device variation bias. The cases were not consecutive. A total of 69 patients were included in the analysis. Data with regard to inotropic use and preoperative hemodynamics were deemed most important in order to define our patient groups and 26 patients whose records were missing or incomplete were excluded. RVD was defined as decrease in RV function or output (cardiac), or both, requiring inotropic support for 14 days or more or need for RVAD support, or both.
Hemodynamic measurements
A pulmonary artery catheter was used to measure capillary wedge pressure (PCWP), pulmonary artery pressure (PAP), right atrial pressure (RAP), cardiac output (CO), and cardiac index (CI). Right ventricular stroke work index (RVSWI) was calculated using the following formula: RVSWI = (mean PAP - mean RAP) x SVI, where stroke volume index (SVI) equals CI divided by heart rate.
Laboratory and transfusion data
Liver function tests, blood urea nitrogen, creatinine, and prothrombin times were evaluated both before and after LVAD implantation. Platelet units are in random donor platelet units. All transfusion data were obtained from the blood bank computer system (Hemocare) records.
Statistical analyses
Data were expressed as mean ± standard deviation. Statistical analyses were performed by the 
2 test or unpaired Student’s t test using the SAS system software (SAS Institute, Inc, Cary, NC). Exact probability values are reported to enable the reader to determine statistical and clinical significance.
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Results |
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Twenty-one (30.4%) of the 69 recipients developed RVD with 1 patient needing RVAD support. This group required inotropic support for a median of 20 days. Forty-eight patients in the non-RVD group had inotropic requirements less than 14 days for a median of 6 days. Preoperative characteristics and laboratory data for each group are summarized in Table 1. There were no significant differences between groups with respect to age, sex, etiology, and duration of support. A total of 37 patients (53.6%) had emergent LVAD implantation after coronary artery bypass graft surgery or percutaneous transluminal coronary angiography or postcardiotomy cardiogenic shock. There was no significant difference in the number of emergent implants between both groups (52.3% versus 54.1%). Preoperatively the RVD group had a significantly higher total bilirubin with a trend toward higher aspartate aminotransferase (AST) and serum creatinine. Preoperative hemodynamics are displayed in Table 2. There was no significant difference in preoperative RAP (14.3 ± 5.4 mm Hg versus 13.7 ± 6.5 mm Hg). The RVD group had a trend toward lower preoperative RVSWI (mm Hg · m-2 · -l, 4.1 ± 3.2 versus 6.1 ± 3.7, p = 0.06) with a larger fraction having an RVSWI less than 4 (52.6% versus 31.2%) indicating severe depression of RV ejection fraction (or depression of RV contractile function; Fig 1). There was no significant difference in CO, CI, left ventricular ejection fraction, RAP, PAP, PCWP, and pulmonary vascular resistance between the two groups. No recipients in the RVD group had mean PAP more than 30 mm Hg as opposed to 13.5% in the non-RVD group, indicating a trend toward lower PAP in the RVD group.
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ICU length of stay was significantly longer in the RVD group (33.6 ± 34.7 days versus 9.1 ± 6.9 days, p = 0.006) as shown in Figure 2. Mean duration of mechanical support was 71.6 ± 56.3 days in the RVD group versus 66.4 ± 41.3 days in the non-RVD group with no significant difference. There was no significant difference in hospital length of stay (46.1 ± 34.1 days versus 33.0 ± 27.9 days, p = 0.15) between the groups. If death is excluded from the analysis, ICU LOS (9.5 ± 7.2 days versus 30.7 ± 29.4 days, p = 0.0003; Fig 2) and hospital LOS (39.3 ± 26.3 days versus 58.4 ± 26.9 days, p = 0.03) were both significantly longer in the RVD group. Recipients without RVD had a significantly lower in-hospital mortality (14.5% versus 42.8%, p = 0.01) and a better survival to transplant (85.4% versus 57.1%, p = 0.01) as shown in Figure 3. In the RVD group, of the 12 patients who survived to transplant, 10 (83.3%) were weaned off inotropic support before transplant, all of whom survived. There was no significant difference between these patients and the non-RVD patients save for a significantly prolonged duration of inotropic support (21.5 ± 12.1 days versus 6.7 ± 3.5 days, p < 0.001). Eleven patients could not be weaned off support and 9 (81.8%) died. In a subgroup analysis, 81.8% (9 of 11) received inhaled NO and had to be returned to the operating room for bleeding, had more packed red blood cells (58.6 ± 20.4 units versus 26.3 ± 27.4 units, p = 0.006) and fresh frozen plasma (39.3 ± 16.3 units versus 17.4 ± 12.1 units, p = 0.003) transfused postoperatively as compared with RVD patients weaned off inotropic agents. Of patients who were successfully bridged to transplant there was no significant difference (75% [8 of 12] in the RVD group versus 62.5% [25 of 40] in the non-RVD group) in the number of recipients discharged home before transplant.
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Comment |
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The ability of the RV to supply the left heart and thus the LVAD with adequate volume is critically related to intrinsic RV contractility and pulmonary vascular resistance (PVR). Factors that influence RVD that worsens after left ventricular support are unclear but include myocardial stunning, ischemia, arrhythmias, and pulmonary vascular resistance. Postischemic RV dysfunction has been observed in 20% to 50% of patients on LVAD support [11]. PVR is usually elevated in longstanding congestive heart failure (CHF) and is further increased in the early postoperative period by the effects of cardiopulmonary bypass and blood product administration [13]. Any of these factors individually or in combination may lead to an impairment of RV contractility or increased RV afterload and subsequent RV dysfunction.
The LVAD unloads the left ventricle and results in a decrease in the reversible component of pulmonary hypertension thereby improving RV stroke volume and LVAD flow [14]. On the other hand increased venous return, which is frequently observed upon insertion, may unmask preexisting RVD caused by ischemia (perioperative myocardial stunning), cardiomyopathy, pulmonary hypertension, or arrhythmias [15, 16]. Intrinsic contractility, pulmonary vascular resistance, ventricular arrhythmias, and volume status are important factors affecting RV function and hence LVAD output. Aggressive volume loading may effectively improve LVAD flows utilizing the RV as a passive chamber similar to the Fontan physiology [9]. Several indices have been studied individually and in combination to predict the occurrence of RVD after LVAD implantation. While elevated RAP have been associated with RVD in previous studies [17], others have found no predictive value of elevated RAP in RVD [12]. A strong association between low preoperative RVSWI and low mean PAP in LVAD recipients requiring a right ventricular assist device (RVAD) has been demonstrated [12]. The same authors also concluded that the need for RVAD support was low (11%) but did not address the occurrence of RVD with subsequent end-organ failure.
Historically it has been shown that elevated pulmonary artery pressures predispose heart transplant recipients to right ventricular failure [18]. However Levin and associates [19] and others have found that elevated right atrial pressures with lower mean PAP were associated with an increased need for right ventricular support [20]. Although previous studies have shown elevated RAP to be a predictor of poor outcome and RVD in LVAD recipients, extensive perioperative use of pulmonary vasodilators (inhaled NO and type III phosphodiesterase inhibitors) and the aggressive use of inotropic agents may have resulted in the lower mean RAP in both groups. It is also possible that patients with more subtle degrees of RVD were included in our analysis and may have resulted in a lower mean RAP. More than half the recipients included in the analysis received inhaled NO perioperatively. There was no significant difference in the number of patients who received NO in both groups and more than two thirds (68.4%) who received it did not develop perioperative RVD. This indicates that the use of NO may have reduced the incidence of pulmonary hypertension and hence RVD. Laboratory data indicative of end-organ failure, ie, deranged liver function tests [12] and increased perioperative transfusion requirement [20] secondary to coagulopathy and liver dysfunction, have been shown to be predictive of the need for right ventricular support.
The ability to predict RVD before LVAD implantation based on available laboratory and hemodynamic indicators would be an invaluable aid with which the development or progression of RVD with subsequent multiorgan failure could be aborted early. Previous attempts to develop a reliable risk factor index have been unsuccessful and unreliable owing to the inadequate number of patients with RVD or failure included in the analyses and the underestimation of the incidence and impact of RVD [12, 17]. The findings in our study emphasize that no single laboratory or hemodynamic variable on its own can reliably predict RVD. We found no association of elevated RAP with RVD. However, low RVSWI as a function of poor RV contractility was strongly associated with RVD. A low mean PAP was more common in the RVD group indicating the inability of a weakened ventricle to generate high pulmonary arterial pressure. Postoperatively the RVD group needed significantly more blood product transfusions with lower LVAD flows.
Although critics may question which arrived first, RVD or bleeding and organ failure, our results indicate that RVD appeared first followed by coagulopathy and bleeding. Typically surgical bleeding manifests within the first 48 hours. There was no significant difference in transfusion requirements in the first 48 hours. However, there was a significantly increased number of transfusions in the RVD group after 48 hours in the later postoperative period. Further, there were significantly more patients who were returned to the operating room for bleeding (mostly nonsurgical) and of these there was no significant difference between the numbers of patients with surgically correctable bleeding. With respect to end-organ dysfunction there was no significant difference in mean preoperative creatinine. There was however a significant increase in mean postoperative creatinine with an increased incidence of CVVH and dialysis in the RVD group. Also mean total bilirubin, which was higher preoperatively in the RVD group, increased further through the perioperative period. That indicates that renal function and liver function did deteriorate over the perioperative period with RV dysfunction being a major contributory factor. The RVD group had a significantly higher morbidity, mortality and a lower survival to transplant. They also had a significantly longer ICU LOS, which translates into increased costs as per our previously published estimates [9]. The postoperative LOS was not significantly higher owing to the higher mortality in the group. On elimination of the deaths, however, both ICU and postoperative LOS were significantly higher in the RVD group. Within the RVD group, those who were weaned off inotropic support had an acceptable survival. This may represent a group who had less severe degrees of RVD and experienced right ventricular recovery. There was no significant difference between these patients and the non-RVD patients save for a significantly prolonged duration of inotropic support. On the other hand the vast majority of the patients who could not be weaned off inotropic agents received inhaled NO, had to be returned to the operating room for bleeding, had more blood products transfused postoperatively, and had an extremely high mortality rate when compared with RVD patients weaned off inotropic agents. These patients represent a group who had severe RVD and may have certainly benefited from RVAD support earlier on or possibly right from the start.
A fair number of patients in this study had emergent implants. Having established an implantable LVAD-based bridge to transplant network along with stringent preoperative risk factor assessment we have shown a significant improvement in survival after failed cardiotomy and the Heartmate is now being used in percutaneous transluminal coronary angioplasty failure/acute myocardial infarction and after cardiogenic shock with a remote chance of cardiac recovery in case the patients can be considered transplant candidates [21]. Our analysis further emphasizes that the incidence of RVD is underestimated with overt RVF being merely the tip of the iceberg. Although this is a large group of LVAD recipients with RVD we analyzed, the study is retrospective. A larger study with adequate power to establish a reliable composite predictive risk factor index to improve outcome in these patients is warranted.
A high index of suspicion with early identification of risk factors for RVD may identify a group of patients who may benefit from biventricular support early on. Although aggressive use of inotropic agents, pulmonary vasodilators, and phosphodiesterase inhibitors may offer support until RV recovery occurs and thus reduce the need for RVAD support, there is a subset of patients with low RVSWI and borderline hepatic and renal function who will not respond and are at a prohibitive risk for severe RVD and failure. In essence failure of these interventions to improve LVAD flow together with the previously described clinical scenario should prompt early RVAD insertion. Until then, RVD should not be underestimated and must be treated aggressively with all available measures with a view to diminish the morbidity, mortality, and cost associated with LVAD implantation.
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