A Novel Link between G6PD Deficiency and Hemolysis Events in Patients Supported with Continuous-Flow Left Ventricular Assist Devices
Continuous-flow left ventricular assist device (CF-LVAD) support is a well-established treatment for end-stage heart failure but little data are available on hemolysis complications. G6PD deficiency is associated with the development of hemolysis during states of high oxidative stress. No data exist on the role of G6PD deficiency in hemolysis during CF-LVAD support. The purpose of this study was to describe hemolysis in patients who have been implanted with a CF-LVAD. In particular, we sought to investigate the relationship of G6PD deficiency with clinical hemolysis events.
Methods and Materials
From October 2005 through October 2011, 85 patients with end-stage heart failure underwent implantation of a CF-LVAD at the University of North Carolina at Chapel Hill. Cases of hemolysis, G6PD deficiency and associated morbidity and mortality were validated by review of medical records. Univariable and multivariable analysis was used to determine independent predictors of hemolysis hospitalizations.
Hemolysis occurred in 13 patients (15%) with average follow-up of 9.9±8.2 months. G6PD levels were available in 34 patients (40%) and were low in 7 (20%), all of whom were blacks (p=0.007). Peak LDH levels at any time during post-LVAD follow-up period were higher in patients with low versus normal G6PD levels (8160±9526 vs. 2534±2919, p=0.01). There was a trend towards more hemolysis events in patients with low versus normal G6PD levels (57% vs. 19% p=0.06). Low G6PD level was the only variable significantly different between patients with and without post-LVAD hemolysis hospitalizations (57% vs. 11% p=0.001; OR 10.7 [95% CI: 1.6-73], p=0.02).
Hemolysis in CF-LVAD supported patients was not uncommon and resulted in important morbidity. To our knowledge, this study is the first to describe an association between low G6PD levels and hemolysis hospitalizations in CF-LVAD supported patients. More studies are needed to elucidate the mechanisms involved.
Available from: Mandeep Mehra
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ABSTRACT: Durable left ventricular assist devices (LVADs) have not only enhanced longevity but also conferred sustained improvements in quality of life, symptom control, and functional capacity in patients with medically refractory advanced heart failure. Problems with device-related infection, bleeding, neurologic events, right-sided heart failure, and device malfunction have dominated the clinical care of patients living on mechanical support. Even as adoption of durable LVADs accelerated globally, we began to encounter a growing dilemma of pump malfunction caused by thrombosis. In early 2011, clinicians began to notice a spike in the incidence of pump thrombosis with the HeartMate II (Thoratec Corp, Pleasanton, CA) LVAD. By 2012, the problem of thrombosis in LVADs began to consume most of the scientific direction as centers and collaborative groups began to dissect this nascent phenomenon. In this perspective, we describe the magnitude and implications of pump thrombosis, discuss secular and management trends in this unique population, attempt to dissect the problem at its root, offer guidance on surveillance and therapeutic principles, and outline issues that deserve our immediate and collaborative attention.
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ABSTRACT: Continuous-flow left ventricular assist devices (LVADs) subject elements of the blood to significant stress, resulting in clinically significant and subclinical hemolysis. We sought to prospectively determine if baseline red cell osmotic fragility of an advanced heart failure patient - influences the hemolytic response to LVAD support. Osmotic fragility assesses the degree of red blood cell hemolysis under varying degrees of osmotic stress. Assays were prospectively obtained on 50 consecutive patients prior to placement of continuous flow LVADs: HeartMate II (n=34), Jarvik 2000 (n=5), HeartWare (n=6). The mean age was 60.2 years, 87% were male, and 47% were nonischemic. The overall median post-LVAD LDH was 583 (427-965) and there was no difference among devices. Mean hemolysis was 15.68 ± 12.96% at 0.45%NaCL (the inflection point of the osmotic fragility hemolysis curve). A scatter plot did not reveal any relationship between pre-op osmotic fragility and post-op LDH. Linear regression confirmed no predictive relationship (p=0.71). In conclusion, preoperative variations in osmotic fragility do not appear to account for differences in hemolysis following VAD placement. Mechanical forces generated by existing LVADs result in similar levels of biochemical hemolysis, as assessed by LDH, despite baseline differences in a patient's osmotic red cell fragility.
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