Feasibility of smaller arterial cannulas in venoarterial extracorporeal membrane oxygenation.

OBJECTIVES: To facilitate venoarterial extracorporeal membrane oxygenation (ECMO) insertion for cardiogenic shock, we recently adopted a strategy of using a 15F arterial cannula in all patients, rather than 1 designed to maximize flow. We aimed to compare the clinical outcomes of these 2 strategies. METHODS: In this retrospective study, 101 consecutive patients supported with ECMO via femoral cannulation between March 2007 and March 2013 were divided into 2 groups: Group L (17F-24F arterial cannula to accommodate full flow [ie, cardiac index of 2.5 L/m(2)/min]; n = 51) and Group S (15F arterial cannula; n = 50). The primary outcomes of interest were patients' overall status at 24 hours of support and cannulation-related adverse events. RESULTS: There were no significant differences in patient demographics, etiology of cardiogenic shock, or severity of illness before ECMO initiation between the 2 groups. Group L had significantly higher ECMO flow than Group S (flow index at 24 hours: 2.2 ± 0.7 vs 1.7 ± 0.3 L/m(2)/min; P < .001). However, there was no significant difference in use of vasoactive medication/hemodynamic parameters/laboratory parameters. Group L had higher incidence of cannulation-related adverse events (35% vs 22% in Group S [P = .14]), particularly in cannulation site bleeding (28% vs 10% [P = .03]). Thirty-day survival was 55% in Group L versus 52% in Group S (P = .77). Bleeding complication occurred in 53% in Group L versus 32% in Group S (P = .03). CONCLUSIONS: Compared with the use of larger cannulas, ECMO with a 15F arterial cannula appears to provide comparable clinical support with reduced bleeding complications.

Acute mechanical circulatory support for fulminant myocarditis complicated by cardiogenic shock.

In fulminant myocarditis complicated by cardiogenic shock, early mechanical circulatory support (MCS) may prevent cardiomyopathy and death. We sought to examine the outcomes of patients with fulminant myocarditis supported with MCS. A retrospective review of patients with acute cardiogenic shock treated with MCS from 2007 to 2013 was conducted, and patients with a diagnosis of fulminant myocarditis were included in this series. At our center, 260 patients received MCS for acute cardiogenic shock, and 11 were implanted for fulminant myocarditis. Eight received the Centrimag biventricular assist device (BIVAD), and three received veno-arterial extracorporeal membrane oxygenator (VA ECMO), though 1 VA ECMO-supported patient was transitioned to BIVAD due to refractory shock. The mean acute support time was 14.7 ± 4.4 days. Two patients required long-term left ventricular assist devices and were further supported for 55 and 112 days. Eight patients recovered with a mean ejection fraction of 54 ± 7 %, and one was successfully transplanted. Eight patients survived to discharge (73 %) with mean follow-up: 292.6 ± 306.8 days. All three deaths were due to neurologic complications. MCS should be considered in patients with fulminant myocarditis complicated by shock. With aggressive medical therapy, early utilization of MCS carries promising outcomes.

Impact of platelet transfusion on hematoma expansion in patients receiving antiplatelet agents before intracerebral hemorrhage.

OBJECTIVES: Patients receiving antiplatelet medications are reported to be at increased risk for hematoma enlargement and worse clinical outcomes following intracerebral hemorrhage (ICH). While platelet transfusions are frequently administered to counteract qualitative platelet defects in the setting of ICH, conclusive evidence in support of this therapeutic strategy is lacking. In fact, platelet transfusions may be associated with adverse effects, and represent a finite resource. We sought to determine the clinical efficacy of platelet transfusion and its impact on systemic complications following ICH in a cohort of patients receiving antiplatelet medications. METHODS: We retrospectively analysed the medical records of 66 patients admitted to our institution from June 2003 to July 2008 who suffered a primary ICH while receiving antiplatelet (acetylsalicylic acid and/or clopidogrel) therapy. The primary outcome was the rate of significant (>25% increase from admission) hematoma expansion in transfused (n=35) versus non-transfused (n=31) patients. Discharge modified-Rankin score (mRS) and the rates of systemic complications were also assessed. RESULTS: There were no statistically significant differences in rates of hematoma expansion between cohorts, nor were there differences in demographic variables, systemic complications or discharge mRS. Subgroup analysis revealed that there was a higher rate of hematoma expansion in the clopidogrel cohort (p=0.034) than in the cohort of patients receiving aspirin alone. DISCUSSION: This study suggests that platelet administration does not reduce the frequency of hematoma expansion in ICH patients receiving antiplatelet medications. This lack of efficacy may relate to transfusion timing, as a significant proportion of hematoma expansion occurs within 6 hours post-ictus. Additionally, the increased rates of hematoma expansion in the clopidogrel cohort may relate to its prolonged half-life. A larger, prospective study is warranted.

HIV-1 clones resistant to a small molecule CCR5 inhibitor use the inhibitor-bound form of CCR5 for entry.

Human immunodeficiency virus type 1 (HIV-1) infection can be inhibited by small molecules that target the CCR5 coreceptor. Here, we describe some properties of clonal viruses resistant to one such inhibitor, SCH-D, using both chimeric, infectious molecular clones and Env-pseudotypes. Studies using combinations of CCR5 ligands, including small molecule inhibitors, monoclonal antibodies (MAbs) and chemokine derivatives such as PSC-RANTES, show that the fully SCH-D-resistant viruses enter target cells by using the SCH-D-bound form of CCR5. However, the way resistance to SCH-D and other small molecule CCR5 inhibitors is manifested depends on the target cell and the nature of the assay (single- vs. multi-cycle). In multi-cycle assays using primary lymphocytes, SCH-D does not inhibit resistant molecular clones, and it can even enhance their infectivity modestly. In contrast, the same viruses (as Env-pseudotypes) are significantly inhibited by SCH-D in single-cycle entry assays using U87-CD4/CCR5 cells, resistance being manifested by incomplete inhibition at high SCH-D concentrations. When a single-cycle, Env-pseudotype entry assay was performed using either U87-CD4/CCR5 cells or PBMC under comparable conditions, entry was inhibited by up to 88% in the former cells but by only 28% in the PBMC. Hence, there are both cell- and assay-dependent influences on how resistance is manifested. We also take this opportunity to correct our previous report that SCH-D-resistant isolates are also substantially cross-resistant to PSC-RANTES [Marozsan, A.J., Kuhmann, S.E., Morgan, T., Herrera, C., Rivera-Troche, E., Xu, S., Baroudy, B.M., Strizki, J., Moore, J.P., 2005. Generation and properties of a human immunodeficiency virus type 1 isolate resistant to the small molecule CCR5 inhibitor, SCH-417690 (SCH-D). Virology 338 (1), 182-199]. A substantial element of this resistance was attributable to the unappreciated carry-over of SCH-D from the selection cultures into analytical assays.