Placement of the Avalon Elite bicaval dual lumen cannula for venovenous extracorporeal membrane oxygenation (VV-ECMO) via the internal jugular vein requires precise positioning of the cannula tip in the inferior vena cava with echocardiography or fluoroscopy guidance. Correct guidewire placement is clearly the key first step in assuring proper advancement of the cannula. We report a case of unexpected wire migration into the right ventricle at the time of final cannula advancement, resulting in right ventricular rupture and tamponade. Transesophageal echocardiography is an important monitoring modality for appropriate placement of the VV-ECMO guidewire and Avalon cannula, and in particular, for early identification of potential complications.

Calpain activation is linked to the cleavage of several cytoskeletal proteins and could be an important contributor to the loss of cardiomyocytes and contractile dysfunction during cardiac pressure overload (PO). Using a feline right ventricular (RV) PO model, we analyzed calpain activation during the early compensatory period of cardiac hypertrophy. Calpain enrichment and its increased activity with a reduced calpastatin level were observed in 24- to 48-h-PO myocardium, and these changes returned to basal level by 1 wk of PO. Histochemical studies in 24-h-PO myocardium revealed the presence of TdT-mediated dUTP nick-end label (TUNEL)-positive cardiomyocytes, which exhibited enrichment of calpain and gelsolin. Biochemical studies showed an increase in histone H2B phosphorylation and cytoskeletal binding and cleavage of gelsolin, which indicate programmed cardiomyocyte cell death. To test whether calpain inhibition could prevent these changes, we administered calpeptin (0.6 mg/kg iv) by bolus injections twice, 15 min before and 6 h after induction of 24-h PO. Calpeptin blocked the following PO-induced changes: calpain enrichment and activation, decreased calpastatin level, caspase-3 activation, enrichment and cleavage of gelsolin, TUNEL staining, and histone H2B phosphorylation. Although similar administration of a caspase inhibitor, N-benzoylcarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VD-fmk), blocked caspase-3 activation, it did not alleviate other aforementioned changes. These results indicate that biochemical markers of cardiomyocyte cell death, such as sarcomeric disarray, gelsolin cleavage, and TUNEL-positive nuclei, are mediated, at least in part, by calpain and that calpeptin may serve as a potential therapeutic agent to prevent cardiomyocyte loss and preserve myocardial structure and function during cardiac hypertrophy.

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Insertion of a left ventricular assist device (LVAD) improves survival and quality of life (QOL) in patients with class IV heart failure failing medical management. However, QOL and survival of patients bridged to LVAD with extracorporeal membrane oxygenation (ECMO) is unknown. Between July 2008 and June 2014, 213 patients underwent insertion of HeartMate II LVAD at two VAD centers without a bridge with a temporary VAD. Extracorporeal membrane oxygenation was used as a bridge before LVAD insertion in 22 Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) 1 patients (ECMO-VAD group). No bridge was used in 21 INTERMACS 1 patients and 170 INTERMACS 2-4 patients (primary LVAD group). Survival was compared between the ECMO-VAD group and INTERMACS 1 patients who underwent a primary LVAD insertion (INTERMACS 1 group). Quality of life was compared between the ECMO-VAD group and the primary LVAD group as a whole. The in-hospital mortality of the ECMO-VAD and INTERMACS1 groups was 23% and 14%, respectively (P = 0.38). The postimplant QOL scores of the ECMO-VAD group were not different compared with the primary LVAD group. Although the ECMO-VAD group consists of critically ill patients, the QOL and survival after discharge were not significantly different compared with patients who were not bridged with ECMO.