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Venous thromboembolism (VTE) is a common complication after intracranial hemorrhage (ICH); the incidence has been reported to vary between 18% to 50% for deep vein thrombosis and between 0.5% to 5% for pulmonary embolism (PE). According to current clinical practice guidelines, patients with acute VTE should receive anticoagulant treatment for at least 3 months in the absence of contraindications. Anticoagulant treatment reduces mortality, prevents early recurrences and improves long-term outcome in patients with acute VTE. However, recent ICH is an absolute contraindication for anticoagulant treatment due to the potential increased risk of hematoma expansion or recurrent ICH. Hematoma expansion occurs in approximately a third of patients within 24 h following the diagnosis of a spontaneous ICH. The risk for recurrent ICH depends on patients' features as well as on the feature of index ICH. Limited evidence is available on the risks of therapeutic anticoagulation started shortly after ICH. Expert consensus around the introduction of therapeutic anticoagulation suggests delaying therapeutic anticoagulation for at least 2 weeks after spontaneous ICH, until the risk re-bleeding becomes acceptable. Vena cava filters should be inserted to reduce the risk for (non) fatal PE until therapeutic anticoagulation can be started; antithrombotic prophylaxis should be started as soon as possible to avoid recurrent VTE after vena cava filter insertion. For patients presenting PE with hemodynamic compromise, percutaneous embolectomy should be considered. Most patients will be able to receive anticoagulant treatment within 4 weeks following spontaneous ICH; direct oral anticoagulants are probably the treatment of choice for those ICH patients tolerating anticoagulant treatment.

Purpose We previously reported experimental advantages of new titanium mesh wrapped inflow cannula for left ventricular assist device (LVAD) to avoid wedge thrombus formation. There was no thrombus formation in any of the explanted LVAD system and around the outside of the inflow cannula after 2 months from LVAD implantation in calves. We had applied this newly developed inflow cannula into the clinical arena with EVAHEART LVAD since 2013. We had clinically evaluated experience of this inflow cannula and showed the clear induction of autologous neointima avoiding wedge thrombus formation for over 5 years from LVAD implantation. Methods Retrospective data were analyzed from 19 patients who underwent EVAHEART LVAD implantation using newly inflow cannula as a bridge to transplant since September 2013 at Tokyo Women's Medical University. Results All patients achieved hospital discharge on LVAD support. 9 patients underwent heart transplantation and 3 of 9 patients were supported over 5 years (5.12-5.45 years) from LVAD implantation. Thromboembolic complications in these patients included 1 cerebral bleeding event, 1 cerebral infarction and 2 transit ischemic attack. In macroscopically findings were no thrombus formation around the inflow cannula. The titanium mesh was completely enveloped with white neointima tissue that appeared to have grown from the ventricular endocardium (Figure). Conclusion The titanium mesh inflow cannula induces autologous neointima avoiding wedge thrombus formation in clinical experience for over 5 years after LVAD implantation.

Background Two implantable continuous-flow left ventricular assist devices (LVADs), DuraHeart (Terumo Heart, Ann Arbor, MI, USA) and EVAHEART (Sun Medical, Nagano, Japan), were approved in Japan in April 2011. We analyzed the midterm outcome of patients implanted with these implantable LVADs at the University of Tokyo Hospital. Methods and results A total of 31 patients who underwent implantation of LVADs (10 DuraHeart, 21 EVAHEART) as a bridge to transplantation at our institution between April 2011 and August 2013 were retrospectively reviewed. All patients were followed up through December 2013. Seven patients underwent conversions from NIPRO paracorporeal LVAD (Nipro, Osaka, Japan) to an implantable LVAD. The mean observation period was 483 ± 239 days (41.0 patient years). Eight patients were transplanted and one patient showed functional recovery with subsequent LVAD explantation. Four patients died due to cerebrovascular accident, empyema, or device malfunction due to pump thrombosis after cerebral bleeding. Kaplan–Meier analysis revealed 6-, 12-, and 24-month survival rates of 93%, 86%, and 86%, respectively. The rates of freedom from cerebrovascular accidents and device-related infections at 1 year after LVAD implantation were 65% and 36%, respectively. Twenty-nine patients were discharged home after LVAD implantation. During the period of this study, there were 59 readmissions (53 urgent, 6 elective) among 22 patients (76%). The overall and urgent readmission rates were 1.66 and 1.49 per patient year, respectively. The common reason for readmission was device-related infection (31%), followed by cerebrovascular accidents (17%). The total out-of-hospital time after the primary discharge was 90%. Conclusions Our midterm survival rate after LVAD implantation is satisfactory. However, patients undergoing LVAD support were often readmitted with adverse events.

Objectives: Adrenomedullin (AM) is a newly discovered vasodilator peptide that participates in the regulation of cerebral blood flow. The aim of this study was to investigate whether circulating AM was increased in infants with prenatal asphyxia who developed intraventricular hemorrhage (IVH). Design and methods: A case-control study was performed on 40 full-term asphyxiated newborns: 20 developed IVH (group A) and 20 did not (group B). Forty term healthy newborns represented the control group. Biochemical laboratory parameters, neurological patterns, cerebral ultrasound scanning, and Doppler velocimetry were assessed at 12 and 72 h from birth. Plasma AM concentration was measured at 12 h from birth by means of a specific RIA. Results: AM levels were significantly higher in group A (20.2 ± 5.2 fmol/ml) than in group B (8.4 ± 2.1 fmol/ml) or controls (9.3 ± 2.6 fmol/ml). In asphyxiated newborns, AM concentration was correlated with middle cerebral artery PI value only in group B. Conclusions: Increased concentration of AM at 12 h from birth in asphyxiated newborns who later developed IVH suggests that this peptide may participate in the loss of cerebral vascular autoregulation in response to hypoxia and could be useful to discriminate, among newborns at risk, those with an adverse neurological outcome.

s S153 and cerebral bleeding rates, a newly developed titanium mesh covered inflow cannula introduced since September 2013. Initial clinical results suggested suppression of both stroke and cerebral bleeding rates within at least acute phase after LVAD implantation, when those complications with previous type (smooth surface) inflow cannulas were observed predominantly. Conclusion: The bridge to heart transplant mechanical circulatory support with EVAHEART LVAD achieved long-term survival without pump replacement as well as with relatively low rate of pump pocket infection, right heart failure, GI bleeding, and hemolysis. The suppression of stroke and cerebral bleeding rates with the newly developed inflow cannulas is expected.

s S153 and cerebral bleeding rates, a newly developed titanium mesh covered inflow cannula introduced since September 2013. Initial clinical results suggested suppression of both stroke and cerebral bleeding rates within at least acute phase after LVAD implantation, when those complications with previous type (smooth surface) inflow cannulas were observed predominantly. Conclusion: The bridge to heart transplant mechanical circulatory support with EVAHEART LVAD achieved long-term survival without pump replacement as well as with relatively low rate of pump pocket infection, right heart failure, GI bleeding, and hemolysis. The suppression of stroke and cerebral bleeding rates with the newly developed inflow cannulas is expected.

The authors present the case of an 83 year-old man with cerebral amyloid angiopathy who had three successive lobar intracerebral hematomas within 4 weeks. There were neither a predisposing familial factor nor cardiovascular risk factors nor any other cause favouring cerebral bleeding. The autopsy revealed amyloid deposits in small cortical and meningeal arteries. No other lesions of the Alzheimer's disease was found.

In patients with severe head injury or multiple trauma a multitude of inflammatory mediators are released. As in cerebral bleeding, elevations of body temperature can be observed even in the absence of bacterial infections. In order to evaluate the diagnostic significance of plasma elastase levels for the exclusion or early detection of infections in the course of the above diseases, quantitative estimations of granulocytic elastase in complex with alpha 1-proteinase inhibitor were carried out in 11 patients using an enzyme-linked immunoassay over a period from 3 to 47 days. Additionally, leukocyte counts were made and body temperatures measured. In all but two cases, elastase levels were elevated at the beginning of the disease and usually decreased over the period of study. In contrast to leukocyte counts and body temperature, the values correlated with the severity of the clinical symptoms. It is concluded that plasma elastase determinations are useful in the differential diagnosis of infection from other causes of elevated body temperatures.