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The extent of the involvement of platelets in venous thromboembolisms (VTE) is still not fully understood. Immature platelets are large, RNA-rich, prothrombotic platelets. They are involved in arterial thromboembolisms and are associated with adverse cardiovascular events. Their role in VTE has not been investigated before. The aim of this study was to assess different platelet parameters including immature platelet fraction (IPF), immature platelet count (IPC), absolute platelet count and platelet aggregation (PA) over time in patients with VTE at time of diagnosis, as well as at 3–10 days and at 90–110 days after diagnosis. 50 healthy volunteers similar in age and sex to patients served as controls at diagnosis. IPF was measured by the Sysmex XE-5000 analyzer, PA was assessed using the Multiplate analyzer. Diagnosis of VTE had no relevant effect on IPF and IPC whereas absolute platelet count and PA were significantly decreased compared to controls. In the course of VTE, IPF decreased significantly, whereas IPC, absolute platelet count and PA increased. In conclusion, VTE was associated with relevant changes of the absolute platelet count and PA at diagnosis, as well as changes in IPF and IPC over time reflecting a relevant and measurable platelet consumption in VTEs. [ABSTRACT FROM AUTHOR]

Purpose: Systematic differences with respect to myocardial perfusion quantification exist between DCE‐MRI and PET. Using the potential of integrated PET/MRI, this study was conceived to compare perfusion quantification on the basis of simultaneously acquired 13NH3‐ammonia PET and DCE‐MRI data in patients at rest and stress. Methods: Twenty‐nine patients were examined on a 3T PET/MRI scanner. DCE‐MRI was implemented in dual‐sequence design and additional T1 mapping for signal normalization. Four different deconvolution methods including a modified version of the Fermi technique were compared against 13NH3‐ammonia results. Results: Cohort‐average flow comparison yielded higher resting flows for DCE‐MRI than for PET and, therefore, significantly lower DCE‐MRI perfusion ratios under the common assumption of equal arterial and tissue hematocrit. Absolute flow values were strongly correlated in both slice‐average (R2 = 0.82) and regional (R2 = 0.7) evaluations. Different DCE‐MRI deconvolution methods yielded similar flow result with exception of an unconstrained Fermi method exhibiting outliers at high flows when compared with PET. Conclusion: Thresholds for Ischemia classification may not be directly tradable between PET and MRI flow values. Differences in perfusion ratios between PET and DCE‐MRI may be lifted by using stress/rest‐specific hematocrit conversion. Proper physiological constraints are advised in model‐constrained deconvolution. [ABSTRACT FROM AUTHOR]

We evaluated safety and long-term outcome of endovascular therapy for steno-occlusive iliac artery disease. All endovascular procedures of iliac artery lesions performed at our institution between 2001 and 2014 (n = 676) were retrospectively analyzed. The overall technical success rate was 99% and yielded 100% for stenoses (n = 596) and 95% for chronic total occlusions (n = 80). Lesion complexity defined by the Trans-Atlantic Inter-Society Consensus (TASC) II classification had no impact on success rates (TASC A + B vs C + D; 99.5% vs 98.6%, P = .359). During a median follow-up of 11 months, the overall rate of restenosis was 9.4%. After 1 and 3 years, the primary patency rates were 94% and 86% and the secondary patency rate was 100%, respectively. The TASC II classification had no impact on long-term patency rates (TASC A þ B vs C þ D; 86% vs 81%). In a multivariable analysis, stent diameter remained the only significant predictor for restenosis (hazard ratio: 0.58; 95% confidence interval: 0.41%-0.81%; P = .002). In this single-center retrospective study, endovascular therapy for steno-occlusive iliac artery disease was associated with high technical and clinical success rates as well as an excellent long-term patency rate irrespective of lesion complexity. [ABSTRACT FROM AUTHOR]

Objectives Studies addressing optimal postprocedural pharmacological management after endovascular stenting of iliofemoral post-thrombotic venous obstruction are lacking. We report our early clinical experience with a combination of rivaroxaban and clopidogrel in patients after iliofemoral post-thrombotic venous obstruction stenting. Methods Demographic, procedural, and follow-up data of nine patients (seven women; mean age of 32 ± 11 years) undergoing 10 procedures for iliofemoral post-thrombotic venous obstruction performed between August 2012 and January 2014 were retrospectively reviewed. After endovascular intervention, all patients were administered 20 mg rivaroxaban once daily (s.i.d.) and 75 mg clopidogrel s.i.d. or every second day depending on the individual drug responsiveness for at least six months. The adenosine diphosphate-induced platelet aggregation (platelet aggregation, in aggregation units × min) was assessed on a Multiplate analyzer. Patency was verified venographically at procedure end and was evaluated with duplex ultrasound in regular follow-ups. Results Iliofemoral venous flow was successfully re-established by percutaneous endovascular angioplasty and stent implantation in nine left-sided and one bilateral iliofemoral post-thrombotic venous obstruction. Under dual treatment strategy of rivaroxaban and clopidogrel with platelet aggregation control (median (range): 285 aggregation units × min (192; 402)), none of the patients experienced restenosis or stent thrombosis, respectively. After a median follow-up of 14 months (range: 6–26 months), the primary patency rate was 100% and no in-stent restenosis, stent occlusion or relevant minor or major bleeding occurred. Conclusion Combined factor Xa inhibition and tailored antiplatelet therapy after stenting of iliofemoral post-thrombotic venous obstruction were safe and performed favorably in terms of vessel patency. [ABSTRACT FROM AUTHOR]

Background--The immune system orchestrates the repair of infarcted myocardium. Imaging of the cellular inflammatory response by 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/magnetic resonance imaging in the heart has been demonstrated in preclinical and clinical studies. However, the clinical relevance of post-MI 18F-FDG uptake in the heart has not been elucidated. The objective of this study was to explore the value of 18F-FDG positron emission tomography/ magnetic resonance imaging in patients after acute myocardial infarction as a biosignal for left ventricular functional outcome. Methods and Results--We prospectively enrolled 49 patients with ST-segment-elevation myocardial infarction and performed 18F-FDG positron emission tomography/magnetic resonance imaging 5 days after percutaneous coronary intervention and follow-up cardiac magnetic resonance imaging after 6 to 9 months. In a subset of patients, 99mTcsestamibi single-photon emission computed tomography was performed with tracer injection before revascularization. Cellular innate immune response was analyzed at multiple time points. Segmental comparison of 18F-FDG-uptake and late gadolinium enhancement showed substantial overlap (κ=0.66), whereas quantitative analysis demonstrated that 18F-FDG extent exceeded late gadolinium enhancement extent (33.2±16.2% left ventricular myocardium versus 20.4±10.6% left ventricular myocardium, P<0.0001) and corresponded to the area at risk (r=0.87, P<0.0001). The peripheral blood count of CD14high/CD16+ monocytes correlated with the infarction size and 18F-FDG signal extent (r=0.53, P<0.002 and r=0.42, P<0.02, respectively). 18F-FDG uptake in the infarcted myocardium was highest in areas with transmural scar, and the standardized uptake valuemean was associated with left ventricular functional outcome independent of infarct size (Δ ejection fraction: P<0.04, Δ end-diastolic volume: P<0.02, Δ end-systolic volume: P<0.005). Conclusions--In this study, the intensity of 18F-FDG uptake in the myocardium after acute myocardial infarction correlated inversely with functional outcome at 6 months. Thus, 18F-FDG uptake in infarcted myocardium may represent a novel biosignal of myocardial injury. [ABSTRACT FROM AUTHOR]

Aims F-18 fluorodeoxyglucose (FDG) myocardial PET imaging is since more than two decades considered to delineate glucose utilization in dysfunctional but viable cardiomyocytes. Late gadolinium enhancement (LGE) MRI was introduced more than a decade ago and identifies increased extravascular space in areas of infarction and scar. Although the physiological foundation differs, both approaches are valuable in the prediction of functional outcome of the left ventricle, but synergistic effects are yet unknown. We aimed to compare the improvement of LV function after 6 months based on the regional FDG uptake and the transmurality of scar by LGE in patients early after acute myocardial infarction (AMI). Methods and results Twenty-eight patients with primary AMI underwent simultaneous PET/MRI for assessment of regional FDG uptake and degree of LGE transmurality 5-7 days after PCI. Follow-up by MRI was performed in 20 patients 6 months later. Myocardium was defined 'PET viable' based on the established threshold of ≥50% FDG uptake compared with remote myocardium or as 'MRI viable' when LGE transmurality of ≤50% was present. Regional wall motion was measured by MRI. Ninety-five dysfunctional segments were further analysed regarding regional wall motion recovery. There was a substantial intermethod agreement for segmental LGE transmurality and reduction of FDG uptake (κ = 0.65). 'PET viable' and 'MRI viable' segments showed a lower wall motion abnormality score (PET: initial: 1.4 ± 0.6 vs. 1.9 ± 0.8, P < 0.008; follow-up: 0.5 ± 0.7 vs. 1.5 ± 1.0, P < 0.0001; MRI: initial: 1.5 ± 0.6 vs. 2.0 ± 0.8, P < 0.002; follow-up: 0.7 ± 0.8 vs. 1.6 ± 1.0, P < 0.0001) and a better regional wall motion improvement (PET: -0.9 ± 0.7 vs. -0.4 ± 0.7, P < 0.0007; MRI: -0.8 ± 0.7 vs. -0.4 ± 0.7, P < 0.009) compared with 'PET non-viable' or 'MRI non-viable' segments, respectively. Eighteen per cent of the dysfunctional segments showed discrepant findings ('PET non-viable' but 'MRI viable'). At follow-up, the regional wall motion of these segments was inferior compared with 'PET viable/MRI viable' segments (1.1 ± 0.8 vs. 0.5 ± 0.7, P < 0.01), had an inferior functional recovery (-0.5 ± 0.6 vs. -0.9 ± 0.7, P < 0.03), but showed no difference compared with concordant 'PET non-viable/MRI non-viable' segments. Conclusion The simultaneous assessment of LGE and FDG uptake using a hybrid PET/MRI system is feasible. The established PET and MRI 'viability' parameter prior to revascularization therapy also predicts accurately the regional outcome of wall motion after AMI. In a small proportion of segments with discrepant FDG PET and LGE MRI findings, FDG uptake was a better predictor for functional recovery. [ABSTRACT FROM AUTHOR]

Objective. We report the case of a 46-year-old woman presenting with acute chest pain in the 20th week of a twin pregnancy after oocyte donation. Case report. The Patient's medical history comprised several cardiovascular risk factors, such as hypertension, obesity, hypercholesterolemia, smoking, and a positive family history. After diagnosis of myocardial infarction, coronary catheterization and stenting was performed. Ten weeks later, Cesarean was indicated because of severe superimposed preeclampsia with lung edema. Mother and babies recovered uneventfully. Conclusion. In respect to increasing rates of higher maternal age and obesity during pregnancy, more attention to maternal health is required, particularly in programs for assisted reproductive techniques. [ABSTRACT FROM AUTHOR]

Current knowledge about the molecular mechanisms of NMDA receptor (NMDAR)-independent long-term potentiation (LTP) in the hippocampus and its function for memory formation in the behaving animal is limited. NMDAR-independent LTP in the CA1 region is thought to require activity of postsynaptic L-type voltage-dependent Ca2+ channels (Cav1.x), but the underlying channel isoform remains unknown. We evaluated the function of the Cav1.2 L-type Ca2+ channel for spatial learning, synaptic plasticity, and triggering of learning-associated biochemical processes using a mouse line with an inactivation of the CACNA1C(Cav1.2) gene in the hippocampus and neocortex (Cav1.2HCKO). This model shows (1) a selective loss of protein synthesis-dependent NMDAR-independent Schaffer collateral/ CA1 late-phase LTP (L-LTP), (2) a severe impairment of hippocampus-dependent spatial memory, and (3) decreased activation of the mitogen-activated protein kinase (MAPK) pathway and reduced cAMP response element (CRE)-dependent transcription in CA1 pyramidal neurons. Our results provide strong evidence for a role of L-type Ca2+ channel-dependent, NMDAR-independent hippocampal L-LTP in the formation of spatial memory in the behaving animal and for a function of the MAPK/CREB (CRE-binding protein) signaling cascade in linking Cav1.2 channel-mediated Ca2+ influx to either process. [ABSTRACT FROM AUTHOR]