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Rupture of tricuspid valve is unusual, occurring mainly in the setting of blunt trauma or endomyocardial biopsy. Spontaneous tricuspid valve chordal rupture is particularly rare. We report herein a case of a patient with severe pulmonary hypertension, on the lung transplantation waiting list, who presented with spontaneous chordal rupture, exacerbation of tricuspid insufficiency and worsening of clinical status. Diagnosis and treatment, along with possible mechanisms for this complication, are discussed. [ABSTRACT FROM AUTHOR]

Background Takotsubo cardiomyopathy, described as transient regional contractile abnormalities limited to the apical and mid-segments of the left ventricle ( LV), has also been reported to involve basal and/or mid LV segments (inverted Takotsubo); fewer reports, however, have addressed right ventricular ( RV) dysfunction. Aim To assess the distribution of regional abnormalities and RV involvement in Takotsubo cardiomyopathy and compare it to the literature. Methods and Results We evaluated 23 patients with both classical and inverted presentations (19 female, aged 64 ± 19 years), including 2 recurrences, totaling 25 episodes. Classical Takotsubo was observed in 15 patients, while 10 had the inverted form. LV ejection fraction ( EF) was lower for classical compared to inverted presentation (30 ± 7 vs. 45 ± 4%, P < 0.001) with higher troponin values (1.3 ± 1.4 vs. 0.5 ± 0.6, P = 0.034). RV abnormalities were found in 7 patients (28%), mainly with classical presentation (6 patients), presenting with mid and apical RV impairment. One patient with inverted Takotsubo had mid- RV involvement. Patients with RV involvement had lower left ventricular ejection fraction ( LVEF) (28 ± 10% vs. 40 ± 10%, P = 0.02), but not when adjusted for presentation type . Overall rate of complications was higher for classical compared to inverted presentation, and not influenced by RV involvement. Conclusion RV contractile abnormalities may follow the same LV regional distribution in Takotsubo cardiomyopathy; the type of presentation rather than the presence of RV dysfunction seems to be responsible for an increased risk of complications and severity of functional impairment. [ABSTRACT FROM AUTHOR]

Objective: Cognitive decline accompanies acute illness and surgery, especially in the elderly. Surgery engages the innate immune system that launches a systemic inflammatory response that, if unchecked, can cause multiple organ dysfunction. We sought to understand the mechanisms whereby the brain is targeted by the inflammatory response and how this can be resolved. Methods: C57BL/6J, Ccr2RFP/+Cx3cr1GFP/+, IkkF/F mice and LysM-Cre/IkkF/F mice underwent stabilized tibial fracture operation under analgesia and general anesthesia. Separate cohorts of mice were tested for systemic and hippocampal inflammation, integrity of the blood-brain barrier (BBB), and cognition. The putative resolving effects of the cholinergic pathway on these postoperative responses were also studied. Results: Peripheral surgery disrupts the BBB via release of tumor necrosis factor-alpha (TNFα), which facilitates the migration of macrophages into the hippocampus. Macrophage-specific deletion of Ikappa B kinase (IKK)β, a central coordinator of TNFα signaling through activation of nuclear factor (NF) κB, prevents BBB disruption and macrophage infiltration in the hippocampus following surgery. Activation of the α7 subtype of nicotinic acetylcholine receptors, an endogenous inflammation-resolving pathway, prevents TNFα-induced NF-κB activation, macrophage migration into the hippocampus, and cognitive decline following surgery. Interpretation: These data reveal the mechanisms for bidirectional communication between the brain and immune system following aseptic trauma. Pivotal molecular mechanisms can be targeted to prevent and/or resolve postoperative neuroinflammation and cognitive decline. ANN NEUROL 2011;70:986-995 [ABSTRACT FROM AUTHOR]

Objective: Although postoperative cognitive dysfunction (POCD) often complicates recovery from major surgery, the pathogenic mechanisms remain unknown. We explored whether systemic inflammation, in response to surgical trauma, triggers hippocampal inflammation and subsequent memory impairment, in a mouse model of orthopedic surgery.Methods: C57BL/6J, knock out (lacking interleukin [IL]-1 receptor, IL-1R(-/-)) and wild type mice underwent surgery of the tibia under general anesthesia. Separate cohorts of animals were tested for memory function with fear conditioning tests, or euthanized at different times to assess levels of systemic and hippocampal cytokines and microglial activation; the effects of interventions, designed to interrupt inflammation (specifically and nonspecifically), were also assessed.Results: Surgery caused hippocampal-dependent memory impairment that was associated with increased plasma cytokines, as well as reactive microgliosis and IL-1beta transcription and expression in the hippocampus. Nonspecific attenuation of innate immunity with minocycline prevented surgery-induced changes. Functional inhibition of IL-1beta, both in mice pretreated with IL-1 receptor antagonist and in IL-1R(-/-) mice, mitigated the neuroinflammatory effects of surgery and memory dysfunction.Interpretation: A peripheral surgery-induced innate immune response triggers an IL-1beta-mediated inflammatory process in the hippocampus that underlies memory impairment. This may represent a viable target to interrupt the pathogenesis of postoperative cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Different vascular abnormalities have been reported under the denomination of 'persistence of the fifth aortic arch.' Detailed studies on experimental embryology raised the discussion about the existence of the fifth aortic arch as an embryological structure, both in humans and mammals. In 1969 the Van Praaghs described the occurrence of double left aortic arch, denominating such anomaly as persistence of the fifth arch. We describe here a female patient showing the presence of an anomalous vessel in parallel with the aortic arch. The finding was occasional, during a preoperative evaluation for cholecystectomy. (Echocardiography 2011;28:E143-E145) [ABSTRACT FROM AUTHOR]

Objective: To investigate the potential role of IkappaB kinase 1 (IKK-1) and IKK-2 in the regulation of nuclear factor kappaB (NF-kappaB) activation and the expression of tumor necrosis factor alpha (TNFalpha), as well as interleukin-1beta (IL-1beta), IL-6, IL-8, vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs), in rheumatoid arthritis (RA)., Methods: Recombinant adenoviruses expressing beta-galactosidase, dominant-negative IKK-1 and IKK-2, or IkappaBalpha were used to infect ex vivo RA synovial membrane cultures and synovial fibroblasts obtained from patients with RA undergoing joint replacement surgery, or human dermal fibroblasts, human umbilical vein endothelial cells (HUVECs), and monocyte-derived macrophages from healthy volunteers. Then, their effect on the spontaneous or stimulus-induced release of inflammatory cytokines, VEGF, and MMPs from RA synovial membrane cells was examined., Results: IKK-2 was not required for lipopolysaccharide (LPS)-induced NF-kappaB activation or TNFalpha, IL-6, or IL-8 production in macrophages, but was essential for this process in response to CD40 ligand, TNFalpha, and IL-1. In synovial fibroblasts, dermal fibroblasts, and HUVECs, IKK-2 was also required for LPS-induced NF-kappaB activation and IL-6 or IL-8 production. In RA synovial membrane cells, IKK-2 inhibition had no effect on spontaneous TNFalpha production but significantly reduced IL-1beta, IL-6, IL-8, VEGF, and MMPs 1, 2, 3, and 13., Conclusion: Our study demonstrates that IKK-2 is not essential for TNFalpha production in RA. However, because IKK-2 regulates the expression of other inflammatory cytokines (IL-1beta, IL-6, and IL-8), VEGF, and MMPs 1, 2, 3, and 13, which are involved in the inflammatory, angiogenic, and destructive processes in the RA joint, it may still be a good therapeutic target.