11 research outputs found

    Outcomes of surgical aortic valve replacement in octogenarians

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    Background: In the era of TAVI, there has been renewed interest in the outcomes of conventional AVR for high-risk patients. This study evaluates the short- and long-term outcomes of AVR in octogenarians. Methods: A retrospective review was performed of all 117 patients aged ≥80 years who underwent AVR, (isolated AVR (n= 60) or AVR + CABG (n= 57),) from August 2005 to February 2011 at Royal Prince Alfred Hospital and Strathfield Hospital. Univariate analysis was used to compare pre- and post-operative variables between younger and older subgroups (age 80-84, n= 82; age 85-89, n= 35 respectively). Long-term survival data was obtained from the National Death Index at the Australian Institute of Health and Welfare and survival curves were constructed using the Kaplan-Meier method. Results: The median age was 83 years (interquartile range, 81-85 years), 46.2% were females, the median EuroSCORE was 10.89% (interquartile range, 8.20-16.45%) and 16.2% of patients had a EuroSCORE ≥20%. The difference between subgroups for history of stroke was significant (p = .042). Post-operative complications included pleural effusion (12.8%), new renal failure (4.3%) and respiratory failure (4.3%). The rate of major adverse events was extremely low, with no cases of stroke. The 30-day mortality rate was 3.4%. There was a significant difference between subgroups for 30-day mortality (p = .007). 38.9% of patients were discharged home, 11.5% were transferred to another hospital and 38.9% spent a period of time in a rehabilitation institution post discharge. In terms of long-term survival, the six-month, one-year and three-year survival was 95.6%, 87.6% and 58.4% respectively. Conclusions: Surgical AVR yields excellent short- and long-term outcomes for potentially high-risk, elderly patients.9 page(s

    Endophenotypical drift in Huntington’s disease:a 5-year follow-up study

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    BACKGROUND: Huntington’s disease (HD) is clinically characterized by progressing motor, cognitive and psychiatric symptoms presenting as varying phenotypes within these three major symptom domains. The disease is caused by an expanded CAG repeat tract in the huntingtin gene and the pathomechanism leading to these endophenotypes is assumed to be neurodegenerative. In 2012/2013 we recruited 107 HD gene expansion carriers (HDGECs) and examined the frequency of the three cardinal symptoms and in 2017/2018 we followed up 74 HDGECs from the same cohort to describe the symptom trajectories and individual drift between the endophenotypes as well as potential predictors of progression and remission. RESULTS: We found higher age to reduce the probability of improving on psychiatric symptoms; increasing disease burden score ((CAG-35.5) * age) to increase the risk of developing cognitive impairment; increasing disease burden score and shorter education to increase the risk of motor onset while lower disease burden score and higher Mini Mental State Examination increased the probability of remaining asymptomatic. We found 23.5% (N = 8) to improve from their psychiatric symptoms. CONCLUSIONS: There is no clear pattern in the development of or drift between endophenotypes. In contrast to motor and cognitive symptoms we find that psychiatric symptoms may resolve and thereby not entirely be caused by neurodegeneration. The probability of improving from psychiatric symptoms is higher in younger age and advocates for a potential importance of early treatment. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13023-021-01967-2

    Decreased CSF oxytocin relates to measures of social cognitive impairment in Huntington's disease patients

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    Objective: Huntington's disease (HD) is an inherited neurodegenerative disease with motor, cognitive and psychiatric symptoms. Non-motor symptoms like depression and altered social cognition are proposed to be caused by dysfunction of the hypothalamus. We measured the hypothalamic neuropeptide oxytocin in plasma and cerebrospinal fluid (CSF) in a cohort of HD gene expansion carriers (HDGECs), compared the levels to healthy HD family controls and correlated oxytocin levels to disease progression and social cognition. Methods: We recruited 113 HDGECs and 33 controls. Psychiatric and cognitive symptoms were evaluated, and social cognition was assessed with the Emotion Hexagon test, Reading the Mind in the Eyes and The Awareness of Social Inference Test. The levels of oxytocin in CSF and blood were analyzed by radioimmunoassay. Results: We found the level of oxytocin in CSF to be significantly lower by 33.5% in HDGECs compared to controls (p = 0.016). When dividing the HDGECs into groups with or without cognitive impairment, we found the oxytocin level to be significantly lower by 30.3% in the HDGECs with cognitive symptoms (p = 0.046). We found a statistically significant correlation between the level of oxytocin and scores on social cognition (Reading the Mind in the Eyes p = 0.0019; Emotion Hexagon test: p = 0.0062; The Awareness of Social Inference Test: p = 0.002). Conclusions: This is the first study to measure oxytocin in the CSF of HDGECs. We find that HDGECs have a significantly lower level of oxytocin compared to controls, and that the level of oxytocin may represent an objective and comparable measure that could be used as a state biomarker for impairment of social cognition. We suggest treatment trials to evaluate a potential effect of oxytocin on social cognition in HD
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