Design: We administered a questionnaire at 2 weeks after discharge to 174 patients undergoing TKA in 10 Australian hospitals. Participants rated pain expectation and severity, use of analgesics and non-pharmacological methods, side-effects,
walking and exercise times, perceptions of analgesics, adequacy of pain management information provided and satisfaction with pain relief.
Results: Of 171 (98%) participants who completed the questionnaire, 88 (52%) reported that the worst pain period occurred during the learn more first 2 weeks at home. During the first 2 weeks at home, the average pain was ‘severe/extreme’ for 40 (23%) participants and 92 (54%) experienced severe pain at least some of the time. Many participants sought further medical help for their pain. Adequate information on analgesics and non-pharmacological
methods for pain relief were reported by only 73% and 47%, respectively. Approximately 20% had negative perceptions about analgesic use. Higher pain severity was associated with lower satisfaction and less time spent walking daily.
Conclusions: Effective pain relief after hospital discharge following TKA is a challenge. Many participants reported significant pain, sought further medical help for pain relief and had inadequate information at discharge to effectively self-manage their postoperative knee pain. (C) 2013 Osteoarthritis Research Society International. Published RG-7388 molecular weight by Elsevier Ltd. All rights reserved.”
“Introduction. Hypertrophic cardiomyopathy (HCM), an inherited
GSK3235025 manufacturer primary cardiac disorder mostly caused by defective sarcomeric proteins, serves as a model to investigate left ventricular hypertrophy (LVH). HCM manifests extreme variability in the degree and distribution of LVH, even in patients with the same causal mutation. Genes coding for renin-angiotensin-aldosterone system components have been studied as hypertrophy modifiers in HCM, with emphasis on the angiotensin (Ang) II type 1 receptor (AT(1)R). However, Ang II binding to Ang II type 2 receptors (AT(2)R) also has hypertrophy-modulating effects.
Methods. We investigated the effect of the functional + 1675 G/A polymorphism (rs1403543) and additional single nucleotide polymorphisms in the 3′ untranslated region of the AT(2)R gene (AGTR2) on a heritable composite hypertrophy score in an HCM family cohort in which HCM founder mutations segregate.
Results. We find significant association between rs1403543 and hypertrophy, with each A allele decreasing the average wall thickness by similar to 0.5 mm, independent of the effects of the primary HCM causal mutation, blood pressure and other hypertrophy covariates (p = 0.020).