Acromioclavicular joint cyst formation

Acromioclavicular joint (ACJ) cysts are an uncommon and unusual sequela associated with shoulder pathophysiology. The majority of literature on ACJ cysts consists of individual case reports with no definitive literature review currently available. In addition to a comprehensive literature review, four clinical cases are presented in this report. First described by Craig (1984), a total of 41 cases have been previously reported in the literature. Of these cases, five occurred with the rotator cuff musculature intact. The remaining 36 cases of ACJ cysts occurred in patients with a complete tear/avulsion of the rotator cuff. Previous attempts at compiling a complete record of all reported cases have combined several distinct conditions into a single category. This article presents two distinct etiologies for the pathogenesis of ACJ cyst formation. In the presence of an intact rotator cuff, a Type 1 cyst can form superficially and be limited to the ACJ. Following a massive or traumatic tear of the rotator cuff, mechanical instability of the humeral head can cause a deterioration of the inferior acromioclavicular capsule (cuff tear arthropathy) and an overproduction of synovial fluid. Overtime, a “geyser” of fluid can form between the glenohumeral and the ACJ, forming a Type 2 cyst. This differentiation and categorization is essential for appropriate classification and treatment. Clin. Anat. 23:145–152, 2010. © 2010 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65052/1/20918_ftp.pd

Midregional proadrenomedullin and its change predicts recurrent major coronary events and heart failure in stable coronary heart disease patients: The LIPID study

Background: Biomarkers may contribute to risk stratification in coronary heart disease (CHD). We examined whether plasma midregional proadrenomedullin (MR-proADM) concentration at baseline and its change over one year predicts long-term outcomes in stable CHD patients. Methods: The LIPID study randomised patients 3–36 months after an acute coronary syndrome with total cholesterol 4.0–7.0 mmol/L (155–271 mg/dL), to placebo or pravastatin 40 mg. Follow-up was 6.0 years. MR-proADM plasma concentrations at baseline and one year later were determined in 7863 and 6658 patients, respectively. These were categorised into quartiles to perform Cox regression analysis, adjusting for baseline parameters. Results: Baseline MR-proADM concentrations predicted major CHD events (non-fatal myocardial infarction or CHD death; hazard ratio (HR) 1.52, 1.26–1.84 for Q4–Q1), CHD death (HR 2.21, 1.67–2.92), heart failure (HR 2.30, 1.78–2.97) and all-cause mortality (HR 1.82, 1.49–2.23). Associations were still significant after adjustment for baseline B-type natriuretic peptide (BNP) concentration. Increase in MR-proADM after one yearwas associated with increased risk of subsequent CHD events (HR 1.34, 1.08–1.66), non-fatalmyocardial infarction (HR 1.50, 1.12–2.03), heart failure (HR 1.78, 1.37–2.30) and all-causemortality (HR 1.31, 1.04–1.64). Associations with heart failure and all-causemortality remained significant after adjusting for baseline and change in BNP concentration. Change in MR-proADM moderately improved risk reclassification for major CHD events (net reclassification improvement (NRI) 3.48%) but strongly improved risk reclassification for heart failure (NRI 5.60%). Conclusions: Baseline and change in MR-proADM concentrations over one year are associated with risk of major clinical events, even after adjustment for BNP concentrations.National Heart Foundation of Australi