Abdel, Matthew

Introduction: One million patients around the world have had total hip arthorplasty with 35% of them having metal-on-metal implants. Although there have been some case reports of cobalt cardiotoxicity from arthroprosthetic cobaltism resulting in dilated cardiomyopathy, incidence of cardiomyopathy and mortality in these patients is unknown. Objective: We therefore sought to determine the incidence of new onset cardiomyopathy (EF <40%) and associated mortality, in patients with metal hip arthroplasty. Methods: We retrospectively examined the records of the patients form our institutional total hip arthroplasty registry (Metal on Metal: MoM, Metal on Polyethylene: MoP, Ceramic on Ceramic: CoC and Ceramic on Polyethylne: CoP). Among 122 patients with baseline and follow up echocardiograms, cobalt and chromium levels were available in 12 patients, none of which developed incident cardiomyopathy. Results: The mean age of the population with metal group (MoM and MoP) was 53 years, predominantly males. During the follow up period of 10 years, the cumulative incidence (KM curve probabilities) of low EF <=40% in our study population was 14% in metal group as compared to 5% in non-metal group (CoC and CoP), (p value 0.51). At 15 years of follow up, among 122 patients, there were16 deaths in the metal group (81) and only 2 deaths in the non-metal group (41) (p value 0.15). Conclusions: In conclusion, although the incidence of cardiomyopathy as well as mortality is low in patients with metal hip arthroplasty and not significantly, further studies maybe needed to assess its effect on diastolic dysfunction.

Abstract The objective of this study was to assess the effects of hypercapnic acidosis on lung cell injury and repair by confocal microscopy in a model of ventilator-induced lung injury. Three groups of normocapnic, hypocapnic, and hypercapnic rat lungs were perfused ex vivo, either during or after injurious ventilation, with a solution containing the membrane-impermeant label propidium iodide. In lungs labeled during injurious ventilation, propidium iodide fluorescence identifies all cells with plasma membrane wounds, both permanent and transient, whereas in lungs labeled after injurious ventilation propidium iodide fluorescence identifies only cells with permanent plasma membrane wounds. Hypercapnia minimized the adverse effects of high-volume ventilation on vascular barrier function, whereas hypocapnia had the opposite effect. Despite CO2-dependent differences in lung mechanics and edema the number of injured subpleural cells per alveolus was similar in the three groups (0.48 ± 0.34 versus 0.51 ± 0.19 versus 0.43 ± 0.20 for hypocapnia, normocapnia, and hypercapnia, respectively). However, compared with normocapnia the probability of wound repair was significantly reduced in hypercapnic lungs (63 versus 38%; p &lt; 0.02). This finding was subsequently confirmed in alveolar epithelial cell scratch models. The potential relevance of these observations for lung inflammation and remodeling after mechanical injury is discussed.