Elevated blood cobalt secondary to metal-on-metal (MoM) hip arthroplasties has been shown to be a risk factor for developing cardiovascular complications including cardiomyopathy. Published case reports document cardiomyopathy in patients with blood cobalt levels as low as 13µg/l (13ppb, 221nmol/l). Clinical studies have found conflicting evidence of cobalt-induced cardiomyopathy in patients with MoM hips. Global longitudinal strain (GLS) is an echocardiography measurement known to be more sensitive than ejection fraction at diagnosing early cardiomyopathies. The extent of cardiovascular injury, as measured by GLS, in patients with elevated blood cobalt levels has not previously been examined. Sixteen patients with documented blood cobalt ion levels above 13µg/l were identified from a regional arthroplasty database. They were matched with eight patients awaiting hip arthroplasty with no history of cobalt implants. All patients underwent electrocardiogram and echocardiogram assessment for signs of cardiomyopathy including GLS. Patients with MoM hip arthroplasties had a mean blood cobalt level of 29µg/l (495nmol/l) compared to 0.01µg/l (0.2nmol/l) in the control group. There was no difference or correlation in ejection fraction (EF), left ventricular (LV) end systolic dimension, LV end diastolic dimension, fractional shortening, ventricular wall thickness or E/e’ ratio. However, GLS was significantly reduced in patients with MoM hip arthroplasties compared to those without (−15.2% v −18%, (MoM v control) p= 0.0125). Pearson correlation demonstrated that GLS is significantly correlated with blood cobalt level (r= 0.8742, p=0.0009). For the first time, this study has demonstrated reduced cardiac function in the presence of normal EF as assessed by GLS in patients with elevated cobalt above 13µg/l. As GLS is a more sensitive measure of systolic function than EF, routine echocardiogram assessment including GLS should be performed in all patients with MoM hip arthroplasties and elevated blood cobalt above 13µg/l. Further work is recommended to assess if these cardiac changes are present in patients with elevated blood cobalt levels below 13µg/l.
Elevated levels of circulating cobalt ions have been linked with a wide range of systemic complications including neurological, endocrine, and cardiovascular symptoms. Case reports of patients with elevated blood cobalt ions have described significant cardiovascular complications including cardiomyopathy. However, correlation between the actual level of circulating cobalt and extent of cardiovascular injury has not previously been performed. This review examines evidence from the literature for a link between elevated blood cobalt levels secondary to metal-on-metal (MoM) hip arthroplasties and cardiomyopathy. Correlation between low, moderate, and high blood cobalt with cardiovascular complications has been considered. Elevated blood cobalt at levels over 250 µg/l have been shown to be a risk factor for developing systemic complications and published case reports document cardiomyopathy, cardiac transplantation, and death in patients with severely elevated blood cobalt ions. However, it is not clear that there is a hard cut-off value and cardiac dysfunction may occur at lower levels. Clinical and laboratory research has found conflicting evidence of cobalt-induced cardiomyopathy in patients with MoM hips. Further work needs to be done to clarify the link between severely elevated blood cobalt ions and cardiomyopathy. Cite this article:
Healthcare associated infections (HAI) pose a major threat to patients admitted to hospitals, and infection rates following orthopaedic arthroplasty surgery are as high as 4%, while the infection rates are even higher after revision surgery. 405 nm High-Intensity Narrow Spectrum (HINS) light has been proven to reduce environmental contamination in hospital isolation rooms, and there is potential to develop this technology for application in orthopaedic surgery. Cultured rat osteoblasts were exposed to 405 nm light to investigate if bactericidal doses of light could be used safely in the presence of mammalian cells. Cell viability was measured by MTT reduction and microscopy techniques, function by alkaline phosphatase activity, and proliferation by the BrdU assay. Exposures of up to a dose of 36 J/cm2 had no significant effect on osteoblast cell viability, whilst exposure of a variety of clinically relevant bacteria, to 36 J/cm2 resulted in up to 100% kill. Exposure to a higher dose of 54 J/cm2 significantly affected the osteoblast cell viability, indicating dose dependency. Work also demonstrated that 405 nm light exposure induces reactive oxygen species (ROS) production in both mammalian and bacterial cells, as shown by fluorescence generated from 6-carboxy-2′,7′-dichlorodihydrofluorescein diacetate dye. The mammalian cells were significantly protected from dying at 54 J/cm2 by catalase, which detoxifies H2O2. Bacterial cells were significantly protected by sodium pyruvate (H2O2 scavenger) and by a combination of free radical scavengers (sodium pyruvate, dimethyl thiourea (·OH scavenger), catalase) at 162 and 324 J/cm2. Thus the cytotoxic mechanism of 405 nm light in mammalian cells and bacteria is likely oxidative stress involving predominantly H2O2 generation, with other ROS contributing to the damage. Additional work describing the potential for incorporation of this antimicrobial light within operating theatre lighting systems will also be discussed, and this, coupled with the cell viability and cytotoxicity results, suggests that 405 nm light could have great potential for continual patient safe decontamination during orthopaedic replacement surgeries and thereby reduce the incidence of infections.