The development of atherosclerosis is a complex process that involves several inflammatory mechanisms. The evolution of a fatty streak to a mature occlusive atheromatous plaque occurs over several decades. However, during acute plaque rupture, to a varying degree, these same inflammatory systems are involved.Evidence exists that suggests a relationship between the activated inflammatory pathways; in the setting of lower respiratory tract or urinary tract infections and cardiac events such as unstable angina or myocardial infarctions.Peripheral vascular disease patients demonstrate atheromatous disease throughout their arterial tree, with coronary artery involvement in a significant proportion of individuals. The stress that a surgical intervention creates may be the catalyst for an acute coronary syndrome through the activation of these inflammatory pathways. Individual responses to the surgical insult are unpredictable and the extent to which the inflammatory mechanisms are stimulated is variable. The measurements of inflammatory biomarkers, such as C-reactive protein, have been associated with adverse short- and long-term mortality in patients who experience an acute coronary syndrome.This review article looks at the previous assessment tools that have been developed over time to try and predict the peri-operative risk of patients undergoing non-cardiac surgery, based on traditional patient parameters. We also explore the use of bio-markers in addition to these characteristics and how future work is being developed to look at the potential use of these to improve individual risk profiles.
We aimed to investigate if major vascular surgery induces LDL oxidation, and whether circulating antibodies against malondialdehyde-modified LDL (MDA-LDL) alter dynamically in this setting. We also questioned relationships between these biomarkers and post-operative cardiovascular events. Major surgery can induce an oxidative stress response. However, the role of the humoral immune system in clearance of oxidized LDL following such an insult is unknown. Plasma samples were obtained from a prospective cohort of 131 patients undergoing major non-cardiac vascular surgery, with samples obtained preoperatively and at 24- and 72 h postoperatively. Enzyme-linked immunoassays were developed to assess MDA-LDL-related antibodies and complexes. Adverse events were myocardial infarction (primary outcome), and a composite of unstable angina, stroke and all-cause mortality (secondary outcome). MDA-LDL significantly increased at 24 h post-operatively (p < 0.0001). Conversely, levels of IgG and IgM anti-MDA-LDL, as well as IgG/IgM-MDA-LDL complexes and total IgG/IgM, were significantly lower at 24 h (each p < 0.0001). A smaller decrease in IgG anti-MDA-LDL related to combined clinical adverse events in a post hoc analysis, withstanding adjustment for age, sex, and total IgG (OR 0.13, 95% CI [0.03–0.5], p < 0.001; p value for trend <0.001). Major vascular surgery resulted in an increase in plasma MDA-LDL, in parallel with a decrease in antibody/complex levels, likely due to antibody binding and subsequent removal from the circulation. Our study provides novel insight into the role of the immune system during the oxidative stress of major surgery, and suggests a homeostatic clearance role for IgG antibodies, with greater reduction relating to downstream adverse events.
Background An atypical presentation of a new diagnosis of undifferentiated CTD highlights the use of cardiac MRI in CTD. In comparison to echocardiogram it can better establish cardiac involvement in CTD which is associated with significant morbidity and mortality. Methods A 49 year old previously well man was referred to rheumatology clinic with symptoms of inflammatory sounding arthralgia, new onset Raynauds, fatigue and 1 stone weight loss. In the interim he presented acutely with dyspnoea and chest pain and was found to be in atrial fibrillation. A chest X-ray was suggestive of pneumonitis and bibasal patchy consolidation. Despite antibiotics the AF persisted, and anticoagulation and rate control was initiated. He represented two weeks later with severe arthralgia, joint swelling and malaise. Bloods showed: CRP 283, ESR 87, lymphopenia but normal renal and liver function. He was pyrexial and tachycardic, but a septic screen was negative and he had limited response to antibiotic therapy. A CT Chest showed extensive lymphadenopathy, bilateral pleural effusions and an enhancing pericardial effusion suggestive of pericarditis, confirmed by echocardiogram. A provisional diagnosis of systemic inflammation secondary to an undifferentiated CTD was made and after initiation of oral prednisolone and colchicine he had significant improvement in symptoms. A repeat CT chest one month later has shown resolution of the mediastinal lymphadenopathy and interstitial changes. Cardiac MRI has confirmed likely infiltrative cardiomyopathy consistent with a connective tissue disease. His ANA is 1:2560 speckled/ nucleolar pattern, ENA negative, anti CCP 55 and Ra Latex 65, DsDNA and complements normal. ACE and ANCA negative and the formal diagnosis of an undifferentiated CTD has been made. Methotrexate was introduced causing resolution of symptoms by 6 months of treatment. Follow up imaging is planned. Results Cardiac MRI (CMR) in CTD is a relatively new imaging modality. Increasingly we are recognising that patients can have abnormalities seen on CMR despite a normal echo. CMR has identified occult cardiac disease in patients with treatment naive CTD which is potentially reversible with immunosuppresion. We also know that despite serological normalisation and systemic improvement of symptoms cardiac involvement can be subclinical. CMR as a non-radiating and non-invasive imaging modality is ideally placed to assess response to treatment in those with CTD related cardiac involvement. Indications for CMR in CTD has been further delineated in guidance from the International consensus group of Cardiac MRI in CTD. Conclusion In our patient identification of his new atrial arrhythmia prompted the instigation of cardiac investigations which culminated in CMR. Close working with cardiology colleagues and subsequent access to their tertiary MDT has meant we have better characterised our patient’s cardiac involvement translating to rapid immunosuppression and planned treatment monitoring with further CMR. Disclosures R. Benson None. L. Waters None. P. Magapu None. H. Sadik None.
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