5 research outputs found
Increasing the Elective Endovascular to Open Repair Ratio of Popliteal Artery Aneurysm
Background: Open repair (OR) for popliteal artery aneurysm (PAA) has recently been challenged by endovascular repair (ER) as the primary choice of treatment. The aim of the present study was to evaluate time trends in treatment modality and compare outcomes between OR and ER among electively operated patients after start of screening in 2010 for abdominal aortic aneurysm (AAA), a disease highly associated with PAA. Methods: Between January 1, 2009, and April 30, 2017, 102 procedures and 36 acute and 66 elective repairs for PAA were identified. Results: Over time, a trend (P =.089) for an increasing elective to acute repair ratio of PAA and an increase in elective ER to OR ratio (P =.003) was found. Among electively repaired PAAs, the ER group was older (P =.047) and had a higher ankle–brachial index (ABI; P =.044). The ER group had fewer wound infections (P =.003), fewer major bleeding complications (P =.046), and shorter in-hospital stay (P <.001). After 1 year of follow-up, the ER group had a higher rate of major amputations (P =.037). Amputation-free survival at the end of follow-up did not differ between groups (P =.68). Among the 17 patients with PAA eligible for AAA screening, 4 (24%) were diagnosed with PAA through the screening program of AAA. Conclusion: The epidemiology of elective repair of PAA has changed toward increased ER, although ER showed a higher rate of major amputations at 1 year. Confounding was considerable and a randomized trial is needed for evaluation of the best therapeutic option
Evaluation of revised classification criteria for giant cell arteritis and its clinical phenotypes
Background: GCA is a systemic vasculitis of the elderly, viewed by many as a disease with multiple and overlapping clinical phenotypes. Retrospective studies have shown differences in clinical presentation between these phenotypes. To reflect the heterogeneity of GCA and novel diagnostic methods, new classification criteria have been proposed. Methods: This is a retrospective study of newly diagnosed patients with GCA at the outpatient rheumatology clinics at Skåne University Hospital (Malmö and Lund) between 2012 and 2018. All patients were evaluated using two sets of classification criteria, the ACR classification criteria from 1990 and a proposed revision of these criteria requiring objective findings (positive biopsy or imaging) for classification. Patients were further classified as one of four widely used clinical phenotypes. Results: A total of 183 patients with a new diagnosis of GCA were identified. The diagnosis was confirmed by one or two experienced rheumatologists in 116 of these patients during a review of medical records. The ACR criteria were more sensitive than the revised criteria (93.1% vs 72.4%), but the revised criteria had higher specificity (94.0% vs 28.4%). The revised criteria tended to have higher sensitivity in the phenotype with constitutional symptoms compared with cranial GCA (P = 0.08). Conclusion: The specificity of the ACR classification criteria for GCA can be improved by using revised criteria requiring objective findings of vasculitis. In addition, the wider symptoms covered by the revised criteria may improve classification of patients with a phenotype characterized by constitutional symptoms
Polygenic Risk Score for Coronary Heart Disease Modifies the Elevated Risk by Cigarette Smoking for Disease Incidence
BACKGROUND: Coronary heart disease (CHD) is a multifactorial disease with both genetic and environmental components. Smoking is the most important modifiable risk factor for CHD. Our aim was to test whether the increased CHD incidence by smoking is modified by genetic predisposition to CHD. METHODS AND RESULTS: Our study included 24 443 individuals from the MDCS (Malmö Diet and Cancer Study). A weighted polygenic risk score (PRS) was created by summing the number of risk alleles for 50 single-nucleotide polymorphisms associated with CHD. Individuals were classified as current, former, or never smokers. Interactions were primarily tested between smoking status and PRS and secondarily with individual single-nucleotide polymorphisms. Then, the predictive use of PRS for CHD incidence was tested among different smoking categories. During a median follow-up time of 19.4 years, 3217 incident CHD cases were recorded. The association between smoking and CHD was modified by the PRS (Pinteraction=0.005). The magnitude of increased incidence of CHD by smoking was highest among individuals in the lowest tertile of PRS (odds ratio, 1.42; 95% confidence interval, 1.29-1.56 per smoking risk category) compared with the highest tertile (odds ratio, 1.20; 95% confidence interval, 1.11-1.30 per smoking risk category). This interaction was stronger among men (Pinteraction=0.001) compared with women (Pinteraction=0.44). The PRS provided a significantly better net reclassification and discrimination on top of traditional risk factors among never smokers compared with current smokers (P<0.001). CONCLUSIONS: Genetic predisposition to CHD modifies the associated increased CHD risk by smoking. The PRS has a better predictive use among never smokers compared with smokers