scholarly journals Atrial inflammation in different atrial fibrillation subtypes and its relation with clinical risk factors

2020 ◽  
Vol 109 (10) ◽  
pp. 1271-1281
Author(s):  
Linghe Wu ◽  
R. W. Emmens ◽  
J. van Wezenbeek ◽  
W. Stooker ◽  
C. P. Allaart ◽  
...  

Abstract Objective Inflammation of the atria is an important factor in the pathogenesis of atrial fibrillation (AF). Whether the extent of atrial inflammation relates with clinical risk factors of AF, however, is largely unknown. This we have studied comparing patients with paroxysmal and long-standing persistent/permanent AF. Methods Left atrial tissue was obtained from 50 AF patients (paroxysmal = 20, long-standing persistent/permanent = 30) that underwent a left atrial ablation procedure either or not in combination with coronary artery bypass grafting and/or valve surgery. Herein, the numbers of CD45+ and CD3+ inflammatory cells were quantified and correlated with the AF risk factors age, gender, diabetes, and blood CRP levels. Results The numbers of CD45+ and CD3+ cells were significantly higher in the adipose tissue of the atria compared with the myocardium in all AF patients but did not differ between AF subtypes. The numbers of CD45+ and CD3+ cells did not relate significantly to gender or diabetes in any of the AF subtypes. However, the inflammatory infiltrates as well as CK-MB and CRP blood levels increased significantly with increasing age in long-standing persistent/permanent AF and a moderate positive correlation was found between the extent of atrial inflammation and the CRP blood levels in both AF subtypes. Conclusion The extent of left atrial inflammation in AF patients was not related to the AF risk factors, diabetes and gender, but was associated with increasing age in patients with long-standing persistent/permanent AF. This may be indicative for a role of inflammation in the progression to long-standing persistent/permanent AF with increasing age. Graphic abstract

2009 ◽  
Vol 132 (2) ◽  
pp. 210-215 ◽  
Author(s):  
Kazumasa Ohara ◽  
Tadakazu Hirai ◽  
Nobuyuki Fukuda ◽  
Kenji Sakurai ◽  
Keiko Nakagawa ◽  
...  

2014 ◽  
Vol 177 (2) ◽  
pp. 666-668 ◽  
Author(s):  
Francesco Perticone ◽  
Angela Sciacqua ◽  
Maria Perticone ◽  
Eliezer J. Tassone ◽  
Giorgio Sesti ◽  
...  

2021 ◽  
Author(s):  
Kelly Chong ◽  
Igor Litvinovich ◽  
Shan Shan Chen ◽  
Yiliang Zhu ◽  
Christos Argyropoulos ◽  
...  

A heated debate in creatinine-based estimated glomerular filtration rate (eGFR) calculation is the inclusion of race alongside biological factors, such as age and gender. Similarly, the race variable was included in the calculation of the Kidney Donor Risk Index (KDRI) as deceased donor kidneys from black donors have historically been shown to be associated with lower allograft or patient survival. Given the current climate of uncertainty with the use of race in nephrology, we sought to answer the question of whether removing the donor race variable from the KDRI would alter its validity to assess allograft and patient survival. Our modeling and analysis showed that removing donor race from the original KDRI did not alter the overall model predictability of allograft failure or patient mortality. Clinical risk factors included in the KDRI have largely accounted for differential risk between black and other donors. Adding donor race into the KDRI only shifts how risk is attributed to these clinical risk factors, without yielding better prediction of outcomes than the model without race.


Author(s):  
Nicholas A. Marston ◽  
Parth N. Patel ◽  
Frederick K. Kamanu ◽  
Francesco Nordio ◽  
Giorgio M. Melloni ◽  
...  

Background: Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) that are associated with an increased risk of stroke. We sought to determine whether a genetic risk score (GRS) could identify subjects at higher risk for ischemic stroke after accounting for traditional clinical risk factors in five trials across the spectrum of cardiometabolic disease. Methods: Subjects who had consented for genetic testing and who were of European ancestry from the ENGAGE AF-TIMI 48, SOLID-TIMI 52, SAVOR-TIMI 53, PEGASUS-TIMI 54, and FOURIER trials were included in this analysis. A set of 32 SNPs associated with ischemic stroke was used to calculate a GRS in each patient and identify tertiles of genetic risk. A Cox model was used to calculate hazard ratios for ischemic stroke across genetic risk groups, adjusted for clinical risk factors. Results: In 51,288 subjects across the five trials, a total of 960 subjects had an ischemic stroke over a median follow-up period of 2.5 years. After adjusting for clinical risk factors, increasing genetic risk was strongly and independently associated with increased risk for ischemic stroke (p-trend=0.009). When compared to individuals in the lowest third of genetic risk, individuals in the middle and top tertiles of genetic risk had adjusted hazard ratios of 1.15 (95% CI 0.98-1.36) and 1.24 (95% CI 1.05-1.45) for ischemic stroke, respectively. Stratification into subgroups revealed the performance of the GRS appeared stronger in the primary prevention cohort with an adjusted HR for the top versus lowest tertile of 1.27 (95% CI 1.04-1.53), compared with an adjusted HR of 1.06 (95% CI 0.81-1.41) in subjects with prior stroke. In an exploratory analysis of patients with atrial fibrillation and CHA 2 DS 2 -VASc of 2, high genetic risk conferred a 4-fold higher risk of stroke and an absolute risk equivalent to those with CHA 2 DS 2 -VASc of 3. Conclusions: Across a broad spectrum of subjects with cardiometabolic disease, a 32-SNP GRS was a strong, independent predictor of ischemic stroke. In patients with atrial fibrillation but lower CHA 2 DS 2 -VASc scores, the GRS identified patients with risk comparable to those with higher CHA 2 DS 2 -VASc scores.


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