Summary statistics from:

Genome-wide association study on coronary artery disease in type 1 diabetes suggests beta-defensin 127 as a risk locus
Antikainen AAV et al. Cardiovasc Res. 2020 Feb 20;cvaa045. doi: 10.1093/cvr/cvaa045. 


CHROM:POS		Chromosome:position (Ref Build GRCh37)
SNP			rsnumber, if available in our data
REF			Reference allele
ALT			Alternative allele
AF			Effect allele frequency
Rsq			Imputation quality (rsq)
SE			Standard error
BETA			Effect size
P			p-value

This study included 5342 Finnish individuals with T1D from the Finnish Diabetic Nephropathy (FinnDiane) study, 
an ongoing nationwide multicentre study with the aim to identify factors leading to diabetic complications. 
The participants were diagnosed with T1D with onset age ≤40 years and insulin treatment initiated within 2 years 
from diagnosis if known. The individuals underwent a thorough clinical examination by the attending physician, 
including blood samples and timed urine collections, at their FinnDiane baseline visit; a subset of patients 
also participated in similar follow-up visits. Further health-related data were obtained from the patients’ 
medical records.

We performed the largest genome-wide association study to date for coronary artery disease in type 1 diabetes, 
comprising 4869 individuals with type 1 diabetes (cases/controls: 941/3928). 

CAD was defined as a hard CAD event by the end of 2015 based on the Finnish Death Registry and Finnish hospital 
discharge registry using ICD codes I21, I22, and I23 for myocardial infarctions; or procedure codes for coronary 
bypass surgery or coronary balloon angioplasty (Supplementary material online, Table S1). Controls were individuals 
without hard CAD events. Only 5% of cases had CAD event before age of 35 years, and thus, controls with age <35 years 
(N = 322) or diabetes duration <15 years (N = 151) were excluded from the case–control CAD analysis, including 4869 
individuals (941 cases and 3928 controls). Among these, 2590 had normoalbuminuria, while 2113 had DKD, defined as 
microalbuminuria (N = 719), macroalbuminuria (N = 544), or end-stage renal disease (i.e. dialysis, kidney transplant, 
or estimated glomerular filtration rate <15 mL/min/1.73 m2; N = 850) at the latest available data point.

The genome-wide genotyping and imputation procedures have been described earlier. In short, 6152 unique Finnish 
individuals with diabetes and their relatives were genotyped at the University of Virginia with HumanCoreExome 
Bead arrays 12-1.0, 12-1.1, and 24-1.0 (Illumina, San Diego, CA, USA). Genotype calling with zCall, sample 
and variant quality control, genotype imputation with minimac3-software and the 1000 Genomes phase 3 reference panel 
were also performed at the University of Virginia. After quality control, 6019 individuals remained; 575 of these did 
not have T1D and/or data on CAD, resulting in 5342 T1D individuals with CAD and GWAS data available.

Association analysis was performed with a score test based on estimated allele dosages using Rvtest (version 20160404).
Calendar year of diabetes onset correlates strongly with the incidence of CAD most likely due to the improvements 
in diabetes management and glycaemic control. We have adjusted the analysis for the calendar year of diabetes onset 
(Supplementary material online, Figure S1), in addition to gender and genotyping batch; and for kinship matrix to 
account for relatedness and population substructure. The top discoveries were reanalysed with DKD as an additional
adjustment covariate. Results were filtered to those in Hardy–Weinberg equilibrium (P ≥ 5 × 10−8) with minor allele 
frequency (MAF) ≥0.01 and imputation quality r2 ≥ 0.6. Suggestive lead single-nucleotide polymorphisms (SNPs) were 
defined as independent SNPs [distance ≥100k base pairs (bp)] with P-value <10−6.