Table 2.

Trans-QTL results.

Variant				Gene		Trans-QTL
GWAS SNP	QTL SNP	Chr	Position	Symbol	Chr	QTL	β	T value	P-value	FDR
rs9675122	rs11658168	chr17	7,406,134	TNNT2a,d	chr1	Transcript	−0.517	−4.27	6.43 × 10−5	0.081
rs9481842	rs9481842	chr6	118,974,798	NKX2-5b	chr5	Transcript	−0.593	−4.27	6.54 × 10−5	0.081
rs34292822	rs11588763	chr1	154,813,584	CYB5R3	chr22	Protein	−0.786	−4.89	6.86 × 10−6	0.113
rs34292822	rs11588763	chr1	154,813,584	NDUFB3c	chr2	Protein	−0.916	−4.44	3.56 × 10−5	0.133
rs9675122	rs11658168	chr17	7,406,134	HIBADH	chr7	Protein	−0.512	−4.43	3.66 × 10−5	0.133
rs34292822	rs11588763	chr1	154,813,584	NDUFA9d	chr12	Protein	−0.752	−4.42	3.85 × 10−5	0.133
rs34292822	rs11588763	chr1	154,813,584	DLAT	chr11	Protein	−0.716	−4.40	4.05 × 10−5	0.133

Significant trans-eQTLs and pQTLs for a FDR < 0.2 (Benjamini-Hochberg procedure to account for multiple comparisons per omic). Two-sided t-tests were performed on 23 transcripts with 74 samples and 152 proteins with 73 samples of human heart right atrial appendage tissue for 108 variants associated with atrial fibrillation from the GWAS catalog (or their proxy, if the GWAS SNP was not measured). Calculations were carried out using the SNP rs11658168 as a proxy for the GWAS SNP rs9675122 as well as rs11588763 instead of the GWAS SNP rs34292822.

eQTL expression quantitative trait loci, pQTL expression quantitative trait loci, QTL quantitative trait loci, FDR false discovery rate, GWAS genome-wide association study, SNP single-nucleotide polymorphism, Chr Chromosome.

^aMutation known to affect cardiovascular phenotypes.

^bMutation known to affect arrhythmias.

^cDifferential expression functional impairment for cardiovascular phenotypes.

^dDifferential expression or functional impairment for arrhythmias; For details to disease links in literature see Supplementary Table 12. Source data are provided as a Source Data file.