Myocardial infarction (MI) had a nominally significant genetic correlation with 31 other traits, of which six had significant evidence (FDR <1%) for a fully or partially genetically causal effect on MI (Table 1); there was no evidence for a genetically causal effect of MI on any other trait. Consistent with previous studies, these traits included LDL[3,13], triglycerides[4] and BMI[30], but not HDL[3]. The effect of BMI was also consistent with prior MR studies [30-33], although these studies did not attempt to account for pleiotropic effects (also see ref. [34], which detected no effect). There was also evidence for a genetically causal effect of high cholesterol, which was unsurprising (due to the high genetic correlation with LDL) but noteworthy because of its strong genetic correlation with MI, compared with LDL and triglycerides. The result for HDL and MI did not pass our significance threshold (FDR <1%), but was nominally significant (p=0.02, Supplementary Table 12); we residualized HDL summary statistics on summary statistics for three established causal risk factors (LDL, BMI and triglycerides), determining that residualized HDL showed no evidence of genetic causality (p=0.8). On the other hand, most of the other traits remained significant (Supplementary Table 13).
