A study of the mesenteric arteries was carried out in 203 unselected autopsies. Although mild degrees of stenosis were common, the incidence of a 'critical stenosis' was rare and no correlation between degrees of stenosis and previous gastrointestinal symptoms could be found. Radiological demonstration of stenosed or blocked visceral arteries remains therefore of doubtful clinical significance.

Epidemiological studies have reported associations between MPB and coronary heart disease (CHD) and related phenotypes such as blood pressure (BP), diabetes (DM) and blood lipid levels. The results vary with regard to the associated hair loss pattern and the assessed CHDsubphenotype and none of the studies has investigated for a shared genetic basis between the traits. Using data from the Heinz Nixdorf Recall study (1,675 men) and a large meta-analysis on MPB (22,518 men), we investigated for an association between MPB and CHD on an epidemiological and genetic level. On an epidemiological level we found weak associations between MPB and CHD (HR¼1.5[0.8-2.7]), DM (PRR¼1.5[1.0;2.1]), BMI (ß¼1.4kg/m2), elevated fasting triglyceride (ß¼8.0mg/dL) and lower HDL-C levels (ß¼-2.7mg/dL). On the genetic level, we found no significant association between a 63 SNP MPB risk score and CHD but the age-stratified analysis revealed a 4% per allele risk increase for CHD and a decrease in fasting triglyceride levels (ß¼-0.5). LD score regression analysis revealed no genome-wide genetic correlation of MPB with 110 (cardio)metabolic or lipid traits. We however identified 7 overlapping associations between MPB and BP; QT-interval length; atrial fibrillation; sudden cardiac arrest; and DM at indiviual loci. While the direction of effect differed between MPB and CHD for the majority of loci, we found identical risk alleles for MPB and BP (FGF5,4q21.21) and sudden cardiac arrest (ATF1,12q13.12). Both, FGF5 and ATF1 regulate cell growth, proliferation and differentiation in hair follicle and cardiac myocytes. Together, our data support the association between MPB and CHD and suggest that FGF5-and ATF1signaling are shared biological pathways.

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