ABCC9, ACTA2, ACTC1, ACTN2, ACVRL1, AKAP9, ANK2, BAG3, CACNA1C, CALM1, CALM2, CASQ2, COL3A1, CSRP3, DES, DMD, DSC2, DSG2, DSP, ENG, FBN1, FHL1, FLNC, GJA5, GLA, HCN4, JUP, KCNA5, KCND3, KCNE1, KCNE2, KCNH2, KCNJ2, KCNQ1, LAMP2, LDB3, LMNA, MYBPC3, MYH11, MYH6, MYH7, MYL2, MYL3, MYPN, NKX2-5, PKP2, PLN, PRKAG2, RBM20, RYR2, SCN10A, SCN1B, SCN5A, SLC2A10, SMAD3, SMAD4, TAZ, TGFB2, TGFB3, TGFBR1, TGFBR2, TMEM43, TNNC1, TNNI3, TNNT2, TPM1, TTN, TTR, VCL
Cardio-vascular diseases are the number one cause of death globally. The chance of developing heart disease increases with age and in addition certain genetic factors also increase the risk. Disease-causing changes in the genome can functionally disrupt the structure of the heart muscle (e.g. in cardiac myopathies). They can also impair the function of ion channels in the heart, which are important for transmitting electrical signals to the heart muscle. This can cause cardiac arrhythmia. Furthermore, pathogenic genetic changes increase the risk of cardiac death by enlarging vessels, splitting vascular walls, or tearing vessels. Identifying these pathogenic changes will ensure that appropriate measures can be taken. The ‘cardio-vascular disease’ module of our Disease Prevention Panel analyzes 69 genes that are involved in cardio-vascular function. Pathogenic changes in these genes tell our doctors whether closer monitoring, lifestyle changes, or therapy are necessary.