Maternally transmitted susceptibility to non–insulin-dependent diabetes mellitus and left ventricular hypertrophy

OBJECTIVES: We studied the association of diabetes transmission with left ventricular hypertrophy (LVH) in patients with non-insulin-dependent diabetes mellitus (NIDDM). BACKGROUND: It is suggested that NIDDM has a strong genetic basis and that maternally transmitted NIDDM is associated with mitochondrial deoxyribonucleic acid (DNA) mutations. However, genetic factors for LVH in NIDDM are unknown. METHODS: We investigated the family history of diabetes and the prevalence of LVH using electrocardiography in 834 patients with NIDDM, of whom 199 also underwent echocardiography. RESULTS: Of the 834 patients, 121 had diabetic mothers, 122 had diabetic fathers and 30 had both. The LVH criterion of S(v1) + R(V5) or R(v6) >35 mm was met in 148 patients. The percentage of patients having diabetic mothers was higher in those with LVH criterion (29%) than without it (16%) (p < 0.001), but the percentage of patients having diabetic fathers was similar in those with LVH (18%) and without it (18%). Compared with the 683 patients with nondiabetic mothers, the 151 patients with diabetic mothers were younger and had earlier onset of diabetes. The percentage of patients having diabetic siblings was also higher in those with diabetic mothers (31%) than in those with nondiabetic mothers (18%) (p < 0.001). On electrocardiograms, the prevalence of LVH was higher in patients with diabetic mothers (28%) than in those with nondiabetic mothers (15%) (p < 0.001). Echocardiograms showed that patients with diabetic mothers had greater left ventricular wall thickness and mass than those with nondiabetic mothers. In multivariate analysis, the family history of diabetes in mothers was an independent factor to LVH, but the family history of diabetes in fathers was not. CONCLUSIONS: Maternal transmission of diabetes was associated with LVH in patients with NIDDM. Some genetic factors of diabetes, such as mitochondrial DNA abnormalities, may contribute to the development of LVH in maternally transmitted NIDDM.