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CLINICAL STUDIES

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

Yukihiko Momiyama, MD^*, Yoshihiko Suzuki, MD^*, Fumitaka Ohsuzu, MD, Yoshihito Atsumi, MD^*, Kempei Matsuoka, MD^* and Mitsuru Kimura, MD^*

^* Division of Internal Medicine, Tokyo Saiseikai Central Hospital, Tokyo, Japan
Division of Medicine I, National Defense Medical College, Saitama, Japan

Manuscript received May 29, 1998; revised manuscript received November 10, 1998, accepted December 23, 1998.

Reprint requests and correspondence: Dr. Yukihiko Momiyama, Division of Internal Medicine, Tokyo Saiseikai Central Hospital, 1-4-17 Mita, Minato-ku, Tokyo 108-0073, Japan

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.

Abbreviations and Acronyms   DNA = deoxyribonucleic acid   ECG = electrocardiogram   HCM = hypertrophic cardiomyopathy   IVS = interventricular septum   LV = left ventricular   LVH = left ventricular hypertrophy   LVIDd = LV end diastolic internal dimension   LVIDs = LV end systolic internal dimension   MELAS = mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes   NIDDM = non–insulin-dependent diabetes mellitus   PWT = posterior wall thickness

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