Incipient cardiomyopathy in young insulin-dependent diabetic patients: a seven-year prospective Doppler echocardiographic study

• Published in: Diabetic medicine Vol. 13; no. 9; p. 834
• Main Authors: Gøtzsche, O, Darwish, A, Gøtzsche, L, Hansen, L P, Sørensen, K E
• Format: Journal Article
• Language: English
• Published: England 01.09.1996
• Subjects: Adolescent; Cardiomyopathies - diagnostic imaging; Cardiomyopathies - epidemiology; Cardiomyopathies - physiopathology; Child; Diabetes Mellitus, Type 1 - diagnostic imaging; Diabetes Mellitus, Type 1 - physiopathology; Diabetic Neuropathies - epidemiology; Diastole; Echocardiography, Doppler; Electrocardiography; Follow-Up Studies; Humans; Prospective Studies; Reference Values; Statistics, Nonparametric; Stroke Volume; Systole; Ventricular Function, Left
• ISSN: 0742-3071
• DOI: 10.1002/(SICI)1096-9136(199609)13:9<834::AID-DIA225>3.0.CO;2-M

Two echo-Doppler cardiographic investigations were performed 7 years apart in 17 insulin-dependent diabetic children without hypertension or nephropathy in order to detect early signs of cardiac abnormalities in this group without ischaemic heart disease. Relative to two matched control groups, the patients had reduced increase in left ventricular size (p < 0.01) and stroke volume (p < 0.05). An initially reduced end systolic wall stress and increased fractional shortening (p < 0.003) was normalized during the 7 years. Concomitant with early signs of autonomic neuropathy and aortic stiffening, left ventricular filling changed with increased velocity during atrial contraction (p < 0.01) correlating to the decreased stroke volumes (r = -0.57, p = 0.016). These early changes could suggest left ventricular restriction but could also reflect a changed sympathetic/parasympathetic balance in diabetic children. A reduced left ventricular cavity size and increased atrial ejection has thus been described in these insulin-dependent children without hypertension, nephropathy or evidence for ischaemic heart disease, suggesting the existence of a metabolically-induced cardiomyopathy.