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Identification of a definite diabetic cardiomyopathy in type 2 diabetes by comprehensive echocardiographic evaluation: A cross‐sectional comparison with non‐diabetic weight‐matched controls
Author(s) -
Ofstad Anne Pernille,
Urheim Stig,
Dalen Håvard,
Orvik Elsa,
Birkeland Kåre I,
Gullestad Lars,
W Fagerland Morten,
Johansen Odd Erik,
Aakhus Svend
Publication year - 2015
Publication title -
journal of diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.949
H-Index - 43
eISSN - 1753-0407
pISSN - 1753-0393
DOI - 10.1111/1753-0407.12239
Subject(s) - medicine , cardiology , diabetic cardiomyopathy , diabetes mellitus , body mass index , diastole , blood pressure , heart failure , subclinical infection , type 2 diabetes , left ventricular hypertrophy , muscle hypertrophy , cardiomyopathy , endocrinology
Background S ubclinical left ventricular ( LV ) dysfunction is prevalent in type 2 diabetes ( T 2 DM ). As obesity has been proposed as one causal factor in the disease process, this could bias the reported prevalences. We wanted to characterize echocardiographic LV dysfunction in obese T 2 DM subjects as compared to non‐diabetic obese controls. Methods O ne hundred patients with T 2 DM without clinical signs of heart failure (29% females, mean ±  SD age 58.4 ± 10.5 years, body mass index ( BMI ) 30.1 ± 5.5 kg/m 2 , blood pressure ( BP ) 141 ± 18/83 ± 9 mmHg) and 100 non‐diabetic controls (29% females) matched for age (58.6 ± 10.5 years), BMI (29.8 ± 4.0 kg/m 2 ) and systolic BP (140 ± 14 mmHg) underwent echocardiography and color tissue D oppler imaging ( TDI ). Diastolic function was evaluated with conventional D oppler recordings and early (e′) and late (a′) myocardial velocities. The ratio between early transmitral filling ( E ) and the corresponding myocardial tissue velocity (e′) served as an index of LV filling pressure. Results T 2 DM patients had more concentric hypertrophy with a relative wall thickness of 0.42 ± 0.07 vs controls 0.38 ± 0.07, P  < 0.001. The T 2 DM group had signs of diastolic dysfunction with lower E / A ratio (0.91 ± 0.27 vs. 1.12 ± 0.38, P  < 0.001), deceleration time (195 ± 49 vs 242 ± 72 ms, P  < 0.001), e′ (5.7 ± 2.0 vs. 6.6 ± 1.8 cm/s, P  = 0.001), and a′ (6.5 ± 2.0 vs. 7.6 ± 1.5 cm/s, P  < 0.001) compared to the controls, and higher E /e′ (13.3 ± 4.7 vs. 11.1 ± 3.5, P  < 0.001). Thus, there were indications of pseudo normalization and increased filling pressure in the T 2 DM group, whereas the controls had evidence for relaxation abnormalities without elevated filling pressure. Conclusion C ompared to a non‐diabetic obese group, more advanced subclinical impairment of diastolic function was seen in T 2 DM .

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