Decreased left ventricular long-axis function may be the earliest stage in subclinical heart failure in Type II diabetes. To assess whether a decrease in SBP (systolic blood pressure) or a change in metabolic control would improve the long-axis function, 48 Type II diabetic patients participating in the CALM II (Candesartan and Lisinopril Microalbuminuria II) study were included in the present study. Patients were examined with tissue Doppler echocardiography at baseline and after 3 and 12 months of follow-up. Corresponding blood pressure, fructosamine and HbA1c (glycated haemoglobin) values were obtained. During the follow-up period, a decrease in SBP of 8 mmHg was seen (from 141±11 mmHg at baseline to 133±12 mmHg; P<0.001) and the peak systolic strain rate was significantly improved (from −1.10±0.25 at baseline to −1.25±0.22; P<0.01). There was a highly significant relationship between the changes in systolic strain rate, HbA1c (P<0.001) and fructosamine (P<0.05), and similarly to changes in left ventricular mass (P<0.05), whereas the correlation to the SBP reduction was not significant. Patients with improved glycaemic control, defined as a reduced HbA1c value after 12 months of follow-up, had a significantly improved strain rate (from −1.07±0.3 s−1 at baseline to −1.32±0.25 s−1; P<0.01) compared with patients with increases in HbA1c (from −1.14±0.25 s−1 at baseline to −1.16±0.27 s−1; P=not significant). The two groups had comparable baseline values of SBP, left ventricular mass, age and disease duration. In conclusion, changes in left ventricular systolic long-axis function are significantly correlated with changes in left ventricular mass, as well as metabolic control, in hypertensive patients with Type II diabetes mellitus.
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July 2006
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Research Article|
June 14 2006
Effects of blood pressure lowering and metabolic control on systolic left ventricular function in Type II diabetes mellitus
Niels H. Andersen;
*Medical Department M (Diabetes and Endocrinology) and The Medical Research Laboratories, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
Correspondence: Dr Niels Andersen (email [email protected]).
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Steen H. Poulsen;
Steen H. Poulsen
†Department of Cardiology, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
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Per L. Poulsen;
Per L. Poulsen
*Medical Department M (Diabetes and Endocrinology) and The Medical Research Laboratories, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
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Søren T. Knudsen;
Søren T. Knudsen
*Medical Department M (Diabetes and Endocrinology) and The Medical Research Laboratories, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
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Kjeld Helleberg;
Kjeld Helleberg
‡Department of Internal Medicine, Viborg County Hospital, DK-8800 Viborg, Denmark
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Klavs W. Hansen;
Klavs W. Hansen
§Department of Internal Medicine, Silkeborg Hospital, DK-8600 Silkeborg, Denmark
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Dines S. Dinesen;
Dines S. Dinesen
*Medical Department M (Diabetes and Endocrinology) and The Medical Research Laboratories, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
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Hans Eiskjær;
Hans Eiskjær
†Department of Cardiology, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
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Allan Flyvbjerg;
Allan Flyvbjerg
*Medical Department M (Diabetes and Endocrinology) and The Medical Research Laboratories, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
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Carl E. Mogensen
Carl E. Mogensen
*Medical Department M (Diabetes and Endocrinology) and The Medical Research Laboratories, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
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Publisher: Portland Press Ltd
Received:
December 15 2005
Revision Received:
February 24 2006
Accepted:
March 03 2006
Accepted Manuscript online:
March 03 2006
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society
2006
Clin Sci (Lond) (2006) 111 (1): 53–59.
Article history
Received:
December 15 2005
Revision Received:
February 24 2006
Accepted:
March 03 2006
Accepted Manuscript online:
March 03 2006
Citation
Niels H. Andersen, Steen H. Poulsen, Per L. Poulsen, Søren T. Knudsen, Kjeld Helleberg, Klavs W. Hansen, Dines S. Dinesen, Hans Eiskjær, Allan Flyvbjerg, Carl E. Mogensen; Effects of blood pressure lowering and metabolic control on systolic left ventricular function in Type II diabetes mellitus. Clin Sci (Lond) 1 July 2006; 111 (1): 53–59. doi: https://doi.org/10.1042/CS20050367
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