Role of Activated Renin-Angiotensin System in Myocardial Fibrosis and Left Ventricular Diastolic Dysfunction in Diabetic Patients Reversal by Chronic Angiotensin II Type 1A Receptor Blockade
Background We attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an improvement of diastolic dysfunction in diabetic patients. Methods and Results Forty-eight type 2 diabetic patients were divided into 2 groups:...
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Published in | Circulation Journal Vol. 71; no. 4; pp. 524 - 529 |
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2007
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Abstract | Background We attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an improvement of diastolic dysfunction in diabetic patients. Methods and Results Forty-eight type 2 diabetic patients were divided into 2 groups: 38 treated with candesartan for 6 months, and 10 without candesartan, as controls. Doppler mitral flow velocity pattern and biomarkers of collagen type I turnover were assessed before and after ARB during a 6-month period. The mitral E/A ratio increased from 0.65±0.11 to 0.75±0.19. The carboxy-terminal propeptide of procollagen type I (PIP), an index of collagen type I synthesis, decreased and the carboxy-terminal telopeptide of collagen type I (CITP), an index of collagen type I degradation, increased following ARB. Consequently, the PIP/CITP ratio, an index of coupling between the synthesis and degradation of collagen type I, decreased. None of the indexes changed in the control group. The change in left ventricular chamber stiffness did not correlate with the change in PICP (r=0.08, p=NS), but it did with the changes in CITP or in the PIP/CITP ratio (r=0.35, p<0.05; r=0.39, p<0.05). Conclusions Chronic ARB improves diastolic dysfunction in diabetic patients, at least partially through the attenuation of myocardial fibrosis, by regulating collagen turnover, particularly by facilitating collagen degradation. (Circ J 2007; 71: 524 - 529) |
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AbstractList | Background We attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an improvement of diastolic dysfunction in diabetic patients. Methods and Results Forty-eight type 2 diabetic patients were divided into 2 groups: 38 treated with candesartan for 6 months, and 10 without candesartan, as controls. Doppler mitral flow velocity pattern and biomarkers of collagen type I turnover were assessed before and after ARB during a 6-month period. The mitral E/A ratio increased from 0.65±0.11 to 0.75±0.19. The carboxy-terminal propeptide of procollagen type I (PIP), an index of collagen type I synthesis, decreased and the carboxy-terminal telopeptide of collagen type I (CITP), an index of collagen type I degradation, increased following ARB. Consequently, the PIP/CITP ratio, an index of coupling between the synthesis and degradation of collagen type I, decreased. None of the indexes changed in the control group. The change in left ventricular chamber stiffness did not correlate with the change in PICP (r=0.08, p=NS), but it did with the changes in CITP or in the PIP/CITP ratio (r=0.35, p<0.05; r=0.39, p<0.05). Conclusions Chronic ARB improves diastolic dysfunction in diabetic patients, at least partially through the attenuation of myocardial fibrosis, by regulating collagen turnover, particularly by facilitating collagen degradation. (Circ J 2007; 71: 524 - 529) BACKGROUNDWe attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an improvement of diastolic dysfunction in diabetic patients. METHODS AND RESULTSForty-eight type 2 diabetic patients were divided into 2 groups: 38 treated with candesartan for 6 months, and 10 without candesartan, as controls. Doppler mitral flow velocity pattern and biomarkers of collagen type I turnover were assessed before and after ARB during a 6-month period. The mitral E/A ratio increased from 0.65+/-0.11 to 0.75+/-0.19. The carboxy-terminal propeptide of procollagen type I (PIP), an index of collagen type I synthesis, decreased and the carboxy-terminal telopeptide of collagen type I (CITP), an index of collagen type I degradation, increased following ARB. Consequently, the PIP/CITP ratio, an index of coupling between the synthesis and degradation of collagen type I, decreased. None of the indexes changed in the control group. The change in left ventricular chamber stiffness did not correlate with the change in PICP (r=0.08, p=NS), but it did with the changes in CITP or in the PIP/CITP ratio (r=0.35, p<0.05; r=0.39, p<0.05). CONCLUSIONSChronic ARB improves diastolic dysfunction in diabetic patients, at least partially through the attenuation of myocardial fibrosis, by regulating collagen turnover, particularly by facilitating collagen degradation. We attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an improvement of diastolic dysfunction in diabetic patients. Forty-eight type 2 diabetic patients were divided into 2 groups: 38 treated with candesartan for 6 months, and 10 without candesartan, as controls. Doppler mitral flow velocity pattern and biomarkers of collagen type I turnover were assessed before and after ARB during a 6-month period. The mitral E/A ratio increased from 0.65+/-0.11 to 0.75+/-0.19. The carboxy-terminal propeptide of procollagen type I (PIP), an index of collagen type I synthesis, decreased and the carboxy-terminal telopeptide of collagen type I (CITP), an index of collagen type I degradation, increased following ARB. Consequently, the PIP/CITP ratio, an index of coupling between the synthesis and degradation of collagen type I, decreased. None of the indexes changed in the control group. The change in left ventricular chamber stiffness did not correlate with the change in PICP (r=0.08, p=NS), but it did with the changes in CITP or in the PIP/CITP ratio (r=0.35, p<0.05; r=0.39, p<0.05). Chronic ARB improves diastolic dysfunction in diabetic patients, at least partially through the attenuation of myocardial fibrosis, by regulating collagen turnover, particularly by facilitating collagen degradation. |
Author | Yamamoto, Kazuhiro Tsujino, Takeshi Kawasaki, Daizo Kosugi, Keisuke Waki, Hidehiko Masuyama, Tohru |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17384453$$D View this record in MEDLINE/PubMed |
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Snippet | Background We attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an... We attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an improvement... BACKGROUNDWe attempted to test the hypothesis that chronic angiotensin II type 1A receptor blockade (ARB) alters myocardial collagen turnover leading to an... |
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SubjectTerms | Aged Angiotensin II Type 1 Receptor Blockers - pharmacology Angiotensin II Type 1 Receptor Blockers - therapeutic use Angiotensin II type 1A receptor blockade Benzimidazoles - pharmacology Benzimidazoles - therapeutic use Blood Pressure - drug effects Blood Pressure - physiology Collagen Collagen - metabolism Diabetes Mellitus, Type 2 - physiopathology Diastolic dysfunction Endomyocardial Fibrosis - drug therapy Endomyocardial Fibrosis - physiopathology Female Humans Hypertension - physiopathology Male Middle Aged Natriuretic Peptide, Brain - blood Receptor, Angiotensin, Type 1 - drug effects Renin-Angiotensin System - drug effects Renin-Angiotensin System - physiology Tetrazoles - pharmacology Tetrazoles - therapeutic use Ventricular Dysfunction, Left - drug therapy Ventricular Dysfunction, Left - physiopathology |
Subtitle | Reversal by Chronic Angiotensin II Type 1A Receptor Blockade |
Title | Role of Activated Renin-Angiotensin System in Myocardial Fibrosis and Left Ventricular Diastolic Dysfunction in Diabetic Patients |
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ispartofPNX | Circulation Journal, 2007, Vol.71(4), pp.524-529 |
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