| Long-term treatment with valsartan improved cyclic variation of the myocardial integral backscatter signal and diastolic dysfunction in hypertensive patients: the echocardiographic assessment. | |
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MedLine Citation:
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PMID: 19015589 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Myocardial fibrosis is the major determinant of diastolic property of the left ventricle (LV). Experimental and clinical studies have suggested that angiotensin receptor blockers attenuate myocardial fibrosis in various heart diseases. The integrated backscatter signal (IBS) represents a promising ultrasonic method for assessing the characterization of myocardial tissue: cardiac cycle-dependent variation of the IBS (IBS-CV) is negatively correlated with myocardial collagen deposition in hypertensive hearts. Using non-invasive echocardiographic techniques, we performed a prospective, multi-center trial to examine whether long-term treatment with valsartan would improve myocardial fibrosis and diastolic dysfunction in hypertensives. This study included 43 hypertensive patients who had impaired diastolic function (transmitral Doppler flow early to late filling velocity ratio [E/A ratio] <1.0) and preserved systolic function (LV ejection fraction [LVEF] >50%). Twelve-month valsartan treatment reduced blood pressure (BP) and LV mass index. Valsartan significantly increased not only IBS-CV but also E/A ratio without changing LVEF. The effects of valsartan were compared between two subgroups: one with low IBS-CV (IBS-CV <5.08 dB [the average of 43 patients at baseline]), the other with high IBS-CV (IBS-CV >5.08 dB). At baseline, BP, LV mass index, LVEF, and E/A ratio were similar in the two groups. Valsartan significantly increased IBS-CV and E/A ratio in the low IBS-CV group, but not in the high IBS-CV group, despite comparable reductions in BP and LV mass. In conclusion, long-term valsartan treatment attenuated myocardial fibrosis and improved diastolic dysfunction in hypertensives. It is suggested that in the low IBS-CV group, improvement of diastolic dysfunction by valsartan may be caused by attenuation of myocardial fibrosis, and not by regression of LV hypertrophy. |
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Authors:
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Yoshihiko Mizuta; Hisashi Kai; Minori Mizoguchi; Katsunori Osada; Nobuhiro Tahara; Hiroyuki Nakaura; Fumitaka Kuwahara; Tsutomu Imaizumi; |
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Publication Detail:
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Type: Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Hypertension research : official journal of the Japanese Society of Hypertension Volume: 31 ISSN: 0916-9636 ISO Abbreviation: Hypertens. Res. Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-11-18 Completed Date: 2009-01-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9307690 Medline TA: Hypertens Res Country: Japan |
Other Details:
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Languages: eng Pagination: 1835-42 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, Division of Cardio-vascular Medicine and Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Angiotensin II Type 1 Receptor Blockers / administration & dosage* Echocardiography* Female Fibrosis Humans Hypertension / complications, drug therapy* Hypertrophy, Left Ventricular / complications, drug therapy, ultrasonography Male Middle Aged Myocardium / pathology Prospective Studies Tetrazoles / administration & dosage* Treatment Outcome Valine / administration & dosage, analogs & derivatives* Ventricular Dysfunction, Left / complications, drug therapy*, ultrasonography* |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin II Type 1 Receptor Blockers; 0/Tetrazoles; 137862-53-4/valsartan; 7004-03-7/Valine |
| Investigator | |
Investigator/Affiliation:
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Tsutomu Imaizumi / ; Hisashi Kai / ; Yoshihiko Mizuta / ; Takahiro Matsumoto / ; Koji Hiyamuta / ; Takafumi Ueno / ; Hideki Yoshiyama / ; Tatsuro Hiraki / |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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