Myocardial fibrosis and diastolic dysfunction in patients with hypertension : results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA)
OBJECTIVES: Hypertensive left ventricular hypertrophy (LVH) is associated with cardiomyocyte hypertrophy and an excess in myocardial collagen. Myocardial fibrosis may cause diastolic dysfunction and heart failure. Circulating levels of the carboxy-terminal propeptide of procollagen type I (PICP), an index of collagen type I synthesis, correlate with the extent of myocardial fibrosis. This study examines myocardial fibrosis in relation to blood pressure, left ventricular mass (LVM), and diastolic function.
METHODS: We examined PICP levels in 115 patients with hypertensive LVH, 38 with hypertension but no hypertrophy, and 38 normotensive subjects. Patients with LVH were subsequently randomly assigned to the angiotensin II type 1 receptor blocker irbesartan or the beta1 receptor blocker atenolol for 48 weeks. Diastolic function was evaluated by tissue velocity echocardiography (n=134). We measured basal septal wall velocities of early (Em) and late (Am) diastolic myocardial wall motion, Em velocity deceleration time (E-decm), and isovolumic relaxation time (IVRTm).
RESULTS: Compared with the normotensive group, PICP was elevated and left ventricular diastolic function was impaired in the hypertensive groups, with little difference between patients with and without LVH. PICP related to blood pressure, IVRTm, Em, and E/Em, but not to LVM. Irbesartan and atenolol reduced PICP similarly. Only in the irbesartan group did changes in PICP relate to changes in IVRTm, and LVM.
CONCLUSION: Myocardial fibrosis and diastolic dysfunction are present in hypertension before LVH develops. The findings with irbesartan suggest a role for angiotensin II in the control of myocardial fibrosis and diastolic function in patients with hypertension with LVH.
| Errataetall: |
CommentIn: J Hypertens. 2008 Jul;26(7):1497; author reply 1497-9. - PMID 18551029 |
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| Medienart: |
Artikel |
| Erscheinungsjahr: |
2007 |
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| Erschienen: |
2007 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:25 |
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| Enthalten in: |
Journal of hypertension - 25(2007), 9 vom: 01. Sept., Seite 1958-66 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Müller-Brunotte, Richard [VerfasserIn] |
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| Anmerkungen: |
Date Completed 24.10.2007 Date Revised 01.12.2018 published: Print CommentIn: J Hypertens. 2008 Jul;26(7):1497; author reply 1497-9. - PMID 18551029 Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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NLM17273827X |
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| 041 | |a eng | ||
| 100 | 1 | |a Müller-Brunotte, Richard |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Myocardial fibrosis and diastolic dysfunction in patients with hypertension |b results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) |
| 264 | 1 | |c 2007 | |
| 336 | |a Text |b txt |2 rdacontent | ||
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| 500 | |a Date Completed 24.10.2007 | ||
| 500 | |a Date Revised 01.12.2018 | ||
| 500 | |a published: Print | ||
| 500 | |a CommentIn: J Hypertens. 2008 Jul;26(7):1497; author reply 1497-9. - PMID 18551029 | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a OBJECTIVES: Hypertensive left ventricular hypertrophy (LVH) is associated with cardiomyocyte hypertrophy and an excess in myocardial collagen. Myocardial fibrosis may cause diastolic dysfunction and heart failure. Circulating levels of the carboxy-terminal propeptide of procollagen type I (PICP), an index of collagen type I synthesis, correlate with the extent of myocardial fibrosis. This study examines myocardial fibrosis in relation to blood pressure, left ventricular mass (LVM), and diastolic function | ||
| 520 | |a METHODS: We examined PICP levels in 115 patients with hypertensive LVH, 38 with hypertension but no hypertrophy, and 38 normotensive subjects. Patients with LVH were subsequently randomly assigned to the angiotensin II type 1 receptor blocker irbesartan or the beta1 receptor blocker atenolol for 48 weeks. Diastolic function was evaluated by tissue velocity echocardiography (n=134). We measured basal septal wall velocities of early (Em) and late (Am) diastolic myocardial wall motion, Em velocity deceleration time (E-decm), and isovolumic relaxation time (IVRTm) | ||
| 520 | |a RESULTS: Compared with the normotensive group, PICP was elevated and left ventricular diastolic function was impaired in the hypertensive groups, with little difference between patients with and without LVH. PICP related to blood pressure, IVRTm, Em, and E/Em, but not to LVM. Irbesartan and atenolol reduced PICP similarly. Only in the irbesartan group did changes in PICP relate to changes in IVRTm, and LVM | ||
| 520 | |a CONCLUSION: Myocardial fibrosis and diastolic dysfunction are present in hypertension before LVH develops. The findings with irbesartan suggest a role for angiotensin II in the control of myocardial fibrosis and diastolic function in patients with hypertension with LVH | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Randomized Controlled Trial | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 7 | |a Adrenergic beta-Antagonists |2 NLM | |
| 650 | 7 | |a Angiotensin II Type 1 Receptor Blockers |2 NLM | |
| 650 | 7 | |a Antihypertensive Agents |2 NLM | |
| 650 | 7 | |a Biphenyl Compounds |2 NLM | |
| 650 | 7 | |a Collagen Type I |2 NLM | |
| 650 | 7 | |a Tetrazoles |2 NLM | |
| 650 | 7 | |a Atenolol |2 NLM | |
| 650 | 7 | |a 50VV3VW0TI |2 NLM | |
| 650 | 7 | |a Irbesartan |2 NLM | |
| 650 | 7 | |a J0E2756Z7N |2 NLM | |
| 700 | 1 | |a Kahan, Thomas |e verfasserin |4 aut | |
| 700 | 1 | |a López, Begoña |e verfasserin |4 aut | |
| 700 | 1 | |a Edner, Magnus |e verfasserin |4 aut | |
| 700 | 1 | |a González, Arantxa |e verfasserin |4 aut | |
| 700 | 1 | |a Díez, Javier |e verfasserin |4 aut | |
| 700 | 1 | |a Malmqvist, Karin |e verfasserin |4 aut | |
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