Abstract:
:The prevalence of left ventricular hypertrophy (LVH) rises with severity of hypertension (HT), age, and obesity. Its prevalence ranges from 20% in mildly hypertensive patients to almost 100% in those with severe or complicated HT. However, the diagnosis of LVH is not straightforward, and the definitions and criteria used in clinical studies lack consistency. While many factors play a role in the onset and progression of LVH, blood pressure (BP) is recognized as a central factor. Twenty-four-hour BP measurements are more closely related to LVH than conventional BP readings taken in the clinician's office. Increased renin-angiotensin system (RAS) activity also plays an important role in the development of LVH, and various studies show a correlation between plasma renin activity and left ventricular mass (LVM). LVH is a recognized marker of HT-related target organ damage, and a strong and independent risk factor for adverse cardiovascular (CV) outcomes. CV risk increases with increasing LVM, and decreases with regression of LVH in response to antihypertensive treatment. Therefore the detection, prevention, and reversal of LVH are important goals in HT management. Most antihypertensive drugs can attenuate BP and LVH. However, each drug class may induce LVH regression to a different extent and these extents seldom correlate with the degree of BP reduction achieved. Data from the few large comparative studies in this area suggest that certain classes of antihypertensive drugs and/or their combinations are more effective than others. In particular, calcium channel blockers and drugs that target the RAS, such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), appear to have a specific effect on LVH, independent of BP reduction. Guidelines, therefore, have recommended these drug classes for the treatment of hypertensive patients with LVH.
journal_name
Am J Hypertensjournal_title
American journal of hypertensionauthors
Ruilope LM,Schmieder REdoi
10.1038/ajh.2008.16subject
Has Abstractpub_date
2008-05-01 00:00:00pages
500-8issue
5eissn
0895-7061issn
1941-7225pii
ajh200816journal_volume
21pub_type
杂志文章,评审abstract::The syndrome of apparent mineralocorticoid excess (AME) is characterized by persistent hypertension and hypokalemia, which is caused by impaired inactivation of cortisol (F) to cortisone (E). The thyroid hormone has been known to influence the F to E conversion leading to efficacious inactivation of F into E. However,...
journal_title:American journal of hypertension
pub_type: 杂志文章
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pub_type: 杂志文章,评审
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journal_title:American journal of hypertension
pub_type:
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更新日期:1994-07-01 00:00:00
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更新日期:2002-06-01 00:00:00
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pub_type: 杂志文章
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pub_type: 临床试验,杂志文章
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更新日期:1991-07-01 00:00:00
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更新日期:2000-09-01 00:00:00
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journal_title:American journal of hypertension
pub_type: 杂志文章
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更新日期:2003-12-01 00:00:00
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journal_title:American journal of hypertension
pub_type: 杂志文章,meta分析
doi:10.1093/ajh/7.8.703
更新日期:1994-08-01 00:00:00
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pub_type: 临床试验,杂志文章,随机对照试验
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journal_title:American journal of hypertension
pub_type: 临床试验,杂志文章,多中心研究,随机对照试验
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更新日期:1990-05-01 00:00:00
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pub_type: 杂志文章
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journal_title:American journal of hypertension
pub_type: 杂志文章
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更新日期:1997-02-01 00:00:00
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pub_type: 杂志文章,随机对照试验
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更新日期:2019-10-16 00:00:00