Treatment of hypertensive left ventricular hypertrophy
(2018) In Current Pharmaceutical Design 24(37). p.4391-4396- Abstract
Background: The development and risk potential of hypertension-induced left ventricular (LV) hypertrophy has been well described in epidemiological studies. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. However, the best treatment strategy is still debated, as well as the appropriate blood pressure target in these patients. Objective: We here review the treatment of LV hypertrophy and the potential benefit on clinical outcomes, against a background of the epidemiology and pathophysiology. Results: Both hemodynamic and non-hemodynamic mechanisms contribute to hypertensive LV hypertrophy, which is characterized by an inappropriate myocardial fibrosis. Stringent blood pressure control reduces LV hypertrophy.... (More)
Background: The development and risk potential of hypertension-induced left ventricular (LV) hypertrophy has been well described in epidemiological studies. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. However, the best treatment strategy is still debated, as well as the appropriate blood pressure target in these patients. Objective: We here review the treatment of LV hypertrophy and the potential benefit on clinical outcomes, against a background of the epidemiology and pathophysiology. Results: Both hemodynamic and non-hemodynamic mechanisms contribute to hypertensive LV hypertrophy, which is characterized by an inappropriate myocardial fibrosis. Stringent blood pressure control reduces LV hypertrophy. Blockers of the renin-angiotensin-aldosterone system may have valuable effects on cardiac and electrophysiological remodelling beyond the effects of blood pressure reduction. Thus, they represent a cornerstone in the treatment of hypertensive LV hypertrophy, but most often other antihypertensive drug classes need to be added. Current guidelines indicate a blood pressure target in most patients with hypertensive LV hypertrophy of 120–130/80 mmHg. Conclusions: LV hypertrophy and myocardial fibrosis are important characteristics of hypertensive heart disease and associated with untoward prognosis. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. New drugs under development may add additional benefit.
(Less)
- author
- Jekell, Andreas ; Nilsson, Peter M. LU and Kahan, Thomas
- organization
- publishing date
- 2018
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Cardiac hypertrophy, Fibrosis, Hypertension, Hypertensive heart disease, Renin-angiotensin-aldosterone system, Treatment
- in
- Current Pharmaceutical Design
- volume
- 24
- issue
- 37
- pages
- 6 pages
- publisher
- Bentham Science Publishers
- external identifiers
-
- pmid:30501597
- scopus:85063298318
- ISSN
- 1381-6128
- DOI
- 10.2174/1381612825666181203092918
- language
- English
- LU publication?
- yes
- id
- 20494231-fcd6-4b39-aae9-924ba7945b74
- date added to LUP
- 2019-04-05 14:41:38
- date last changed
- 2024-06-11 07:59:43
@article{20494231-fcd6-4b39-aae9-924ba7945b74,
abstract = {{<p>Background: The development and risk potential of hypertension-induced left ventricular (LV) hypertrophy has been well described in epidemiological studies. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. However, the best treatment strategy is still debated, as well as the appropriate blood pressure target in these patients. Objective: We here review the treatment of LV hypertrophy and the potential benefit on clinical outcomes, against a background of the epidemiology and pathophysiology. Results: Both hemodynamic and non-hemodynamic mechanisms contribute to hypertensive LV hypertrophy, which is characterized by an inappropriate myocardial fibrosis. Stringent blood pressure control reduces LV hypertrophy. Blockers of the renin-angiotensin-aldosterone system may have valuable effects on cardiac and electrophysiological remodelling beyond the effects of blood pressure reduction. Thus, they represent a cornerstone in the treatment of hypertensive LV hypertrophy, but most often other antihypertensive drug classes need to be added. Current guidelines indicate a blood pressure target in most patients with hypertensive LV hypertrophy of 120–130/80 mmHg. Conclusions: LV hypertrophy and myocardial fibrosis are important characteristics of hypertensive heart disease and associated with untoward prognosis. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. New drugs under development may add additional benefit.</p>}},
author = {{Jekell, Andreas and Nilsson, Peter M. and Kahan, Thomas}},
issn = {{1381-6128}},
keywords = {{Cardiac hypertrophy; Fibrosis; Hypertension; Hypertensive heart disease; Renin-angiotensin-aldosterone system; Treatment}},
language = {{eng}},
number = {{37}},
pages = {{4391--4396}},
publisher = {{Bentham Science Publishers}},
series = {{Current Pharmaceutical Design}},
title = {{Treatment of hypertensive left ventricular hypertrophy}},
url = {{http://dx.doi.org/10.2174/1381612825666181203092918}},
doi = {{10.2174/1381612825666181203092918}},
volume = {{24}},
year = {{2018}},
}