Advanced

Treatment of hypertensive left ventricular hypertrophy

Jekell, Andreas; Nilsson, Peter M. LU and Kahan, Thomas (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)
Please use this url to cite or link to this publication:
author
organization
publishing date
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
  • 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
2019-09-17 04:51:19
@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},
  keyword      = {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},
  volume       = {24},
  year         = {2018},
}