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Published on: September 25, 2017
Treatment of Hypertensive Left Ventricular Hypertrophy
Andreas Jekell1, Peter M Nilsson2, Thomas Kahan1
1Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden.
Insights
Hypertension can cause left ventricular (LV) hypertrophy, a condition that can be reversed with treatment to lower cardiovascular risk. Optimal blood pressure targets and treatment strategies for LV hypertrophy are still under investigation.
Area of Science:
- Cardiology
- Hypertension Research
- Cardiac Remodeling
Background:
- Hypertension-induced left ventricular (LV) hypertrophy is a significant risk factor for cardiovascular events.
- Regression of LV hypertrophy is associated with reduced cardiovascular morbidity and mortality.
- Optimal treatment strategies and blood pressure targets for hypertensive LV hypertrophy remain subjects of debate.
Purpose of the Study:
- To review current treatment strategies for LV hypertrophy.
- To evaluate the potential benefits of different treatments on clinical outcomes.
- To provide an overview of the epidemiology and pathophysiology of hypertensive LV hypertrophy.
Main Methods:
- Review of epidemiological studies on hypertension and LV hypertrophy.
- Analysis of pathophysiological mechanisms contributing to hypertensive LV hypertrophy.
- Evaluation of current treatment guidelines and pharmacological approaches.
Main Results:
- Both hemodynamic and non-hemodynamic factors contribute to hypertensive LV hypertrophy, often involving myocardial fibrosis.
- Strict blood pressure control is effective in reducing LV hypertrophy.
- Renin-angiotensin-aldosterone system blockers show promise for cardiac remodeling benefits beyond blood pressure reduction, often requiring combination therapy.
Conclusions:
- LV hypertrophy and myocardial fibrosis are key indicators of hypertensive heart disease with poor prognosis.
- Reversing LV hypertrophy significantly improves cardiovascular outcomes.
- Emerging pharmacological agents may offer additional therapeutic advantages.
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.
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