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Left ventricular and microvascular hypertrophy in essential hypertension: clinical relevance and prognostic
1Institute of Clinical Pharmacology, University Hospital, Frankfurt/Main, Germany.
Insights
Essential hypertension causes cardiac and vascular changes. Angiotensin-converting enzyme inhibitors effectively reduce left ventricular hypertrophy, highlighting the renin-angiotensin-aldosterone system
Area of Science:
- Cardiology
- Hypertension Research
- Vascular Biology
Background:
- Essential hypertension leads to cardiac and vascular structural/functional changes.
- Left ventricular hypertrophy is an independent risk factor for cardiovascular events and mortality.
- Cardiovascular remodeling is influenced by mechanical stress, neuro-humoral stimuli, and genetics.
Purpose of the Study:
- To review the therapeutic goal of reversing cardiac hypertrophy in hypertensive patients.
- To discuss the role of the renin-angiotensin-aldosterone system in cardiac diseases.
- To explore the reversibility of small vessel alterations and their association with left ventricular hypertrophy regression.
Main Methods:
- Review of existing literature on hypertension, cardiac hypertrophy, and vascular remodeling.
- Analysis of the efficacy of various antihypertensive drugs, particularly ACE inhibitors.
- Discussion of morphological changes in small resistance arteries and their impact.
Main Results:
- Antihypertensive drugs, especially ACE inhibitors, can normalize myocardial hypertrophy.
- The renin-angiotensin-aldosterone system plays a crucial role in cardiac diseases.
- Small vessel alterations contribute to persistent hypertension and may be reversible.
Conclusions:
- Regression of cardiac hypertrophy is a significant therapeutic objective in hypertension.
- ACE inhibitors demonstrate potent effects on myocardial hypertrophy, underscoring the importance of the RAAS.
- Reversibility of vascular changes and their link to cardiac hypertrophy regression warrant further investigation.
Abstract:
A considerable number of patients with essential hypertension develop cardiac and vascular structural and functional alterations, indicating an adaptation to the persistently elevated blood pressure. Besides the mechanical stress, neuro-humoral stimuli and possibly the genetic disposition contribute to the process of cardiovascular hypertrophy and remodeling. Left ventricular hypertrophy has been identified as an independent risk factor for cardiovascular events and mortality in these patients and therefore regression of cardiac hypertrophy seems to be a meaningful therapeutic goal. A normalization of myocardial hypertrophy can be achieved with various antihypertensive drugs and combinations, where angiotensin-converting enzyme inhibitors seem to be the most powerful substances. This observation emphasizes the role of the renin-angiotensin-aldosterone system in cardiac diseases. Morphological changes in small resistance arteries do not only represent an adaptation to an elevated peripheral resistance, moreover, they contribute to the persistence of the increase in blood pressure. Investigations on the potential reversibility of small vessel alterations in humans as well as the association with regression of left ventricular hypertrophy will be discussed in this review.