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Published on: December 11, 2017
The therapeutic role of RAS blockade in chronic heart failure
Christian M Werner1, Michael Böhm
1Kardiologische Forschung Kardiologie, Angiologie und Internistische Intensivmedizin Innere Medizin - Universitätsklinikum des Saarlandes Kirrberger Str. D-66421 Homburg, Germany. cwerner@med-in.uni-saarland.de
Insights
Renin-angiotensin system (RAS) blockade, using ACE inhibitors or ARBs, benefits cardiovascular disease stages. RAS inhibition is key for managing chronic heart failure (CHF) and preventing cardiac decompensation.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Cardiovascular disease progresses from risk factors to chronic heart failure (CHF).
- Neuroendocrine activation drives left ventricular remodeling and CHF symptoms.
- Renin-angiotensin system (RAS) plays a critical role in cardiovascular disease progression.
Purpose of the Study:
- To review the therapeutic role of RAS inhibitors in chronic heart failure (CHF).
- To discuss the benefits of RAS blockade across the cardiovascular disease continuum.
Main Methods:
- Literature review of studies on RAS inhibitors in CHF.
- Analysis of mechanisms linking RAS to myocardial damage and CHF progression.
Main Results:
- RAS blockade with ACE inhibitors and/or ARBs is beneficial at all stages of cardiovascular disease.
- Combined RAS blockade is particularly effective in patients with recurrent cardiac decompensations.
- RAS inhibition is a cornerstone therapy for neuroendocrine blockade in CHF.
Conclusions:
- RAS inhibitors are crucial for managing chronic systolic left ventricular dysfunction.
- Targeting the RAS is essential for mitigating cardiovascular disease progression and improving CHF outcomes.
Abstract:
Cardiovascular disease represents a continuum that starts with risk factors such as hypertension and progresses to atherosclerosis, end-organ damage, and ultimately to chronic heart failure (CHF) and premature death. Renin-angiotensin system (RAS) blockade with angiotensin converting enzyme (ACE) inhibitors and/or angiotensin II type 1 receptor blockers (ARBs) has turned out to be beneficial at all stages of this continuum. Several mechanisms govern the progression of structural myocardial damage to end-stage CHF. Chronic neuroendocrine activation fosters left ventricular remodeling and dilatation and leads to clinical symptoms of CHF via forward/backward failure. RAS inhibition is a cornerstone of neuroendocrine blockade in CHF patients, and combined RAS blockade is especially effective in patients presenting with repetitive cardiac decompensations. This review focuses on the therapeutic role of inhibitors of different RAS components in chronic heart failure caused by systolic left ventricular dysfunction.
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