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Published on: December 11, 2017
Current limitations in treatment of heart failure: new avenues and treatment options
1Medizinische Hochschule Hannover, Germany. Drexler.Helmut@MH-Hannover.de
Insights
Despite current treatments, chronic heart failure outcomes remain poor. Future therapies targeting neuroendocrine activation and energy depletion may improve heart failure progression.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Chronic heart failure (CHF) is a leading cause of mortality in Western countries.
- Current standard treatments (ACE inhibitors, beta-blockers, spironolactone) offer limited efficacy in improving survival and symptom relief for CHF patients.
Purpose of the Study:
- To review current limitations in heart failure management.
- To explore potential future therapeutic strategies for chronic heart failure.
Main Methods:
- Literature review of current heart failure treatments and pathophysiology.
- Analysis of novel pathophysiologic pathways implicated in heart failure progression.
Main Results:
- Existing treatments for chronic heart failure have significant limitations.
- Novel therapeutic targets include the neuroendocrine system (catecholamines, angiotensin II, cytokines, endothelins), calcium homeostasis, and energy metabolism.
Conclusions:
- Interventions targeting newly identified pathophysiologic aspects of heart failure show promise.
- Future drug development could focus on modulating these pathways to delay or reduce heart failure progression.
Abstract:
Chronic heart failure is one of the main causes of death in western countries. Despite state-of-the-art treatment including angiotensin-converting enzyme inhibitors, beta-blockers, and spironolactone, survival and relief from symptoms still are unacceptably poor in patients with chronic heart failure. The present article gives an overview of current limitations in the treatment of heart failure and points out possible treatment options in the future. It seems possible to reduce or at least delay progression of heart failure by adding drugs that interfere with novel pathophysiologic aspects in heart failure activation of the neuroendocrine system, including catecholamines, angiotensin II, cytokines, and endothelins, as well as alteration of calcium homeostasis and energy depletion.
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