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Mechanisms involved in the hemodynamic alterations in congestive heart failure as a basis for a rational
J Marín1, E Marín, M A Gutiérrez-Iñiguez
1Servicio de Farmacología Clínica, Hospital Universitario Clínica Puerta de Hierro, c/ San Martín de Porres, 4, 28035-Madrid, Spain.
Insights
Congestive heart failure (CHF) treatment aims to improve quality of life and prolong survival by managing neurohumoral activation. Current and novel drug therapies target compensatory mechanisms to improve patient prognosis.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Congestive heart failure (CHF) is a significant cardiological issue.
- Neurohumoral activation is a key compensatory mechanism in CHF that can worsen prognosis.
- Effective treatment is crucial for improving quality of life and survival rates.
Purpose of the Study:
- To outline current and emerging therapeutic strategies for managing congestive heart failure.
- To address the complexities of neurohumoral activation in CHF.
Main Methods:
- Review of established and novel pharmacological agents used in CHF treatment.
- Discussion of symptomatic and disease-modifying therapeutic approaches.
Main Results:
- Established drugs include ACE inhibitors, diuretics, digoxin, and beta-agonists.
- Emerging therapies encompass angiotensin II receptor antagonists, novel beta-blockers, and agents targeting specific pathways like vasopressin and endothelin.
Conclusions:
- CHF management requires addressing both symptoms and neuroendocrine changes.
- A range of pharmacological options, both current and novel, are available to improve CHF outcomes.
Abstract:
Congestive heart failure is a complex syndrome and one of the major cardiological problems of our time. It is characterized by an important neurohumoral activation to compensate for the reduction of cardiac output and blood pressure, that worsens the prognosis with time. The aim of the treatment is focused on how to improve the quality of life and how to prolong survival. Usually, treatment, either symptomatic or directed to control the neuroendocrine compensatory changes, is necessary. The drugs currently used are angiotensin-converting enzyme inhibitors, diuretics, digoxin, and beta-adrenoceptor agonists. In addition, new drugs, such as angiotensin II receptor antagonists, beta-adrenoceptor antagonists, ibopamine, Ca(2+) antagonists, neutral endopeptidase inhibitors, vasopressin antagonists, Ca(2+)-sensitizers with cyclic AMP-dependent or -independent mechanisms, and endothelin antagonists, are also being used.
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