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[Clinical aspects of differential drug therapy of chronic heart failure]
E Erdmann1, D Beuckelmann, M Böhm
1Medizinische Klinik I, Universität München.
Insights
Modern chronic heart failure treatment combines diuretics, digitalis, and ACE-inhibitors for improved prognosis. Optimal heart rate management remains complex, influenced by calcium handling in failing hearts.
Area of Science:
- Cardiology
- Pharmacology
Context:
- Chronic heart failure (CHF) management has evolved significantly with ACE-inhibitors improving patient outcomes.
- Diuretics are crucial for reducing mortality in CHF, while the role of cardiac glycosides requires further clarification.
Purpose:
- To outline a comprehensive treatment strategy for chronic heart failure across all disease stages.
- To discuss the impact of heart rate on myocardial oxygen consumption and contractility in CHF.
- To explore the role of calcium handling in the force-frequency relation in heart failure.
Summary:
- Current evidence suggests a combination therapy of diuretics, digitalis, and ACE-inhibitors is superior to stepwise drug addition for CHF.
- Elevated heart rate in CHF exacerbates ischemia and reduces contractility due to increased oxygen demand.
- Beta-blocker effects on heart rate do not consistently improve CHF symptoms or hemodynamics; optimal heart rate is disease-dependent.
Impact:
- This integrated approach to CHF treatment aims to optimize patient prognosis and reduce mortality.
- Understanding the mechanisms of disordered force-frequency relation, particularly Ca2+ handling, is key to future therapeutic advancements.
Abstract:
Treatment of chronic heart failure with ACE-inhibitors has greatly improved the prognosis. In addition to ACE-inhibitors, diuretics seem to be necessary to decrease mortality, whereas the importance of cardiac glycosides has not been demonstrated unequivocally. Nevertheless, modern treatment of chronic heart failure in all stages should be a combination of diuretics, digitalis, and ACE-inhibitors rather than a stepwise addition of drugs depending on the severity of the disease. An increased heart rate leads to increased myocardial O2-consumption, decreased O2-supply, ischemia, and reduced contractility. Betablocker-induced reduction of heart rate does, however, not necessarily improve symptoms or hemodynamic conditions. The optimal heart rate in large failing hearts is not known yet. Probably, it is dependent on the type and severity of myocardial disease or impairment. In this respect, the sarcoplasmatic release and uptake of Ca2+ plays the most important role in the disordered force-frequency-relation in chronic heart failure.