Heart failure (HF) is clinical syndrome that develops and progresses as a result of the overexpression of biologically active molecules that are sufficient to cause deleterious effects on the heart and circulation. Over the past 2 decades the adherence to practice guidelines for treating HF, including the use of angiotensin-converting enzyme inhibitors/angiotensin-receptor antagonists and /β-blockers, has resulted in improved survival for patients. However, despite the use of these evidence-based strategies that block the deleterious effects of neurohormonal activation, the overall mortality for HF remains unacceptably high. Unfortunately, when patients remain symptomatic despite having their medical and/or device therapies optimized, the "next steps" to improving patient morbidity are not at all clear. Thus, there remains an unmet need with respect to the treatment of HF patients. The concept that cardiac remodeling represents an important mechanism for disease progression in HF is reviewed, as well as discussion of several novel treatment strategies with respect to devices that are intended to prevent worsening cardiac remodeling.
- Heart failure
- Neurohumoral activation