- Conventional strategies and emerging novel therapies are both needed to offset the rising toll of heart failure (HF)
- Risk stratification is aided by communicating with patients to assess compliance and understanding the role of biomarkers in prognosis and monitoring
- State-of-the-art pharmacotherapy for heart failure with reduced ejection fraction (HFrEF) offers a well-defined, evidence-based suite of guideline-directed medical therapies (GDMT)
- GDMT can be augmented by novel devices and strategies such as cardiac resynchronization, catheter-based therapies and emerging neuromodulation approaches
Despite decades-long progress in patient outcomes, heart failure (HF) remains a management challenge characterized by a clinical natural history of steady functional decline. However, an expanding number of gold-standard approaches and novel treatments now offer a powerful HF management suite.
Heart failure with preserved ejection fraction (HFpEF) is an urgent public health problem and no proven therapies currently exist. HFpEF is associated with high mortality and morbidity and affects 50% of HF patients. Therefore, a focus on HFrEF options in this review is clinically relevant.
Characterizing and Communicating HF
The average HF patient has five comorbidities; three of the most common are hypertension, ischemic heart disease and diabetes. All must be accurately characterized to anticipate possible interactions with HF therapies when applying conventional guideline-directed medical therapies (GDMTs).
Clear communication of prognosis is key to motivating patients to comply with GDMTs and lifestyle recommendations that reduce risks. Clinical factors and laboratory measures such as age, atrial fibrillation, levels of creatinine and biomarkers such as B-type natriuretic peptide, help characterize a patient’s prognosis and monitor conditions.
Gold standards: pharmacotherapies
Patients with HFrEF suffer a maladaptive neurohormonal activation that typically responds well to a number of pharmacotherapies that target the renin-angiotensin-aldosterone system. Other treatments for HFrEF patients are angiotensin-converting enzyme (ACE) inhibitors. Most HFrEF patients respond to angiotensin receptor blockers (ARBs), which are especially useful in treating patients for whom ACE inhibitors are contraindicated due to cough or angioedema. For maximal safe effect, it is important with ACE inhibitors and ARBs to titrate dose to levels achieved in clinical trials, or to the maximally-tolerated individual patient dose.
Game-changers: cardiac resynchronization, neuromodulation
Newer and novel approaches to HF management have the potential to manage key pathways and physiologies. CRT can improve ventricular systolic function and reduce mitral regurgitation, and can be an effective mediator of reverse remodeling with reduction in chamber dimensions.
New and emerging neuromodulation therapies can also impact the autonomic nervous system to shift the sympathovagal signaling to effect cardiovascular remodeling and improve outcomes. Among promising therapies are:
- vagal nerve stimulation
- carotid baroreceptor stimulation
- spinal cord stimulation
- renal denervation
Clinicians face an expanding array of HF therapies and must master both the old and the new—the gold standards and the game changers—to improve morbidity and mortality of their HF patients.
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