Myocardial infarction, heart failure and sympathetic nervous system activity: new pharmacological approaches that affect neurohumoral activation

BACKGROUND: Myocardial infarction (MI) is a leading cause of death among adults and MI survivors have increased risk of developing heart failure. MI is accompanied by acute sympathetic nervous system activation, which becomes persistent in heart failure patients. OBJECTIVE: We establish whether current and investigated therapies affect sympathetic activation after MI and in heart failure patients. METHODS: We reviewed the literature on the mechanisms of sympathetic nervous system activation and effects of standard and investigated treatments on adrenergic activation after MI and in heart failure patients. RESULTS/CONCLUSION: Angioplasty and beta-blockers result in a decrease of adrenergic activation after acute MI; in heart failure patients, medications that affect renin-angiotensin-aldosterone system modulate sympathetic activation. Endothelin receptors agonists, adenosine receptors antagonists, arginine vasopressin antagonists, cardiac myosin activators, natriuretic peptide analogues, vasopeptide inhibitors, renin inhibitors, tyrosine kinase inhibitors and dopamine receptors inhibitors were tested in heart failure settings. They target better management of neurohumoral activation.