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.


CONCLUSIONS
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.
Ciarka
Agnieszka
A
Free University of Brussels, Erasme Hospital, Cardiology Department, 808 Route de Lennik, 1070 Brussels, Belgium. aciarka@ulb.ac.be
van de Borne
Philippe
P
Pathak
Atul
A
D000818:Animals; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D004364:Pharmaceutical Preparations; D013564:Sympathetic Nervous System / Q000187:drug effects*
D004364:Pharmaceutical Preparations