Rationale for beta-adrenergic blocking drugs in cardiomyopathy.
Activation of the sympathetic nervous system has traditionally been regarded as an important compensatory mechanism that helps to maintain myocardial contractility in severe heart failure. Recent findings suggest that increased catecholamine levels are linked to decreased beta-adrenergic receptor density and myocardial damage. Thus, rather than aiding the failing heart, increased myocardial exposure to catecholamines may actually contribute to further deterioration in myocardial function. Beta-adrenergic blocking drugs may ameliorate these harmful effects and paradoxically result in improved ventricular performance.
Fowler
M B
MB
Bristow
M R
MR
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy / Q000503:physiopathology; D002395:Catecholamines / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D011943:Receptors, Adrenergic, beta