TY - JOUR
T1 - Basic mechanisms of disease progression in the failing heart
T2 - The role of excessive adrenergic drive
AU - Mann, D. L.
N1 - Funding Information:
From the Cardiology Section, Department of Medicine, Veterans Administration Medical Center, and Baylor College of Medicine, Houston, TX. Supported in part by research funds from the Department of VeteransA ffairs. Address reprint requests to Douglas L. Mann, MD, Cardiology Research (151C), VA Medical Center, 2002 Holcombe Blvd, Houston, TX 77030. Copyright © 1998 by W.B. Saunders Company 0033-0620/98/4101 - 1001 $8.00/0
PY - 1998
Y1 - 1998
N2 - This review examines experimental evidence that suggests that excessive adrenergic stimulation of the heart may actually contribute to the untoward natural history of congestive heart failure. The basic mechanisms for catecholamine-mediated cardiac toxicity are discussed, as well as relatively new evidence that catecholamine-mediated toxicity is the result of β- adrenoceptor-mediated cyclic adenosine monophosphate-dependent calcium overload of the cardiac myocyte. The studies reviewed herein provide a plausible biological rationale for the use of β-adrenergic blocking agents in patients with heart failure.
AB - This review examines experimental evidence that suggests that excessive adrenergic stimulation of the heart may actually contribute to the untoward natural history of congestive heart failure. The basic mechanisms for catecholamine-mediated cardiac toxicity are discussed, as well as relatively new evidence that catecholamine-mediated toxicity is the result of β- adrenoceptor-mediated cyclic adenosine monophosphate-dependent calcium overload of the cardiac myocyte. The studies reviewed herein provide a plausible biological rationale for the use of β-adrenergic blocking agents in patients with heart failure.
UR - http://www.scopus.com/inward/record.url?scp=0031875199&partnerID=8YFLogxK
U2 - 10.1016/S0033-0620(98)80025-X
DO - 10.1016/S0033-0620(98)80025-X
M3 - Article
C2 - 9715817
AN - SCOPUS:0031875199
SN - 0033-0620
VL - 41
SP - 1
EP - 8
JO - Progress in cardiovascular diseases
JF - Progress in cardiovascular diseases
IS - 1 SUPPL.
ER -