(Circulation. 1998;97:1529-1531.)
© 1998 American Heart Association, Inc.
What Have We Learned From the Calcium Channel Blocker Controversy?
Robert M. Califf, MD;
; Judith M. Kramer, MD
From the Division of Cardiology and the Division of General Internal
Medicine, Department of Medicine, Duke University Medical Center and Health
Systems, Durham, NC.
Correspondence to Robert M. Califf, MD, Director, Duke Clinical Research Institute, 2024 W Main St, Durham, NC 27705.
Key Words: Editorials • drugs • trials
Hundreds
of thousands of patients around the world have been treated with drugs
that antagonize the function of calcium channels. The development of
these drugs was based on the remarkable scientific discovery of calcium
channels, the identification of methods to antagonize their effects,
and the development of compounds to block
them.1 2 As concepts of the pathophysiology and
treatment of hypertension and atherosclerosis evolved
in parallel with the science of calcium channels, an approach to
determining whether these therapies have clinical benefit was
developed.
In the treatment of hypertension, the strategy for therapeutic
evaluation has been based on the simple concept that lowering blood
pressure will result in a decrease in the incidence of stroke,
myocardial infarction, renal failure, and death.2
In the treatment of angina, a more complex set of concepts has
prevailed. Three factors have formed the framework for evaluating
therapies for angina: (1) the role of coronary vasospasm in the
production of myocardial
ischemia,3 (2) the belief that reduction
in myocardial ischemia over a specified time interval or
improvement in exercise time on a treadmill provided strong evidence of
an overall health benefit,4 and (3) more
difficult extrapolations related to preservation of cellular function
during myocardial ischemia.5 The
synthesis of these factors has led to the acceptance of a
reduction in frequency of angina or an improvement in exercise time as
adequate evidence of a desirable clinical benefit of a therapy for
angina.
On the basis of these constructs, a variety of compounds were developed
that had disparate . . . [Full Text of this Article]
This article has been cited by other articles:
|
|
|
|
 
M. D.M Engelmann and S. Pehrson
Quality of life in nonpharmacologic treatment of atrial fibrillation
Eur. Heart J.,
August 1, 2003;
24(15):
1387 - 1400.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. R. Kizer and S. E. Kimmel
Epidemiologic Review of the Calcium Channel Blocker Drugs: An Up-to-date Perspective on the Proposed Hazards
Arch Intern Med,
May 14, 2001;
161(9):
1145 - 1158.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. M. Psaty, N. S. Weiss, C. D. Furberg, T. D. Koepsell, D. S. Siscovick, F. R. Rosendaal, N. L. Smith, S. R. Heckbert, R. C. Kaplan, D. Lin, et al.
Surrogate End Points, Health Outcomes, and the Drug-Approval Process for the Treatment of Risk Factors for Cardiovascular Disease
JAMA,
August 25, 1999;
282(8):
786 - 790.
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Temple
Are Surrogate Markers Adequate to Assess Cardiovascular Disease Drugs?
JAMA,
August 25, 1999;
282(8):
790 - 795.
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. A. Heidenreich, K. M. McDonald, T. Hastie, B. Fadel, V. Hagan, B. K. Lee, and M. A. Hlatky
Meta-analysis of Trials Comparing {beta}-Blockers, Calcium Antagonists, and Nitrates for Stable Angina
JAMA,
May 26, 1999;
281(20):
1927 - 1936.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Langer, K. B. Michels, B. A. Rosner, J. E. Manson, M. J. Stampfer, A. M. Walker, W. C. Willett, and C. H. Hennekens
Safety of Calcium Channel Blockers in Cardiovascular Disease • Response
Circulation,
December 22, 1998;
98
(25):
2932 - 2935.
[Full Text]
[PDF]
|
|
|
