Circulation, Vol 84, 1130-1135, Copyright © 1991 by American Heart Association
ME Brickner, JE Willard, EJ Eichhorn, J Black and PA Grayburn
BACKGROUND. This study was performed to determine whether chronic cocaine
abuse is associated with left ventricular hypertrophy in humans. METHODS
AND RESULTS. A consecutive series of 40 chronic cocaine abusers 23-44 years
old who were enrolled in an inpatient drug rehabilitation program were
considered for the study. Subjects with elevated resting blood pressure (n
= 4) or a history of hypertension (n = 3) were excluded. Technically
adequate two-dimensional echocardiograms were obtained in 30 cocaine
abusers and 30 age- and race-matched normal control subjects. All subjects
were men, and the groups were similar with regard to resting blood
pressure, height, weight, and body surface area. All echocardiograms were
read in blinded fashion, and left ventricular mass was calculated by the
area-length method. Left ventricular cavity dimensions and wall motion were
normal in all subjects. Left ventricular mass index was higher in the
cocaine group (103 +/- 24 versus 77 +/- 14 g/m2, p = 0.0001). Posterior
wall thickness was increased (1.2 cm or more) in 13 cocaine abusers (43%)
compared with four controls (p = 0.0099). CONCLUSIONS. Chronic cocaine
abuse is associated with increased left ventricular mass index and wall
thickness. Left ventricular hypertrophy may provide a substrate
facilitating the development of myocardial ischemia and/or arrhythmias in
cocaine abusers.
ARTICLES
Left ventricular hypertrophy associated with chronic cocaine abuse
Department of Internal Medicine, University of Texas Southwestern Medical School, Dallas.
This article has been cited by other articles:
![]() |
J. McCord, H. Jneid, J. E. Hollander, J. A. de Lemos, B. Cercek, P. Hsue, W. B. Gibler, E. M. Ohman, B. Drew, G. Philippides, et al. Management of Cocaine-Associated Chest Pain and Myocardial Infarction: A Scientific Statement From the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology Circulation, April 8, 2008; 117(14): 1897 - 1907. [Full Text] [PDF] |
||||
![]() |
F. Moritz, C. Monteil, M. Isabelle, F. Bauer, S. Renet, P. Mulder, V. Richard, and C. Thuillez Role of reactive oxygen species in cocaine-induced cardiac dysfunction Cardiovasc Res, October 1, 2003; 59(4): 834 - 843. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Henning and Y. Li Cocaine Produces Cardiac Hypertrophy by Protein Kinase C Dependent Mechanisms Journal of Cardiovascular Pharmacology and Therapeutics, June 1, 2003; 8(2): 149 - 160. [Abstract] [PDF] |
||||
![]() |
R. A. Lange and L. D. Hillis Cardiovascular Complications of Cocaine Use N. Engl. J. Med., August 2, 2001; 345(5): 351 - 358. [Full Text] [PDF] |
||||
![]() |
R. J. Henning, J. Silva, V. Reddy, S. Kamat, M. B. Morgan, Yong Xiang Li, and S. Chiou Cocaine Increases {beta}-Myosin Heavy-Chain Protein Expression in Cardiac Myocytes Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 2000; 5(4): 313 - 322. [Abstract] [PDF] |
||||
![]() |
J. E. Hollander The Management of Cocaine-Associated Myocardial Ischemia N. Engl. J. Med., November 9, 1995; 333(19): 1267 - 1272. [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1991 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |