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(Circulation. 1995;91:1888-1890.)
© 1995 American Heart Association, Inc.

Articles

Angiotensin-Converting Enzyme and Lipoprotein(a) as Risk Factors for Myocardial Infarction

Edgar Haber, MD

From the Center for the Prevention of Cardiovascular Disease, Harvard School of Public Health and Harvard Medical School, Boston, Mass.

Correspondence to Edgar Haber, MD, Harvard School of Public Health, 677 Huntington Ave, Boston, MA 02115.

Key Words: angiotensin • enzymes • myocardial infarction • lipoproteins

	Introduction

 
In this issue Badenhop et al¹ present a study of genetic markers in schoolchildren and death from coronary artery disease or myocardial infarction or a history of coronary artery bypass surgery or angioplasty in their grandparents. The study shows a correlation between these end points and both an angiotensin-converting enzyme (ACE) genotype and the plasma concentration of lipoprotein(a) [Lp(a)]. These observations remind us that we do not fully understand the risk factors governing coronary artery disease. Over many years, a wealth of studies have identified smoking, hypertension, sex, increased low-density lipoprotein (LDL) cholesterol, diabetes mellitus, and a sedentary lifestyle as having a significant impact on the incidence of arteriosclerosis and myocardial infarction or stroke. Yet data from the Framingham Study show that the probability of developing one of the manifestations of coronary artery disease within 10 years is 6% for a 50-year-old man without any of the known risk factors; for a 60-year-old man in the same condition, the probability is 9%.² It is not surprising, then, that the identification of other risk factors for arteriosclerosis and its consequences —especially those factors for which a positive linkage exists between a genetic locus and disease—remains the focus of considerable research activity. Of particular interest in the context of the report by Badenhop et al¹ are the plasma concentrations of angiotensin II and Lp(a).

Angiotensin II is a potent vasoconstrictor, cardiac inotropic agent, and smooth muscle cell growth factor. Elevated levels of angiotensin II have been recognized for some time to correlate . . . [Full Text of this Article]

This article has been cited by other articles:

				D. R.J. Singer, C. G. Missouris, and S. Jeffery Angiotensin-Converting Enzyme Gene Polymorphism: What to Do About All the Confusion? Circulation, August 1, 1996; 94(3): 236 - 239. [Full Text]