From the Department of Cardiovascular Pathology (A.P.B., A.F., Y.-h.L.,
R.V.), Armed Forces Institute of Pathology, Washington, DC; Louisiana State
University, New Orleans (G.T.M.); and the University of Maryland, Baltimore
(J.S.).
Correspondence to Renu Virmani, MD, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000.
BackgroundTraditional risk factors
have been linked to atherosclerotic heart disease in women. However,
the effect of risk factors and menopausal status on the mechanism of
sudden coronary death is unknown.
Methods and ResultsWe examined 51 cases of sudden
coronary death and 15 hearts from women who died of trauma.
Coronary deaths were divided into four mechanisms of death:
ruptured plaque with acute thrombus (n=8), eroded plaque with acute
thrombus (n=18), stable plaque with healed infarct (n=18), and stable
plaque without infarction (n=7). Vulnerable plaques prone to rupture
were defined as those with a thin, fibrous cap infiltrated by
macrophages and were quantitated in coronary deaths and
control subjects. Total cholesterol (TC), HDL
cholesterol, glycosylated hemoglobin, cigarette smoking,
and hypertension were determined in each case. Compared with control
subjects, women with plaque ruptures had elevated TC (270±55 versus
194±44 mg/dL, P=0.002), and those with erosions were
more likely to be smokers (78% versus 33%, P=0.01).
Women with stable plaque and healed infarct had elevated glycosylated
hemoglobin (10.2±5.0% versus 6.4±0.4% in control subjects,
P=0.001) and were more likely to be hypertensive (50%
versus 15% in control subjects, P=0.03). By
multivariate analysis, cigarette smoking was
associated with plaque erosion (P=0.03, odds ratio
[OR] 21), glycoslyated hemoglobin with stable plaque and healed
infarct (P=0.03, OR 41), TC with plaque rupture
(P=0.02, OR 7), and hypertension with stable plaque with
healed infarct (P=0.02, OR 15). Seven of 8 plaque
ruptures occurred in women >50 years of age versus 3 of 18 erosions
(P=0.001). In cases of coronary death,
vulnerable plaques were associated with elevated
cholesterol (P=0.002) and age >50 years
(P=0.002), independent of other risk factors.
ConclusionsIn women, traditional risk factors have distinct
effects on the mechanisms of sudden coronary death, which vary
by menopausal status. Effective risk factor modification may therefore
differ between younger and older women and may be targeting different
mechanisms of plaque instability.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Effect of Risk Factors on the Mechanism of Acute Thrombosis and Sudden Coronary Death in Women
Key Words: thrombosis death, sudden risk factors women
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