(Circulation. 1995;91:948-950.)
© 1995 American Heart Association, Inc.
Articles |
Rapid Angiographic Progression of Coronary Artery Disease in Patients With Elevated Lipoprotein(a)
From the Department of Cardiology (W. Terres, E. Tatsis, C.W.H.) and Lipid Laboratory, the Department of Medicine (B.P., F.U.B., U.B.), University Hospital Eppendorf, Hamburg, Germany.
Correspondence to Wolfram Terres, MD, Department of Cardiology, Medical Clinic, University Hospital Eppendorf, Martinistr 52, 20246 Hamburg, FRG.
Background The mechanisms underlying rapid angiographic progression of coronary artery disease are still unknown. Intravascular thrombosis with or without plaque rupture may be involved.
Methods and Results In a prospective study in 79 patients
with coronary artery disease and at least one coronary diameter
stenosis 
50%, possible risk factors for rapid progression were
investigated. Quantitative coronary angiography was performed twice at
a mean time interval of 66±25 days. Rapid progression of coronary
disease defined as (1) an increase >10% in stenosis severity in at
least one stenosis 50%, (2) occurrence of a new stenosis 50%, or
(3) occlusion of a formerly patent vessel was found in 21 patients
(27%). Between patients with rapid progression and those without,
there were no significant differences in sex distribution, age, smoking
history, frequency of hypertension or diabetes mellitus, and serum LDL
cholesterol, HDL cholesterol, and apolipoprotein B concentrations. In
contrast, serum lipoprotein(a) [Lp(a)] concentrations 25 mg/dL
were
found in 14 of 21 patients (67%) with rapid progression of coronary
artery disease but in only 19 of 58 (33%) in the group without
progression (P=.007). The respective median Lp(a)
concentrations were 66 mg/dL (range, 2 to 139) and 13 mg/dL (range, 2
to 211; P=.01).
Conclusions Lp(a) appears to be a risk factor for the rapid angiographic progression of coronary artery disease. The pathophysiological link between Lp(a) and rapid progression may be an interference with thrombolysis through the partial structural homology of Lp(a) with plasminogen.
Key Words: lipoproteins • coronary disease • stenosis • risk factors • angiography
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