Original Contributions |
From the Department of Medicine, State University at New York at Stony Brook.
AbstractThe serum lipoprotein(a)
[Lp(a)] level is a known risk factor for
arteriosclerotic coronary artery disease.
However, its association with restenosis after
percutaneous transluminal coronary angioplasty
(PTCA) is controversial. We hypothesized that the Lp(a) level is a
significant risk factor for restenosis after angioplasty
through a pathophysiological mechanism leading to
excess thrombin generation or inhibition of
fibrinolysis. We designed a prospective study of the
relation of Lp(a) to outcome after PTCA, in which we measured selected
laboratory variables at entry and collected clinical, procedural,
lesion-related, and outcome data pertaining to restenosis.
Restenosis was defined as >50% stenosis of the target
lesion by angiography or as ischemia in the target vessel
distribution by radionuclide-perfusion scan. Before the patients
underwent PTCA, blood was obtained by venipuncture for
measurement of Lp(a), total cholesterol,
thrombin-antithrombin (TAT) complex,
2-antiplasminplasmin (APP) complex, and
plasminogen activator inhibitor-1
(PAI-1). Evaluable outcome data were obtained on 162 subjects, who form
the basis of this report. Restenosis occurred in 61 subjects
(38%). The Lp(a) level was not correlated significantly with TAT, APP,
PAI-1, or the TAT-APP ratio. Levels of TAT, APP, and PAI-1 were not
statistically different in the patients with versus those without
restenosis. The median ratio of TAT to APP was 2-fold higher in
the restenosis group, and this difference approached
statistical significance (P=0.07).
Univariate analysis was performed for the
association of clinical, lesion-related, and procedural risk factors
with restenosis. Lp(a) levels did not differ significantly in
the restenosis versus no-restenosis group, whether
assessed categorically (>25 mg/dL versus <25 mg/dL) or as a
continuous variable by Mann-Whitney U test. The
number of lesions dilated and the lack of family history of premature
heart disease were significantly associated with restenosis
(P=0.002 and P=0.008, respectively). A
history of diabetes mellitus was of borderline significance
(P=0.055). By multiple logistic regression
analysis, the number of lesions dilated was the only
variable significantly associated with restenosis
(P=0.03). We conclude that the number of lesions dilated
during PTCA is a significant risk factor for restenosis,
whereas the serum Lp(a) level was not a significant risk factor for
restenosis in our patient population. The TAT to APP ratio
merits further study as a possible risk factor for restenosis.
Key Words: lipoprotein(a) angioplasty thrombin plasmin antiplasmin
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B Jorgensen, S Simonsen, K Endresen, K Forfang, T Egeland, A.T Hostmark, and E Thaulow Luminal loss and restenosis after coronary angioplasty. The role of lipoproteins and lipids Eur. Heart J., October 1, 1999; 20(19): 1407 - 1414. [Abstract] [PDF] |
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