Lipoprotein(a) level does not predict restenosis after percutaneous transluminal coronary angioplasty.
The 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, alpha2-antiplasmin-plasmin (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.
Alaigh
P
P
Department of Medicine, State University at New York at Stony Brook, USA.
Hoffman
C J
CJ
Korlipara
G
G
Neuroth
A
A
Dervan
J P
JP
Lawson
W E
WE
Hultin
M B
MB
D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D015331:Cohort Studies; D003327:Coronary Disease / Q000097:blood* / Q000628:therapy*; D005260:Female; D005341:Fibrinolysin / Q000032:analysis; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011379:Prognosis; D011446:Prospective Studies; D012008:Recurrence; D018709:Statistics, Nonparametric; D000979:alpha-2-Antiplasmin / Q000032:analysis
D015415:Biomarkers; D017270:Lipoprotein(a); D017395:Plasminogen Activator Inhibitor 1; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; D000990:Antithrombin III; D010447:Peptide Hydrolases; D005341:Fibrinolysin