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 arte riosclerotic coronary artery disease. However, its association with re stenosis after percutaneous transluminal coronary angioplasty (PTCA) i s controversial. We hypothesized that the Lp(a) level is a significant risk factor for restenosis after angioplasty through a pathophysiolog ical 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 varia bles 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 tar get vessel distribution by radionuclide-perfusion scan. Before the pat ients underwent PTCA, blood was obtained by venipuncture for measureme nt of Lp(a), total cholesterol, thrombin-antithrombin (TAT) complex, a lpha(2)-antiplasmin-plasmin (APP) complex, and plasminogen activator i nhibitor-1 (PAI-1). Evaluable outcome data were obtained on 162 subjec ts, who form the basis of this report. Restenosis occurred in 61 subje cts (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 n ot statistically different in the patients with versus those without r estenosis. The median ratio of TAT to APP was 2-fold higher in the res tenosis group, and this difference approached statistical significance (P=0.07). Univariate analysis was performed for the association of cl inical, lesion-related, and procedural risk factors with restenosis. L p(a) levels did not differ significantly in the restenosis versus no-r estenosis 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 d isease were significantly associated with restenosis (P=0.002 and P=0. 008, respectively). A history of diabetes mellitus was of borderline s ignificance (P=0.055). By multiple logistic regression analysis, the n umber of lesions dilated was the only variable significantly associate d with restenosis (P=0.03). We conclude hat the number of lesions dila ted during PTCA is a significant risk factor for restenosis, whereas t he serum Lp(a) level was not a significant risk factor for restenosis in our patient population. The TAT to APP ratio merits further study a s a possible risk factor for restenosis.