RAPID ANGIOGRAPHIC PROGRESSION OF CORONARY-ARTERY DISEASE IN PATIENTS WITH ELEVATED LIPOPROTEIN(A)

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 greater than or equal to 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 greater than or equal to 50%, (2) occurrence of a new stenosis greater than or equal to 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 greater than or equal to 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.