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

Background The mechanisms underlying rapid angiographic progression of coronary artery disease are still unknown. Intravascular thrombosis w ith 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%, po ssible risk factors for rapid progression were investigated. Quantitat ive coronary angiography was performed twice at a mean time interval o f 66+/-25 days. Rapid progression of coronary disease defined as (1) a n 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 thos e 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 conce ntrations. In contrast, serum lipoprotein(a) [Lp(a)] concentrations gr eater 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 media n Lp(a) concentrations were 66 mg/dL (range, 2 to 139) and 13 mg/dL (r ange, 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 homolog y of Lp(a) with plasminogen.