Lipoprotein (a) is increased in acute coronary syndromes (unstable angina pectoris and myocardial infarction), but it is not predictive of the severity of coronary lesions

Lipoprotein (a) [Lp(a)] concentrations were determined in 365 patients undergoing coronary angiography for stable angina (n = 159), unstable angina (n = 99), recent myocardial infarction (n = 45), and nonischemic heart disease (cardiomyopathy or valvular disease, n = 62, non‐IHD). Mean ± SD and median Lp(a) concentrations in stable angina (29.9 ± 29.2; 22 mg/dl) did not differ from those in non‐IHD (26.9 ± 26.3; 17), but were significantly lower than in patients with unstable angina (52.7 ± 36.6; 58) and myocardial infarction (44.8 ± 36.4; 34) (p < 0.01). Coronary angiography revealed that 261 patients, including 4 patients in the non‐IHD group, had significant (≥ 50%) coronary lesions. Lp(a) was higher in patients with (41 ± 35; 32) than in those without (28 ± 27; 19) angiographic evidence of significant coronary stenosis (p < 0.05) and showed a weak univariate correlation with the angiographic index (Total Score) of the severity of the disease (r = 0.106; p < 0.05). However, in the subgroup of 303 patients with stable/unstable angina or myocardial infarction, Lp(a) was predictive neither of angiographic presence nor of severity of coronary disease. Patients were then ranked according to the Total Score values. Among patients with comparable angiographic severity of coronary artery disease, Lp(a) appeared to be remarkably higher in patients with acute ischemic syndromes (unstable angina, myocardial infarction) than in patients with stable angina. In conclusion, Lp(a) was roughly twice as high in acute (unstable angina, myocardial infarction) than in chronic (stable angina) ischemic syndromes, but there was no difference between chronic stable angina and non‐IHD. Serum level determination of Lp(a) made a poor contribution in predicting the extent of coronary artery disease.