Lipoprotein(a) is related to the extent of lesions in the coronary vasculature and to unstable coronary syndromes.

BACKGROUND: Lp(a) is a highly atherogenic particle with a prothrombotic effect. Until now its relation to the extent and severity of the atheromatic lesions had not been established by standard procedures. HYPOTHESIS: This study examined the correlation of Lp(a) to the extent and severity of coronary artery disease (CAD) and its relation to unstable clinical events (not including sudden death). METHODS: In 202 patients undergoing coronary angiography, plasma lipids were measured with the usual procedures and Lp(a) with the enzyme-linked immunosorbent assay. The extent of CAD was expressed in the number of diseased vessels and its severity in terms of the severity coefficient and the obstruction coefficient. RESULTS: A very strong relationship between LP(a) and the number of diseased vessels (p = 0.0007) signifying diffuse atherosclerosis, but no relation with the severity of the lesions. was found. However, it was the only lipid that correlated significantly with the number of totally occluded vessels (p = 0.0003). The thrombogenic ability of Lp(a) was manifested by increased incidence of myocardial infarction and unstable angina episodes in patients with elevated Lp(a) (p = 0.0157). CONCLUSION: Elevated Lp(a) predisposes to the extent of CAD and total occlusions but not to the severity of lesions. Patients with increased Lp(a) levels and unstable angina are at increased danger of suffering myocardial infarction. Thus, Lp(a) may predispose to plaque destabilization and thrombosis of noncritical lesions.

Clinical and electrocardiographic predictors of recurrent atrial fibrillation.

Patients with frequent episodes of paroxysmal atrial fibrillation (AF) are prone to develop permanent AF and have an increased thromboembolic risk. We have previously shown that P wave dispersion (P dispersion), defined as the difference between the maximum and the minimum P wave duration, and maximum P wave duration (P maximum) can distinguish patients with paroxysmal lone AF. The ability of those ECG markers and of other clinical and ECG variables to detect patients at risk for recurrent AF was tested in 88 patients, aged 64 +/- 12 years. All patients had a history of symptomatic episodes of AF during the last 2 years and had not previously received any antiarrhythmic prophylaxis. P maximum and P dispersion were calculated from a 12-lead surface ECG recorded in all patients during sinus rhythm. A computerized ECG system was used and P maximum and P dispersion were calculated on screen from the averaged complexes of all 12 leads. Age (P = 0.01), history of organic heart disease (P = 0.03), P maximum (P < 0.001), minimum P wave duration (P = 0.05), and P dispersion (P < 0.001) were found to be significant univariate predictors of recurrent AF, whereas only P maximum (P < 0.001) and age (P = 0.037) remained significant independent predictors of frequent AF paroxysms in the multivariate analysis. It is concluded that advanced age and prolonged P wave duration may be used as predictors of frequently relapsing AF. Therefore, simple AF predictors exist that could possibly distinguish the patients in whom prophylaxis with antiarrhythmic medicines should be instituted.