ASSOCIATION OF SERUM LIPOPROTEIN(A) LEVELS AND APOLIPOPROTEIN(A) SIZEPOLYMORPHISM WITH TARGET-ORGAN DAMAGE IN ARTERIAL-HYPERTENSION

Objective.-To investigate the association between lipoprotein(a) [Lp(a )] and other plasma lipids and apolipoproteins and target-organ damage (TOD) in patients with arteria[ hypertension. Design.-Cross-sectional study of a case series. Setting.-University medical center. Participa nts.-Lipoprotein(a) and apolipoproteins were analyzed in 277 untreated patients with mild to moderate essential hypertension and in 102 heal thy controls. Apolipoprotein(a) [apo(a)] phenotypes were additionally analyzed in an independent sample set of 106 hypertensive and 105 cont rol subjects. Main Outcome Measures.-Staging of TOD obtained according to World Health Organization guidelines by clinical evaluation, and l aboratory tests including measurments of creatinine clearance, protein uria, ophthalmoscopy, electrocardiography, echocardiography, and ultra sound examination of major arteries; levels of lipids, apolipoproteins , Lp(a), fibrinogen, and apo(a) phenotypes. Results.-Blood pressure, d uration of hypertension, and levels of total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, Lp(a), and fibrinogen were significantly related to the presence and severity of TOD in univariat e analysis. Stepwise multivariate analysis showed Lp(a) levels (P<.001 ) to be the best discriminator of the presence of TOD, followed by sys tolic blood pressure (P<.001), duration of hypertension (P=.01), and l ow-density lipoprotein cholesterol (P=.04). The Lp(a) levels were rela ted to TOD independent of the level of blood pressure. We confirmed th is association between Lp(a) concentrations and severity of TOD in a s econd independent sample set and observed a significantly higher frequ ency of low-molecular-weight apo(a) isoforms with increasing severity of TOD (P=.02). Conclusions.-Lipoprotein(a) and apo(a) phenotype are s ensitive indicators of the severity of TOD in patients with essential hypertension, and their evaluation might permit identification of hype rtensive subjects liable to the development of organ damage. The highe r frequency of low-molecular-weight apo(a) isoforms in patients with T OD demonstrates a genetically determined risk for the development of T OD in hypertensive patients.