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Coronary events have a close association with a low HDL/hypertriglyceridemia (LHDL/HTG) phenotype. As enzymes that hydrolyze triglyceride-rich lipoproteins are associated with a modulation of both HDL cholesterol and triglycerides, we have tested the hypothesis that mutations in the genes encoding lipoprotein lipase (LPL) or hepatic lipase (HTGL) may contribute to the formation of coronary atherosclerosis and, thus, of coronary heart disease (CHD). The entire coding and boundary regions of LPL and HTGL genes were analyzed by direct sequencing in 20 patients with both LHDL/HTG and diagnosed CHD. In the LPL gene six different polymorphisms were identified with same frequencies observed in the general population. In the HTGL gene, besides several polymorphisms, we identified three missense mutations: Asn37His, Val73Met, and Ser267Phe. Population screening using allele specific PCR identified Val73Met as a polymorphism while the two others were absent from 100 control individuals. One of the mutations (Ser267Phe) is known to cause HTGL deficiency and is associated with type III hyperlipoproteinemia. Since this dyslipoproteinemia meets the criteria of LHDL/HTG, it is intriguing to speculate that missense mutations in HTGL may play a role in the pathogenesis of this atherogenic phenotype.

Objective: To investigate the different effects of hypertension, hyperlipidaemia and atherosclerosis on the visco-elastic properties of large arteries., Design: Vessel wall properties were determined in patients who had been subjected for the first time to coronary arteriography. Normotensive patients with no coronary disease (n = 15), one-vessel disease (n = 15) or two- or three-vessel disease (n = 15), 15 treated hypertensive patients (mean +/- SEM duration of hypertension 9.6 +/- 1.7 years) with no coronary disease and normocholesterolaemia and 15 healthy controls were matched for blood pressure, age and sex., Methods: Arterial distension of the common carotid artery was determined by using a multigate Doppler system. The blood pressure curve was recorded by finger plethysmography., Results: The end-diastolic diameter was significantly higher in the hypertensives (P<0.05) but not significantly different in the normotensives compared with the controls. Arterial distensibility was significantly lower in the hypertensive group [(13.3 +/- 0.8) x 10(-3)/kPa] than in the controls [(19.1 +/- 1.5) x 10(-3)/kP; P<0.01), in the group with no coronary disease [(18.8 +/- 1.3) x 10(-3)/kPa; P<0.01] and in those with one-vessel disease [(17.7 +/- 1.4) x 10(-3)/kPa; P<0.05]. Arterial distensibility was not significantly lower in the hypertensives than in the group with two- or three-vessel disease [(15.0 +/- 1.0) x 10(-3)/kPa; NS). No significant correlation was found between cholesterol or lipoprotein(a) levels and arterial distensibility in the normotensive patients., Conclusions: Hypertension is the predominant factor affecting the visco-elastic properties of large arteries. Arterial compliance is significantly altered only in extensive atherosclerosis.