Essential Hypertension

Approximately 50% of patients with essential hypertension are insulin resistant/hyperinsulinemic [75], and it is this subset of patients with essential hypertension that have the atherogenic lipoprotein phenotype characteristic of individuals with the IRS: high TG and low HDL-C concentrations, smaller and denser LDL-particles, and an exaggerated degree of postprandial lipemia [69]. Furthermore, there is evidence that it is these patients in whom essential hypertension is present as a component of the IRS that are at the greatest CVD risk [76-79]. The importance of the link between the dyslipidemia present in insulin-resistant/hyperinsulinemic patients with essential hypertension and CVD has received considerable support from results of the Copenhagen Male Study. In one publication [78], Jeppesen and colleagues demonstrated that blood pressure, per se, was less predictive of CVD in individuals with the characteristic dyslipidemia of the IRS - a high TG and a low HDL-C concentration - than in those without these changes in lipid metabolism. These findings support the view that the development of CVD in individuals with a high TG and low HDL-C concentration was independent of differences in baseline systolic or diastolic blood pressure. In contrast, the higher either systolic (p < 0.001) or diastolic (p < 0.03) blood pressure was at the beginning of the study, the greater the incidence of CVD in those without the dyslipidemia of the IRS.

In a second study [79], participants in the prospective Copenhagen Male Study were divided into three groups on the basis of their fasting plasma TG and HDL-C concentrations. Individuals, whose plasma TG and HDL-C concentrations were in the upper third or lower third, respectively, of the whole population, were assigned to the high TG-low HDL-C group. At the other extreme, a low TG-high HDL-C group was composed of those individuals whose plasma TG and HDL-C concentrations were in the lower third and upper third, respectively, of the study population for these two lipid measurements. The intermediate group consisted of those participants whose lipid values did not qualify them for either of the two extreme groups. The results of their analysis indicated that the development of CVD in patients with hypertension in the lowest TG and highest HDL-C category was no different than in nor-motensive individuals with a similar lipoprotein profile, and the greatest incidence of CVD was seen in patients with hypertension who also were in the highest TG and HDL-C group.

Based upon these findings, it seems reasonable to suggest that lowering blood pressure is a necessary, but not sufficient, approach to reducing CVD in patients in whom essential hypertension is present as one of the manifestations of the IRS. Thus, at the simplest, the choice of drugs used to lower blood pressure should be selected with awareness of their possible deleterious effect on the adverse CVD risk factors often present in patients high blood pressure. For example, it is probably not the best approach to treat a patient, who has a high TG and a low HDL-C concentration, with more than 12.5 mg of hydrochlorothiazide, and in the absence of a previous myocardial infarct, to use a beta-blocker. More importantly, aggressive treatment of the dyslipidemia, if present, seems to be highly justified. It must be emphasized that there is no evidence that this approach will decrease CVD risk in hypertriglyceridemic patients with essential hypertension. On the other hand, given the evidence that the atherogenic lipoprotein profile of the

IRS greatly increases CVD risk [24,25,70,71], and the results of the VA-HIT and Helsinki Heart studies [72-74], it would seem prudent to aggressively treat hypertriglyceridemia when present in patients with essential hypertension.

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