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Lipid Lowering: Another Method of Reducing Blood Pressure?

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Lipid Lowering: Another Method of Reducing Blood Pressure? Journal of Human Hypertension (2002) 16, 753–760 & 2002 Nature Publishing Group All rights reserved 0950-9240/02 $25.00 www.nature.com/jhh REVIEW ARTICLE Lipid lowering: another method of reducing blood pressure? AS Wierzbicki Lipid Unit, Department of Chemical Pathology, St Thomas’ Hospital, London, UK Modern management of cardiovascular risk depends on pulse wave velocity. This blood pressure action may assessment of cardiovascular risk factors. Hypertension account for some of the clinical effects of lipid-lowering and hyperlipidaemia are synergistic risk factors for drugs on cardiovascular risk. Thus, lipid lowering may cardiovascular events. Both show a degree of cross- provide an additional method of correcting hypertension correlation through sharing mechanisms of pathogen- in some high-risk patients. However, data from large- esis including insulin resistance and endothelial dys- scale intervention trials are either absent or ambiguous. function. This article reviews the common pathways Definitive large-scale trials to investigate the antihyper- leading to dyslipidaemia and hypertension and the tensive effects of lipid-lowering drugs are required, effects diet and lipid-lowering drug therapies have had although end point studies examining the interaction of on correcting blood pressure in patients with essential lipid-lowering and antihypertensive drugs to determine hypertension. Both statins and fibrates have shown a optimum combinations are already under way. capability to lower blood pressure by up to 8/5 and 15/ Journal of Human Hypertension (2002) 16, 753–760. 10 mmHg respectively, in some small-scale clinical trials doi:10.1038/sj.jhh.1001483 and have effects on arterial wall structure and hence Keywords: cholesterol; cardiovascular risk; statin; fibrate; review; hypertension Introduction obese.2–4 In secondary hypertension, disorders asso- ciated with chronic renal failure cause a mixed Hyperlipidaemia and hypertension are common hyperlipidaemia or, in the case of nephrotic syn- conditions that both contribute synergistically to drome, hypercholesterolaemia.3 Hypertension and cardiovascular risk. The management of cardiovas- hyperlipidaemia may be related at a deeper level as cular risk now forms the principal function of both insulin resistance is a common feature in the lipid and hypertension clinics, and this article will pathogenesis of both conditions.5,6 In epidemiologi- address what benefits over and beyond risk reduc- cal studies, where hypertension has been linked to tion can be achieved by management of the causes of hyperlipidaemia, the principal factors seem to be hyperlipidaemia and, in particular, whether lipid- insulin resistance and saturated fat intake (ie plasma lowering drugs have direct effects on blood pressure. cholesterol) (Table 1).7 Endothelial dysfunction has been described in association with hypertension in many studies; it also has strong associations with Epidemiology insulin resistance, dyslipidaemia, and other cardio- vascular risk factors.8 Indeed, hypertension and Surveys of hypertensive patients routinely identify hypercholesterolaemia act synergistically as cardio- other cardiovascular risk factors in this population. vascular risk factors, although the exact mechanisms If lipids have effects in blood pressure, it would be are obscure but certainly include both insulin expected that patients with hyperlipidaemia would resistance and endothelial dysfunction. show a greater incidence of hypertension. The common occurrence of both syndromes is often noted but, given the high prevalence of both Dietary management hyperlipidaemia and hypertension, is often dismissed as coincidental.1 Up to 40% of hyperten- Lifestyle strategies are employed in the management sive patients have hyperlipidaemia and 40% are of both hyperlipidaemia and hypertension, and both diets have remarkable similarities. Both aim to stop smoking, reduce saturated fat intake, reduce alcohol Correspondence: AS Wierzbicki, Department of Chemical Pathol- consumption, increase fruit and fibre intake, and ogy, St. Thomas’ Hospital, Lambeth Palace Road, London SE1 6 7EH, UK. improve exercise tolerance. The only difference is Received 13 March 2002; revised and accepted 2 September 2002 in the salt restriction, which is not routinely advised Lipid lowering and blood pressure AS Wierzbicki 754 Table 1 Epidemiological studies that have identified links between hypertension and hypercholesterolaemia. After Goode et al7 Study Numbers Lipid factors Possible pathology Tecumseh Community 3064 TC, TG IRS, saturated fat Southern California 4839 TC, TG IRS, saturated fat Framingham 5127 TC Saturated fat Tromso 16 744 TC, LDL, VLDL-C IRS, saturated fat LRC prevalence 7747 TG, VLDL-C IRS Williams 6128 LDL Saturated fat Abbreviation: total cholesterol (TC); triglyceride (TG); low-density-lipoprotein cholesterol (LDL-C); very-low-density-lipoprotein cholesterol (VLDL-C); insulin resistance syndrome (IRS). for patients with hyperlipidaemia. Diet remains over and above low HDL, and apolipoprotein C2 in controversial in the management of hyperlipidaemia men.17 In the Utah study, which included patients as many intervention trials have shown only mini- with familial combined hyperlipidaemia (FCH) mal effects on the surrogate endpoint of cholesterol and familial hypercholesterolaemia (FH), SLC reduction. Yet trials with polyunsaturated fatty activity also correlated strongly with blood acids achieve a 0.6 mmol/l reduction in cholesterol pressure and lipids.18,19 Both these epidemiological as opposed to 0.15–0.3 mmol/l achieved with low- studies linked SLC to triglycerides, insulin cholesterol diet.9 The Mediterranean diet as used in resistance, and lipoprotein lipase activity as have 605 patients in the Lyons Diet Heart Study10 or studies in patients with type V hyperlipidaemia.20 polyunsaturated fatty acid supplements used in The Utah study population defined a subgroup GISSI-P in 11 374 patients11 showed reductions in of up to 10% of patients with essential hypertension coronary events of 40–70 and 20%, respectively. The who had a phenotype of dyslipidaemia allied role of diet in hypertension is also controversial with hypertension with a strong genetic component. though again many studies show a reduction in This group was termed familial dyslipidaemic blood pressure of 5 mmHg with diets rich in hypertension (FDH). Studies in patients with polyunsaturated fatty acids, which did not translate FCH have persistently shown the presence of into significant benefits in coronary events or hypertension in 30–40% of patients, suggesting a strokes probably due to the inadequate size of the lower penetrance for hypertension compared to studies.12 The most recent of these was the dietary dyslipidaemia in this group.21 Recently, a study in approaches to the hypertension study (DASH) in a colony of 634 baboons colony localised the gene 459 patients with a blood pressure 4160/80 mmHg, behind SLC activity to baboon chromosome 5, a which showed reductions of 11.6/5.3 mmHg in homologue of human chromosome 4.22 Genetic hypertensive patients as opposed to 3.5/2 mmHg in mapping studies of hypertension in FCH kindreds nonhypertensive patients with a low-cholesterol also show quantitative trait linkage of SLC activity and low-salt diet.13 to human chromosome 4p in the region containing a fatty acid hydrolase (CD36) and a-adducin and secondary loci at chromosome 8p near the Sodium–lithium countertransport and familial lipoprotein lipase gene and for diastolic blood dyslipidaemic hypertension pressure chromosome 19 close to the apolipoprotein B locus.21 Many, but not all, studies, have shown Surrogate markers for hypertension have been an association between a-adducin polymorphisms defined. The most currently investigated are the and hypertension in cross-sectional studies23 and a effects of hyperlipidaemia on nitric oxide produc- few have implicated the fatty acid hydrolase tion and paracrine hormone production by the CD 36.24 endothelium (vide infra). However, other markers These studies suggest that a subgroup of patients also show a relationship between hyperlipidaemia with essential hypertension are also dyslipidaemic. and hypertension. Sodium–lithium countertran- This may comprise up to 10% of patients with sport is an ill-understood membrane transport hypertension. The treatment of FCH is well estab- marker associated with hypertension and insulin lished with the use of statins, fibrates, or often a resistance.14,15 It has been shown to be a prospective combination of both. However, no studies have marker for hypertension in the Gubbio study.16 The measured the blood pressure response to lipid- kinetics of SLC activity show similar correlations lowering therapy using accurate methods in this with ethnicity, hypertension, and cardiovascular patient group. risk.14 Sodium–lithium countertransport is highly ge- netically inherited and shows a 65–80% heritability Endothelium and hyperlipidaemia in various cohort studies.14 The Rochester study of 900 patients showed that SLC activity modelled as a The interaction of lipids and the endothelium has recessive monogenic trait predicted blood pressure been extensively reviewed in many publications, Journal of Human Hypertension Lipid lowering and blood pressure AS Wierzbicki 755 and shows a strong relationship between endothe- decrease in albuminuria was seen in patients with lial function and cholesterol or oxidised cholesterol nephrotic syndrome with fibrate therapy compared levels.25,26 Although the direct
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