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Impact of Lipid and ACE Inhibitor Therapy on Cardiovascular Disease and Metabolic Abnormalities in the Diabetic and Hypertensive Patient

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Impact of Lipid and ACE Inhibitor Therapy on Cardiovascular Disease and Metabolic Abnormalities in the Diabetic and Hypertensive Patient Journal of Human Hypertension (1997) 11, 9–16 1997 Stockton Press. All rights reserved 0950-9240/97 $12.00 Impact of lipid and ACE inhibitor therapy on cardiovascular disease and metabolic abnormalities in the diabetic and hypertensive patient JR Sowers Division of Endocrinology, Metabolism and Hypertension, Wayne State University School of Medicine, Detroit, MI, USA Hypertension is often accompanied by a variety of meta- abnormal more atherogenic LDL cholesterol particle. bolic abnormalities. These metabolic abnormalities Dyslipidemia interacts with associated hemodynamic include insulin resistance, dyslipidemia and abnormali- (ie, hypertension) and metabolic (ie, increased platelet ties of the coagulation-fibrinolytic system predisposing aggregation and PAI-1 levels) in a multiplicative manner to a procoagulent state. The nexus for all of these potentiating cardiovascular and renal disease. Accord- abnormalities may be central (visceral) obesity. The dys- ingly, lipid therapy should be aggressive to attenuate lipidemia accompanying hypertension consists of low these medical complications of essential hypertension. HDL cholesterol, elevated triglyceride levels and an Keywords: diabetes; cardiovascular disease; lipids; ACE inhibitors Introduction lin levels11 (Table 1). In the Rancho Bernardo Study, those persons with type II diabetes and impaired Ischemic heart disease (IHD) impacts more than 12 glucose tolerance had higher triglycerides and lower million people, and remains the highest cause of HDL compared with normal controls.13 Similar death in the US. Lipid abnormalities, cigarette observations have been made in other populations.14 smoking and hypertension are known modifiable Genetics studies, including twin, parent–child stud- risk factors for IHD.1–7 Furthermore, the risk for IHD ies, large scale family, and candidate gene studies is markedly increased with multiple risk factors, provide substantial evidence for a genetic basis for especially if diabetes is one of those risk factors.4,5,8– the relationship between hypertension/diabetes and 12 Diabetes is often accompanied by hypertension, other accompanying metabolic abnormalities.11,15–17 which is twice as frequent in individuals with this There is higher heritability in estimates twins than metabolic disorder as in those without.9–11 This arti- in pedigrees for blood pressure (BP), very low den- cle reviews the impact of dyslipidemia and other sity lipoproteins (VLDL), LDL, and BMI.15 In one metabolic abnormalities that often accompany dia- study it was estimated that 70% of adults with betes mellitus and hypertension, and therapeutic hypertension before age 55 have siblings or parents strategies which address metabolic as well as hemo- with hypertension, and 12% of all hypertensive dynamic abnormalities. patients have familial dyslipidemic hypertension.17 Thus, both hypertension and dyslipidemic con- ditions appear to have a genetic basis, and both have Genetic basis for lipid abnormalities been linked to insulin resistance.11 The genetic accompanying diabetes/hypertension Hypertensive persons matched for age and body mass index (BMI) with normotensive individuals Table 1 Lipoprotein abnormalities seen in patients with hyper- have been reported to have lower high density lipo- tension and diabetes mellitus proteins (HDL), higher low-density lipoprotein 1. Elevated plasma levels of VLDL, LDL, and (LDL) levels, as well as increased postprandial insu- lipoprotein(a). 2. Decreased plasma HDL cholesterol. 3. Elevated plasma triglyceride levels. 4. Increased lipoprotein oxidation. 5. Increased lipoprotein glycation. 6. Increased small, dense LDL cholesterol products. 7. Decreased lipoprotein lipase activity. Correspondence: Dr JR Sowers, Director, Division of Endocrin- 8. Increased Lp(a) levels. ology, Metabolism and Hypertension, Wayne State University School of Medicine, UHC-4H 4201 St Antoine, Detroit, MI VLDL indicates very-low-density lipoprotein; HDL, high-den- 48201, USA sity lipoprotein. Impact of lipid and ACE inhibitor therapy JR Sowers 10 locus more commonly associated with poor glycemic control.29,30 Lp(a) is a complex lipo- diabetes/hypertension and accompanying dyslipide- protein particle that contains one LDL cholesterol mia (high triglycerides, low HDL cholesterol, and coupled to one molecule of apolipoprotein a (apo [a] small dense LDL particles) is closely linked to the and apo B-100 through a sulfhydryl bond). Apo(a) LDL receptor and to the insulin receptor locus.17–19 is highly homologous to plasminogen but without Indeed, in coronary sibships, three-fourths of those its protease activity.31,32 Accordingly, it does not with early coronary disease have lipid abnormalities possess the ability to catalyze the conversion of associated with the familial dyslipidemic hyperten- fibrinogen and fibrin to degradable products.31,32 sion syndrome.11,17 Sequencing of DNA has shown L(a) potentiates thrombosis because it inhibits the a point mutation for the enzyme lipoprotein lipase binding of plasminogenic binding proteins on the that contributes to high VLDL/low HDL and poss- surface of endothelial cells, thus inhibiting the con- ibly hypertension.17 In an investigation examining version of plasminogen to plasmen and thus the relationship between HDL cholesterol and the fibrinogen and fibrin degradation. Lp(a) also inhibits variable region flanking the human insulin gene, one fibrinolysis, possibly via fibrin binding attributable class of alleles was associated with a family history to the kringle repeats of apo(a), Lp(a) may delay of both diabetes and IHD.18 In children from the thrombolysis and contribute to the progression of Bogalusa cohort, postprandial insulin levels were atherosclerotic plaques.31–34 Plasma levels of Lp(a) positively correlated with fasting serum cholesterol have been observed to be elevated with increasing and VLDL.20 Thus, there is mounting evidence for a age, LDL-cholesterol levels33 and hyperglycemia.34 genetic basis for the association of insulin resistance Similar to LDL, Lp(a) can undergo oxidative modi- and dyslipidemia.21 In turn, both of these abnormali- fication and has been localized in atherosclerotic ties are associated with hypertension and type II dia- lesions,33 suggesting a direct participation.5 While it betes mellitus.9–12,22–24 seems likely that lowering of Lp(a), could decrease atherosclerotic vascular disease risk, currently there Elevated VLDL and serum triglycerides are no data to support this notion. Niacin and post- menopausal estrogen therapy, but not other lipid High serum triglyceride levels are associated with therapies have been demonstrated to lower increased IHD risk,21,25 and often elevated in associ- Lp(a),5,31,32 but additional investigation is needed to ation with insulin resistance.21 Viseral or ‘android’ determine the relevance of this effect. obesity is associated with insulin resistance, elev- ated VLDL, reduced HDL and an increased propen- sity to IHD.22–26 Compared with adipocytes located Post-translational modification of lipoproteins peripherally (ie, gluteofemoral), visceral adipocytes associated with diabetes mellitus display greater sensitivity to lipolytic hormones.27 Hyperglycemia contributes to acceleration of athero- The consequent increased lipolysis in visceral obes- sclerosis, in part, by resulting in glycooxidation of ity, in turn, causes increased free fatty acid (FFA) lipoprotein particles (Table 1).4,5,35–37 In the diabetic turnover into the portal and systemic circulations. state, the generation of reactive oxygen species Delivery of increased FFA to the liver inhibits hep- (ROS) or free radicals by vascular intimal macro- atic clearance of circulating insulin, and stimulates phages and vascular smooth muscle cells (VSMC) hepatic glycogenesis as well as synthesis and release results in oxidative modification of lipoproteins and of triglyceride-rich lipoprotein (VLDL).11,21 vascular structural proteins. Oxidation of LDL modi- Increased levels of FFA are, in turn, associated with fies not only the fatty acid and lipoprotein content reduced insulin sensitivity.28 This relationship is of this particle, but also the amino acid side chains explained by the observation that increases in FFA of apo B, analogous to the modification produced by oxidation elevated the mitochondrial ratio of acetyl- acetylation.35 As a result, oxidized LDL (ox-LDL) is CoA to CoA, which suppresses pruvate dihydro- no longer recognized by the classical LDL receptor, genase (PDH) directly, and phosphofructo 1-kinase but by macrophage scavenger receptors which and hexokinase activities indirectly via citrate and enhances ox-LDL uptake into vascular tissue.35,36 glucose 6-phosphate (C-6-P) accumulation, and Once taken up by foam cells, ox-LDL is poorly resultant inhibition of glucose uptake and oxi- degraded leading to further accumulation. Ox-LDL dation.28 Further, as a result of the consequent is also toxic to endothelial cells, altering both struc- decrease in insulin sensitivity, there is decreased ture and function.35,36 Ox-LDL also stimulates the activity of endothelial bound lipoprotein lipase in production of chemoattracts thereby increasing skeletal muscle and adipocytes, and it is this lipo- migration and binding of monocytes to damaged protein lipase that is responsible for the metabolism endothelium. In addition, antibodies to ox-LDL may of triglyceride rich particles. Thus, triglyceride lev- be involved in the latter stages of atheroma forma- els increase because of increased hepatic production tion.35
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