IMPAIRED MICROVASCULAR REACTIVITY IN NON-DIABETIC PRIMARY HYPERTENSION IS INVERSELY RELATED TO LOW HDL CHOLESTEROL AND REDUCED GLUCOSE TOLERANCE

Abstract

Objective: Type 2 diabetes and the metabolic syndrome is characterized by dyslipidaemia with low HDL-cholesterol and skin microvascular dysfunction. The associations of glucose and lipid abnormalities with microvascular dysfunction in hypertension are not well studied. Design and method: We studied untreated hypertensive patients (n = 71, 55 ± 13 years, 34% women) with no overt cardiovascular disease, dyslipidaemia, or diabetes. Arterial endothelial function was studied by forearm post-ischemic flow mediated vasodilatation (FMD), and glyceryl trinitrate (GTN) for nonspecific dilation; and in smaller resistance arteries by change in reflection index (RI) by pulse wave analysis and terbutaline. Skin microvascular reactivity was assessed by laser Doppler fluxmetry and local iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), and by maximum reactive hyperaemia by heating. Triglyceride glucose index (TyG), defined as: Ln [fasting plasma glucose x plasma triglycerides], was used as a measure of glucose tolerance. Results: Mean BP was 154/93 mmHg, fasting LDL, HDL, triglycerides and glucose 3.48 ± 0.92, 1.40 ± 0.40, 1.16 ± 0.86 and 5.40 ± 0.55 mmol/L, respectively; and TyG 6.74 ± 0.59. The FMD (mean 5.8 ± 4.3%)-to-GTN (mean 14.7 ± 6.9%) ratio related to HDL (r = 0.30, P = 0.018). The RI change (mean 7.0 ± 3.0%) related inversely to HDL (r = −0.42, P < 0.001). Ach peak flux increase (mean 483 ± 380%) related to HDL (r = 0.28, P = 0.021), whereas SNP (679 ± 395%) and heat mediated (906 ± 491%) peak flux increase did not. Changes in cutaneous vascular conductance (CVC) by Ach related to HDL (r = 0.27, P = 0.025). Changes in CVC by local heating related to the LDL-to-HDL ratio (r = −0.30, P = 0.018). Changes in, FMD, GTN, and RI change did not relate to TyG. However, in skin microcirculation, peak flux increase and the change in CVC to Ach tended to relate inversely to TyG (r = −0.22, P = 0.069 and r = −0.22, P = 0.071), while responses to SNP and heat did not. LDL showed no relations to the vascular function indices studied. Conclusions: In contrast to arterial endothelial function, impaired microvascular reactivity relates inversely to low HDL-cholesterol and reduced glucose tolerance in patients with uncomplicated hypertension. These findings, in consort with observations in type 2 diabetes and in familial combined hyperlipidaemia, suggest that impaired microvascular function is an early finding in dyslipidaemia and with impaired glucose tolerance.