Effect of Antihypertensive Treatment on PlasmaFibrinogen and Serum HDL Levelsin Patients with Essential Hypertension

Abstract

The influence of hypertension, and its treatment, on circulating lipid and fibrinogen (Fib) concentrations in patients with essential hypertension was investigated. The lipid profile and Fib levels were measured in 353 patients (131 men) with essential hypertension. Their median age was 60 years (range: 18-85 years). All patients had normal results from liver, renal, and thyroid function tests. There were 162 patients (45.9%) who were not receiving antihypertensive treatment. Of the remaining patients, 117 were taking 'lipid-hostile' beta-blockers, thiazide diuretics) antihypertensives and 74 were taking 'lipid-neutral' (angiotensin-converting enzyme inhibitors, calcium channel blockers, angiotensin-II receptor blockers) agents. Patients who were taking 'lipid-hostile' antihypertensive drugs had significantly higher plasma Fib concentrations when compared with those taking 'lipid-neutral' antihypertensives or those not receiving antihypertensive treatment. These differences were not attributable to established factors that influence plasma Fib levels, since when smokers and patients with diabetes mellitus and/or vascular disease were excluded, the difference remained significant. In addition, in these more homogeneous groups, patients receiving 'lipid-neutral' treatment had significantly higher serum high-density lipoprotein (HDL) cholesterol levels when compared with both those taking 'lipid-hostile' antihypertensives and untreated ones. There were no significant differences in the other lipid variables, independently of the presence/absence or the type of antihypertensives. These results suggest that antihypertensive drugs have additional effects, beyond lowering blood pressure, on other vascular risk factors, like Fib and HDL. These effects may depend on the type of drug used.

Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint reduction in hypertension study

“…The observation that losartan-based compared with atenolol-based treatment was associated with higher HDL-C and lower non-HDL-C throughout the study confirms previous reports [6,10] that beta-adrenergic receptor blockers have negative effects on lipid metabolism, whereas angiotensin-converting enzyme inhibitors [20] and angiotensin II receptor blockers have neutral [21] or positive [22] effects. These treatment differences in HDL-C and non-HDL-C were independent of baseline characteristics and weight changes during treatment as well as statin and hydrochlorothiazide treatment.…”

“…It is generally accepted that beta-adrenergic receptor blockers [1][2][3] and diuretics [4,5] have negative [6] or neutral [7] effects on lipid metabolism, whereas angiotensin II receptor blockers have neutral [8] or slightly positive effects [9,10]. Because hypertension is part of the metabolic syndrome, patients with hypertension either have dyslipidemia or are at risk of developing dyslipidemia.…”

Dyslipidaemia, Hypercoagulability and the Metabolic Syndrome

“…During the past decade, there is accumulating evidence that antihypertensive drugs have additional effects, beyond lowering BP, on other vascular risk factors, like fibrinogen and HDL [134]. These effects may be mediated by a variety of mechanisms, including altering insulin sensitivity [135].…”

Antihypertensive pharmacogenetic effect of fibrinogen-beta variant −455G>A on cardiovascular disease, end-stage renal disease, and mortality: the GenHAT study

“…Overall, studies have shown that ACE inhibitors (including lisinopril) lower plasma fibrinogen concentrations, while other classes such as diuretics and calcium channel blockers do not have this effect. [22–25] While no mechanism has been clearly elucidated to explain why ACE inhibitors lead to fibrinogen lowering, it has been postulated that it may be related to inhibition of the hepatic synthesis of fibrinogen [24]. Because of this differential effect of medication class on plasma fibrinogen, there is reason to suspect a pharmacogenetic effect of the FGB gene on cardiovascular disease outcomes.…”