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Black and Hispanic older adults in the United States have higher prevalence of hypertension, less adequate treatment, less consistent blood pressure control, and worse cardiovascular outcomes than their white counterparts. Genetic differences are insufficient to explain these disparities-various social, economic, and environmental factors notably contribute. Racial and ethnic differences in living circumstances, household income, access to appropriate care, food security, educational attainment, and tobacco use all negatively impact long-term hypertension outcomes in minoritized older adults. To remedy these inequities, the search for solutions must include a complete assessment of the social, racial, and cultural components of the problem., Competing Interests: Disclosures S. D. Nesbitt, MD, MS, serves as a site principal investigator for a clinical trial sponsored by Ablative Solutions. S. V. Carter has nothing to disclose., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Purpose of Review: The purpose of this review is to discuss the unique mechanism of firibastat, a new antihypertension medication. Hypertension continues to be a highly prevalent public health issue., Recent Findings: Firibastat is a novel agent developed to treat hypertension. As the first member in the class of centrally acting agents to target the brain renin angiotensin system, firibastat offers new pathways to consider and enhances the regimen of agents currently available to treat hypertension. Recent clinical trials have demonstrated effectiveness and safety in mild hypertension as well as resistant hypertension. This review introduces firibastat as a new therapeutic class of treatment for hypertension focused on the renin angiotensin system in the brain. Early studies have shown a significant reduction in blood pressure with minimal side effects particularly in patients who are difficult to treat., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Despite existing therapy, successful control of hypertension in the United States is estimated at less than 50%. In blacks, hypertension occurs earlier, is more severe, controlled less often and has a higher morbidity and mortality than in whites. Blacks are also less responsive to monotherapy with angiotensin-I converting enzyme inhibitors or angiotensin-II receptor type 1 blockers. Obesity, higher salt-sensitivity and low plasma renin activity are possible reasons of this poor blood pressure (BP) control, especially in blacks. The aim of the study was to assess efficacy and safety of firibastat, a first-in-class aminopeptidase A inhibitor preventing conversion of brain angiotensin-II into angiotensin-III, in BP lowering in a high-risk diverse hypertensive population., Methods: Two hundred fifty-six overweight or obese hypertensive patients, including 54% black and Hispanic individuals, were enrolled in a multicenter, open-label, phase II study. After a 2-week wash-out period, subjects received firibastat for 8 weeks (250 mg BID orally for 2 weeks, then 500 mg BID if automated office blood pressure (AOBP) >140/90 mm Hg; hydrochlorothiazide 25 mg QD was added after 1 month if AOBP ≥160/110 mm Hg). The primary end point was change from baseline in systolic AOBP after 8 weeks of treatment, and secondary end points include diastolic AOBP, 24-hour mean ambulatory BP and safety., Results: Firibastat lowered systolic AOBP by 9.5 mm Hg ( P<0.0001) and diastolic AOBP by 4.2 mm Hg ( P<0.0001). 85% of the subjects did not receive hydrochlorothiazide and were treated with firibastat alone. Significant BP reduction was found across all subgroups regardless age, sex, body mass index, or race. Systolic AOBP decreased by 10.2 mm Hg ( P<0.0001) in obese patients, by 10.5 mm Hg ( P<0.0001) in blacks, and 8.9 mm Hg ( P<0.0001) in nonblacks. Most frequent adverse events were headaches (4%) and skin reactions (3%). No angioedema was reported. No change in potassium, sodium, and creatinine blood level were observed., Conclusions: Our results demonstrate the efficacy of firibastat in lowering BP in a high-risk diverse population where monotherapy with angiotensin-I converting enzyme inhibitors or angiotensin-II receptor type 1 blockers may be less effective and support the strategy to further investigate firibastat in subjects with difficult-to-treat or potentially resistant hypertension., Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique Identifier: NCT03198793.

Background: Previous studies reported increased white blood cell counts (WBCCs), an inflammatory marker, in hypertension, prehypertension and metabolic syndrome. Evidence suggests that inflammation precedes blood pressure (BP) elevation and may contribute to incident hypertension. Angiotensin receptor blockers (ARBs) may reduce inflammation. We analyzed WBCC trends in TRial Of Preventing HYpertension (TROPHY) to determine if this inflammatory marker predicted incident hypertension in prehypertensive individuals and whether randomized assignment to the ARB candesartan (391 individuals) for 2 years, lowered WBCC compared with placebo-treated controls (381 individuals)., Methods: A new analysis of TROPHY trial data., Results: In the total population, baseline BMI correlated with WBCC (r = 0.185, P < 0.0001), neutrophils (r = 0.135, P < 0.001) and lymphocytes (r = 0.204, P < 0.0001). Baseline triglycerides also correlated significantly with inflammatory markers. Despite a wide range of home BP (HBP) values, HBP did not correlate with baseline WBCC counts. After 2 years, candesartan decreased placebo corrected HBP by -5.5/-2.5 mmHg, (P < 0.0001), but WBCC, neutrophil and lymphocyte counts were not different in placebo and in candesartan groups. Baseline WBCC, neutrophils and lymphocyte counts did not predict incident hypertension in the placebo group., Conclusion: In TROPHY, candesartan lowered BP but did not alter WBCC. Baseline WBCC did not predict incident hypertension. Our findings do not support the hypothesis that inflammation contributes to incident hypertension or that ARB treatment suppresses inflammation. The significant independent association of WBCC with baseline BMI and triglycerides is consistent with the evidence that obesity and insulin resistance are associated with inflammation. The findings highlight the importance of effective lifestyle modification in prehypertension to reduce inflammatory cardio-metabolic risk and suppress transition to hypertension.

In the prospective, open-label, titrate-to-goal Blood Pressure Control in All Subgroups With Hypertension (BP-CRUSH) study, 999 patients with hypertension uncontrolled on monotherapy (mean age, 55.6 ± 11.4 years; baseline blood pressure [BP], 153.7 ± 9.2/91.9 ± 8.6 mm Hg) were switched to fixed-dose amlodipine/olmesartan medoxomil (AML/OM) 5/20 mg. Patients were uptitrated every 4 weeks to AML/OM 5/40 mg and 10/40 mg to achieve BP < 120/70 mm Hg. Patients were subsequently uptitrated every 4 weeks to AML/OM+hydrochlorothiazide (HCTZ) 10/40+12.5 mg and 10/40+25 mg to achieve BP <125/75 mm Hg. The primary end point, the cumulative percentage of patients achieving seated systolic BP < 140 mm Hg (< 130 mm Hg for patients with diabetes) by week 12, was 75.8%. The mean (± standard error) BP changes from baseline during the titration periods ranged from -14.2±0.4 mm Hg/-7.7 ± 0.3 mm Hg for AML/OM 5/20 mg to -25.1 ± 0.7 mm Hg/-13.7 ± 0.4 mm Hg for AML/OM+HCTZ 10/40+25 mg. By week 20, the cumulative BP threshold of <140/90 mm Hg was achieved by 90.3% of patients. An ambulatory BP monitoring substudy (n=243) showed that 24-hour efficacy was maintained. Treatment-emergent adverse events (TEAEs), mostly mild to moderate in severity, occurred in 529 patients (53.0%). Drug-related TEAEs occurred in 255 patients (25.5%). This well-tolerated, treat-to-goal algorithm enabled a large proportion of patients with uncontrolled hypertension on monotherapy to safely achieve BP control on single-pill AML/OM combination therapy or triple therapy with the addition of HCTZ. ., (© 2011 Wiley Periodicals, Inc.)

Since the first International Society on Hypertension in Blacks consensus statement on the "Management of High Blood Pressure in African American" in 2003, data from additional clinical trials have become available. We reviewed hypertension and cardiovascular disease prevention and treatment guidelines, pharmacological hypertension clinical end point trials, and blood pressure-lowering trials in blacks. Selected trials without significant black representation were considered. In this update, blacks with hypertension are divided into 2 risk strata, primary prevention, where elevated blood pressure without target organ damage, preclinical cardiovascular disease, or overt cardiovascular disease for whom blood pressure consistently <135/85 mm Hg is recommended, and secondary prevention, where elevated blood pressure with target organ damage, preclinical cardiovascular disease, and/or a history of cardiovascular disease, for whom blood pressure consistently <130/80 mm Hg is recommended. If blood pressure is ≤10 mm Hg above target levels, monotherapy with a diuretic or calcium channel blocker is preferred. When blood pressure is >15/10 mm Hg above target, 2-drug therapy is recommended, with either a calcium channel blocker plus a renin-angiotensin system blocker or, alternatively, in edematous and/or volume-overload states, with a thiazide diuretic plus a renin-angiotensin system blocker. Effective multidrug therapeutic combinations through 4 drugs are described. Comprehensive lifestyle modifications should be initiated in blacks when blood pressure is ≥115/75 mm Hg. The updated International Society on Hypertension in Blacks consensus statement on hypertension management in blacks lowers the minimum target blood pressure level for the lowest-risk blacks, emphasizes effective multidrug regimens, and de-emphasizes monotherapy.

Context: Aldosterone has been shown to exert a central sympathoexcitatory action in multiple animal models, but evidence in humans is still lacking., Objectives: Our objective was to determine whether hyperaldosteronism causes reversible sympathetic activation in humans., Methods: We performed a cross-sectional comparison of muscle sympathetic nerve activity (SNA, intraneural microelectrodes) in 14 hypertensive patients with biochemically proven primary aldosteronism (PA) with 20 patients with essential hypertension (EH) and 18 age-matched normotensive (NT) controls. Seven patients with aldosterone-producing adenoma (APA) were restudied 1 month after unilateral adrenalectomy., Results: Mean blood pressure values in patients with PA and EH and NT controls was 145 ± 4/88 ± 2, 150 ± 4/90 ± 2, and 119 ± 2/76 ± 2 mm Hg, respectively. The major new findings are 2-fold: 1) baseline SNA was significantly higher in the PA than the NT group (40 ± 3 vs. 30 ± 2 bursts/min, P = 0.014) but similar to the EH group (41 ± 3 bursts/min) and 2) after unilateral adrenalectomy for APA, SNA decreased significantly from 38 ± 5 to 27 ± 4 bursts/min (P = 0.01), plasma aldosterone levels fell from 72.4 ± 20.3 to 11.4 ± 2.3 ng/dl (P < 0.01), and blood pressure decreased from 155 ± 8/94 ± 3 to 117 ± 4/77 ± 2 mm Hg (P < 0.01)., Conclusion: These data provide the first evidence in humans that APA is accompanied by reversible sympathetic overactivity, which may contribute to the accelerated hypertensive target organ disease in this condition.

Uncontrolled blood pressure (BP) remains a leading contributor to cardiovascular disease and mortality worldwide. Although current practice guidelines recommend treating patients with hypertension to defined BP goals, the approach is not widely implemented, and BP control in clinical practice is much worse than that attained in clinical trials. Recent and ongoing clinical trials are utilizing more aggressive approaches with combination therapy as initial treatment. This article discusses the problem of therapeutic or clinical inertia when attempting to control hypertension and highlights differences in BP control rates between clinical trials and real-world practice. Additionally, the rationale for an ongoing treat-to-goal study using a fixed-dose combination of amlodipine/olmesartan medoxomil in patients with hypertension not controlled on monotherapy is provided.

Three important principles have emerged from recent epidemiologic and clinical studies in hypertension. First, patients with hypertension most often have other cardiovascular risk factors such as obesity and diabetes. Second, hypertension remains grossly undertreated. Third, at blood pressure levels once considered "high-normal," early organ damage may already be taking place in patients with multiple risk factors that, without treatment, can eventually lead to cardiovascular morbidity and mortality. The concept of evaluating global or overall risk is gaining wide acceptance, and US treatment guidelines may soon reflect these findings and assist clinicians in identifying individuals who are most likely to benefit from therapy. Results from clinical trials suggest that among the various pharmacologic agents available to treat hypertension, blockers of the renin-angiotensin system are effective in type 2 diabetes and chronic kidney disease, conditions that often occur in conjunction with hypertension.

Prehypertension, defined by Seventh Joint National Committee (JNC 7) as a blood pressure (BP) 120-139/80-89 mm Hg, was controversial. Approximately 31-37% of US adults are prehypertensive, and approximately 12-14% have BP of 130-139/85-89 mm Hg or ;Stage 2' prehypertension, is associated with approximately 3-fold greater likelihood of developing hypertension and roughly twice the cardiovascular events than BP <120/80 mm Hg. Lifestyle change is the only intervention recommended for most prehypertensives. When fully implemented, lifestyle changes lower BP and prevent cardiovascular events, but evidence for community-wide effectiveness is limited. The Trial of Preventing Hypertension (TROPHY) documented that angiotensin receptor blockade safely lowers BP and prevents and/or delays hypertension in Stage 2 prehypertensives. Prehypertensives with diabetes or nephropathy are at high risk and should receive antihypertensive treatment according to JNC 7. Epidemiological data suggest that the number needed to treat to prevent a cardiovascular event in these at-risk Stage 2 prehypertensives is similar to Stage 1 hypertensives when both groups have one or more concomitant risk factors. Clinical trials are urgently needed to address this question. In the absence of clinical trials data, we believe it is prudent for the concerned clinician to consider initiating antihypertensive pharmacotherapy in selected Stage 2 prehypertensive patients at significant absolute risk for progression to hypertension and cardiovascular events.

The Trial of Preventing Hypertension (TROPHY) demonstrated the feasibility of possibly reducing the incidence of hypertension with the angiotensin receptor blocker candesartan compared with placebo. The long-term benefits of pharmacologic therapy in high-normal blood pressure, or prehypertension are not known, and the long-term effect on health-related quality of life (HRQL) has not been determined. An analysis of covariance model was used to assess treatment differences from baseline in the HRQL scores using Short Form (SF)-36, and component measures at subsequent visits. Of the 809 randomized patients, 734 had both baseline and > or =1 HRQL follow-up assessment: 95% (379 of 397) of patients receiving candesartan and 91% (355 of 388) of patients receiving placebo. There were no statistically significant between-group differences in least-squares mean physical component survey and mental component survey scores or the individual scales at each scheduled visit relative to baseline values (P >.05). In TROPHY, patients with prehypertension had relatively high baseline HRQL, and HRQL was maintained with the angiotensin receptor blocker candesartan over both the 2-year treatment period and a total 4-year trial period.

Purpose of Review: Prehypertension is a recognized stage of blood pressure but treatment standards have not yet been established. This review will focus on the treatment considerations in prehypertension., Recent Findings: Previous approaches to prehypertensive blood pressure have focused on the role of nonpharmacologic modalities alone. The recently published Trial of Preventing Hypertension (TROPHY) is the first study of pharmacologic intervention in this category of blood pressure., Summary: TROPHY forged new territory in the area of pharmacologic treatment for prehypertension. The safety and tolerability of the angiotensin receptor blocker treatment in the trial offer a new option to clinicians attempting to avoid the ravages of hypertension in the patients they treat. Furthermore the stage is properly set for additional research in treatments for prehypertension.

The Trial of Preventing Hypertension (TROPHY) investigated pharmacologic intervention in patients with prehypertension. TROPHY confirmed that treatment with candesartan 16 mg can prevent or postpone the development of hypertension, demonstrating a 66.3% reduction in hypertension incidence relative to placebo (26.8% absolute reduction) at 2 years, and a 15.6% reduction in hypertension incidence relative to placebo (9.8% absolute reduction) at 4 years. Further analyses of TROPHY may help to delineate the mechanisms behind this result more specifically, including those relating to components of the metabolic syndrome and markers of inflammation and early vascular change. The rate of progression and the concurrence of risk factors make a strong case for the development of a directive for closer follow-up and treatment. The potential for success in reducing cardiovascular events is great, given the prevalence of prehypertension and the likelihood of progression.

Background: Prehypertension is considered a precursor of stage 1 hypertension and a predictor of excessive cardiovascular risk. We investigated whether pharmacologic treatment of prehypertension prevents or postpones stage 1 hypertension., Methods: Participants with repeated measurements of systolic pressure of 130 to 139 mm Hg and diastolic pressure of 89 mm Hg or lower, or systolic pressure of 139 mm Hg or lower and diastolic pressure of 85 to 89 mm Hg, were randomly assigned to receive two years of candesartan (Atacand, AstraZeneca) or placebo, followed by two years of placebo for all. When a participant reached the study end point of stage 1 hypertension, treatment with antihypertensive agents was initiated. Both the candesartan group and the placebo group were instructed to make changes in lifestyle to reduce blood pressure throughout the trial., Results: A total of 409 participants were randomly assigned to candesartan, and 400 to placebo. Data on 772 participants (391 in the candesartan group and 381 in the placebo group; mean age, 48.5 years; 59.6 percent men) were available for analysis. During the first two years, hypertension developed in 154 participants in the placebo group and 53 of those in the candesartan group (relative risk reduction, 66.3 percent; P<0.001). After four years, hypertension had developed in 240 participants in the placebo group and 208 of those in the candesartan group (relative risk reduction, 15.6 percent; P<0.007). Serious adverse events occurred in 3.5 percent of the participants assigned to candesartan and 5.9 percent of those receiving placebo., Conclusions: Over a period of four years, stage 1 hypertension developed in nearly two thirds of patients with untreated prehypertension (the placebo group). Treatment of prehypertension with candesartan appeared to be well tolerated and reduced the risk of incident hypertension during the study period. Thus, treatment of prehypertension appears to be feasible. (ClinicalTrials.gov number, NCT00227318.)., (Copyright 2006 Massachusetts Medical Society.)

The excess risk for hypertension in black Americans continues to be a major health concern. Although there is considerable information regarding these disease trends, many of the major underpinnings of the etiology of hypertension remain unclear. The excess mortality in blacks due to heart disease, renal failure, and stroke is clearly directly related to the excess burden of hypertension. Amid the recent findings about the pathophysiology of hypertension, some clear differences in the effects of overweight, salt sensitivity, and vascular biology emerge along ethnic lines. These differences may shed some light on the development of more effective treatment strategies. Based on our current knowledge, aggressive management of hypertension in blacks is critical. This review highlights what is known about various factors affecting hypertension and its treatment in black Americans.

Background: The Trial of Preventing Hypertension (TROPHY) Study is designed to establish whether treating high normal blood pressure with a low-dose angiotensin receptor blocker, candesartan cilexetil, for 2 years reduces the rate of progression to hypertension compared with placebo treatment over a 4-year observation period. We are presenting the baseline cardiovascular risk factor profile of the 809 subjects randomized in the TROPHY Study. The risk factors in this analysis were as follows: cholesterol >or=200 mg/dl; LDL-cholesterol >or=160 mg/dL; HDL-cholesterol or=150 mg/dL; body mass index >or=25 kg/m2 (overweight and obese), fasting insulin >or=20 mU/mL; heart rate >or=80 beats/min; hematocrit >or=43.5 % (men) and >or=41.2% (women)., Methods: The TROPHY Study is a 4-year randomized, placebo-controlled, multicenter clinical trial of 809 subjects with high normal blood pressure (BP), which is currently in progress., Results: The participants of the TROPHY study (mean age 49+/-8.1 years) with high normal BP (mean 134+/-4/85+/-4 mm Hg) had additional cardiovascular risk factors. Of the group, 96% had at least one, 81% had two or more, and 13% had five or more additional risk factors., Conclusions: Our data from individuals with high normal BP suggests clearly that the risk of cardiovascular disease begins to rise before the diagnosis of hypertension is evident. The overall risk in such subjects reflects both the rising BP and other concurring factors. It appears that truly low-risk hypertension only rarely exists.

Hypertension is a multifaceted disease that may present somewhat differently in various populations. It is clear that hypertensive treatment reduces cardiovascular, renal, and cerebrovascular outcomes for all patients, yet recent clinical trial data suggest that some groups may benefit more than others from specific drug intervention. Furthermore, these data justify specific approaches for some special populations. This article reviews important features of the presentation, rationale for treatment, and treatment recommendations for the treatment of hypertension in special populations. The special populations addressed include diabetic patients, the elderly, and women.

Objective: Hypertension and insulin resistance might be associated through peripheral vascular hypertrophy/rarefaction which compromises skeletal muscle blood flow and decreases glucose uptake, inducing insulin resistance. We hypothesized that treatment with losartan as compared to atenolol would improve insulin sensitivity through regression of peripheral vascular hypertrophy/rarefaction., Methods: In 70 hypertensive patients with electrocardiographic left ventricular hypertrophy, we measured minimal forearm vascular resistance (MFVR) by plethysmography and insulin sensitivity (M/IG) by a 2-h isoglycemic hyperinsulinemic clamp at baseline and after 1, 2 and 3 years of blinded treatment with atenolol- or losartan-based regimens., Results: Blood pressures were reduced similarly in the two treatment groups. After 3 years, MFVR was increased (3.7 versus 3.2 mmHg x min x 100, P < 0.05) and M/IG decreased (8.6 versus 12.1 l/kg x mmol x min, P < 0.05) in patients treated with atenolol, whereas MFVR and M/IG were unchanged (3.5 versus 3.5 mmHg x min x 100 and 12.6 versus 11.1 l/kg x mmol x min, both P = NS) in patients treated with losartan. As compared to atenolol, losartan treatment was associated with less increase in MFVR (4.3 versus 27%, P < 0.05) and less decrease in M/IG (24 versus -14%, P < 0.01). The relative change in M/IG was inversely associated with the relative change in MFVR (r = -0.16, P < 0.05) independently of the relative change in body mass index (r = -0.29, P < 0.001)., Conclusions: As compared to atenolol, losartan treatment was associated with less peripheral vascular hypertrophy/rarefaction and higher insulin sensitivity. The relative change in MFVR and M/IG were inversely related, supporting the hypothesis that peripheral vascular changes in hypertension may induce insulin resistance. The ability of losartan to preserve insulin sensitivity may explain the lower incidence of new onset diabetes in patients treated with losartan in the LIFE study.

The excess risk of hypertension in black Americans continues to be a major health concern. Although there is considerable information regarding these disease trends, much of the major underpinnings of the etiology of hypertension remain unclear. The excess mortality in blacks due to heart disease, renal failure, and stroke are clearly directly related to the excess burden of hypertension. Amid the recent findings about the pathophysiology of hypertension, some clear differences in the effects of overweight, salt sensitivity, and vascular biology emerge along ethnic lines. These differences may shed some light on the development of more effective treatment strategies. Based on our current knowledge, aggressive management of hypertension in blacks is critical. This review highlights what is known about various factors affecting hypertension and its treatment in black Americans.

Prehypertension, defined by Seventh Joint National Committee (JNC 7) as a blood pressure (BP) 120—139/80—89 mm Hg, was controversial. Approximately 31—37% of US adults are prehypertensive, and ∼12—14% have BP of 130—139/85—89 mm Hg or `Stage 2' prehypertension, is associated with ∼3-fold greater likelihood of developing hypertension and roughly twice the cardiovascular events than BP <120/80 mm Hg. Lifestyle change is the only intervention recommended for most prehypertensives. When fully implemented, lifestyle changes lower BP and prevent cardiovascular events, but evidence for community-wide effectiveness is limited. The Trial of Preventing Hypertension (TROPHY) documented that angiotensin receptor blockade safely lowers BP and prevents and/or delays hypertension in Stage 2 prehypertensives. Prehypertensives with diabetes or nephropathy are at high risk and should receive antihypertensive treatment according to JNC 7. Epidemiological data suggest that the number needed to treat to prevent a cardiovascular event in these at-risk Stage 2 prehypertensives is similar to Stage 1 hypertensives when both groups have one or more concomitant risk factors. Clinical trials are urgently needed to address this question. In the absence of clinical trials data, we believe it is prudent for the concerned clinician to consider initiating antihypertensive pharmacotherapy in selected Stage 2 prehypertensive patients at significant absolute risk for progression to hypertension and cardiovascular events. [ABSTRACT FROM PUBLISHER]

We have seen relationships between whole blood viscosity (WBV) and components of the metabolic cardiovascular syndrome in borderline hypertensive young men and suggested that sympathetic nervous system (SNS) activity may be a mediator. In the present study we aimed to test this hypothesis in established hypertension and to investigate the relationship between WBV and cardiac dimensions. Unmedicated patients (n = 42) with stage II-III hypertension and electrocardiographic left ventricular hypertrophy (LVH) underwent hyperinsulinemic isoglycemic glucose clamp to assess glucose disposal rate (GDR) and echocardiographic studies. WBV, plasma catecholamines and insulin were measured in arterialized venous blood. WBV at high shear rate correlated with baseline plasma adrenaline (r = 0.33, p = 0.04) and fasting insulin (r = 0.34, p = 0.04) while there was a negative trend for GDR (r = -0.21, p = 0.2). WBV at low shear rate correlated with plasma adrenaline (r = 0.49, p = 0.002) and resting heart rate (r = 0.36, p = 0.02). WBV was higher in smokers than in non-smokers (p = 0.02) and in males than in females (p = 0.02). Fasting insulin independently explained 12% of the variation in WBV at high shear, while baseline adrenaline independently explained 17% of the variation in WBV at low shear. Systolic blood pressure explained 31% of the variation in LV mass index. Thus, we demonstrate positive relationships between blood viscosity versus plasma adrenaline and fasting insulin in hypertensive patients with LVH. We suggest that adrenergic activity may increase hematocrit and viscosity and hence reduce insulin sensitivity. [ABSTRACT FROM AUTHOR]