Angiotensin, inflammation, hypertension, and cardiovascular disease

Luft, Friedrich C.

doi:10.1007/s11906-001-0082-y

Cited by 48 publications

(30 citation statements)

References 54 publications

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“…28 In patients with T2DM and albuminuria, overactivation of the RAS occurs and angiotensin II mediates a number of effects from increased collagen synthesis to proliferation of smooth muscle cells, arterial wall fibrosis, accumulation and activation of inflammatory cells, and increased vascular permeability, which result in premature vascular and renal complications. 42 We confirmed in this study our previous observation that, as monotherapy, valsartan results in a significantly greater reduction in albuminuria than that obtained by amlodipine despite similar brachial BP lowering effects in T2DM. 2 We found no relationship between the change in arterial stiffness and the reduction in albuminuria with valsartan, suggesting that blockade of the AT 1 receptor affects these 2 variables through different mechanisms.…”

Section: Discussionsupporting

confidence: 90%

Valsartan Improves Arterial Stiffness in Type 2 Diabetes Independently of Blood Pressure Lowering

Smith²,

et al. 2008

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Abstract-Increased arterial stiffness, as estimated from aortic pulse wave velocity (Ao-PWV), and albuminuria are independent predictors for cardiovascular disease in type 2 diabetes mellitus (T2DM). Whether angiotensin receptor blockers (ARBs), drugs with cardio-renal protective effects, improve Ao-PWV to a greater extent than other equipotent antihypertensive medications remains unclear. After a 4-week washout phase, we compared the effects of valsartan (nϭ66), an ARB, with that of amlodipine (nϭ65), a calcium channel blocker on Ao-PWV in 131 T2DM patients with pulse pressure (PP) Ն60 mm Hg and raised albumin excretion rate (AER) in a 24-week randomized, double-blind, parallel group study. Hydrochlorothiazide (HCTZ) 25 mg/d was added to valsartan 160 mg and amlodipine 5 mg/od uptitrated to 10 mg/od after 4 weeks to ensure equivalent BP control. After 24 weeks brachial and central aortic PP had fallen to a similar extent with attained mean (SD) brachial and central PP of 61.6 (13.6) and 47.3 (14.1) mm Hg in the valsartan/HCTZ group and 61.5 (12.2) and 47.3 (9.9) mm Hg in the amlodipine group, respectively. Ao-PWV showed a significantly greater reduction, mean (95% CI), Ϫ0.9 m/s (Ϫ1.4 to Ϫ0.3) for valsartan/HCTZ compared to amlodipine (Pϭ0.002). AER fell significantly only with Val/HCTZ from 30.8(20.4, 46.5) to 18.2(12.5, 26.3) mcg/min, (Pϭ0.01) with between treatment difference in favor of Val/HCTZ of Ϫ15.3mcg/min (PϽ0.001). Changes in AER and Ao-PWV were not correlated. Valsartan/HCTZ improves arterial stiffness and AER to a significantly greater extent than amlodipine despite similar central and brachial BP control. These 2 effects, which appear independent of each other, may explain the specific cardio-renal protective properties of ARBs. Key Words: type 2 diabetes Ⅲ hypertension Ⅲ arterial stiffness Ⅲ albuminuria Ⅲ angiotensin receptor blockers C ardiovascular disease (CVD) is the main cause of death in patients with type 2 diabetes mellitus (T2DM). 1 In T2DM angiotensin type 1 (AT 1 ) receptor blockers (ARB) reduce albumin excretion and prevent the progression of diabetic renal disease, 2,3 and inhibition of the renin angiotensin system (RAS) may also provide cardio-protective benefits. 4,5 These effects would appear independent of the brachial blood pressure lowering action of these drugs. [2][3][4][5] However, some authors have questioned whether antihypertensive drugs offer cardio-renal protection beyond blood pressure lowering. 6,7 In T2DM systolic hypertension is often associated with albuminuria, and both are strong predictors of CVD mortality and morbidity and progressive renal failure. 8 Recent evidence indicates that increased arterial stiffness, involving accelerated vascular aging of the aorta, is a powerful and independent risk factor for early mortality and provides prognostic information above and beyond traditional CVD risk factors such as blood pressure itself, age, gender, diabetes, smoking, and cholesterol. 9,10 As arterial stiffness is the principal determinant of pulse pressure (PP), a...

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Section: Discussionsupporting

confidence: 90%

Valsartan Improves Arterial Stiffness in Type 2 Diabetes Independently of Blood Pressure Lowering

Smith²,

et al. 2008

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“…Inflammation has been linked to both calcific valvular disease 15 and to hypertension. 16 However, even in patients without valvular disease, atrial arrhythmias were independently predictive of CRP elevation after adjusting for hypertension.…”

Section: Discussionmentioning

confidence: 97%

C-Reactive Protein Elevation in Patients With Atrial Arrhythmias

et al. 2001

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Background-Atrial fibrillation (AF) may persist due to structural changes in the atria that are promoted by inflammation.C-reactive protein (CRP), a marker of systemic inflammation, predicts cardiovascular events and stroke, a common sequela of AF. We hypothesized that CRP is elevated in patients with atrial arrhythmias. Methods and Results-Using a case-control study design, CRP in 131 patients with atrial arrhythmias was compared with CRP in 71 control patients. Among arrhythmia patients, 6 had frequent atrial ectopy or tachycardia, 86 had paroxysmal AF, 39 had persistent AF lasting Ͼ30 days, and 70 had lone arrhythmias. CRP was higher in arrhythmia than in control patients (median, 0.21 versus 0.096 mg/dL; PϽ0.001). Arrhythmia patients in AF within 24 hours before sampling had higher CRP than those in sinus rhythm (0.30 versus 0.15 mg/dL; PϽ0.001). CRP in controls was not different than in patients with atrial ectopy or tachycardia. Lone arrhythmia patients had a CRP of 0.21 mg/dL, which was not significantly lower than arrhythmia patients with structural heart disease (CRP, 0.23 mg/dL) but higher than controls (Pϭ0.002). Persistent AF patients had a higher CRP (0.34 mg/dL) than paroxysmal AF patients (0.18 mg/dL; Pϭ0.008); both groups had higher CRP levels than controls (PՅ0.005). Conclusions-CRP is elevated in AF patients. This study is the first to document elevated CRP in non-postoperative arrhythmia patients. These findings are reinforced by stepwise CRP elevation with higher AF burden. Although the cause of elevated CRP levels in AF patients remains unknown, elevated CRP may reflect an inflammatory state that promotes the persistence of AF.

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“…12 In our study, valsartan and ramipril reduced the levels of IL-6 and IL-8 during hemodialysis. Angiotensin II stimulates IL-6 production and release [31][32][33] ; therefore, ramipril and valsartan have likely reduced IL-6 by preventing the formation or action of angiotensin II. The finding that ramipril treatment increased levels of IL-1b and decreased IL-10, an anti-inflammatory cytokine, however, suggests that ramipril had an additional proinflammatory effect.…”

Section: Discussionmentioning

confidence: 99%

Comparative Effects of Angiotensin-Converting Enzyme Inhibition and Angiotensin-Receptor Blockade on Inflammation during Hemodialysis

Gamboa¹,

Pretorius²,

Todd-Tzanetos³

et al. 2012

Journal of the American Society of Nephrology

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Biomarkers of oxidative stress and inflammation predict cardiovascular events in maintenance hemodialysis patients. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) reduce cardiovascular mortality in the general population, but their benefit in maintenance hemodialysis patients is not fully explored. To test whether ACE inhibitors and ARBs differentially affect markers of oxidative stress, inflammation, and fibrinolysis during hemodialysis, we conducted a randomized, doubleblind, placebo-controlled 333 crossover study. We randomly assigned 15 participants undergoing hemodialysis to placebo, ramipril (5 mg/d), and valsartan (160 mg/d) for 7 days, with a washout period of 3 weeks in between the treatments. On the morning of the seventh day of drug treatment, participants underwent serial blood sampling during hemodialysis. Neither ramipril nor valsartan affected BP during hemodialysis. Ramipril increased IL-1b concentrations (P=0.02) and decreased IL-10 concentrations (P=0.04) compared with placebo. Valsartan and ramipril both lowered IL-6 levels during dialysis (P,0.01 for each compared with placebo). Valsartan increased F 2 -isoprostane levels, and ramipril suggested a similar trend (P=0.09). Valsartan and ramipril both lowered D-dimer levels (P,0.01 for both), whereas only ramipril seemed to prevent a rise in vWf levels (P=0.04). In summary, during hemodialysis, valsartan induces a greater anti-inflammatory effect compared with ramipril, although ramipril seems to prevent dialysis-induced endothelial dysfunction as measured by levels of vWf. A prospective clinical trial is necessary to determine whether ACE inhibitors and ARBs also differ with respect to their effects on cardiovascular mortality in this population. 23: 334-342, 201223: 334-342, . doi: 10.1681 In ESRD patients, cardiovascular death accounts for .50% of overall mortality and the risk of cardiovascular death is 30 times higher than in the general population. 1,2 Moreover, patients undergoing maintenance hemodialysis (MHD) have a 5-year survival rate of 10% after acute myocardial infarction. 3 Traditional risk factors, as used in Framingham risk scoring, only explain half of the excessive cardiovascular mortality observed in ESRD patients, 4 and it is thought that other factors contribute to the high cardiovascular mortality among ESRD patients. J Am Soc NephrolIncreased oxidative stress and inflammation may contribute to accelerated atherosclerosis and cardiovascular events in patients with MHD. 5,6 Markers of oxidative stress, such as F 2 -isoprostanes, are increased in MHD patients. 7,8 Inflammatory markers, particularly IL-1, IL 6, and TNFa, are also elevated in MHD patients and are associated with

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Angiotensin, inflammation, hypertension, and cardiovascular disease

Cited by 48 publications

References 54 publications

Valsartan Improves Arterial Stiffness in Type 2 Diabetes Independently of Blood Pressure Lowering

Valsartan Improves Arterial Stiffness in Type 2 Diabetes Independently of Blood Pressure Lowering

C-Reactive Protein Elevation in Patients With Atrial Arrhythmias

Comparative Effects of Angiotensin-Converting Enzyme Inhibition and Angiotensin-Receptor Blockade on Inflammation during Hemodialysis

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