Hg Reduction In Blood Pressure Research Articles

Economic Evaluation of Blood Pressure Monitoring Techniques in Patients With Hypertension

Blood pressure monitoring is critical to the timely diagnosis and treatment of hypertension. At-home self-monitoring techniques are highly effective in managing high blood pressure; however, evidence regarding the cost-effectiveness of at-home self-monitoring compared with traditional monitoring in clinical settings remains unclear. To identify and synthesize published research examining the cost-effectiveness of at-home blood pressure self-monitoring relative to monitoring in a clinical setting among patients with hypertension. A systematic literature search of 5 databases (PubMed, MEDLINE, Embase, EconLit, and CINAHL) followed by a backward citation search was conducted in September 2022. Full-text, peer-reviewed articles in English including patients with high blood pressure (systolic blood pressure ≥130 mm Hg and diastolic blood pressure ≥80 mm Hg) at baseline were included. Data from studies comparing at-home self-monitoring with clinical-setting monitoring alternatives were extracted, and the outcomes of interest included incremental cost-effectiveness and cost-utility ratios. Non-peer-reviewed studies or studies with pregnant women and children were excluded. To ensure accuracy and reliability, 2 authors independently evaluated all articles for eligibility and extracted relevant data from the selected articles. Of 1607 articles identified from 5 databases, 16 studies met the inclusion criteria. Most studies were conducted in the US (6 [40%]) and in the UK (6 [40%]), and almost all studies (14 [90%]) used a health care insurance system perspective to determine costs. Nearly half the studies used quality-adjusted life-years gained and cost per 1-mm Hg reduction in blood pressure as outcomes. Overall, at-home blood pressure monitoring (HBPM) was found to be more cost-effective than monitoring in a clinical setting, particularly over a minimum 10-year time horizon. Among studies comparing HBPM alone vs 24-hour ambulatory blood pressure monitoring (ABPM) or HBPM combined with additional support or team-based care, the latter were found to be more cost-effective. In this systematic review, at-home blood pressure self-monitoring, particularly using automatic 24-hour continuous blood pressure measurements or combined with additional support or team-based care, demonstrated the potential to be cost-effective long-term compared with care in the physical clinical setting and could thus be prioritized for patients with hypertension from a cost-effectiveness standpoint.

POSC165 Cost-Effectiveness Analysis of Free Anti-Hypertensive Medicines on Blood Pressure Among HIV Positive Patients at IDI

To determine the cost effectiveness of free anti-hypertensive drug intervention on HIV patients with hypertension. 1.To determine the impact of increased access to free-anti-hypertensive on median blood pressure. 2.To identify the factors associated with hypertension control among HIV patients receiving free-anti-hypertensive drugs. 3.To determine the cost per mm Hg reduction in blood pressure (BP).

Renal denervation in hypertension patients: Proceedings from an expert consensus roundtable cosponsored by SCAI and NKF.

Renal denervation in hypertension patients: Proceedings from an expert consensus roundtable cosponsored by SCAI and NKF.

Effect of Cystamine on Blood Pressure and Vascular Characteristics in Spontaneously Hypertensive Rats

Background: Tissue transglutaminase (t-TG) has been implicated in small artery remodelling. The aim of this study was to determine if cystamine, an inhibitor of t-TG, could reduce blood pressure in spontaneously hypertensive rats (SHR) and if so to what extent this is mediated through small arteries. Methods: In vitro inhibition of t-TG, with cystamine, was studied in organ culture and wire myograph setups in small mesenteric arteries obtained from SHR. In vivo treatment with cystamine (80 mg/kg/day) or amlodipine (10 mg/kg/day) was performed with osmotic pumps in adult SHR, and hemodynamic parameters determined with telemetry. Plasma concentrations of cystamine were determined with a liquid chromatography setup. Small arteries were harvested following administration of cystamine, and structural as well as functional characteristics were determined. Results: SHR small arteries showed inward remodelling following in vitro activation. Administration of cystamine caused attenuation of the inward remodelling induced by activation. In vivo administration of cystamine caused a 9 ± 2 mm Hg reduction in blood pressure, but with no detectable alterations in small artery structure. Conclusion: t-TG is potentially involved in vascular remodelling of SHR small arteries and results support a possible role for t-TG in blood pressure control.

Blood pressure-dependent and independent effects of amlodipine and angiotensin receptor blockers on the risk of stroke

Calcium channel blockers (CCBs) by the use of amlodipine substantially reduce the risk of stroke, and the benefit of initial treatment with this drug versus other antihypertensive drugs could be largely, though not entirely, explained by blood pressure differences between randomized groups of trials [1]. When contrasted with a long-acting CCB, amlodipine, angiotensin receptor blockers (ARBs) are less effective in lowering blood pressure and also demonstrate inferiority for the prevention of stroke [1]. It remains uncertain, however, whether mechanisms independent of blood pressure also affect the size of the treatment benefit, and there have been few formal attempts to investigate any such classand drug-specific effects. Using data from trials of amlodipine or ARBs that were included in recent meta-analyses [2,3], we conducted analyses to determine the relative contribution of blood-pressure-dependent and independent mechanisms to the reduction in risk of stroke produced by these drugs. Instead of comprehensive electronic and manual searches, we identified 10 and 17 odds ratios (ORs) for stroke from randomized controlled trials of amlodipine (77,093 individuals) and ARBs (104,360 individuals), respectively, from the comprehensive metaanalyses [2,3] (Table 1). We used sophisticated methods designed by the Blood Pressure Lowering Treatment Trialists’ Collaboration (BPLTTC) [4]. For each trial, the mean difference in follow-up systolic blood pressure levels between the randomized groups was sought. The association between the difference in follow-up systolic blood pressure levels and the log OR for stroke was investigated using random-effects meta-regression analysis with inverse variance weighting. Initially, using a single regression model, separate regression lines were fitted for trials in which amlodipine or ARBs were the treatment. The slopes of these lines were compared, so as to test for a differential effect of blood pressure reduction on risk in trials of amlodipine compared with ARBs. If these slopes were not significantly different (pN0.05), a parallel lines regression model was fitted, which assumes equal effects of blood pressure reduction with amlodipine and ARBs. Using this model, the null hypothesis of no separation between the 2 parallel lines was tested to explore whether there was evidence of a differential effect of amlodipine and ARBs independent of blood pressure lowering. Assumptions of linear associations between differences in follow-up blood pressure levels and log ORs were tested using standard graphical methods. Analyses were carried out using the metareg routine in STATA version 8.0 (Stata Corporation, College Station, Texas). In the single regression model, the association between the magnitude of reduction in blood pressure and the size of relative risk reduction were similar for amlodipine and ARBs (p=0.326). In the parallel lines regression model, treatment with amlodipine or ARBs achieved a 4.0% (95% confidence interval [CI]; 1.2% to 7.0%; p=0.007) reduction in the risk for each 1 mm Hg reduction in blood pressure (Fig. 1). At zero blood pressure reduction, the estimated relative risk reduction with amlodipine was 11.9% (95% CI, 4.4% to 18.7%; p=0.004). However, ARBs did not confer any additional protection beyond that conferred by blood pressure reduction alone. There was a significant difference between amlodipine and ARBs in terms of their likelihood of providing protection independent of blood pressure lowering (p=0.010), suggesting greater protection with amlodipine than ARBs. The size of blood pressure reduction achieved with amlodipine or ARBs was directly associated with the size of the reductions in the risk of stroke. In addition, although treatment with amlodipine provided an additional 11.9% relative risk reduction beyond that explained by the observed blood pressure differences, no such effect was observed for ARBs. This cerebroprotective effect of amlodipine was significantly greater than any such effect produced by ARBs. These findings extend those previously reported by Wang et al. [1], who plotted only 5 ORs for amlodipine trials and 5 ORs for ARB trials and performed meta-regression analyses separately for trials involving amlodipine and ARB groups. The present analyses provide much more reliable information about the blood pressure-dependent and independent effects of amlodipine and ARBs. The analyses included 10 ORs for amlodipine trials and 17 ORs for ARB trials and involved more sophisticated statistical methods (parallel lines regression model) specifically aimed at the identification of blood pressure-dependent and independent components of the treatment effects. For the risk of stroke, metaregression analyses by the BPLTTC [4] showed similar blood pressure-dependent effects of angiotensin-converting enzyme inhibitors and ARBs but no blood pressure-independent effects for both drug classes. Maximization of the benefit for stroke may be achieved with a regimen that includes amlodipine together with other drugs in an effort to optimize the size of the blood pressure reduction achieved. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology (Shewan and Coats 2010;144:1–2).

Weight Loss and Blood Pressure Control (Pro)

Overweight is an increasingly prevalent condition throughout the world. Current estimates, which are probably conservative, indicate that at least 500 000 000 people worldwide are overweight as defined by a body mass index (BMI) of between 25.0 and 29.9 and an additional 250 000 000 are obese with a BMI of 30.0 or higher.1 In the United States, recent data indicate that as much as 66% of the adult population is overweight or obese.2 Overweight and obesity are established risk factors for cardiovascular disease (CVD), stroke, noninsulin dependent diabetes (NIDDM), certain cancers, and numerous other disorders.3,4,5,6,7 It is also a risk factor for hypertension.8 Hypertension, defined as a systolic blood pressure in excess of 140 mm Hg or a diastolic blood pressure higher than 90 mm Hg, is also a globally increasing public health concern. Roughly 1 billion individuals worldwide are estimated to exhibit clinically significant elevated blood pressure with about 50 million of those residing in the United States.8 Hypertension, in turn, is associated with increased risk for CVD, stroke, renal disease, and all-cause mortality.9,10,11,12 The JNC VII report defines Stage 1 hypertension as blood pressure levels between 140 and 159 mm Hg systolic and 90 and 99 diastolic. Additionally, the report establishes a category of Prehypertension (Systolic blood pressure between 120 and 140 mm Hg or diastolic between 80 and 89 mm Hg). These 2 blood pressure classifications are deemed to be appropriate primary targets for lifestyle modification interventions, including weight loss. Higher levels of blood pressure, or stage 1 hypertension that is maintained over a long period, should be addressed primarily with medications or other physician directed treatments. There is a positive relationship between overweight or obesity and blood pressure and risk for hypertension. As early as the 1920s, a significant …

Effect of angiotensin receptor blockade and antihypertensive drugs on diastolic function in patients with hypertension and diastolic dysfunction: a randomised trial

Diastolic dysfunction might represent an important pathophysiological intermediate between hypertension and heart failure. Our aim was to determine whether inhibitors of the renin-angiotensin-aldosterone system, which can reduce ventricular hypertrophy and myocardial fibrosis, can improve diastolic function to a greater extent than can other antihypertensive agents. Patients with hypertension and evidence of diastolic dysfunction were randomly assigned to receive either the angiotensin receptor blocker valsartan (titrated to 320 mg once daily) or matched placebo. Patients in both groups also received concomitant antihypertensive agents that did not inhibit the renin-angiotensin system to reach targets of under 135 mm Hg systolic blood pressure and under 80 mm Hg diastolic blood pressure. The primary endpoint was change in diastolic relaxation velocity between baseline and 38 weeks as determined by tissue doppler imaging. Analyses were done by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00170924. 186 patients were randomly assigned to receive valsartan; 198 were randomly assigned to receive placebo. 43 patients were lost to follow-up or discontinued the assigned intervention. Over 38 weeks, there was a 12.8 (SD 17.2)/7.1 (9.9) mm Hg reduction in blood pressure in the valsartan group and a 9.7 (17.0)/5.5 (10.2) mm Hg reduction in the placebo group. The difference in blood pressure reduction between the two groups was not significant. Diastolic relaxation velocity increased by 0.60 (SD 1.4) cm/s from baseline in the valsartan group (p<0.0001) and 0.44 (1.4) cm/s from baseline in the placebo group (p<0.0001) by week 38. However, there was no significant difference in the change in diastolic relaxation velocity between the groups (p=0.29). Lowering blood pressure improves diastolic function irrespective of the type of antihypertensive agent used.

Analysis of Recent Papers in Hypertension Jan Basile, MD, Senior Editor

Analysis of Recent Papers in Hypertension Jan Basile, MD, Senior Editor

Myocardial PKC beta2 and the sensitivity of Na/K-ATPase to marinobufagenin are reduced by cicletanine in Dahl hypertension.

Marinobufagenin (MBG), an endogenous ligand of alpha-1 Na/K-ATPase, becomes elevated and contributes to hypertension in NaCl-loaded Dahl-S rats (DS). Protein kinase C (PKC) phosphorylates alpha-1 Na/K-ATPase and increases its MBG sensitivity. Cicletanine, an antihypertensive compound with PKC-inhibitory activity, reverses MBG-induced Na/K-ATPase inhibition and vasoconstriction. We hypothesized that increased PKC levels in sodium-loaded hypertensive DS would sensitize alpha-1 Na/K-ATPase to MBG and that PKC inhibition by cicletanine would produce an opposite effect. We studied the effects of cicletanine on systolic blood pressure, left ventricular PKC isoforms, cardiac alpha-1 Na/K-ATPase levels, and sensitivity to MBG in hypertensive DS. Seven DS received 50 mg x kg(-1) x d(-1) cicletanine, and 7 DS received vehicle during 4 weeks of an 8% NaCl diet. Vehicle-treated rats exhibited an increase in blood pressure, left ventricular mass, MBG excretion (74+/-11 vs 9+/-1 pmol/24 h, P<0.01), myocardial alpha-1 Na/K-ATPase protein, and PKC beta2 and delta. The sensitivity of Na/K-ATPase to MBG was enhanced at the level of high-affinity binding sites (IC50, 0.8 vs 4.4 nmol/L, P<0.01). Cicletanine-treated rats exhibited a 56-mm Hg reduction in blood pressure (P<0.01) and a 30% reduction in left ventricular weight, whereas cardiac alpha-1 Na/K-ATPase protein and MBG levels were unchanged. In cicletanine-treated rats, PKC beta2 was not increased, the sensitivity of Na/K-ATPase to MBG was decreased (IC50=20 micromol/L), and phorbol diacetate-induced alpha-1 Na/K-ATPase phosphorylation was reduced versus vehicle-treated rats. In vitro cicletanine treatment of sarcolemma from vehicle-treated rats also desensitized Na/K-ATPase to MBG, indicating that this effect was not solely attributable to a reduction in blood pressure. Thus, PKC-induced phosphorylation of cardiac alpha-1 Na/K-ATPase is a likely target for cicletanine treatment.

Nonpharmacologic Approaches to Therapy for Hypertension

To provide an overview of nondrug therapeutic modalities for management of hypertension. We review four strategies that involve lifestyle changes--weight reduction, moderation of sodium intake, physical activity, and moderation of alcohol consumption--that can potentially have a blood pressure-lowering effect. Several clinical trials have shown that a weight loss of 10 to 20% will significantly decrease blood pressure. An average of 1 to 2 mm Hg reduction in blood pressure may occur per kilogram of weight lost. Although sodium restriction has less effect on blood pressure than does weight reduction, a decrease in sodium intake to <100 mmol/day can yield a mean blood pressure reduction of 3 to 5 mm Hg systolic and 2 to 3 mm Hg diastolic. Exercise regimens have demonstrated convincing antihypertensive effects. In recent randomized studies, the average reduction in blood pressure ranged from 5 to 15 mm Hg for systolic measurements and 5 to 10 mm Hg for diastolic readings. Alcohol consumption has been shown to have one of the strongest associations with blood pressure among the potentially modifiable risk factors for hypertension. An average of 1 mm Hg decrease in blood pressure has been noted per one drink/day reduction in consumption. Lifestyle changes that can decrease blood pressure are important because they may not only eliminate the need for drug treatment but also decrease other cardiovascular risk factors.

Long-term Effects of Antihypertensive Agents on Proteinuria and Renal Function

Although many studies have examined the effects of antihypertensive agents on proteinuria and glomerular filtration rate in patients with kidney disease, many questions remain unresolved. These questions include whether the effects of agents differ, whether their effects are similar in diabetic and nondiabetic patients with renal disease, and whether the effects of any agents are independent of blood pressure reductions. We conducted a meta-analysis of studies obtained with MEDLINE and bibliographies from comprehensive reviews but included only investigations with follow-up times of at least 6 months. We combined data (1) in an analysis of randomized controlled trials, (2) in a separate univariate analysis of controlled and uncontrolled trials, and (3) using weighted multiple linear regression. In 14 randomized controlled trials, angiotensin-converting enzyme inhibitors caused a greater decrease in proteinuria (pooled mean [95% confidence intervals], -0.51[-0.68 to -0.35], ln [treatment/control]), improvement in glomerular filtration rate (0.13 mL/min per month [0.10 to 0.16 mL/min per month]), and decline in mean arterial pressure (-4.0 mm Hg [-4.9 to -3.0 mm Hg]) compared with controls. In a multivariate analysis of controlled and uncontrolled trials, each 10-mm Hg reduction in blood pressure decreased proteinuria (regression coefficient [95% confidence interval] -0.14 [-0.22 to -0.06] ln [after/before]), but angiotensin-converting enzyme inhibitors (-0.45 [-0.58 to -0.32]) and nondihydropyridine calcium antagonists (-0.38 [-0.70 to -0.06]) were associated with additional declines in proteinuria that were independent of blood pressure changes and diabetes. Each 10-mm Hg reduction in blood pressure caused a relative improvement in glomerular filtration rate (0.18 mL/min per month [0.04 to 0.31 mL/min per month]), but among diabetic patients there was a tendency for dihydropyridine calcium antagonists to cause a relative reduction in glomerular filtration rate (-0.68 mL/min per month [-1.31 to -0.04 mL/min per month]). Long-term beneficial effects of antihypertensive agents on proteinuria and glomerular filtration rate are proportional to blood pressure reductions and are similar in diabetic and nondiabetic patients with renal disease. In addition, angiotensin-converting enzyme inhibitors, and possibly nondihydropyridine calcium antagonists, have additional beneficial effects on proteinuria that are independent of blood pressure reductions.

Antihypertensive actions of the novel nonpeptide endothelin receptor antagonist SB 209670.

Indirect evidence has implicated endothelin-1 in the pathogenesis of hypertension. In the present study we examined such a role directly with SB 209670, a novel nonpeptide endothelin receptor antagonist. The antihypertensive and hemodynamic effects of SB 209670 were examined in conscious, unrestrained spontaneously hypertensive (SHR), normotensive Wistar-Kyoto (WKY), and renin-hypertensive rats. Sustained intravenous infusion of SB 209670 (10 micrograms.kg-1.min-1 for 6 hours) produced a significant, reversible reduction in mean arterial pressure in SHR but not in WKY rats. The antihypertensive response to 10 micrograms.kg-1.min-1 SB 209670 (approximately 25 mm Hg reduction in blood pressure) was associated with bradycardia (16% decrease in heart rate) but only a minimal reduction (3%) in cardiac output, because stroke volume was evaluated (by 15%). Therefore, the antihypertensive effect of SB 209670 resulted from a decrease (13%) in total peripheral resistance. A sustained antihypertensive effect could also be observed after intraduodenal administration of SB 209670 (3 mg/kg) in conscious SHR (reduction of approximately 35 mm Hg 5 hours after administration). SB 209670 (3 mg/kg intravenous bolus) did not alter the pressor response or tachycardia observed in pithed SHR after stimulation of thoracolumbar sympathetic outflow. SB 209670 was also antihypertensive in renin-hypertensive rats, lowering blood pressure to an extent similar to that observed in SHR. Thus, the data presented provide evidence to support a role for endothelin-1 in the pathophysiology of two animal models of hypertension.

Rostral ventrolateral medulla as a site for the central hypertensive action of kinins.

In the present study, we focused on the rostral ventrolateral medulla as a possible site of action for kinins because of its established importance in the central regulation of the cardiovascular system. Unilateral microinjections of 100 pmol to 4 nmol bradykinin into the rostral ventrolateral medulla produced dose-dependent increases in mean arterial pressure in Sprague-Dawley (SD) rats, Wistar-Kyoto (WKY) rats, and spontaneously hypertensive rats (SHR). The dose-response curves for the hypertensive responses to bradykinin in SD and WKY rats were essentially the same, whereas the hypertensive effect of bradykinin was significantly greater in SHR than in either SD or WKY rats. The kinin B2 receptor antagonists D-Arg0,Hyp3,Thi5,8,D-Phe7-bradykinin and Hoe 140 inhibited the hypertensive responses to bradykinin in both SHR and WKY rats. The hypertensive effect of 500 pmol bradykinin was reduced 65 +/- 5% after 4 nmol of D-Arg0, Hyp3,Thi5,8,D-Phe7-bradykinin in SHR and 50 +/- 16% in WKY rats, whereas 1 nmol Hoe 140 abolished the hypertensive effect of 500 pmol bradykinin injected into the rostral ventrolateral medulla. Microinjection of D-Arg0,Hyp3,Thi5,8,D-Phe7-bradykinin produced prolonged dose-dependent decreases in mean arterial pressure and heart rate. Blood pressure decreased 70 +/- 8 mm Hg and heart rate decreased 49 +/- 9 beats per minute in SHR, whereas in WKY rats mean arterial pressure decreased 12 +/- 4 mm Hg, with no change in heart rate. In a similar fashion, Hoe 140 caused a 51 +/- 7 and 17 +/- 3 mm Hg reduction in blood pressure in SHR and WKY rats, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Central and peripheral inhibition of angiotensin converting enzyme (ACE) in the SHR: correlation with the antihypertensive activity of ACE inhibitors.

A series of five structurally distinct ACE inhibitors were evaluated for their ability to inhibit tissue ACE activity in the SHR after oral administration. In the first series of experiments, the ACE inhibitors captopril, enalapril, pentopril, CGS 14824A and CGS 16617 were given to groups of SHR at doses that produced a 15 to 20 mm Hg reduction in blood pressure within 1 hour. Under these conditions of dose and time, only captopril significantly inhibited brain ACE activity (43%), whereas inhibition of serum ACE activity ranged from 72% to 99% with these agents. Inhibition of aortic ACE activity ranged from 54% to 87%, and lung ACE inhibition varied from 50% to 83%. In the second series of experiments, SHR were administered higher doses of each ACE inhibitor such that these compounds produced peak reductions in blood pressure (-25 mm Hg to -33 mm Hg) within a range of 2 to 6 hours. When tissue ACE activity was measured at the time corresponding to peak reduction in blood pressure, all five ACE inhibitors produced a significant inhibition of brain ACE activity ranging from 21% to 76%. Serum ACE activity was almost completely inhibited by these agents, with the exception of captopril (62% inhibition). The inhibition of aortic ACE activity ranged from 79% to 99%, while the inhibition of lung ACE activity did not increase under these conditions. These data suggest that ACE inhibitors may exert their maximal antihypertensive effects by inhibiting ACE in vascular tissues and brain.