A prospective, randomized, open-label, active-controlled, clinical trial to assess central haemodynamic effects of bisoprolol and atenolol in hypertensive patients

Park, Sungha; Rhee, Moo Yong; Lee, Sung Yun; Park, Seung Woo; Jeon, Dongwoon; Kim, Byung‐Wook; Kwan, Jun; Choi, Donghoon

doi:10.1097/hjh.0b013e32835e8f5b

Cited by 18 publications

(11 citation statements)

References 21 publications

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“…18,19 However, recently the X-CELLENT study was unable to show different central and peripheral blood pressure effects by indapamid, candesartan, and amlodipine, 20 as did the CHAMPION trial comparing beta-blockers with different receptor affinities. 21 Thus, some, but not all, antihypertensive medications may exert different effects on central and brachial blood pressure. Another important issue is whether central and brachial blood pressure reductions are equally important for prevention of adverse events.…”

Section: Discussionmentioning

confidence: 99%

Central Hemodynamics Are Associated With Cardiovascular Disease and Albuminuria in Type 1 Diabetes

Theilade

Hansen

Rossing

2014

American Journal of Hypertension

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backgroundWe sought to investigate associations between central hemodynamic parameters (estimated from radial pulse wave analyses (PWAs)), cardiovascular disease (CVD), and albuminuria in type 1 diabetes. methodsWe conducted an observational study of 636 type 1 diabetes patients. Central hemodynamics were measured by PWA as central aortic systolic pressure (CASP), central aortic pulse pressure (CPP), central aortic diastolic pressure (CADP), and subendocardial viability ratio (SEVR). CVD included revascularization, myocardial infarction, peripheral arterial disease, and stroke. Albuminuria was urinary albumin excretion rate ≥30 mg/24 hours. We computed standardized odds ratios (ORs) adjusted for sex, age, mean arterial pressure (MAP), heart rate, height, estimated glomerular filtration rate, glycated hemoglobin (HbA 1c ) total cholesterol, antihypertensive medication, and smoking. At follow-up, development of end-stage renal disease (ESRD) and mortality was traced through electronic medical records. resultsPatients were aged a mean of 54 ± 13 years, and 289 (45%) were women. The mean ± SD was 118 ± 17 mm Hg for CASP, 75 ± 10 mm Hg for CADP, 43 ± 14 mm Hg for CPP, and 150 ± 32 for SEVR. In fully adjusted models, increased CASP and CPP and decreased CADP and SEVR were associated with presence of CVD (n = 132; P ≤ 0.02) and presence of albuminuria (n = 335; P < 0.001). During follow-up, median (range) (2.8 (0.7-3.8) years), SEVR predicted ESRD or mortality combined (n = 26) after adjustment for sex, age, and MAP (P = 0.001), whereas CASP, CPP, and CADP did not (P ≥ 0.13). conclusionsIn type 1 diabetes patients, increased CASP and CPP and decreased CADP and SEVR were independently associated with history of CVD and albuminuria. Furthermore, SEVR predicted mortality and ESRD during follow-up. Future studies are needed to determine whether targeting central hemodynamics improves outcome.

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Section: Discussionmentioning

confidence: 99%

Central Hemodynamics Are Associated With Cardiovascular Disease and Albuminuria in Type 1 Diabetes

Theilade

Hansen

Rossing

2014

American Journal of Hypertension

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“…Conflicting results regarding the effect of beta‐blockers on central BP have been published: a decrease in central systolic pressure and pulse pressure , a decrease in central systolic and diastolic but not pulse pressure and a decrease in central diastolic pressure have been reported. The results on the effects of non‐vasodilating beta‐blockers on pulse wave velocity (PWV), a marker of arterial stiffness, have also been controversial.…”

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confidence: 99%

Haemodynamic Influences of Bisoprolol in Hypertensive Middle‐Aged Men: A Double‐Blind, Randomized, Placebo‐Controlled Cross‐Over Study

Suojanen

Haring

Tikkakoski

et al. 2017

Basic Clin Pharma Tox

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Treatment with beta-blockers appears to show inferior reduction in central versus peripheral blood pressure. We aimed to examine simultaneous changes in central and peripheral blood pressure, vascular resistance, cardiac function and arterial stiffness during beta-blockade. Haemodynamics were investigated after 3 weeks of bisoprolol treatment (5 mg/day) in a double-blind, randomized, placebo-controlled cross-over trial in never-treated 16 Caucasian males with grade I-II primary hypertension using continuous tonometric pulse wave analysis and whole-body impedance cardiography. Bisoprolol decreased radial (134/80 versus 144/89 mmHg) and aortic blood pressure (122/80 versus 130/90 mmHg) and heart rate (57 versus 68 beats/min) when compared with placebo (p < 0.05 for all). Ejection duration (336 versus 316 ms) and stroke volume (109 versus 98 ml) were increased (p < 0.01 for all), while cardiac output was not significantly changed (6.2 versus 6.6 l/min). Bisoprolol decreased pulse wave velocity (7.8 versus 8.9 m/s, p < 0.001), but after adjustment for blood pressure, the decrease was not significant (8.16 versus 8.52 m/s, p = 0.464). The treatment reduced pulse pressure amplification from central to peripheral circulation (30 versus 38%, p = 0.002). No differences were observed in systemic vascular resistance, augmentation index, aortic characteristic impedance or total arterial stiffness after bisoprolol versus placebo. Bisoprolol decreased central and peripheral blood pressure and pulse wave velocity in male individuals with grade I to grade II hypertension. The decrease in pulse wave velocity was related to the antihypertensive effect. Reduced pulse pressure amplification indicates that peripheral blood pressure was reduced more efficiently than central blood pressure.

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“…It is important to recognize that although the patients recruited in GENRES were similar to those in PEAR in terms of having mild-to-moderate hypertension and of similar age and baseline BP, there were two significant differences between these two studies. The β-blocker used in GENRES was bisoprolol 5 mg/day, which is considered equivalent to atenolol 50 mg/day [18]. This is half the dose that was used in PEAR participants.…”

Section: Discussionmentioning

confidence: 99%

PTPRD gene associated with blood pressure response to atenolol and resistant hypertension

Gong

McDonough

Beitelshees

et al. 2015

Journal of Hypertension

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Objective The aim of this study is to identify single-nucleotide polymorphisms (SNPs) influencing blood pressure (BP) response to the β-blocker atenolol. Methods Genome-wide association analysis of BP response to atenolol monotherapy was performed in 233 white participants with uncomplicated hypertension in the pharmacogenomic evaluation of antihypertensive responses study. Forty-two polymorphisms with P less than 10−5 for association with either diastolic or systolic response to atenolol monotherapy were validated in four independent groups of hypertensive individuals (total n = 2114). Results In whites, two polymorphisms near the gene PTPRD (rs12346562 and rs1104514) were associated with DBP response to atenolol (P = 3.2 × 10−6 and P = 5.9 × 10−6, respectively) with directionally opposite association for response to hydrochlorothiazide in another group of 228 whites (P = 0.0018 and P = 0.00012). A different polymorphism (rs10739150) near PTPRD was associated with response to atenolol in 150 black hypertensive individuals (P = 8.25 ×10−6). rs12346562 had a similar trend in association with response to bisoprolol (a different β-blocker) in 207 Finnish men in the genetics of drug responsiveness in essential hypertension study. In addition, an intronic single-nucleotide polymorphism (rs4742610) in the PTPRD gene was associated with resistant hypertension in whites and Hispanics in the international verapamil SR trandolapril study (meta-analysis P = 3.2 × 10−5). Conclusion PTPRD was identified as a novel locus potentially associated with BP response to atenolol and resistant hypertension in multiple ethnic groups.

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A prospective, randomized, open-label, active-controlled, clinical trial to assess central haemodynamic effects of bisoprolol and atenolol in hypertensive patients

Abstract: In this study, there was no significant difference between bisoprolol and atenolol in terms of reduction of aortic pulse pressure after 12 weeks of treatment.

Cited by 18 publications

References 21 publications

Central Hemodynamics Are Associated With Cardiovascular Disease and Albuminuria in Type 1 Diabetes

Central Hemodynamics Are Associated With Cardiovascular Disease and Albuminuria in Type 1 Diabetes

Haemodynamic Influences of Bisoprolol in Hypertensive Middle‐Aged Men: A Double‐Blind, Randomized, Placebo‐Controlled Cross‐Over Study

PTPRD gene associated with blood pressure response to atenolol and resistant hypertension

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