Adverse influence of bisoprolol on central blood pressure in the upright position: a double-blind placebo-controlled cross-over study

Suojanen, Lauri; Haring, Antti; Tikkakoski, Antti; Huhtala, Heini; Kähönen, Mika; Eräranta, Arttu; Mustonen, Jukka; Pörsti, Ilkka

doi:10.1038/s41371-019-0188-9

Cited by 7 publications

(19 citation statements)

References 41 publications

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“…The PA group presented with the typical characteristics of aldosterone excess [3], and only four PA patients and seven EH patients were taking spironolactone during the recordings. In addition to age, BMI, sex, plasma lipids and glucose, the medicated groups were matched for the use of beta adrenoceptor blockers, as this class drugs interferes with both cardiac function and regulation of systemic vascular resistance [35]. Figure 1, except that in extracellular water analyses, BMI was replaced with lean body mass, and in PWV analyses, the results were also adjusted for mean aortic blood pressure; *P < 0.05, **P < 0.01, ***P < 0.001 In separate previous reports, PA has been associated with increased ECW volume [5,6], increased cardiac output [36] and increased large arterial stiffness [9,10,37] (see Supplementary Table S1 for a summary of haemodynamic findings in PA).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Primary aldosteronism: Higher volume load, cardiac output and arterial stiffness than in essential hypertension

et al. 2020

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Background. The diagnostics of primary aldosteronism (PA) are usually carried out in patients taking antihypertensive medications. We compared haemodynamics between medicated PA, medicated essential hypertension (EH), never-medicated EH and normotensive controls (n = 130 in all groups). Methods. The hypertensive groups were matched for age (53 years), sex (84 male/46 female) and body mass index (BMI) (30 kg m À2); normotensive controls had similar sex distribution (age 48 years, BMI 27 kg m À2). Haemodynamics were recorded using whole-body impedance cardiography and radial pulse wave analysis, and the results were adjusted as appropriate. Radial blood pressure recordings were calibrated by brachial blood pressure measurements from the contralateral arm. Results. Radial and aortic systolic and diastolic blood pressure was similar in PA and never-medicated EH, and higher than in medicated EH and normotensive controls (P ≤ 0.001 for all comparisons). Extracellular water balance was~4% higher in PA than in all other groups (P < 0.05 for all), whilst cardiac output was~8% higher in PA than in medicated EH (P = 0.012). Systemic vascular resistance and augmentation index were similarly increased in PA and both EH groups when compared with controls. Pulse wave velocity was higher in PA and never-medicated EH than in medicated EH and normotensive controls (P ≤ 0.033 for all comparisons). Conclusions. Medicated PA patients presented with corresponding systemic vascular resistance and wave reflection, but higher extracellular water volume, cardiac output and arterial stiffness than medicated EH patients. Whether the systematic evaluation of these features would benefit the clinical diagnostics of PA remains to be studied in future.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Primary aldosteronism: Higher volume load, cardiac output and arterial stiffness than in essential hypertension

et al. 2020

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“…Это можно объяснить тем, что у лиц с повышенной жесткостью сосудов бисопролол, вызывая снижение ЧСС, удлиняет обе фазы сердечного цикла, способствует наложению центральной и отраженной пульсовых волн непосредственно перед окончанием систолы. Все это приводит к повышению цПД и оказывает неблагоприятное влияние на коронарный кровоток [5,7]. Ивабрадин, напротив, обладая сопоставимым с бисопрололом пульсурежающим эффектом, в меньшей степени влияет на продолжительность систолы, что способствует сдвигу времени наложения пульсовых волн в сторону диастолы и, соответственно, уменьшению ПД в аорте [4,19,26].…”

Section: Discussionunclassified

“…Ивабрадин, напротив, обладая сопоставимым с бисопрололом пульсурежающим эффектом, в меньшей степени влияет на продолжительность систолы, что способствует сдвигу времени наложения пульсовых волн в сторону диастолы и, соответственно, уменьшению ПД в аорте [4,19,26]. Полученные данные согласуются с выводами не давно завершившегося в Финляндии двойного слепого перекрестного исследования (2019), свидетельствующего о негативном влиянии бисопролола на параметры цПД у пациентов с начальными стадиями АГ [5].…”

Section: Discussionunclassified

“…Увеличение ЧСС рассматривают в качестве независимого предиктора неблагоприятного прогноза у больных артериальной гипертензией (АГ), ишемической болезнью сердца (ИБС) и хронической сердечной недостаточностью (ХСН) [4]. В связи с этим, представляет интерес изучение клинической эффективности бета-адреноблокаторов (β-АБ), уменьшающих ЧСС, риск повторного инфаркта миокарда, инсульта, сердечно-сосудистой смерти и смерти от любых причин [4,5].…”

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Heart rate-lowering therapy in gout patients with stable coronary artery disease: focus on ivabradine

Kushnarenko¹,

Александровна²,

Мишко³

et al. 2020

Russ J Cardiol

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Aim. To study the effect of ivabradine and bisoprolol on cardiac hemodynamics and diastolic remodeling in gout patients with coronary artery disease and hypertension and without left ventricular systolic dysfunction.Material and methods. The open randomized parallel clinical trial of 35 men with intercritical gout at the age of 41,4±3,3 years, with class II-III stable angina, hypertension and sinus rhythm without data suggestive of heart failure was performed. All patients included in the study were randomly divided into two groups: eighteen patients took bisoprolol at a dose of 2,5 to 10 mg/day, 17 subjects received bisoprolol 2,5 mg/day with ivabradine (Coraxan, SERVIER, France) 5 mg 2 times a day. Adjustment of the therapy was carried out every 2 weeks until the target heart rate (HR) was reached at 55-60 beats/min and then remained unchanged until 12 weeks of therapy. All patients underwent echocardiography, 24-hour Holter and central aortic blood pressure monitoring, and 3-minute cycle ergometer test with a power of 25, 50, 75 and 100 watts.Results. There was a comparable decrease in the maximum and minimum 24-hour average heart rates in patients receiving only bisoprolol and those taking bisoprolol+ivabradine. Patients taking bisoprolol+ivabradine had a decrease of central systolic and diastolic blood pressure (BP). Pulse pressure in the bisoprolol group increased by 17,7% (p=0,02), and when ivabradine was added, on the contrary, it decreased by 7,0% (p=0,04). Twelve-week therapy with beta-blockers and ivabradine was accompanied by an effective decrease in the pulse wave velocity in both groups (p<0,05). All gout patients did not have a decrease of systolic function and there was an improvement in diastolic remodeling with beta-blockers and ivabradine therapy.Conclusion. The results obtained indicate that the addition of ivabradine to bisoprolol leads to an effective decrease in heart rate, an improvement in arterial stiffness and exercise tolerance. Combination therapy with ivabradine is accompanied by an improvement in clinical outcomes using lower doses of bet-blockers, which requires further study and a double-blind controlled study.

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Individual changes of central blood pressure in response to upright posture: different hemodynamic phenotypes

Suojanen

Koskela

Wilenius

et al. 2021

Journal of Hypertension

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Objectives: Most studies about upright regulation of blood pressure have focused on orthostatic hypotension despite the diverse hemodynamic changes induced by orthostatic challenge. We investigated the effect of passive head-up tilt on aortic blood pressure.Methods: Noninvasive peripheral and central hemodynamics in 613 volunteers without cardiovascular morbidities or medications were examined using pulse wave analysis, whole-body impedance cardiography and heart rate variability analysis.Results: In all participants, mean aortic SBP decreased by À4 (À5 to À3) mmHg [mean (95% confidence intervals)] and DBP increased by 6 (5-6) mmHg in response to upright posture. When divided into tertiles according to the supineto-upright change in aortic SBP, two tertiles presented with a decrease [À15 (À14 to À16) and À4 (À3 to À4) mmHg, respectively] whereas one tertile presented with an increase [R7 (7-8) mmHg] in aortic SBP. There were no major differences in demographic characteristics between the tertiles. In regression analysis, the strongest explanatory factors for upright changes in aortic SBP were the supine values of, and upright changes in systemic vascular resistance and cardiac output, and supine aortic SBP. Conclusion:In participants without cardiovascular disease, the changes in central SBP during orthostatic challenge are not uniform. One-third presented with higher upright than supine aortic SBP with underlying differences in the regulation of systemic vascular resistance and cardiac output. These findings emphasize that resting blood pressure measurements give only limited information about the blood pressure status.

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Adverse influence of bisoprolol on central blood pressure in the upright position: a double-blind placebo-controlled cross-over study

Cited by 7 publications

References 41 publications

Primary aldosteronism: Higher volume load, cardiac output and arterial stiffness than in essential hypertension

Primary aldosteronism: Higher volume load, cardiac output and arterial stiffness than in essential hypertension

Heart rate-lowering therapy in gout patients with stable coronary artery disease: focus on ivabradine

Individual changes of central blood pressure in response to upright posture: different hemodynamic phenotypes

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