{"id":"964f77456252","type":"article","url":"https://hartvaat.nl/2016/06/01/selectieve-hartfrequentieverlaging-met-ivabradine-verhoogt-centrale-bloeddruk-bi/","title":"Selectieve hartfrequentieverlaging met ivabradine verhoogt centrale bloeddruk bij stabiel coronairlijden","title_en":"Selective Heart Rate Reduction With Ivabradine Increases Central Blood Pressure in Stable Coronary Artery Disease.","category":"hypertensie","category_label":"Hypertensie","professions":["apotheker","cardioloog"],"tags":["aficamten","bloeddrukbehandeling","hfpef","hfref","ivabradine","stabiel-coronairlijden"],"journal":"Hypertension (Dallas, Tex. : 1979)","doi":"10.1161/HYPERTENSIONAHA.116.07250","source_url":"https://doi.org/10.1161/HYPERTENSIONAHA.116.07250","authors":["Stefano F Rimoldi","Franz H Messerli","David Cerny","Steffen Gloekler","Tobias Traupe","Stéphane Laurent","Christian Seiler"],"significance":6,"published":"2016-06-01","source_date":"2016-06-01","image":"","kennis":["https://hartvaat.nl/kennis/hypertensie/witte-jas-hypertensie/","https://hartvaat.nl/kennis/hypertensie/hypertensie-en-diabetes/"],"congress":"","summary_en":"This study showed that ivabradine paradoxically increases central blood pressure despite reducing heart rate in patients with stable coronary disease, raising questions about the hemodynamic consequences of selective heart rate reduction.","created":"2026-07-03T10:26:08Z","updated":"2026-07-03T13:25:29Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Studie die aantoonde dat ivabradine de centrale bloeddruk verhoogt bij stabiel coronairlijden, in tegenstelling tot de verwachte gunstige hemodynamische effecten. Klinisch relevante bevinding voor het ivabradinebeleid.","abstract_original":"Heart rate (HR) lowering by β-blockade was shown to be beneficial after myocardial infarction. In contrast, HR lowering with ivabradine was found to confer no benefits in 2 prospective randomized trials in patients with coronary artery disease. We hypothesized that this inefficacy could be in part related to ivabradine's effect on central (aortic) pressure. Our study included 46 patients with chronic stable coronary artery disease who were randomly allocated to placebo (n=23) or ivabradine (n=23) in a single-blinded fashion for 6 months. Concomitant baseline medication was continued unchanged throughout the study except for β-blockers, which were stopped during the study period. Central blood pressure and stroke volume were measured directly by left heart catheterization at baseline and after 6 months. For the determination of resting HR at baseline and at follow-up, 24-hour ECG monitoring was performed. Patients on ivabradine showed an increase of 11 mm Hg in central systolic pressure from 129±22 mm Hg to 140±26 mm Hg (P=0.02) and in stroke volume by 86±21.8 to 107.2±30.0 mL (P=0.002). In the placebo group, central systolic pressure and stroke volume remained unchanged. Estimates of myocardial oxygen consumption (HR×systolic pressure and time-tension index) remained unchanged with ivabradine.The decrease in HR from baseline to follow-up correlated with the concomitant increase in central systolic pressure (r=-0.41, P=0.009) and in stroke volume (r=-0.61, P<0.001). In conclusion, the decrease in HR with ivabradine was associated with an increase in central systolic pressure, which may have antagonized possible benefits of HR lowering in coronary artery disease patients. CLINICAL TRIALSURL: http://www.clinicaltrials.gov. Unique identifier NCT01039389."}