Acute, sympathetic-independent increases in heart rate by way of cardiac pacing raises aortic and brachial blood pressure with increased cardiac output and arterial stiffness

Objective. Whilst the effects of heart rate (HR) on the cardiovascular system have been studied cross-sectionally or during exercise, the effect of acute, sympathetic-independent changes in HR on arterial stiffness, cardiac output (CO), mean pressure (MAP) and total peripheral resistance (TPR) has not previously been studied.

Methods. Sixteen subjects (aged 70 to 79 years, 3 female) with in situ permanent cardiac pacemakers or implantable cardioverter defibrillators were studied. Each subject was paced in a random order at 60 to 100 beats per minute (bpm) in 10 bpm increments. At each heart rate, TPR and CO were derived from measured finger arterial pressure waveform (Finometer®). Brachial (b) and central aortic (c) systolic (SBP), diastolic (DBP), MAP, and aortic augmentation index (AIx) were determined by brachial cuff-based pulse wave analysis, and carotid-femoral pulse wave velocity (PWV) measured using a thigh cuff and carotid tonometry (SphygmoCor® XCEL). Aortic to brachial pulse pressure amplification (PPA) was calculated.

Results. All parameters except for TPR and cSBP changed significantly with HR (Table, data presented as mean ± sem). This indicated that HR-driven changes in MAP were due to increased CO, not changes in TPR. PWV showed an increase with increasing HR. However, this was not significant once corrected for changes in MAP (PWVc, Table).

Conclusion. Acute, sympathetic-independent increases in HR through cardiac pacing raises CO, which in turn increases MAP and results in increased arterial stiffness.