Effects of pacing modality on noninvasive assessment of heart rate dependency of indices of large artery function

Abstract

Studies investigating the relationship between heart rate (HR) and arterial stiffness or wave reflections have commonly induced HR changes through in situ cardiac pacing. Although pacing produces consistent HR changes, hemodynamics can be different with different pacing modalities. Whether the differences affect the HR relationship with arterial stiffness or wave reflections is unknown. In the present study, 48 subjects [mean age, 78 ± 10 (SD), 9 women] with in situ cardiac pacemakers were paced at 60, 70, 80, 90, and 100 beats per min under atrial, atrioventricular, or ventricular pacing. At each paced HR, brachial cuff-based pulse wave analysis was used to determine central hemodynamic parameters, including ejection duration (ED) and augmentation index (AIx). Wave separation analysis was used to determine wave reflection magnitude (RM) and reflection index (RI). Arterial stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV). Pacing modality was found to have significant effects on the HR relationship with ED (P = 0.01), central aortic pulse pressure (P = 0.01), augmentation pressure (P < 0.0001), and magnitudes of both forward and reflected waves (P = 0.05 and P = 0.003, respectively), but not cfPWV (P = 0.57) or AIx (P = 0.38). However, at a fixed HR, significant differences in pulse pressure amplification (P < 0.001), AIx (P < 0.0001), RM (P = 0.03), and RI (P = 0.03) were observed with different pacing modalities. These results demonstrate that although the HR relationships with arterial stiffness and systolic loading as measured by cfPWV and AIx were unaffected by pacing modality, it should still be taken into account for studies in which mixed pacing modalities are present, in particular, for wave reflection studies.

Ivabradine and endothelium: an update

“…Many previous studies have shown the interaction between HR, Ea, and arterial stiffness, both in animal models and in humans. 21–29 These data are consistent with ours, suggesting that blood vessels can adapt to increased mechanic wall stress changing their structure, benefitting from ivabradine-induced HR reduction, with a final improvement of Ea and VAC. According to previous evidence, the effect might be predominantly on the arterial system and less on LV end-systolic elastance (Ees).…”

Atenolol’s Inferior Ability to Reduce Central vs Peripheral Blood Pressure Can Be Explained by the Combination of Its Heart Rate-Dependent and Heart Rate-Independent Effects

“…Until the participant's HR remained over 40 bpm, the investigational drugs could exert their HR-lowering and other effects without any restriction by the pacemaker. e rationale of using the middle and high HR levels was to study drug effects in a situation where their pharmacological HR-lowering capacity had been nonpharmacologically eliminated by pacing, a relatively neutral method in hemodynamic terms, but the drugs' other effects, including HR-independent effects, on hemodynamics were preserved [16]. To our knowledge, elimination of BB-or ivabradine-induced HR reduction by pacing has only rarely been done earlier and for purposes different from ours [17][18][19].…”

Effect of increasing heart rate on finger photoplethysmography fitness index (PPGF) in subjects with implanted cardiac pacemakers

“…(iii) We did not take into account the effects of different types of pacing modalities to investigate effects of HR changes on PPGF. Previous studies found that atrial pacing (Ap), ventricular pacing (Vp) and sequential atrioventricular pacing (ApVp) have different impact on haemodynamic changes such as ejection duration and central pulse pressure, while no change for PWV and augmentation index [36]. Since the PPGF was also independently determined by PWV, it is suggested that changes in PPGF due to HR changes may not be so different between different types of pacing modalities.…”