Why the study?
The study was conducted to investigate the dynamic relationships among heart rate and systemic hemodynamics in everyday life.
Does heart rate correlate with systemic blood pressure, stroke volume index, and systemic vascular resistance index in individuals with normal and elevated blood pressure?
Does heart rate correlate with systemic blood pressure, stroke volume index, and systemic vascular resistance index in individuals with normal and elevated blood pressure?
Heart rate is decoupled from blood pressure through continuous counter-regulation of stroke volume and systemic vascular resistance, suggesting hemodynamic measurements should be corrected for heart rate.
May support HR correction in hemodynamic assessments; hypothesis-generating for BP counter-regulation mechanisms.
To investigate the dynamic relationships among Heart Rate (HR) and systemic hemodynamics in everyday life, we performed 24-h ambulatory pulse wave analyses (Mobil-O-Graph) in individuals with normal and elevated BP ( n = 116) and in a double-blinded cross-over study where HR was varied pharmacologically ( n = 24). In the whole cohort and in the low [24-h mean Systolic BP (SBP) < 135 mmHg] and high (SBP ≥ 135 mmHg) groups, mean HR did not correlate with mean SBP but did correlate strongly and negatively with Stroke Volume Index (SVI) and Systemic Vascular Resistance Index (SVRI) over 24 h and during night-time and daytime periods (all p < 0.000). SVI varied by about 0.2 mL/m 2 per bpm in both BP groups, while SVRI varied by about 0.03 and 0.01 mmHg.s.m 2 /mL per bpm in the high and low BP groups, respectively, p < 0.001). On stepwise multiple linear regression, there was greater sensitivity of SVI to HR in Blacks and younger individuals, and greater sensitivity of SVRI to HR with age in addition to higher SBP. In a crossover study (monotherapy for 1 month each with nebivolol or valsartan), BP was constant throughout, while SVI and SVRI varied inversely with HR as in the main cohort with similar intercepts and coefficients; the regression equations on either drug predicted the same SVI or SVRI at HR of 70 bpm. We conclude that the decoupling of BP from HR is facilitated by the continuous counter-regulation of SVI and SVRI against HR and that HR is the primary hemodynamic setpoint. These findings have implications for pathogenetic studies and imply that hemodynamic measurements should be corrected for HR.
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Izzo et al. (2019) studied this question.
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