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/m2 per bpm in both BP groups, while SVRI varied by about 0.03 and 0.01 mmHg.s.m2/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.
Windkessel (WK) models have often been used to simulate the arterial circulation. We studied a critical characteristic of WK function, the arterial pressure-decay constant tau, to test whether all arterial regions share the same WK characteristics, which should theoretically be related to arterial stiffness. We performed carotid and forearm arterial tonometry (Sphygmocor) and modeled arterial pressure (P) as A + (SBP − A)·exp[−(t − t0)/tau], where A = minimum pressure, SBP = systolic BP, t = time, t0 = start of decay). Model validity was supported by strong between-site correlations for t0 and A. We also measured central and peripheral Pulse Wave Velocity (PWV, Colin VP1000) and calculated arterial compliances (1/PWV2) in the heart-femoral (hf) and femoral-ankle (fa) regions. For the full cohort [n = 98, mean (SD): age 50 (20) years, weight 81 (17) kg, BP 135/77 (17/12) mmHg, 38% female], carotid and forearm taus were different [283 (126) vs. 199 (88) ms, p < 0.000] and uncorrelated (r2 = 0.01). Although hf and fa arterial compliances were well correlated (p < 0.000), neither was closely correlated with carotid or forearm tau (r2 < 0.06). In a subset (n = 22), carotid and brachial blood flow (Ultramark 9) were measured and regional WK compliances were calculated (= tau/regional resistance). Carotid blood flow [571 (216) vs. 117 (84) mL/min, p < 0.000] and WK compliance [0.031 (0.017) vs. 0.004 (0.004) mL/mmHg, p < 0.000] were much higher than corresponding forearm values. We conclude that: (1) tau and WK compliance are regional, not systemic indicators, (2) neither carotid nor forearm tau reflects large artery stiffness, and (3) a single WK model cannot adequately describe the arterial circulation.
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