The human sympathetic nervous system: its relevance in hypertension and heart failure

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Analysis and Interpretation of 24-h Blood Pressure Profiles: Appropriate Mathematical Models May Yield Deeper Understanding

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Automated-auscultatory (Hybrid) sphygmomanometers for clinic blood pressure measurement: a suitable substitute to mercury sphygmomanometer as reference standard?

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Alterations of cardiovascular complexity during acute exposure to high altitude: A multiscale entropy approach

Stays at high altitude induce alterations in cardiovascular control and are a model of specific pathological cardiovascular derangements at sea level. However, high-altitude alterations of the complex cardiovascular dynamics remain an almost unexplored issue. Therefore, our aim is to describe the altered cardiovascular complexity at high altitude with a multiscale entropy (MSE) approach. We recorded the beat-by-beat series of systolic and diastolic blood pressure and heart rate in 20 participants for 15 min twice, at sea level and after arrival at 4554 m a.s.l. We estimated Sample Entropy and MSE at scales of up to 64 beats, deriving average MSE values over the scales corresponding to the high-frequency (MSEHF) and low-frequency (MSELF) bands of heart-rate variability. We found a significant loss of complexity at heart-rate and blood-pressure scales complementary to each other, with the decrease with high altitude being concentrated at Sample Entropy and at MSEHF for heart rate and at MSELF for blood pressure. These changes can be ascribed to the acutely increased chemoreflex sensitivity in hypoxia that causes sympathetic activation and hyperventilation. Considering high altitude as a model of pathological states like heart failure, our results suggest new ways for monitoring treatments and rehabilitation protocols

Blood pressure variability and silent cerebral damage in essential hypertension

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Determination of Baroreflex Sensitivity during the Modified Oxford Maneuver by Trigonometric Regressive Spectral Analysis

BACKGROUND: Differences in spontaneous and drug-induced baroreflex sensitivity (BRS) have been attributed to its different operating ranges. The current study attempted to compare BRS estimates during cardiovascular steady-state and pharmacologically stimulation using an innovative algorithm for dynamic determination of baroreflex gain. METHODOLOGY/PRINCIPAL FINDINGS: Forty-five volunteers underwent the modified Oxford maneuver in supine and 60° tilted position with blood pressure and heart rate being continuously recorded. Drug-induced BRS-estimates were calculated from data obtained by bolus injections of nitroprusside and phenylephrine. Spontaneous indices were derived from data obtained during rest (stationary) and under pharmacological stimulation (non-stationary) using the algorithm of trigonometric regressive spectral analysis (TRS). Spontaneous and drug-induced BRS values were significantly correlated and display directionally similar changes under different situations. Using the Bland-Altman method, systematic differences between spontaneous and drug-induced estimates were found and revealed that the discrepancy can be as large as the gain itself. Fixed bias was not evident with ordinary least products regression. The correlation and agreement between the estimates increased significantly when BRS was calculated by TRS in non-stationary mode during the drug injection period. TRS-BRS significantly increased during phenylephrine and decreased under nitroprusside. CONCLUSIONS/SIGNIFICANCE: The TRS analysis provides a reliable, non-invasive assessment of human BRS not only under static steady state conditions, but also during pharmacological perturbation of the cardiovascular system

Sodium intake and hypertension

The close relationship between hypertension and dietary sodium intake is widely recognized and supported by several studies. A reduction in dietary sodium not only decreases the blood pressure and the incidence of hypertension, but is also associated with a reduction in morbidity and mortality from cardiovascular diseases. Prolonged modest reduction in salt intake induces a relevant fall in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group, with larger falls in systolic blood pressure for larger reductions in dietary salt. The high sodium intake and the increase in blood pressure levels are related to water retention, increase in systemic peripheral resistance, alterations in the endothelial function, changes in the structure and function of large elastic arteries, modification in sympathetic activity, and in the autonomic neuronal modulation of the cardiovascular system. In this review, we have focused on the effects of sodium intake on vascular hemodynamics and their implication in the pathogenesis of hypertensio

Left ventricular ejection time, not heart rate, is an independent correlate of aortic pulse wave velocity.

Salvi P, Palombo C, Salvi GM, Labat C, Parati G, Benetos A. Left ventricular ejection time, not heart rate, is an independent correlate of aortic pulse wave velocity. J Appl Physiol 115: 1610–1617, 2013. First published September 19, 2013; doi:10.1152/japplphysiol.00475.2013.— Several studies showed a positive association between heart rate and pulse wave velocity, a sensitive marker of arterial stiffness. However, no study involving a large population has specifically addressed the dependence of pulse wave velocity on different components of the cardiac cycle. The aim of this study was to explore in subjects of different age the link between pulse wave velocity with heart period (the reciprocal of heart rate) and the temporal components of the cardiac cycle such as left ventricular ejection time and diastolic time. Carotid-femoral pulse wave velocity was assessed in 3,020 untreated subjects (1,107 men). Heart period, left ventricular ejection time, diastolic time, and early-systolic dP/dt were determined by carotid pulse wave analysis with high-fidelity applanation tonometry. An inverse association was found between pulse wave velocity and left ventricular ejection time at all ages (25 years, r2 0.043; 25–44 years, r2 0.103; 45–64 years, r2 0.079; 65–84 years, r2 0.044; 85 years, r2 0.022; P 0.0001 for all). A significant (P 0.0001) negative but always weaker correlation between pulse wave velocity and heart period was also found, with the exception of the youngest subjects (P0.20). A significant positive correlation was also found between pulse wave velocity and dP/dt (P 0.0001). With multiple stepwise regression analysis, left ventricular ejection time and dP/dt remained the only determinant of pulse wave velocity at all ages, whereas the contribution of heart period no longer became significant. Our data demonstrate that pulse wave velocity is more closely related to left ventricular systolic function than to heart period. This may have methodological and pathophysiological implications