Abstract:Background-The effect of moderate left ventricular systolic dysfunction (LVSD) on ventricular/vascular coupling and the aortic pressure waveform (AoPW) has been well described, but the effect of severe LVSD has not. Methods and Results-We used noninvasive, high-fidelity tonometry of the radial artery and a mathematical transfer function to generate the AoPW in 25 treated patients with LVSD (mean LV ejection fraction, 24Ϯ8.8%; range, 11% to 40%; 21 patients Ͻ30%). Pulse wave analysis of the AoPW was used to cha… Show more
“…Therefore, in these patients arterial wave reflections induce a negative influence on flow rather than a positive influence on pressure. 27) This deleterious effect of wave reflections has been described in patients with LVSD by Denardo, et al 28) They reported a decrease in all components of central and peripheral blood pressure compared with normal subjects with a reduction in ED, in reflected wave amplitude, and in Ew of LV effort. It must be pointed out that these authors considered patients with severe LV impairment (mean LVEF = 24%) to be comparable to our LVSD patient subgroup of 12 patients with more compromised LV function (mean LVEF = 29%).…”
SummaryCentral aortic pressure waveform (AoPW) is the summation of a forward-traveling wave generated by the left ventricle and a backward-traveling wave caused by the reflection of the forward wave. The aim of this study was to evaluate the effect of ventricular-vascular coupling on the morphology of AoPW in chronic heart failure patients with different degrees of left ventricular systolic dysfunction (LVSD) using pulse wave analysis (PWA). PWA of AoPW and left ventricular (LV) function were evaluated by applanation tonometry in 26 control subjects, in 12 patients with left ventricular ejection fraction (LVEF) ≤ 30%, and in 14 patients with LVEF > 30%. Augmentation pressure, augmentation index, wasted energy, and ejection duration were lower in patients with LVEF ≤ 30% than in those with LVEF > 30% and in control subjects. Furthermore, augmentation index showed an inverse correlation with Doppler mitral E-wave amplitude (r = -0.40; P = 0.04) and E/A ratio (r = -0.42; P = 0.03) and a direct correlation with deceleration time of mitral E-waves (r = 0.39; P = 0.04). In patients with severe LVSD (LVEF ≤ 30%), aortic wave reflections negatively interfere with LV function and induce a shortening of ejection duration. In contrast, AoPW is similar in patients with moderate LVSD (LVEF > 30%) and in control subjects. (Int Heart J 2014; 55: 526-532) Key words: Arterial stiffness, Heart failure, Ejection fraction, Pulse pressure H igh brachial pulse pressure (PP), commonly considered a marker of arterial stiffness, has been shown to predict adverse outcomes in patients with left ventricular (LV) systolic dysfunction.1,2) However, in patients with advanced systolic heart failure, the association between PP and outcome is reversed and a low PP is an independent predictor of all cause and cardiovascular death.3,4) It is conceivable that different pathophysiological mechanisms may underlie the opposite prognostic significance of PP in patients with LV systolic dysfunction (LVSD) and different severity of cardiac function impairment.Several sets of data support the greater importance of the central rather than peripheral blood pressure profile in patients with various cardiovascular diseases. A central blood pressure profile offers a more direct measure of LV load and arterial stiffness and provides useful clinical information independently from peripheral PP. [5][6][7][8] The central aortic pressure wave is composed of a forward-traveling wave generated by LV ejection and a late-arriving reflected wave from the periphery. Normally, wave reflections arrive during diastole, when LV has completed the ejection and contribute to coronary perfusion. As arterial stiffness increases, the velocity of forward and reflected waves increases so that the reflected wave arrives earlier to the heart and boosts pressure in late systole with an extra pulsatile workload on the left ventricle.9,10) The availability of noninvasive methods to accurately measure central blood pressure and flow has increased interest in gaining a further understan...
“…Therefore, in these patients arterial wave reflections induce a negative influence on flow rather than a positive influence on pressure. 27) This deleterious effect of wave reflections has been described in patients with LVSD by Denardo, et al 28) They reported a decrease in all components of central and peripheral blood pressure compared with normal subjects with a reduction in ED, in reflected wave amplitude, and in Ew of LV effort. It must be pointed out that these authors considered patients with severe LV impairment (mean LVEF = 24%) to be comparable to our LVSD patient subgroup of 12 patients with more compromised LV function (mean LVEF = 29%).…”
SummaryCentral aortic pressure waveform (AoPW) is the summation of a forward-traveling wave generated by the left ventricle and a backward-traveling wave caused by the reflection of the forward wave. The aim of this study was to evaluate the effect of ventricular-vascular coupling on the morphology of AoPW in chronic heart failure patients with different degrees of left ventricular systolic dysfunction (LVSD) using pulse wave analysis (PWA). PWA of AoPW and left ventricular (LV) function were evaluated by applanation tonometry in 26 control subjects, in 12 patients with left ventricular ejection fraction (LVEF) ≤ 30%, and in 14 patients with LVEF > 30%. Augmentation pressure, augmentation index, wasted energy, and ejection duration were lower in patients with LVEF ≤ 30% than in those with LVEF > 30% and in control subjects. Furthermore, augmentation index showed an inverse correlation with Doppler mitral E-wave amplitude (r = -0.40; P = 0.04) and E/A ratio (r = -0.42; P = 0.03) and a direct correlation with deceleration time of mitral E-waves (r = 0.39; P = 0.04). In patients with severe LVSD (LVEF ≤ 30%), aortic wave reflections negatively interfere with LV function and induce a shortening of ejection duration. In contrast, AoPW is similar in patients with moderate LVSD (LVEF > 30%) and in control subjects. (Int Heart J 2014; 55: 526-532) Key words: Arterial stiffness, Heart failure, Ejection fraction, Pulse pressure H igh brachial pulse pressure (PP), commonly considered a marker of arterial stiffness, has been shown to predict adverse outcomes in patients with left ventricular (LV) systolic dysfunction.1,2) However, in patients with advanced systolic heart failure, the association between PP and outcome is reversed and a low PP is an independent predictor of all cause and cardiovascular death.3,4) It is conceivable that different pathophysiological mechanisms may underlie the opposite prognostic significance of PP in patients with LV systolic dysfunction (LVSD) and different severity of cardiac function impairment.Several sets of data support the greater importance of the central rather than peripheral blood pressure profile in patients with various cardiovascular diseases. A central blood pressure profile offers a more direct measure of LV load and arterial stiffness and provides useful clinical information independently from peripheral PP. [5][6][7][8] The central aortic pressure wave is composed of a forward-traveling wave generated by LV ejection and a late-arriving reflected wave from the periphery. Normally, wave reflections arrive during diastole, when LV has completed the ejection and contribute to coronary perfusion. As arterial stiffness increases, the velocity of forward and reflected waves increases so that the reflected wave arrives earlier to the heart and boosts pressure in late systole with an extra pulsatile workload on the left ventricle.9,10) The availability of noninvasive methods to accurately measure central blood pressure and flow has increased interest in gaining a further understan...
“…The complete pulse pressure waveform is known to provide valuable information for diagnostics and therapy of cardiovascular diseases such as arteriosclerosis, hypertension and left ventricular systolic dysfunction [37][38][39][40] . Many hemodynamic parameters such as arterial index, upstroke time, stroke volume variation and cardiac output can be directly calculated or estimated in real time from the pressure waveforms 41,42 .…”
The ability to measure subtle changes in arterial pressure using devices mounted on the skin can be valuable for monitoring vital signs in emergency care, detecting the early onset of cardiovascular disease and continuously assessing health status. Conventional technologies are well suited for use in traditional clinical settings, but cannot be easily adapted for sustained use during daily activities. Here we introduce a conformal device that avoids these limitations. Ultrathin inorganic piezoelectric and semiconductor materials on elastomer substrates enable amplified, low hysteresis measurements of pressure on the skin, with high levels of sensitivity (B0.005 Pa) and fast response times (B0.1 ms). Experimental and theoretical studies reveal enhanced piezoelectric responses in lead zirconate titanate that follow from integration on soft supports as well as engineering behaviours of the associated devices. Calibrated measurements of pressure variations of blood flow in near-surface arteries demonstrate capabilities for measuring radial artery augmentation index and pulse pressure velocity.
“…9 In the presence of LV systolic dysfunction, the load imposed by the reflected wave may be predominantly associated with a pronounced decrease and early cessation of flow 21 and shortening of the ejection period. 22 In contrast to early systole, when systolic pressure and "diastolic" geometry (thin wall and large cavity) occur, myocardial fiber shortening and ejection of blood determine a progressive change in LV geometry, which causes a decrease in myocardial stress (despite rising pressure) during mid-to-late systole, such that wall stress tends to reach its lowest ejection-phase value in end systole. 19 This sequence of events appears to be ideal for the myocardium to handle the additional load imposed by wave reflections and may be compromised in ventricles with depressed ejection fraction.…”
Abstract-The mechanical load imposed by the systemic circulation to the left ventricle is an important determinant of normal and abnormal cardiovascular function. Left ventricular afterload is determined by complex time-varying phenomena, which affect pressure and flow patterns generated by the pumping ventricle. Left ventricular afterload is best described in terms of pressure-flow relations, allowing for quantification of various components of load using simplified biomechanical models of the circulation, with great potential for mechanistic understanding of the role of central hemodynamics in cardiovascular disease and the effects of therapeutic interventions. In the second part of this tutorial, we review analytic methods used to characterize left ventricular afterload, including analyses of central arterial pressure-flow relations and windkessel modeling (pressure-volume relations). Conceptual descriptions of various models and methods are emphasized over mathematical ones. Our review is aimed at helping researchers and clinicians obtain and interpret results from analyses of left ventricular afterload in clinical and epidemiological settings. (Hypertension. 2010;56:563-570.)Key Words: afterload Ⅲ noninvasive Ⅲ input impedance Ⅲ arterial load T he mechanical load imposed by the systemic circulation to the left ventricle (LV) is an important determinant of normal and abnormal cardiovascular function. With the availability of noninvasive methods to accurately measure central pressure and flow, as well as computational tools for their analysis, there is great potential for their application in order to gain further mechanistic understanding of the role of central hemodynamics in cardiovascular disease. In the first part of this tutorial, we reviewed noninvasive methods to measure aortic pressure and flow, introduced basic concepts of analyses of pressure/flow relations in the time and frequency domains based on simple models of wave conduction and reflection, and briefly discussed wave reflections in the arterial tree. In this article, we review modeling of the arterial system as a windkessel, techniques for analyses of human arterial pressure-flow relations and considerations for interpreting hemodynamic indices in the context of research studies and individual hemodynamic assessments.
The Arterial WindkesselIn addition to considering the arterial tree as a system of tubes with wave travel and reflection (or as a transmission line network), one might address it in terms of "windkessel" model components. Frank proposed the original windkessel model as a resistance and compliance (C) pair (2-element windkessel), meant to represent small vessel resistance and large artery compliance, respectively. 1 In the arterial system, total resistance to flow originates predominantly from small arteries, whereas most of the summed compliance is provided by large arteries. This is not a perfect distinction, because large arteries impose some resistance and smaller vessels provide some compliance, whereas the model only measu...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.