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The pressure phase plane (PPP), defined by dP(t)/dt versus P(t) coordinates has revealed novel physiologic relationships not readily obtainable from conventional, time domain analysis of left ventricular pressure (LVP). We extend the methodology by introducing the normalized pressure phase plane (nPPP), defined by 0 ≤ P ≤ 1 and -1 ≤ dP/dt ≤ +1. Nor...
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... RVP data [P(t)] were converted to digital data (Fig. 2d), and the time derivative of pressure (dP/dt) vs. time data sets were digitally smoothed using a five-point average to suppress small noise (Fig. 2e). As shown in Fig. 2f, the loop in the pressure-phase plane (PPP; by replacing displacement x with pressure P) also traces a clockwise path, reflecting events of the cardiac cycle 20,21 . The PPP configuration is not affected by the heart rate, but analogously determined by the amplitude of Pmax -Pmin, and the angular velocity of ω, which affects dP/dt_max and dP/dt_min. ...
The aims of the present study were to develop and check the utility and feasibility of a novel right ventricular (RV) functional index (RV angular velocity; RVω, s−1) derived from the angular velocity in harmonic oscillator kinematics obtained from the RV pressure waveform. We hypothesized that RVω reflects the myocardial performance index (MPI), which represents global RV function. A total of 132 consecutive patients, ranging in age from 3 months to 34 years with various cardiac diseases were included in this prospective study. RVω was defined as the difference between the peak derivative of pressure (dP/dt_max − dP/dt_min) divided by the difference between the maximum and minimum pressure (Pmax – Pmin). RVω showed significant negative correlations with the pulsed-wave Doppler-derived myocardial performance index (PWD-MPI) and the tissue Doppler imaging-derived MPI (TDI-MPI) (r = −0.52 and −0.51, respectively; both p < 0.0001). RVω also showed significant positive correlations with RV fractional area change (RVFAC) and RV ejection fraction (RVEF) (r = 0.41 and 0.39, respectively; both p < 0.0001), as well as a significant negative correlation with tricuspid E/e′ (r = −0.19, p = 0.0283). The clinical feasibility and utility of RVω for assessing global RV performance, incorporating both systolic and diastolic function, were demonstrated.
... The meaning of load-independence has been further characterized by the mathematical modeling of time-varying elastance in kinematic terms (Oommen et al. 2003), leading to the first analytic proof that in-vivo elastance could be a load-independent index of contractility. Additional load-independent LV chamber attributes have been characterized by Ghosh and Kov acs (2013) by normalizing the pressure phase plane such that 0 ≤ P(t) ≤ 1 and À1 ≤ dP/dt ≤ 1. They observed that peak ÀdP/dt, corresponding to the peak rate of cross-bridge dissociation during isovolumic relaxation, is inscribed very close to 61% of the peak pressure of the previous cardiac cycle. ...
... Our method for normalizing high fidelity LV pressure data has been previously described by Ghosh and Kov acs (2013). We normalized LV pressure for each cardiac cycle according to: P N ðtÞ ¼ ðPðtÞ À P min Þ ðP max À P min Þ Such that P min = 0 and P max = 1 after normalization. ...
... We normalized LV pressure for each cardiac cycle according to: P N ðtÞ ¼ ðPðtÞ À P min Þ ðP max À P min Þ Such that P min = 0 and P max = 1 after normalization. As noted by Ghosh and Kov acs (2013), this method of pressure normalization has revealed that P N at the peak rate of cross-bridge dissociation during LV isovolumic relaxation has load-independent attributes. ...
Left ventricular (LV) pressure?volume (P?V) loop analysis is the gold standard for chamber function assessment. To advance beyond traditional P?V and pressure phase plane (dP/dt-P) analysis in the quest for novel load-independent chamber properties, we introduce the normalized P?V loop. High-fidelity LV pressure and volume data (161 P-V loops) from 13 normal control subjects were analyzed. Normalized LV pressure (PN) was defined by 0?? P(t) ? 1. Normalized LV volume (VN) was defined as VN=V(t)/Vdiastasis, since the LV volume at diastasis (Vdiastasis) is the in-vivo equilibrium volume relative to which the LV volume oscillates. Plotting PN versus VN for each cardiac cycle generates normalized P-V loops. LV volume at the peak LV ejection rate and at the peak LV filling rate (peak ?dV/dt and peak +dV/dt, respectively) were determined for conventional and normalized loops. VN at peak +dV/dt was inscribed at 64???5% of normalized equilibrium (diastatic) volume with an inter-subject variation of 8%, and had a reduced intra-subject (beat-to-beat) variation compared to conventional P-V loops (9% vs. 13%, respectively; P?<?0.005), thereby demonstrating load-independent attributes. In contrast, VN at peak ?dV/dt was inscribed at 81???9% with an inter-subject variation of 11%, and had no significant change in intra-subject (beat-to-beat) variation compared to conventional P-V loops (17% vs. 17%, respectively; P?=?0.56), therefore failing to demonstrate load-independent tendencies. Thus, the normalized P-V loop advances the quest for load-independent LV chamber properties. VN at the peak LV filling rate (?sarcomere length at the peak sarcomere lengthening rate) manifests load-independent properties. This novel method may help to elucidate and quantify new attributes of cardiac and cellular function. It merits further application in additional human and animal physiologic and pathophysiologic datasets.
We hypothesized that KPA, a harmonic oscillator kinematics-derived spring constant parameter of the pulmonary artery pressure (PAP) profile, reflects PA compliance in pediatric patients. In this prospective study of 33 children (age range = 0.5-20 years) with various cardiac diseases, we assessed the novel parameter designated as KPA calculated using the pressure phase plane and the equation KPA = (dP/dt_max)(2)/([Pmax - Pmin])/2)(2), where dP/dt_max is the peak derivative of PAP, and Pmax - Pmin is the difference between the minimum and maximum PAP. PA compliance was also calculated using two conventional methods: systolic PA compliance (sPAC) was expressed as the stroke volume/Pmax - Pmin; and diastolic PA compliance (dPAC) was determined according to a two-element Windkessel model of PA diastolic pressure decay. In addition, data were recorded during abdominal compression to determine the influence of preload on KPA. A significant correlation was observed between KPA and sPAC (r = 0.52, P = 0.0018), but not dPAC. Significant correlations were also seen with the time constant (τ) of diastolic PAP (r = -0.51, P = 0.0026) and the pulmonary vascular resistance index (r = -0.39, P = 0.0242). No significant difference in KPA was seen between before and after abdominal compression. KPA had a higher intraclass correlation coefficient than other compliance and resistance parameters for both intra-observer and inter-observer variability (0.998 and 0.997, respectively). These results suggest that KPA can provide insight into the underlying mechanisms and facilitate the quantification of PA compliance.
The laws of fluid dynamics govern vortex ring formation and precede cardiac development by billions of years, suggesting that diastolic vortex ring formation is instrumental in defining the shape of the heart. Using novel and validated magnetic resonance imaging measurements, we show that the healthy left ventricle moves in tandem with the expanding vortex ring, indicating that cardiac form and function is epigenetically optimized to accommodate vortex ring formation for volume pumping. Healthy hearts demonstrate a strong coupling between vortex and cardiac volumes (R2 = 0.83), but this optimized phenotype is lost in heart failure, suggesting restoration of normal vortex ring dynamics as a new, and possibly important consideration for individualized heart failure treatment. Vortex ring volume was unrelated to early rapid filling (E-wave) velocity in patients and controls. Characteristics of vortex-wall interaction provide unique physiologic and mechanistic information about cardiac diastolic function that may be applied to guide the design and implantation of prosthetic valves, and have potential clinical utility as therapeutic targets for tailored medicine or measures of cardiac health.
Despite Leonardo da Vinci's observation (circa 1511) that "the atria or filling chambers contract together while the pumping chambers or ventricles are relaxing and vice versa", the dynamics of four-chamber heart function, and of diastolic function in particular, are not generally appreciated. We view diastolic function (DF) from a global perspective while characterizing it in terms of causality and clinical relevance. Our models derive from the insight that global diastolic function is ultimately a result of forces generated by elastic recoil, modulated by cross-bridge relaxation, and load. The interaction between recoil and relaxation results in physical wall motion that generates pressure gradients that drive fluid flow, while epicardial wall motion is constrained by the pericardial sac. Traditional DF indexes (τ, E/E', etc.) are not derived from causal mechanisms and are interpreted as approximating either stiffness or relaxation, but not both, thereby limiting the accuracy of DF quantification. Our derived kinematic models of isovolumic relaxation and suction-initiated filling are extensively validated, quantify the balance between stiffness and relaxation, and provide novel mechanistic physiologic insight. For example, causality based modeling provides load-independent indexes of DF and reveals that both stiffness and relaxation modify traditional DF indexes. The method has revealed that the in-vivo LV equilibrium volume occurs at diastasis, predicted novel relationships between filling and wall motion, and quantified causal relationships between ventricular and atrial function. In summary, by using governing physiologic principles as a guide, we define what global diastolic function is, what it is not, and how to measure it.
Copyright © 2015, American Journal of Physiology - Heart and Circulatory Physiology.
