Coronary waves during valsalva maneuver measured during catheterization

The mechanical interactions between heart contraction and perfusion of the heart are difficult to study in humans because of the restrictions in inducing changes in hemodynamic and cardiac mechanics parameters during catheterization. We hypothesize that the Valsalva maneuver can induce such alterations in the cardiac-coronary mechanical interaction and that these variations can be studied with the Wave Intensity Analysis. In order to interpret eventual changes in the wave intensity, a deep understanding of the effect of the Valsalva maneuver on the coronary circulation is needed. A particular attention has to be payed on the effect of the control of the microvascular resistance that is known to compensate for eventual alterations in the surrounding hemodynamic conditions when vessel tone is intact. In the catheterization laboratory, coronary pressure and flow velocity signals were recorded simultaneously by a new guidewire developed by Volcano Corporation. Aortic pressure, left ventricular pressure and ECG were acquired by the catheterization laboratory setup and recorded together with coronary hemodynamic signals. Left ventricular performance parameters were derived per beat from the noninvasive recording of the finger pressure using the Nexfin monitor developed by BMEYE B.V. In order to match the output data of coronary hemodynamic and left ventricular performance parameters, a dedicated program has been written in Delphi. An analysis of the per-beat data was performed in order to study the relative dependence of the parameters during the Valsalva maneuver. Pilot results of the Wave Intensity Analysis were obtained with an existing custom-made program also written in Delphi. Our study shows that the Valsalva maneuver caused a profound stress in the whole cardiovascular system. The well-known changes of the aortic pressure were transmitted also to the left ventricle and the coronary microcirculation. The data show that this stress caused a small but significant decrease in the flow velocity. As expected, the microvascular resistance varied with the same pattern as the coronary pressure trying to keep the flow constant. With respect to the decrease in stroke volume, cardiac output and contractility, the left ventricular performance was strongly compromised: pulse pressure generation and cardiac contraction were almost annulled. The decrease in systolic left ventricular pressure of almost 40% and the 2 fold increase in the end-diastolic left ventricular pressure confirm the decrease in the pumping action. Consequentially, the oxygen consumption of the heart decreased to 40% of the baseline level but only after an initial increase at the onset of the strain by 10%. The results also show that the timing of variation of the parameters was not the same. Especially the left ventricular end-diastolic pressure changed more rapidly than the perfusion pressure. Pilot results on Wave Intensity Analysis (WIA) show that the Valsalva maneuver gave rise to changes in the Wave Intensity pattern suggesting that the speed of the reflected waves has indeed been altered. Our results agree with previous studies that reveal a slight decrease in the flow velocity due to the Valsalva maneuver. Nevertheless, our results contradict the belief that ascribes the decrease in flow velocity to the decrease in oxygen consumption. We assume that the flow decrease is due to mechanical factors, especially the rise of left ventricular end-diastolic pressure. The results shown on WIA are pilot results and some work is still needed in this direction to obtain more information on the coronary-cardiac interaction. However, these results give confidence about the use of the Valsalva maneuver as an intervention affecting external parameters and thus they are useful in the study of coronary-cardiac interaction in humans.

Novel non-invasive techniques for hemodynamic monitoring

Orestis Vardoulis

The monitoring of hemodynamic parameters is crucial for optimal patient management and treatment. However, established methods are often invasive and possibly inapplicable to sensitive age groups. Novel, non-invasive techniques have the potential to transform cardiovascular (CV) assessment, offering reduced hospitalization periods, lower infection risk and decreased staff-to-patient ratio. Cardiac output (CO) monitoring provides valuable insight on global tissue perfusion. To overcome limitations of traditional methods, a novel technique was proposed. Taking into account the basic principles of CV physiology we derived an equation where the required variables can be extracted non-invasively. The novel technique was validated in a controlled, in silico, environment against previously established wave analysis methods. Subsequent data analysis showed that the new method yielded superior accuracy and precision. The new method was further evaluated in vivo using a 2D transthoracic echocardiography protocol for CO estimation. The corresponding comparison showed that the SVB method provides highly reproducible and accurate estimates of CO when compared to ultrasound. The estimation of pulse transit time (PTT) affects critically the accuracy and precision of pulse wave velocity (PWV) measurements. We proposed the "Diastole-Patching" method (DPm), which estimates PTT based on a signal region in the diastolic foot of the wave and is more robust against noisy arterial waveforms. DPm and previously established techniques were tested with a computational model of the arterial tree where the "real" values of PWV are known. The novel method yielded the highest agreement, accuracy and precision even when the waves were distorted with noise. The technique was further evaluated against the corresponding â"reference" algorithm of a commercially available device with in vivo acquired waves. DPm yielded more precise and reproducible measurements of PWV. Total Systemic Compliance (CT) expresses the ability of the arterial system to dilate and store blood during cardiac ejection. Our aim was to develop a relationship between aPWV and CT. The proposed, generalized Bramwell-Hill model of the systemic arterial tree estimates CT by a single non-invasive measurement of PWV. The proposed scheme was found to accurately estimate CT from aPWV. The mechanical properties of woven Dacron grafts differ significantly from the human aorta. As a result, aortic graft implantation changes the aortic geometry and mechanical properties, thus affecting blood pressure and wave reflections. A dedicated cardiovascular model was developed to include graft geometry and in vitro measured Dacron properties. It was found that aortic reconstruction affected aortic hemodynamics. For the proximal graft, the primary reason for pulse pressure rise is augmentation of the forward wave. For the distal graft, the pulse pressure rise is associated with augmented wave reflections resulting from the compliance mismatch between the aorta and the distal graft. To conclude, this body of work has shown that given the current computational tools and biosensors, it is possible to design and validate a set of non-invasive techniques that will provide valuable clinical insight for a wide gamut of cardiovascular diseases.

EPFL2014

Predicting systolic and diastolic aortic blood pressure and stroke volume in the intact sheep

Patrick Segers, Nikolaos Stergiopulos, Nico Westerhof

We developed a mathematical model describing the interaction between the heart and the arterial system. The model was constructed and tested on basis of invasive hemodynamic data in six sheep. Data from a first group of three animals (49 cardiac cycles) were used to assess a template time-varying elastance curve for the left ventricle, while the baseline steady-state data of a second group of three animals were used to assess reference cardiac and arterial parameters in sheep. The model is fully characterized by nine parameters, which were converted into 6 dimensionless numbers using the Buckingham pi theorem. The model was then used to generate LV pressure and volume and aortic pressure and flow for 86 conditions obtained by varying parameters 50 to 200% of their reference value. Systolic (SBP) and diastolic (DBP) blood pressure and stroke volume (SV) were determined from these model-generated curves and multiple linear regression analysis yielded the following expressions: SBP = Pisovolumic [0.638 - 0.0773 Emax C + 0.0507 RC/T] (r2 = 0.89); DBP = Pisovolumic [0.438-0.0712 Emax C + 0.0655RC/T] (r2 = 0.88) and SV = LVEDV [1.265-1.040 LVEDV/(LVEDV - Vd) + 0.125 Emax C-0.0777RC/T] (r2 = 0.93) with Pisovolumic = Emax (LVEDV - Vd), Emax and Vd being the slope and intercept of the end-systolic pressure-volume relation, R and C the total peripheral resistance and compliance, LVEDV the left ventricular end-diastolic volume, and T the cardiac cycle length. These expressions were validated using data from the second group of three animals obtained during vena cava occlusion at baseline and during administration of dobutamine (61 cycles). The correlation between measured and predicted values was 0.98, 0.97 and 0.92 for SBP, DBP and SV, respectively. Compared to the measured values, SBP and DBP were, on average, underestimated by 5 and 6mmHg, respectively, and SV overestimated by 1.4 ml. We conclude that the derived expressions for blood pressure and stroke volume remain valid in the intact sheep for various hemodynamic conditions, and, taking into account their dimensionless form, may hold in other species and in humans.

2001

Pressure and Flow Wave Propagation in Patient-Specific Models of the Arterial Tree

Philippe Reymond

Blood flow in the arterial circulation induces hemodynamic forces that play an important role in various forms of vascular diseases. Temporal variation of the wall shear stress seems to play a significant role in atherogenesis and plaque stability. Flow induced wall shear stress has been linked to growth and possibly rupture of the aneurysm wall. Hemodynamic forces are patient-specific and difficult to assess in the clinic. At present, there is no in vivo measurement technique that enables measurement of hemodynamic forces to the degree of precision needed. However, when imaging modalities used frequently in clinical routine re-create high-definition, patient geometric quantification of the blood vessel, they can be employed as a base for creating predictive hemodynamic models. Which in the case of understanding healthy vs. pathologic blood flow within the cerebral or systemic circulation, renders this an interesting approach. First, we developed a "generic 1D" distributed model of the human arterial tree including the primary systemic arteries and coupled this to a heart model. The fluid mechanics equations were solved numerically to obtain pressure and flow throughout the arterial tree. A nonlinear viscoelastic constitutive law for the arterial wall was considered while distal vessels were terminated with a three-element Windkessel model. The coronary arteries were modeled assuming a systolic flow impediment proportional to ventricular varying elastance. The model predictions were validated with noninvasive measurements of pressure and flow performed in young volunteers. Flow in the large arteries was visualized with magnetic resonance imaging, cerebral flow detected with ultrasound Doppler and blood pressure measured with applanation tonometry. Model predictions at different arterial locations compared well to measured flow and pressure waves at the same anatomical points. Thus, the generic 1D model reflected the flow and pressure measurements of the "average subject" of our volunteer population. Following the same approach as the generic 1D model, we built and validated a patient-specific model. In this case, geometric data, flow and pressure measurements were obtained for one person. The model predicted pressure and flow waveforms in good agreement with the in-vivo measurements with regards to wave shape and features. Comparison with a generic 1-D model has shown that the patient-specific model better predicted pressure and flow at specific arterial sites. Overall, the patient-specific 1-D model was able to predict pressure and flow waveforms in the main systemic circulation, whereas this was not always the case for a generic 1-D model. The inherent underestimation of energy losses of the 1-D wave propagation model, due to bifurcations, non-planarity and complex geometry, were examined. The 1-D model was compared to a rigid wall 3-D computational fluid dynamic model. Newtonian and non-Newtonian blood properties were studied and the longitudinal pressure distribution along the arteries was compared with the 1-D patient-specific model mean pressure prediction. The results indicated that pressure drop is significant only in small diameter vessels such as the precerebral and cerebral arteries. In these vessels the 1-D model in comparison to 3-D models consistently underestimated pressure drop. The complex flow patterns resulting from asymmetry and bifurcation yield shear stresses in the 3-D model that were greater than the 1-D model. A 3-D unsteady fluid structure interaction simulation in a patient-specific model was performed to simultaneously capture the flow details, given by the 3-D model, and wave propagation phenomena, provided by the 1-D model. The 3-D unsteady fluid structure interaction approach is the most computationally intense and cumbersome, but it allows physiological simulations with a high level of detail and accuracy. For instance, this approach could be relevant to obtain blood flow details in regions that are prone to atherosclerotic plaques or development of aneurysms. The 3-D fluid structure interaction simulation was performed for a patient-specific aorta. Important clinical parameters such as wall shear stress were quantified and significant differences were found in comparison to the rigid wall 3-D simulation indicating the relevance of a fluid structure interaction approach. A comparison of the fluid structure interaction to an equivalent 1-D model resulted in good reproduction of the pressure and flow waveforms. The effect of a decreased compliance of the arterial tree on hemodynamical parameters has been assessed with the use of a 1-D model. Local, proximal aorta and global stiffening of the arterial tree were modeled and led to two different mechanisms that contribute to the increase in central pulse pressure. They probably both contribute to systolic hypertension and their relative contribution depends on the topology of arterial stiffening and geometrical alterations taking place in aging or in disease. All these patient-specific models are about to being in use in a clinical environment and will be useful for providing better diagnostics and treatment planning in a near future.

EPFL2011