Endografting of the descending thoracic aorta increases ascending aortic input impedance and attenuates pressure transmission in dogs.

OBJECTIVES: Endografting is being used to manage aneurysms, dissections and acute traumatic disruptions of the thoracic aorta. The acute effects of such interventions on ventricular afterload and on pressure wave transmission characteristics are not well known. METHODS: In five dogs, a 55 mm endograft was introduced into the descending aorta, just distal to the left subclavian artery, with oversizing of 20%. Following formaldehyde induced complete heart block, the hearts were paced (30-120bpm). The ascending aortic pressures and flows were recorded using Millar micro-tip manometers and ultrasonic flowmeters, respectively. Arterial pressures proximal and distal to the stent site were also recorded. For each heart rate, parameters of a modified Windkessel (SVR: systemic vascular resistance, Z0: characteristic impedance, C: total arterial compliance) were estimated. The pulse wave velocity (PWV) and reflection coefficient (Gamma) were calculated from the pressure wave transfer functions. RESULTS: The Z0 (0.25+/-0.05 vs 0.41+/-0.06 mmHg/ml s(-1), P<.05) was increased and C was decreased (0.45+/-0.07 vs 0.28+/-0.04 ml/mmHg, P<0.001) following endograft placement. SVR tended to increase (P=.06) and ascending aortic Gamma was unchanged. The PWV increased (418+/-67 vs 755+/-135 cm/s, P<.05) and the distal Gamma decreased (0.09+/-0.10 vs -0.49+/-0.07, P<.05). CONCLUSIONS: Endografting in the proximal descending aorta cause unfavorable changes in the ascending aortic input impedance and an increase in the PWV through the grafted segment, consistent with an increase in the modulus of elasticity. The grafts produce a negative Gamma at the distal end, an uncommon occurrence in the systemic circulation. Whether this change is of sufficient magnitude to result in post-graft dilation is unknown.

Late systolic pressure augmentation: role of left ventricular outflow patterns.

Late systolic augmentation of the ascending aortic pressure waveform is believed to be caused by particular impedance patterns but also could be caused by particular left ventricular outflow patterns. Using a linear mathematical model of the entire human arterial tree, we derived realistic impedance patterns by altering 1) Young's modulus of the arterial wall of the individual branches, 2) peripheral reflection coefficients, and 3) distal compliances at the terminations. These calculated impedance patterns were then coupled to realistic left ventricular outflow patterns determined by unique 1) end-diastolic and end-systolic pressure-volume relationships, 2) preload-recruitable stroke work relationships, and 3) shortening paths simulated by altered aortic flow contours. As determined by the ratio of the individual parameter coefficient of determination (r(2)) to the overall model r(2), late systolic pressure augmentation was more strongly determined by left ventricular outflow patterns than by arterial impedance parameters (r(2) ratio: 53% vs. 33%). Thus left ventricular outflow patterns are at least as important as impedance parameters in determining late systolic pressure augmentation in this model.

On-line synthesis of the human ascending aortic pressure pulse from the finger pulse.

Although systolic pressure in the ascending aorta (AA) can be determined accurately from the radial arterial waveform using a single generalized transfer function (TF) of the upper limb, a better on-line methods is needed for accurate noninvasive synthesis of the AA pressure contour to characterize left ventricular contractile function and ventricular-vascular coupling. AA, tonometric carotid (CA), and photoplethysmographic finger (FA) arterial pressure waveforms were recorded in 12 subjects (10 male, aged 59.1+/-10.3 years, mean+/-SD) during cardiac catheterization. The AA-FA TF was estimated using (1) a single generalized TF (GAA), (2) individualized TFs directly determined from CA-FA recordings in each patient (DAA), and (3) individualized TFs computed from CA-FA recordings in each patient with a mathematical model of the human upper limb (MAA). AA pressure waveforms were synthesized from FA recordings in real time using convolution windows derived from these TFs. Under steady state conditions, the root mean square error (RMSE) between measured and synthesized AA was lower by DAA (3.3+/-1.3 mm Hg) and MAA (3.9+/-1.2 mmHg) than by GAA (4.8+/-2.0 mm Hg, P<.05). During dynamic load alteration induced by the Valsalva maneuver, however, the MAA method performed better (5.4+/-2.8 mm Hg) than both the GAA (5.8+/-3.3 mm Hg, P<.05) and DAA (6.5+/-2.7 mm Hg, P<.01) methods. The beat-to-beat AA contour can be accurately and noninvasively synthesized on-line using individualized TFs. During dynamic load alteration, individualized TFs derived with an upper limb arterial model provide greater accuracy.

A system for analysis of arterial blood pressure waveforms in humans.

Recent developments in arterial hemodynamics have indicated that the human arterial pressure waveform contains more information than is available from conventional sphygmomanometry. This information includes indices describing left ventricular systolic function and arterial properties. A cheap and reliable system was designed and implemented using readily available hardware for recording, analysis, and storage of arterial pressure waveforms. The system embodies an online technique for synthesizing ascending aortic pressure waveform from recordings made at different peripheral sites of the human arterial system. Eighteen indices are then derived from arterial pressure waveforms. This system can be used in an outpatient clinic for assisting in current pharmacological management of cardiovascular disease. It can also be extended to the critical care area, where the extra information provided aid in assessing the patient's condition.

Derivation of the ascending aortic-carotid pressure transfer function with an arterial model.

To devise a method of deriving the ascending aortic pressure waveform from the noninvasively determined carotid arterial waveform, ascending aortic and carotid arterial pressures were recorded in 13 patients aged 58.5 +/- 10.0 (SD) yr. A single viscoelastic tube terminated with a modified windkessel was used to model the carotid arterial system. For each patient the model parameters, characteristic impedance of the tube (Z0), reflection coefficient at the termination (gamma), and time constant of the windkessel (tau), were estimated by minimizing the root-mean-square error between the measured and predicted carotid waveforms, with the ascending aortic pressure waveform as input. The resulting arterial parameters were realistic: Z0 = 729.5 +/- 246.8 dyn.s.cm-3, gamma = 0.75 +/- 0.19, and tau = 0.16 +/- 0.17 s. A generalized model constructed with these mean parameters yielded a smaller error between predicted and measured carotid arterial pressures (3.4 +/- 1.3 mmHg) than between ascending aortic pressure and measured carotid arterial pressure (4.4 +/- 1.6 mmHg, P < 0.01) and also reproduced the carotid wave contour indexed by the ratio of late systolic to early systolic peak amplitude: predicted = 1.26 +/- 0.05 and measured = 1.24 +/- 0.16 vs. aortic = 1.55 +/- 0.19.

Pressure wave propagation in a multibranched model of the human upper limb.

The influence of the large arteries and the peripheral load on pressure wave propagation in the human upper limb was investigated in an anatomically realistic multibranched model based on linear transmission theory. To mimic vascular changes seen in life, the viscoelastic properties of large arteries and the peripheral load properties (represented as modified windkessels) were altered as follows: Young's modulus (from 10.9 x 10(6) to 15.3 x 10(6) dyn/cm2) and phase (from 0 to 15 degrees) of the complex elastance, windkessel time constant (from 0 to 0.6 s), and peripheral reflection coefficient (from 0 to 0.95). The relationship between the central aortic and peripheral radial pressure waveforms was analyzed in the time and the frequency domain. Results indicate that the large arterial properties have less influence (peak systolic pressure changed by 3% and peak of transfer function changed by 29%) than the properties of the peripheral load (systolic pressure changed by 14% and peak of transfer function changed by 74%) on the pressure wave propagation in the upper limb.

Functional origin of reflected pressure waves in a multibranched model of the human arterial system.

The effects of wave travel and wave reflection were simulated in a mathematical model of the whole arterial tree consisting of 142 uniform transmission line segments. The arterial model was partitioned into three separate segments: upper limbs, trunk, and lower limbs. Aging was simulated by increasing average pulse wave velocities of these segments (10.9-12.9, 8.0-11.7, and 9.0-11.3 m/s for upper limbs, trunk, and lower limbs, respectively). Reflection coefficients at the terminal elements were altered to simulate vasodilation (0.0) and vasoconstriction (0.95). The impedance patterns and spatial distribution of pressure waveforms generated by the model simulating aging and vasoconstriction were similar to in vivo measurements by other investigators. Reflected pressure waves from each segment reached the ascending aorta and contributed differently to the late systolic peak on the aortic pressure wave. Aging does not alter the origin of these reflected pressure waves in the trunk. Aortic impedance and pressure wave changes induced by simulation of dilation of splanchnic bed were similar to those observed experimentally with nitroglycerin.

An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.

Amplification of the pressure pulse between central and peripheral arteries renders pressure values in the upper limb an inaccurate measure of ascending aortic (AA) pressure. Accuracy could be improved by allowance for such amplification. Transfer functions (TF) for pressures between AA and brachial artery (BA):(BATF) and between AA and radial artery (RA):(RATF) were derived from high-fidelity pressure recordings obtained at cardiac catheterization in 14 patients under control conditions, and after sublingual nitroglycerine 0.3 mg. There was no significant difference in BATF under control conditions and with nitroglycerine; hence results were pooled. Control and nitroglycerine results were also pooled to obtain a single RATF. BATF and RATF moduli peaked at 5 Hz and 4 Hz, reaching 2.5 and 2.8 times the value at zero frequency respectively. Frequency-dependent changes in modulus and phase of BATF and RATF were attributable to wave travel and reflection in the upper limb. BATF and RATF were compared to published transfer functions and those derived from analysis of aortic and brachial or radial pressure waves in previous publications. Results were similar. Our BATF and RATF were used to synthesize AA pressure waves from published peripheral pulses. Correspondence was close, especially for systolic pressure which differed by 2.4 +/- 1.0 (mean +/- SEM) mmHg, whereas recorded systolic pressure differed by 20.4 +/- 2.6 (mean +/- SEM) mmHg between central and peripheral sites. Results indicate that in adult humans a single generalized TF can be used with acceptable accuracy to determine central from peripheral pressure under different conditions.(ABSTRACT TRUNCATED AT 250 WORDS)