Pulse-wave velocity was measured in isolated canine common carotid arteries using sinusoidal frequency pulses of 1, 2, 5, 10, 15 and 20 Hz at 50, 100 and 150 mmHg. It was found that the pulse-wave velocity was independent of frequency and dependent on pressure. Using the Moens-Korteweg equation, the predicted pulse-wave velocity (y) was compared with measured pulse-wave velocity (x). A good correspondence was found (y = 1.063 x - 0.337, with a correlation coefficient of 0.963). The propagation velocity of the significant harmonic components of the pulsatile pressure waveform is the same for heart rates up to 120 beats/min.

Pulse wave velocity (PWV) was measured in situ in 11 isolated canine common carotid arteries. Seven arteries exhibited a linear PWV vs. pressure function at pressures ranging from 0 to 200 mmHg. Four arteries yielded a linear relationship between PWV and pressure between 1 and 100 mmHg; for these vessels the relationship was nonlinear at higher pressures. Seven arteries (five from the group which was linear up to 200 mmHg and two from the group which was linear up to 100 mmHg) were excised and pressure/volume measurements were made in vivo. Using pressure/volume data, the Moens-Korteweg equation was evaluated as a predictor of the PWV vs. pressure relationship over the linear region. An expression was developed to enable prediction of the pressure/volume relationship using the coefficients at the linear PWV vs. pressure function, and these predictions were evaluated. We found that, for this range, the Moens-Korteweg equation provides a very good basis for predicting the increase in PWV with increasing bias pressure. In addition, we found that the pressure/volume relationship of common carotid arteries is well represented by an exponential of the form V/V 0 = Ke αf(P) , which was derived as the inverse solution to the Moens-Korteweg equation.*

A new pacing technique is described that permits high fidelity recording of the paced ventricular evoked response, including cardiac depolarization. Integration of the paced R wave yields the ventricular depolarization gradient (GD), which is dependent on activation sequence and the spatial dispersion of activation times. GD was studied in 27 dogs to determine the effects of treadmill exercise at fixed rate pacing (n = 10), elevation of heart rate in the absence of stress (n = 20), epinephrine at fixed rate (n = 6), and exercise in the presence of normal chronotrophic response (n = 7). Low level exercise (1 mph, 2 min, 15 degrees) at a fixed heart rate produced significant (P less than 0.0005) decreases in GD that averaged -10.8 +/- 4.0% (mean +/- SD). The rate of change in GD was faster at the onset of exercise than at its cessation (P less than 0.0005). Artificial elevation of heart rate at rest produced significant (P less than 0.0005) increases in GD; mean sensitivity of GD to rate was 0.27 +/- 0.12%/beats/min. Intravenous injection of epinephrine produced significant (P less than 0.001) decreases in GD at two dosage levels (2.5 and 5.0 micrograms/kg) when evaluated at two baseline pacing rates (150 and 190 beats/min); mean changes in GD were -20.64 +/- 0.53% (2.5 micrograms/kg at 150 beats/min), -25.19 +/- 4.20% (5.0 micrograms/kg at 150 beats/min), -14.18 +/- 5.19% (2.5 micrograms/kg at 190 beats/min), and -24.22 +/- 4.94% (5.0 micrograms/kg at 190 beats/min). Sensitivity of GD to epinephrine was dose-dependent (P less than 0.01) at each baseline rate, but was independent (P greater than 0.05) of the rate itself. In the presence of a normal chronotropic response, GD remained unchanged (P greater than 0.5) during exercise in spite of significant elevation in heart rate (105.0 to 167.1 beats/min, P less than 0.001). These data suggest the presence of an intrinsic negative-feedback control mechanism that maintains GD constant in the healthy heart during homeostatic disturbance. Applications in closed-loop rate adaptive pacing are described.

A new method of evoked response detection, previously demonstrated in the ventricle, has been studied in the atrium at the time of routine pacemaker implant in 16 patients. The atrial evoked response was readily detectable in all patients due to excellent recovery from poststimulus polarization. In six patients, as experimental threshold-tracking pacemaker was used to automatically verify atrial capture and to generate strength-duration curves. It is concluded that this pacing technique is both simple and reliable, and that automatic atrial threshold tracking is feasible.

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