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Enhanced External Counterpulsation Treatment Improves Arterial Wall Properties and Wave Reflection Characteristics in Patients With Refractory Angina

Department of Medicine/Cardiology, University of Florida College of Medicine, Gainesville, Florida.

View larger version (8K): [in a new window]   Figure 1 The early part of the ascending aortic pressure wave, with amplitude (Pi – Pd), is generated by the left ventricular (LV) ejection (flow) wave. This forward-traveling pressure wave is dependent upon central (elastic) arterial stiffness and pulse wave velocity (PWV) and is not influenced by wave reflections. The later part of the pressure wave, with amplitude (Ps – Pi), is generated by the reflected wave arriving from the lower body during systole and adding to the forward pressure wave. This wave is dependent upon the elastic properties of the entire arterial tree and PWV. Pulse pressure = (Pi – Pd) + (Ps – Pi) = (Ps – Pd), and augmentation index (AIa) = (Ps – Pi)/(Ps – Pd). AIa is dependent on the elastic properties of the entire arterial tree, transmission velocity of the reflected wave, and distance to the major reflecting site. tp is inversely related to arterial stiffness and is the round-trip travel time of the pressure wave from the heart to the periphery and back; tr is the systolic duration of the reflected wave. Wasted LV pressure energy (2.09 tr[Ps – Pi]) and tension-time-index (area under the systolic portion of the pressure wave) are measures of myocardial oxygen demand. The broken curve is the pressure or flow wave without reflections.

View larger version (31K): [in a new window]   Figure 2 Noninvasive recordings of radial artery pressures waves (left) and synthesized aortic pressure waves (right) before and after EECP treatment in a 58-year-old woman with stable refractory angina. Arrows on the radial pressure wave denote the beginning of the reflected wave, and those on the aortic pressure wave denote the beginning and peak of the reflected wave.

View larger version (23K): [in a new window]   Figure 3 Effects of enhanced external counterpulsation (EECP) treatment on indices of estimated arterial pulse wave velocity and arterial stiffness. EECP caused an increase in travel time of the reflected wave, tp/2, from 68 ± 8.0 ms to 74 ± 6.6 ms (p < 0.001) and a decrease in augmentation index (AIa) from 27 ± 10% to 19 ± 10% (p < 0.001).

View larger version (23K): [in a new window]   Figure 4 Effects of enhanced external counterpulsation (EECP) treatment on indices of estimated myocardial oxygen demand. EECP caused a decrease in tension-time index (TTI) from 23 ± 5.1 x 102 units to 19 ± 3.9 x 102 units (p < 0.001) and a decrease in wasted LV energy from 56 ± 16 x 102 dyne-s-cm–2 to 36 ± 13 x 102 dyne-s-cm–2 (p < 0.001).