Skeletal muscle extraaortic counterpulsation. A true arterial counterpulsation

Reduction of left ventricular work load during systole, a critical component of arterial counterpulsation, has not previously been documented for skeletal muscle-powered extraaortic counterpulsation. To assess its capacity for afterload reduction, a skeletal muscle extraaortic counterpulsator was connected to the thoracic aorta and counterpulsated. Canine hearts (n = 7) were instrumented with left ventricular Millar catheters (Millar Instruments, Inc., Houston, Tex.) for pressure measurements and with piezoelectric ultrasonic crystals for measurement of the left ventricular minor axis dimension and wall thickness. During systole, skeletal muscle extraaortic counterpulsation resulted in a significant change in all three determinants of left ventricular circumferential wall stress compared with control conditions (no counterpulsation). Pressure decreased (peak systole, 100 +/- 5 versus 75 +/- 6 mm Hg; p less than 0.05 by paired t test), minor axis dimension decreased (end systole, 46.4 +/- 1.1 versus 45.8 +/- 1.1 mm; p less than 0.05 by paired t test), and wall thickness increased (end systole, 10.4 +/- 0.7 versus 10.6 +/- 0.7 mm; p less than 0.05 by paired t test). Left ventricular wall stress/dimension work loops showed a shift downward and to the left, a shift consistent with afterload reduction. The mean systolic left ventricular wall stress was significantly reduced, from 67.3 +/- 10.6 to 47.7 +/- 8.1 10(3) dyne/cm2 (p less than 0.05 by paired t test). Skeletal muscle extraaortic counterpulsation increased the diastolic aortic pressure from 72 +/- 6 to 105 +/- 8 mm Hg (p less than 0.05 by paired t test). Our data, which documented the counterpulsator's direct effects on left ventricular functional mechanics, showed that skeletal muscle extraaortic counterpulsation is capable of both diastolic augmentation of arterial pressure and systolic unloading of the left ventricle. Skeletal muscle extraaortic counterpulsation has potential application for ventricular unloading in the treatment of chronic end-stage heart failure.