Three-dimensional transmural mechanical interaction between the coronary vasculature and passive myocardium in the dog.

The "garden hose" effect of coronary perfusion on diastolic left ventricular (LV) mechanics has been proposed to cause changes in systolic function by altering diastolic sarcomere length. We measured transmural distributions of three-dimensional shape change using radiopaque markers implanted in the LV free wall of eight isolated arrested canine hearts as functions of coronary arterial perfusion pressure (Pp) and LV pressure (PLV) and related these deformations to the local muscle fiber architecture. Increased Pp from 0 to 110 mm Hg produced a 10% reduction in LV chamber volume (P < .01) and 25% to 40% decreases in local three-dimensional wall strain at matched PLV, indicating myocardial stiffening. Significant decreases in the magnitudes of local deformation occurred preferentially in the cross-fiber and radial directions (P < .02), with no change in fiber strain. This suggests that changing coronary Pp does not alter diastolic fiber length; hence, the Frank-Starling law may not mediate the Gregg effect. Since the myocardial microvessels are primarily oriented parallel to the muscle fibers, the observed myocardial stiffening occurs in the directions transverse to the microvessels rather than along their length. Local myocardial wall volume in the unloaded LV demonstrated a uniform 5% increase from the unperfused state to Pp of 50 mm Hg. With further increases in Pp up to 110 mm Hg, the change in regional wall volume from the unperfused state developed a substantial transmural gradient increasing by 7% at the epicardium and 15% at the subendocardium. This reflects a significant increase (P < .02) in intramyocardial coronary capacitance from epicardium to endocardium, which may be related to a transmural gradient in coronary distensibility or vascularity.