A new hypothesis on the mechanism of calcification formed on a blood-contacted polymer surface

Calcification on a blood-contacting polymer surface in an artificial heart is one of the most serious problems. Recently, we maintained a goat with a total artificial heart (AH) for 532 days without systemic anticoagulation. Sac-type blood pumps coated with segmented polyurethane and incorporating jellyfish valves, thin polymer membrane valves, were used in the experiment. The pump was exchanged for a new one on the 312th day on the left side and the 414th day on the right side. They were analyzed with a scanning electron microscope (SEM) and an X-ray microanalyzer. The valve membrane after 312 days of pumping revealed plastic deformation expanding toward upstream between the spokes by creep fatigue with blood pressure difference when the valve closed. Calcification on the membrane was concentrated in the limited portions that received a strong stretching force: the upstream side of the membrane between the spokes and downstream side of the membrane on the spokes. Slight or no calcification was observed on the opposite side of the membrane that received a compression force, and no calcification was found on nonmoving parts such as the center of the membrane and spokes. A new hypothesis on the mechanism of calcification at the portion that received repeated stretching force was raised. The repeated stretching force would extend the polymer membrane, causing some loosening between polymer molecules and generating microgaps. The blood protein and phospholipid would invade into these microgaps, which would then attract Ca ions followed by phosphate ions to make their complexation. The hypothesis could well explain the calcification phenomena on a blood-contacting polymer surface, and gave a good clue on how to protect from calcification.