Inhibition of calcification with citric acid in pericardial bioprosthetic heart valve material: a preliminary report

• Published in: The Journal of heart valve disease Vol. 13; no. 4; p. 697
• Main Authors: Sucu, Nehir, Tamer, Lulufer, Aytacoglu, Barlas, Polat, Ayse, Dondas, H Ali, Gul, Ali, Dikmengil, Murat, Atik, Ugur
• Format: Journal Article
• Language: English
• Published: England 01.07.2004
• Subjects: Animals; Bioprosthesis; Calcinosis - metabolism; Calcinosis - prevention & control; Calcium - metabolism; Cattle; Chelating Agents - pharmacology; Citric Acid - pharmacology; Disease Models, Animal; Heart Valve Prosthesis; Heart Valve Prosthesis Implantation; Male; Models, Cardiovascular; Pericardium - drug effects; Pericardium - metabolism; Pericardium - surgery; Rats; Rats, Wistar; Severity of Illness Index
• ISSN: 0966-8519

Although current bioprosthetic heart valves have low thrombogenicity and favorable hemodynamic properties, their durability remains unsatisfactory. Valve failure usually occurs from calcific degeneration. The study aim was to investigate the effect of a chelating agent, citric acid (CA), on calcification in bovine pericardium. Freshly excised bovine pericardium was dissected free from adhering fat tissue and cut into 1- cm2 pieces; these were rinsed in phosphate-buffered saline solution (PBS), transferred into +4 degrees C PBS containing 0.625% glutaraldehyde (GA) for initial fixation, and then allocated to two groups. Control samples received the same treatment in a fresh solution for 5 days. The other samples underwent an additional fixation step in PBS (pH = 7.4, 37 degrees C) containing 3.8% CA for a period of 48 h (30 ml/g tissue) and were then transferred into freshly prepared PBS + 0.625% GA solution at 37 degrees C for a further 3 days. To investigate calcification rate, pericardial patches were inserted into the dorsal pouches of 15 juvenile male Wistar rats for 42 days. Tissue calcium levels were measured with atomic absorption spectrophotometer, and also assessed histopathologically. The calcium content of CA-treated pericardium was significantly lower than that of controls (66.4 +/- 33.5 and 111.4 +/- 27.2 mg/g, respectively; p = 0.000). In general, the degree of calcification in histological sections agreed well with results of the chemical analyses. Control pericardial tissues showed moderate to severe solid mineral depositions, predominantly parallel to the implant surface, whereas only minor traces of calcium were found in CA-treated tissues. These preliminary data suggest that calcific degeneration in bovine pericardium may be reduced by using CA as a chelating agent.