Citric acid as a decalcifying agent for the excised calcified human heart valves.

OBJECTIVE: Cardiac valvular pathologies are frequently encountered as mechanical and functional disorders due to the calcification of the valves whatever the etiologies are. This pathophysiologic table usually ends up with valvular replacement. In this study, we aimed to decrease/eliminate the calcium in the excised calcified human heart valves by using citric acid in vitro hence bringing about the question for possible oral treatment of calcification of the valves by citric acid ingestion. METHODS: Fourteen pieces of mitral and/or aortic valves excised from 12 patients undergoing valve replacement were placed in a freshly prepared phosphate buffered saline solution containing 0.625% glutaraldehyde at +4 0C for 48 h. They were rinsed with 0.9% NaCl and divided into two groups; study and control. Control tissues were further treated in a freshly prepared solution with identical properties for another 5 days. Study tissues were placed into a solution containing 3.8% citric acid (pH 7.4) and kept for 48 h at +37 degrees C, then rinsed with 0.9% NaCl and transferred into a fresh solution containing 0.625% glutaraldehyde with phosphate buffer at 37 0C for 3 more days. Specimens were biochemically and histopathologically evaluated and compared using Mann Whitney U test. RESULTS: Calcium and phosphate levels in the study group were lower than in the control group (852.5+/-913.41 microg g-1 vs 413.05+/-519.53 microg g-1, p=0.001 and 207.6+/-321.86 microg g-1 vs 124.4+/-289.48 microg g-1, p=0.035, respectively). Malondialdehyde and protein level values were changed insignificantly in the control and study groups. Histopathologic evaluation showed that collagen and elastin fibers were similar in both groups. In the study group, irregular and fusiform calcific formations around the collagen fibers were significantly decreased. CONCLUSIONS: Decalcifying human heart valves in vitro conditions with citric acid without an adverse change to the morphology of the valvular tissue specimens is meaningful. We believe that forwarding and looking for the answer to the question "whether systemic application of citric acid could lead to the decalcification and/or reduction of calcification in the native human heart valves" would be expressive.

Prevention of calcification with TPEN in pericardial bioprosthetic heart valve material.

OBJECTIVE: Calcification is a frequent cause of the clinical failure of bioprosthetic heart valves fabricated from glutaraldehyde pretreated bovine pericardium. The major object of the present study is to prevent calcification of pericardial bioprosthetic heart valve materials with TPEN. METHODS: Bovine pericardium was cut into 2-cm 2 pieces, rinsed in phosphate-buffered saline solution, transferred into +4 degrees C phosphate-buffered saline containing 0.625% glutaraldehyde for initial fixation for 48 h, and allocated into two groups. Control samples were treated in an identical fresh solution for five more days. Others underwent additional fixation in phosphate-buffered saline 2microM TPEN for 48 h. They were then transferred into phosphate-buffered saline + 0.625% glutaraldehyde solution at 37 degrees C (pH 7.4) for three more days. Pericardial patches were inserted into the dorsal pouches of 18 juvenile male Wistar rats as control and study groups. Rats were divided into two groups and sacrificed consecutively by the end of 9th and 12th weeks. The biomechanical properties and calcium contents of explanted tissues were tested and were also assessed histopathologically. RESULTS: The difference in the calcium contents of the control and study groups' pericardial tissues at the 9th, and 12th weeks were statistically significant (p=0.0001, p=0.0001). The comparison of calcium contents between controls of 9th and 12th weeks and study groups' of the 9th and 12th weeks pericardial tissues were also significant (p=0.0001 and p=0.0001). Histopathologic and biomechanical assessment also supported these findings. CONCLUSION: Calcific degeneration of glutaraldehyde-fixed bovine pericardium can be reduced by using TPEN without any effect on durability.

Hearing loss in patients undergoing coronary artery bypass grafting with or without extracorporeal circulation.

BACKGROUND: Our aim was to investigate the differences in postoperative hearing thresholds in patients undergoing coronary artery bypass grafting with (Group I, n=20) or without (Group II, n=17) extracorporeal circulation. MATERIAL/METHODS: 37 patients undergoing coronary artery bypass grafting with or without extracorporeal circulation were prospectively evaluated in terms of hearing threshold changes with the intention of documenting hearing losses postoperatively. The t-test for two independent variables was used for statistical analysis. RESULTS: Hearing threshold changes were detected in 9 Group I patients (45%) and 3 Group II patients (17.65%). The difference between the two groups was statistically significant (p=0.0426). CONCLUSIONS: Postoperative hearing threshold changes, not necessarily revealed by clinical examinations, are encountered after coronary artery bypass grafting operations. Extracorporeal circulation usage seems to bring an additional risk in terms of hearing loss.

Comparison and evaluation of experimental mediastinitis models: precolonized foreign body implants and bacterial suspension inoculation seems promising.

BACKGROUND: Post-sternotomy mediastinitis (PSM) is a devastating surgical complication affecting 1-3% of patients that undergo cardiac surgery. Staphylococcus aureus is one of the most commonly encountered bacterial pathogen cultured from mediastinal samples obtained from patients with PSM. A component of the membrane of the gram positive bacteria, lipoteichoic acid, stimulates the blood monocytes and macrophages to secrete cytokines, radicals and nitrogen species leading to oxido-inflammatory damage. This seems to be responsible for the high mortality rate in PSM. For the evaluation of the pathogenesis of infection or for the investigation of alternative treatment models in infection, no standard model of mediastinitis seems to be available. In this study, we evaluated four mediastinitis models in rats. METHODS: The rats were divided into four groups to form different infection models. Group A: A suspension of 1 x 107 colony-forming units Staphylococcus aureus in 0,5 mL was inoculated from the right second intercostal space into the mediastinum. Group B: A hole was created in the right second intercostal space and a piece of stainless-steel implant with a length of 0.5 cm was inserted into the mediastinum and a suspension of 1 x 107 cfu bacteria in 0,5 mL was administered via the tail vein. Group C: Precolonized stainless-steel implant was inserted into the mediastinum. Group D: Precolonized stainless-steel implant was inserted into the mediastinum and the bacteria suspension was also injected into the mediastinum. On the 10th day, rats were sacrificed and the extension of infection in the mediastenae was evaluated by quantitative cultures. Myeloperoxidase activity (MPO) and malondialdehyde (MDA) levels were determined in the sera to evaluate the neutrophil activation and assess the inflammatory oxidation. RESULTS: The degree of infection in group C and D were 83.3% and 100% respectively (P < 0.001). MDA levels were significantly higher in these two groups than the others (P < 0.001). CONCLUSION: Infected implants and high bacterial concentration administration were the two important components that played a significant role in the outcome of a successful infection in mediastinum in a rat model.