[Reconstructive surgery of the mitral and tricuspid valves with a Cosgrove-Edwards flexible ring]. / Chirurgia ricostruttiva delle valvole mitrale e tricuspide con anello flessibile di Cosgrove-Edwards.

BACKGROUND: Mitral and tricuspid valve asymmetric annular dilation represents the most important mechanism which produces insufficiency. Recent computerized in vitro and in vivo three-dimensional models have been developed in order to better understand the competing factors (annular dilation, displacement of papillary muscles, left and right ventricular geometry). The leading cause of mitral and tricuspid competence is a sphincteric action of both annuli, during systole and diastole, the loss of which produces asymmetric dilation and therefore the absence of cusp coaptation. The Cosgrove-Edwards dynamic ring corrects, alone or in combination with other procedures on the valves, this patho-anatomic feature in a physiological way by restoring the normal annular dimensions and the sphincteric movements during the cardiac cycle. METHODS: Between June 1998 and May 1999, 30 adult patients underwent mitral (n = 20, Group I) or tricuspid valve repair (n = 10, Group II). Regurgitation was due to a degenerative disease in 13 Group I patients and to ischemic (n = 3), congenital (n = 2) or dilated cardiomyopathy (n = 2) in the others. In Group II the leading cause of insufficiency was functional regurgitation in 7 patients and organic in 3. Associated procedures were carried out in 4 Group I patients and in all Group II patients. Regurgitation was evaluated by transesophageal echocardiography before, during and 3 months after operation. The maximal regurgitant area (MRA) and the grade of insufficiency were evaluated using the equation: MRA < 2 cm2 = grade 0, MRA > 2 < 4 cm2 = 1+, MRA > 4 < 7 cm2 = grade 2+, MRA > 7 < 10 cm2 = 3+, MRA > 10 cm2 = 4+. RESULTS: The operative mortality was 0%. One Group I patient died 3 months after operation due to bronchopneumonia. No patient was reoperated on for plasty failure in both groups during the follow-up. Mitral insufficiency was absent (grade 0) in 17 Group I patients and mild (grade 1+) in 3 at the end of operation. At 3-month postoperative transesophageal echocardiographic control mitral insufficiency was absent in 14 patients, mild (1+) in 4 and moderate (2+) in 2. MRA was 3 cm2 in the 2 patients operated on for dilated cardiomyopathy and < 3 cm2 in the others. Preoperative tricuspid insufficiency of grade 4+ in all Group II patients became absent in 9 of them either at the end of operation or at 3-month postoperative control. CONCLUSIONS: The Cosgrove-Edwards dynamic ring as isolated device or in combination with other plasty mitral or tricuspid procedures is a safe, simple, and reproducible method to restore the distorted motion of valvular annuli. It preserves the sphincteric mechanism of the valve and allows for the coaptation of cusps. Although in a small number of patients and for a short period of follow-up our experience corroborates what other more consistent series of patients operated on have shown.

Effect of glutathione monoethyl ester on glutathione level and cardiac energetics in reperfused pig heart.

The GSH level in myocardial tissue represents an important defense mechanism against oxygen toxicity. Since the ischemia-induced depletion of GSH might favour the cytotoxicity of oxygen-derived free radicals produced during reperfusion, we assessed the effects of the GSH donor, glutathione monoethylester, in anaesthetized pigs subjected to 90 minutes of coronary occlusion followed by 30 minutes reperfusion. The drug was infused intracoronarily at a dose of 1 mg/ml (0.5 ml/min) throughout the experimental period. After coronary occlusion and reperfusion, we found a decrease in GSH, ADP, ATP and phosphocreatine levels in reperfused compared with non-ischemic tissue. Less evident were the differences in mitochondrial function, there being only a reduction in the reperfused tissue of the respiratory control index and state 3 respiration values when pyruvate was used as substrate. The infusion with glutathione monoethylester decreased the depletion of tissue GSH and improved the GSH/GSSG ratio, particularly in the non-ischemic tissue. Moreover, the drug decreased the mitochondrial dysfunction at the level of pyruvate utilization and partially prevented the fall in ATP in the reperfused tissue. This study confirms a possible protective effect of glutathione monoethylester in the prevention of reperfusion-induced myocardial damage.