Cardiopulmonary bypass (CPB) produces an inflammatory response due to the interaction of blood with a foreign body surface. The lungs are most affected by this inflammatory response. Pentoxifylline (PTX), a phosphodiesterase inhibitor and an inhibitor of leukocyte activation, is used to minimize damage in lungs where leukocytes play an important role. Twenty patients with mitral valve stenosis with planned mitral valve surgery were included in the study. The ten patients receiving pentoxifylline (PTX group) were administered 400 mg PTX orally TID for 3 days preoperatively and, following anesthetic induction, a 300 mg PTX infusion was given. The ten patients receiving no PTX were the control group (CT). Platelet and leukocyte counts, mean pulmonary arterial pressure (mPAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI), pulmonary vascular resistance (PVR), alveolar-arterial PO2 gradient (AaDO2) were measured just before and after CPB, and 2 h postoperatively. The number of the leukocytes increased in the blood samples drawn 15 min after CPB in both groups and 2 h postoperatively showed no statistical change. The number of platelets had decreased significantly at the end of the CPB in both groups and, 2 h postoperatively, there was a further decrease in the blood count in the control group (P < 0.05). There was no significant difference in either the preoperative or postoperative PAP, PAWP, and CI. Pulmonary vascular resistance increased in both groups following the CPB (CT, before: 136 +/- 44, after: 177 +/- 94 dyne. sec.cm-5; PTX, before: 151 +/- 82, after 182 +/- 43 dynes.sec.cm-5). Two hours postoperatively, a considerable increase continued in the control group (CT 219 +/- 170 dynes.sec. cm-5), while there was an insignificant increase in the PTX group (PTX 193 +/- 51 dynes.sec.cm-5) (P < 0.05). The alveolar-arterial PO2 gradient increased after the CPB in both groups but a moderate decrease was observed 2 h postoperatively. In lung biopsy specimens taken before and after the CPB, there was marked leukocyte sequestration in the control group, whereas the number of leukocytes was seen to be insignificant in the PTX group (P < 0.005). This dosage regimen of PTX inhibits the postoperative increase in PVR and greatly minimized leukocyte sequestration in the lung due to CPB.

Patients with giant left atrium were divided into 2 groups retrospectively. Group 1 comprised 10 patients with compression symptoms who received left atrial plication after mitral valve replacement. Group 2 comprised 31 patients without symptoms of compression who did not receive plication. Age, sex, ejection fraction, and left ventricular end-diastolic pressure were similar in the 2 groups preoperatively. Left atrial diameter reduction was not significantly different between the 2 groups. Mean left atrial diameter was 80.41 ± 15.08 mm preoperatively and 66.64 ± 13 mm postoperatively in group 1. In group 2, the mean values were 80 ± 8.95 and 66.1 ± 8.14 mm, respectively. Postoperatively, no differences were observed in ejection fraction or left ventricular end-diastolic pressure between the 2 groups. Left atrial diameter was over 80 mm in 12 patients in group 2 and it did not reduce postoperatively to below 65 mm in 11 of these patients. On the other hand, only 7 of 19 patients with a left atrial diameter below 80 mm preoperatively did not reduce to values below 65 mm (p = 0.04). Therefore, in cases of giant left atrium with a left atrial diameter below 80 mm, plication might not be necessary.

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