Leukocyte depletion during cardiopulmonary bypass has been demonstrated in animal experiments to improve pulmonary function. Conflicting results have been reported, however, with clinical depletion by arterial line filter of leukocytes at the beginning of cardiopulmonary bypass. In this study, we examined whether leukocyte depletion from the residual heart-lung machine blood at the end of cardiopulmonary bypass would improve lung function and reduce the postoperative inflammatory response. Thirty patients undergoing elective heart operations were randomly allocated to a leukocyte-depletion group or a control group. In the leukocyte-depletion group (n = 20), all residual blood (1.2 to 2.1 L) was filtered by leukocyte-removal filters and reinfused after cardiopulmonary bypass, whereas in the control group an identical amount of residual blood after cardiopulmonary bypass was reinfused without filtration (n = 10). Leukocyte depletion removed more than 97% of leukocytes from the retransfused blood (p < 0.01) and significantly reduced circulating leukocytes (p < 0.05) and granulocytes (p < 0.05) compared with the control group. Levels of the inflammatory mediator thromboxane B2 determined at the end of operation (p < 0.05) were significantly lower in the depletion group than in the control group, whereas no statistical differences in interleukin-6 levels were found between the two groups. After operation, pulmonary gas exchange function (arterial oxygen tension at a fraction of inspired oxygen of 0.4) was significantly higher in the leukocyte-depletion group 1 hour after arrival to the intensive care unit (p < 0.05) and after extubation (p < 0.05). There were no statistical differences between the two groups with respect to postoperative circulating platelet levels and blood loss, and no infections were observed during the whole period of hospitalization. These results suggest that leukocyte depletion of the residual heart-lung machine blood improves postoperative lung gas exchange function and is safe for patients who are expected to have a severe inflammatory response after heart operations.

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Extensive myocardial bridging in the left anterior descending coronary artery was found in a 46 year old survivor of sudden cardiac near-death. Positron emission tomography and dobutamine stress echocardiography revealed ischaemia in the myocardium distal to the bridging. Spasm was excluded as cause of the ischaemia by intracoronary infusion of acetylcholine. Further evaluation of the haemodynamic importance of the bridging using intracoronary Doppler flow velocity measurements revealed an abnormal flow reserve. Dobutamine stress during coronary angiography caused increased mechanical compression during diastole. This was accompanied by multiple premature ventricular contractions. After a debridging operation the flow velocity reserve was normal. The abnormalities found during dobutamine stress had disappeared. Unexpectedly, a spasm was inducible. This may have been due to local oedema or scar formation after the operation. For the evaluation of the haemodynamic importance of myocardial bridging, intracoronary Doppler flow velocity measurements and angiography during dobutamine stress may be helpful in clinical decision making. (Heart 1997;77:280-282) Keywords: dobutamine stress; coronary flow reserve; myocardial bridging; sudden cardiac death Sudden cardiac death in young and middle aged subjects may be caused by (congenital) abnormalities of the coronary arteries. In this report a case of extreme myocardial bridging was found as the precipitating factor for ventricular arrhythmia in a survivor of sudden cardiac near-death.Case A 46 year old man collapsed during lunch in a factory canteen. Cardiopulmonary resuscitation was started immediately. On the arrival of the ambulance ventricular fibrillation was present. After defibrillation, sinus rhythm and adequate circulation were established. In the hospital the heart rate was 50 beats/min, blood pressure 130/70 mm Hg, and the patient respired spontaneously.