interleukin-8 and Mitral-Valve-Insufficiency

Leukocytopenia can be caused by depressed production, increased peripheral destruction, or excessive peripheral pooling. Leukocyte margination is one of the mechanisms responsible for excessive peripheral pooling. A reversible leukocyte margination is caused by an increase in pro-inflammatory cytokines. However, there are limited data for this phenomenon in clinical conditions. We describe a case of unexpected transient leukocytopenia after exchanging an extracorporeal membrane oxygenation (ECMO) system used to treat severe cardiogenic pulmonary edema. To assess the cause of the leukocytopenia, the serum concentrations of pro-inflammatory cytokines and selectins were measured. The concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 were markedly, but transiently, elevated in relation to the leukocytopenia. The transient leukocytopenia with pulmonary margination appeared to be caused by a steep surge of pro-inflammatory cytokines stimulated by hypoxia/reoxygenation during the exchange of the ECMO system. This case may suggest the mechanisms responsible for leukocytopenia in the clinical entity referred to as "systemic inflammatory response syndrome"

Topics: Chordae Tendineae; Cytokines; Dyspnea; Extracorporeal Membrane Oxygenation; Heart Valve Diseases; Humans; Hypoxia; Interleukin-6; Interleukin-8; Intra-Aortic Balloon Pumping; Leukopenia; Male; Middle Aged; Mitral Valve Insufficiency; Positive-Pressure Respiration; Pulmonary Edema; Rupture, Spontaneous; Systemic Inflammatory Response Syndrome; Tumor Necrosis Factor-alpha

In patients with atrial septal defect in whom pulmonary hypertension could develop as a consequence of left-to-right shunt, the extent of neutrophil-mediated lung injury induced by cardiopulmonary bypass (CPB) is related to the degree of increase in the preoperative pulmonary artery pressure. In the present study, we investigated the relationship between levels of granulocyte elastase (GEL) after CPB and preoperative pulmonary hemodynamics or changes in pulmonary function after the operation in patients with mitral valve disease, in whom pulmonary hypertension could develop as a result of pulmonary venous congestion. The plasma levels of GEL were measured before and after CPB in patients who underwent mitral valve replacement. Respiratory index (RI) was evaluated preoperatively and postoperatively. Preoperative pulmonary hemodynamics were determined within one month of the operation. Granulocyte elastase level rose significantly after CPB from baseline (134.3 +/- 44.6 mg/L versus 2042.1 +/- 1215.0 mg/L; p <0.001). Peak level of GEL was significantly correlated with preoperative systolic pulmonary artery pressure (r = 0.71; p = 0.020), mean pulmonary artery pressure (r = 0.64; p = 0.046), pulmonary capillary wedge pressure (r = 0.68; p = 0.032), and pulmonary-to-systemic arterial pressure ratio (r = 0.64; p = 0.045), but not with the hemodynamic variables for pulmonary blood flow or pulmonary resistance. Moreover, the value of (Postoperative RI - Preoperative RI)/Preoperative RI was positively correlated with the peak level of GEL (r = 0.76; p = 0.011). In conclusion, in patients with mitral valvular disease, as in those with atrial septal defect, the increase in GEL level after CPB is proportional to the increase in preoperative pulmonary artery pressure, which may cause the accordant pulmonary vascular damage.

Topics: Aged; Cardiopulmonary Bypass; Female; Heart Valve Prosthesis Implantation; Hemodynamics; Humans; Interleukin-6; Interleukin-8; Intraoperative Period; Leukocyte Elastase; Lung Diseases; Male; Middle Aged; Mitral Valve Insufficiency; Mitral Valve Stenosis; Predictive Value of Tests; Pulmonary Circulation; Vascular Diseases