Tumor necrosis factor alpha serum levels and inflammatory response in acute ischemic stroke patients.

Experimental evidence indicates that tumor necrosis factor alpha (TNF-alpha) is involved in brain damage following ischemic injury. The present study was designed to monitor serum TNF-alpha levels in acute stroke patients and to correlate TNF-alpha levels with lesion size, neurological impairment and vascular risk factors. In 41 patients with ischemic stroke, serum TNF-alpha levels were serially measured by a solid enzyme amplified sensitivity immunoassay (EASIA) in the first 10 days after stroke onset. Serum fibrinogen and C-reactive protein (CRP), white blood cell (WBC) and neutrophil counts were determined on the same days to monitor acute phase response changes. Lesion size was calculated on computed tomograms by a computer-assisted procedure. Neurological impairment was evaluated on the Canadian Neurological Scale. Forty age-matched subjects were used as controls. Compared to baseline, TNF-alpha levels significantly increased during the study ( p=0.0001), peaking on day 7. Peak TNF-alpha levels did not correlate with neurological impairment or lesion size. Multivariate analysis showed that sex, age, vascular risk factors and infectious complications did not influence TNF-alpha levels. Fibrinogen, CRP, WBC and neutrophil concentrations increased, indicating an acute phase response occurred after stroke. In conclusion, serum TNF-alpha levels showed an early and prolonged increase after stroke onset, unrelated to lesion size, neurological impairment, age, sex, vascular risk factors or infectious complications. Serum increase of TNF-alpha may be explained as part of the acute phase response occurring in stroke patients.

Association between myocardial right ventricular relaxation time and pulmonary arterial pressure in chronic obstructive lung disease: analysis by pulsed Doppler tissue imaging.

This study assessed right ventricular function in chronic obstructive lung disease and pulmonary hypertension by Doppler tissue imaging. Doppler echocardiography of the right ventricle and Doppler tissue imaging of the tricuspid annulus were performed in 63 subjects: 20 healthy controls, 20 with lung disease, and 23 with both lung disease and pulmonary hypertension. Two-dimensional tricuspid systolic plane excursion was lower in patients with pulmonary hypertension than in the other 2 groups. Doppler tricuspid inflow measurements distinguished patients in both of the diseased groups from the control subjects, but they did not differentiate patients with pulmonary hypertension from those without it. The ratio of peak E-wave to peak A-wave velocities derived by Doppler tissue imaging was significantly lower and the myocardial acceleration time longer in both groups of lung disease than in the control group. Only myocardial relaxation time distinguished the 3 groups (all P <.01); a gradual increase in time occurred, with the shortest time seen in controls, a longer time in patients with chronic obstructive lung disease without pulmonary hypertension, and the longest time in patients with lung disease and pulmonary hypertension. In the overall population including subjects with at least minimal tricuspid regurgitation, myocardial relaxation time was positively related to pulmonary systolic pressure. In conclusion, Doppler tissue imaging distinguishes subsets of patients affected by lung disease with or without pulmonary hypertension and identifies patients with different levels of pulmonary artery systolic pressure.