The aim of this study was to evaluate the diagnostic criteria and angiographic classifications of Takayasu arteritis by presenting the clinical, angiographic, and prognostic findings and a prospective follow-up of 78 patients. Occlusive thromboaortopathy or Takayasu arteritis is a large vessel vasculitis. The disease is systemic with an autoimmune and genetic etiology. The complete clinical and angiographic manifestations are reported for 78 cases based on diagnostic criteria of the American College of Rheumatology with a mean 6 +/- 3.2 years follow-up. The mean age was 34.7 and female:male ratio was 3.6:1. According to National Institute of Health criteria, 61.5% of patients were in the acute phase of disease with systemic symptoms such as fever, weight loss, malaise, and elevated C-reactive protein levels. Immunologic markers, such as antinuclear antibody and antineutrophil cytoplasmic antibodies, were negative. The tuberculin test result was positive in 47%. Vascular bruit was present in 89%. Almost all patients had stenoses, occlusions, or aneurysmatic changes of the aorta and its main branches. Hypertension was detected in 58% and left ventricular hypertrophy was initially present in 22 (28%) patients. The angiographic manifestations were classified as type I, cervicobrachial type with 20 cases (25.6%); type II, thoracoabdominal type with 13 cases (16.6%); type III, peripheral type with 10 cases (12.8%); and type IV, generalized type with 35 cases (44.8%). The coronary arteries were involved in 6 cases, pulmonary arteries in 11 initially 5 in follow-up (16 cases), and renal arteries in 28 cases, respectively. A good correlation of the clinical manifestations and the prognosis was observed. During follow-up, five patients suffered from myocardial infarction, six had cerebrovascular accident, seven patients underwent aortic valve replacement, and six patients died (mortality rate, 7.6%). The specificity and sensitivity of diagnostic criteria were 94% and 76%, respectively. In contrast to ours and Nasu's classification in the new classification of Numano, some angiographic types and subtypes of Takayasu arteritis are not present in our patients.

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We studied the effect of atrial pacing induced myocardial ischemia on levels of soluble L-selectin (sL-selectin) and generation of neutrophil derived reactive oxygen species (ROS) in 10 patients with coronary artery disease (CAD) and stable angina and in six individuals without CAD. Myocardial ischemia was measured metabolically by lactate sampling from the coronary sinus (CS) and arterial blood at each pacing step. Before each pacing step, at peak pacing and shortly after cessation, plasma concentrations of sL-selectin and generation of ROS using the chemiluminescence method were measured in CS and femoral artery blood. Baseline sL-selectin levels in CS samples were significantly lower in the CAD compared to the control group (547 +/- 80 vs 836 +/- 82 ng/mL, P = 0.03). At peak pacing, nine of ten patients with CAD developed myocardial ischemia (lactate extraction ratio at rest 28% +/- 7%, at peak pacing -16% +/- 6%). In these patients, luminol-enhanced chemiluminescence (CL, 0.88 +/- 0.45 vs 1.9 +/- 0.9 cpm x 10(5), P = 0.09) and levels of sL-selectin (547 +/- 80 vs 764 +/- 86 ng/mL, P = 0.03) from naive neutrophils increased significantly in CS blood suggesting a potent in vivo activation of neutrophils. In control patients, incremental pacing caused neither myocardial ischemia nor a significant change of chemiluminescence or of sL-selectin levels. In conclusion, myocardial ischemia induced by pacing tachycardia is able to activate neutrophils in patients with chronic stable coronary artery disease leading to increased generation of ROS and shedding of L-selectin into the coronary circulation.

We studied the effect of atrial pacing-induced myocardial ischemia on the generation of oxygen free radicals (OFR) in 8 patients with verified coronary artery disease (CAD) and in a control group of 4 patients without coronary atherosclerosis. Myocardial ischemia was measured metabolically by simultaneous lactate sampling from coronary sinus (CS) and arterial blood. Generation of OFR from purified viable polymorphonuclear neutrophils (PMN) was assessed by means of the chemiluminescence (CL) method. At peak pacing, 7 of 8 patients with CAD exhibited transient myocardial ischemia (mean lactate extraction ratio at rest: 23.6 +/- 7.7 vs 5.21 +/- 5.1% at peak pacing, p = 0.012). In these patients, unstimulated PMN harvested from the CS depicted a significant increase of luminol-enhanced CL (from 1.06 +/- 0.54 to 2.15 +/- 1.28 cpm x 10(5), p = 0.012) after atrial pacing. There was no additional effect from further ex vivo stimulation with phorbol myristate acetate. This finding underscores the role of myocardial ischemia as a potent endogenous activator of PMN function and may have implications in the pathogenesis and progression of atherosclerosis.

Objectives: Critically ill patients often require mechanical ventilatory support and increased inspiratory 0 2 concentration. Experimentally, continuous breathing of 100% 02 in animals leads to progressive irreversible damage to the lung, ARDS and death. In critical care units 100% 0 2 is often administered for several hours. The mechanism of hyperoxia induced lung injury is unclear. The objective of this study is to explore inflammatory mediator responses following breathing 100% 0 2 in humans. Ten healthy subjects aged 32-46 breathed 100% 0 2 for 60 minutes. Minute ventilation, arterial 02 saturation, blood pressure, heart rate and EKG were continually monitored. Methods: Interleukin-1 beta (IL-1(3) and Interleukin-1 receptor antagonist (IL-ira) were determined by ELISA in the supernatant of whole blood incubated with Endotoxin by the method of Nerad and Dinarello, before (To), at the end of 60 minutes of 100% Oz breathing (F6o) and at 90 (Tso) and 180 (Ttso) minutes following resumption of air breathing. Results: pg/ml 02 Breathing Air Breathing To