Effects of statins on oxidative stress and primed polymorphonuclear leukocytes in hyperlipidemic patients.

Inflammation and oxidative stress are among the factors that have been implicated in the pathogenesis of hyperlipidemia. In metabolic syndrome and hyperlipidemic patients, peripheral polymorphonuclear leukocytes (PMNL) are primed and they release uncontrolled superoxide that contributes to oxidative stress and inflammation. Recent studies have demonstrated that the anti-hyperlipidemic drug, Atrovastatin effects improvement in endothelial function, exhibits anti-oxidative characteristics and reduces lipid markers of oxidation. To evaluate possible nontraditional effects of treatment with Atrovastatin on PMNL priming, oxidative stress and inflammation in hyperlipidemia, 50 non-smoking hyperlipidemic patients were treated for 6 months with Atrovastatin and compared to age and gender-matched healthy controls. PMNL priming was assessed by the rate of superoxide release from separated, phorbol ester-stimulated PMNL and by PMNL-CD11b levels. Inflammation was reflected by blood inflammatory markers including albumin, transferrin, C-reactive protein (CRP) and fibrinogen levels, white blood cells (WBC), PMNL counts and PMNL apoptosis. Atrovastatin treatment showed a reduction in PMNL priming, PMNL apoptosis, fibrinogen and CRP levels concomitant with decreased lipid levels. Atrovastatin may be preferred for hyperlipidemic patients owing to its combined anti-PMNL priming and anti-inflammatory effects in addition to its anti-atherogenic effects.

Reduction of blood loss from diagnostic sampling in critically ill patients using a blood-conserving arterial line system.

STUDY OBJECTIVE: To demonstrate the utility of a new blood-conserving arterial line system in reducing blood loss associated with blood drawing in the critical care setting. DESIGN: Prospective, randomized, crossover comparison between two arterial line systems. SETTING: Medical intensive care unit (ICU); tertiary care teaching institution. PATIENTS: Thirty-one patients who required invasive arterial blood pressure monitoring throughout their ICU course. INTERVENTIONS: For ICU days 1 to 2, patients were randomized to receive either a conventional arterial line system or a new blood-conserving arterial line system. On ICU days 3 to 7, patients with a conventional arterial line were crossed over to the blood-conserving arterial line, and vice versa. Laboratory blood volumes, mixed discard volumes, and blood discard volumes were then recorded to document how much blood loss is associated with each aspect of the blood sampling process. RESULTS: The mean total volume of blood sent to the laboratory for testing was 257.4 ml. As a result of "clearing the line" over the 7-day period, patients with the conventional arterial line system lost a mean volume of 340.2 ml of blood mixed with heparinized saline solution more than patients with the blood-conserving arterial line. In terms of the blood component of the blood-heparinized saline solution mixture, use of the conventional arterial line was associated with an average of 156.8 ml more blood discarded than with the blood-conserving arterial line. CONCLUSION: The new blood-conserving arterial line system provides a simple and effective method for reducing blood loss related to diagnostic sampling in the critical care setting.

Evaluation of a new blood-conserving arterial line system for patients in intensive care units.

OBJECTIVE: To evaluate blood samples obtained from a new blood-conserving arterial line system for the presence of hemodilution or heparin contamination. DESIGN: Prospective, clinical trial. SETTING: A coronary intensive care unit in a tertiary-care teaching hospital. PATIENTS: Cardiovascular patients in whom invasive arterial blood pressure monitoring was indicated. INTERVENTIONS: Paired blood samples were obtained from a conventional arterial line system and a new blood-conserving arterial line system for the measurement of hematocrit and partial thromboplastin time, and compared to evaluate for the presence of either hemodilution or heparin contamination. MEASUREMENTS AND MAIN RESULTS: A Bland-Altman bias analysis of the variability between the two blood draw methods was performed. The analysis indicated that a) a randomly determined partial thromboplastin time obtained from the blood-conserving arterial line would lie between 3.32 and -5.11 of the partial thromboplastin time taken from the conventional arterial line value with 95% confidence; and b) a randomly determined hematocrit obtained from the blood-conserving arterial line would lie between 1.97 and -1.85 of the hematocrit taken from the conventional arterial line value with 95% confidence. CONCLUSIONS: We concluded that a) blood samples obtained with the blood-conserving arterial line demonstrate no evidence of hemodilution or heparin contamination; b) the blood-conserving arterial line provides blood samples without the need for an initial volume of blood to be discarded; c) the blood-conserving arterial line provides a means for blood conservation in the intensive care setting.

Survival after a first episode of ventricular tachycardia or fibrillation.

Recent outcome analyses in ventricular tachycardia (VT) and ventricular fibrillation (VF) have included patients undergoing electrophysiological study (EPS) at tertiary care centers. The selection process involved could introduce bias in the reported populations. We analyzed the outcome of 42 consecutive patients (aged 63 +/- 11 years) admitted to a coronary care unit within 48 hours of a first episode of VT/VF not associated with reversible causes. All patients recovered neurologically and were candidates for EPS. Nine patients (21%) died during the initial hospitalization (none had EPS), and another nine died during a follow-up of 17 +/- 12 months. Actuarial survival at 1 and 2 years was 64% and 62%, respectively. By Cox's model, congestive heart failure functional Class III-IV (P = 0.008; hazard ratio = 3.7) was the only independent prognostic factor. Among patients discharged, subsequent survival did not depend on the performance of EPS or on the antiarrhythmic therapeutic modalities used. Mortality after a first episode of VT/VF is high. Severe congestive heart failure is the most powerful prognostic factor. Studies including successfully referred patients undergoing EPS may not reflect the true natural history of patients with VT/VF.

Atrial natriuretic factor in patients with right ventricular infarction.

To determine the possible role of atrial natriuretic factor in right ventricular infarction, serial measurements of this hormone were performed in 21 patients with acute inferior myocardial infarction. All patients underwent enzymatic, electrocardiographic, echocardiographic and coronary arteriographic studies. Ten patients also had right heart hemodynamic measurements. Eight patients had evidence of an associated right ventricular infarction (Group I) and 13 patients did not (Group II). Enzymatically estimated infarct size, presence of left heart failure and arrhythmias were similar in both groups. Mean arterial pressure in Group I (72.1 +/- 4.4 mm Hg) was significantly lower (p = 0.02) than in Group II (89.5 +/- 4.6 mm Hg). Seven (88%) of the eight patients in Group I had elevated right atrial pressures and a higher incidence than Group II of prolonged hypotension (75%) and right ventricular dysfunction (75%) clinically and by echocardiography. Plasma atrial natriuretic factor levels (mean values +/- SEM in pg/ml) for days 1, 2, 3 and 7 after infarction were, respectively: 152 +/- 30, 165 +/- 48, 199 +/- 27 and 189 +/- 31 for Group I versus 55 +/- 9, 55 +/- 11, 61 +/- 13 and 77 +/- 20 for Group II. The difference between groups was significant for days 1 (p less than 0.05), 3 and 7 (p less than 0.01) and not significant for day 2 (p = 0.07). These findings show that atrial natriuretic factor elevation is part of the neurohumoral response to right ventricular infarction and are consistent with the hypothesis that atrial natriuretic factor may play a pathophysiologic role in the right ventricular infarct syndrome.