natriuretic-peptide--brain and Venous-Insufficiency

To study trends in systemic inflammatory factors and aminoterminal brain natriuretic propeptide (NT-proBNP) in the blood of patients with stage IIA and IIB chronic heart failure (CHF) during therapy aimed at reducing venous congestion.. The study enrolled 52 patients with postinfarction cardiosclerosis (PICS). Clinical, echocardiographic and laboratory studies were conducted. The levels of TNF-alpha, IL-6, IL-10 and C-reactive protein (CRP) were measured by enzyme immunoassay. The concentration of endotoxin (ET) was estimated by the end-point chromogenic LAL test, that of NT-proBNP--by immunochromotographic assay.. In the patients with CHF, clinical signs of pulmonary venous congestion are associated with a statistically significant increase in the blood levels of TNF-alpha and CRP, those of systemic venous congestion are related to a further rise in TNF-alpha levels and elevation of blood concentrations of NT-proBNP, ET and IL-10. Treatment-related reduction in pulmonary venous congection is associated with a decrease in the levels of TNF-alpha, CRP and IL-6; that in systemic venous congestion--with lower concentrations of NT-proBNP, TNF-alpha and ET.. Specific changes in the levels of systemic inflammatory factors and NT-proBNP were found in patients with CHF in the presence of pulmonary and systemic venous congestion. Treatment aimed at elimination of the latter leads to reduction in the levels of systemic inflammatory factors and NT-proBNP.

Topics: C-Reactive Protein; Chronic Disease; Coronary Circulation; Cytokines; Female; Heart Failure; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Peptide Fragments; Severity of Illness Index; Systemic Inflammatory Response Syndrome; Treatment Outcome; Venous Insufficiency

Edema is a common clinical sign that may indicate numerous pathologies. As a sequela of imbalanced capillary hemodynamics, edema is an accumulation of fluid in the interstitial compartment. The chronicity and laterality of the edema guide evaluation. Medications (e.g., antihypertensives, anti-inflammatory drugs, hormones) can contribute to edema. Evaluation should begin with obtaining a basic metabolic panel, liver function tests, thyroid function testing, brain natriuretic peptide levels, and a urine protein/creatinine ratio. Validated decision rules, such as the Wells and STOP-Bang (snoring, tired, observed, pressure, body mass index, age, neck size, gender) criteria, can guide decision-making regarding the possibility of venous thromboembolic disease and obstructive sleep apnea, respectively. Acute unilateral lower-extremity edema warrants immediate evaluation for deep venous thrombosis with a d-dimer test or compression ultrasonography. For patients with chronic bilateral lower-extremity edema, duplex ultrasonography with reflux can help diagnose chronic venous insufficiency. Patients with pulmonary edema or elevated brain natriuretic peptide levels should undergo echocardiography to assess for heart failure. Lymphedema is often a clinical diagnosis; lymphoscintigraphy can be performed if the diagnosis is unclear. Treatment of edema is specific to the etiology. Diuretics are effective but should be used only for systemic causes of edema. Ruscus extract and horse chestnut seed demonstrate moderate-quality evidence to improve edema from chronic venous insufficiency. Compression therapy is effective for most causes of edema.

Topics: Edema; Humans; Lymphedema; Natriuretic Peptide, Brain; Primary Health Care; Venous Insufficiency