Sildenafil is more selective pulmonary vasodilator than prostaglandin E1 in patients with pulmonary hypertension due to heart failure.

In some patients, heart failure (HF) is associated with increased pulmonary vascular resistance (PVR). The magnitude and the reversibility of PVR elevation affect the HF management. Sildenafil has been recently recognized as potent PVR-lowering drug in HF. The aim of the study was to compare hemodynamic effects and pulmonary selectivity of sildenafil to prostaglandin E(1) (PGE(1)). Right-heart catheterization was performed in 13 euvolemic advanced HF patients with elevated PVR (6.3+/-2 Wood's units). Hemodynamic parameters were measured at the baseline, during i.v. infusion of PGE1 (alprostadil 200 ng · kg(-1) · min(-1)) and after 40 mg oral dose of sildenafil. Both drugs similarly reduced systemic vascular resistance (SVR), but sildenafil had higher effect on PVR (-28 % vs. -49 %, p = 0.05) and transpulmonary pressure gradient than PGE(1). The PVR/SVR ratio--an index of pulmonary selectivity, did not change after PGE(1) (p = 0.7) but it decreased by -32 % (p = 0.004) after sildenafil. Both drugs similarly reduced pulmonary artery mean and wedge pressures and increased cardiac index (+27 % and +28 %). Sildenafil led more often to transplant-acceptable PVR while causing smaller drop of mean systemic pressure than PGE(1). In conclusion, vasodilatatory effects of sildenafil in patients with heart failure are more pronounced in pulmonary than in systemic circulation.

[Infection and atherosclerosis]. / Infekce a ateroskleróza.

Atherosclerosis is a chronic inflammation and the cause of most cardiovascular diseases. It is the main cause of death in the Western world today, even though growing incidence of atherosclerosis-related diseases has been recently observed in developing countries, too. In many patients with atherosclerosis, however, traditional risk factors for atherosclerosis are not identifiable. This has renewed the interest, in recent years, in the links between atherosclerosis and environmental exposures, including infectious agents. Infection was identified as as risk factor for atherosclerosis in the first half of the 20th century. Experimental and clinical studies have shown that infection can stimulate atherogenic processes and that there are significant interactions between infection and traditional risk factors. Yet there are questions concerning etiology, pathogenesis and appropriate interventions which remain unanswered. The following article provides an overview of the role of the infectious agents in atherosclerosis and discusses possible intervention strategies.

Hyperlipoproteinemia impairs endothelium-dependent vasodilation.

Atherogenic lipoproteins can cause endothelial dysfunction in the initial stage of atherogenesis. In our study we examined 134 patients with defined hyperlipoproteinemia (non-HDL cholesterol>4.1 mmol/l or triglycerides>2.5 mmol/l or taking any of lipid lowering drugs)--94 men and 40 women. The subgroup of controls of comparable age contained 54 normolipidemic individuals--30 men and 24 women. Patients with hyperlipoproteinemia revealed significantly lower ability of endothelium-dependent flow-mediated vasodilation (EDV) measured on brachial artery (4.13+/-3.07 vs. 5.41+/-3.82 %; p=0.032) and higher carotid intima media thickness than normolipidemic controls (0.68+/-0.22 vs. 0.58+/-0.15 mm; p=0.005). In regression analysis, EDV correlated significantly with plasma concentrations of oxLDL (p<0.05) HDL-cholesterol (p<0.05), Apo A1 (p<0.05), ATI (p<0.01) and non-HDL cholesterol (p<0.05). Patients with hyperlipoproteinemia showed higher plasma levels of oxLDL (65.77+/-9.54 vs. 56.49+/-7.80 U/l; p=0.015), malondialdehyde (0.89+/-0.09 vs. 0.73+/-0.08 micromol/l; p=0.010) and nitrites/nitrates (20.42+/-4.88 vs. 16.37+/-4.44 micromol/l; p=0.018) indicating possible higher long-term oxidative stress in these patients.

[Detecting and evaluating hyperaluminemia in 3 dialysis centers]. / Vyhledávání a hodnocení hyperaluminémie ve trech dialyzacních strediscích.

We have investigated plasma aluminium level in normal conditions and after application of 40 mg of desferrioxamine per one kilogram of body weight in 101 patients with different content of aluminium in dialysate solution. At 20 to 120 months of exposure by dialysate with aluminium content higher than 20 micrograms/l in an average the plasma aluminium level reached 80 micrograms/l in an average and after desferrioxamine application 211 micrograms/l. Plasma aluminium level varied between 80 to 250 micrograms/l in 16 patients with osteomalacia proved by bone biopsy. Oral ingestion of aluminium dosed 500 mg/day may result in significantly high plasma aluminium level. Desferrioxamine test proved significant accumulation of aluminium in some cases with low level of plasma aluminium, and further proved significant accumulation of aluminium in tissues at long time desferrioxamine treatment. Plasma aluminium levels 40 to 80 micrograms/l may be of clinical relevance. Aluminium level was determined by means of atomic absorption spectroscopy in graphite furnace with the accuracy +/- 3.0 micrograms/l.