PubMed Health⌕ Search

Biomedical subjects

Ales Blinc

Publications and source records attributed to Ales Blinc.

9 recordsLinked to original sources
PubMed2006

Peripheral arterial disease and ankle-brachial pressure index as predictors of mortality in residents of Metlika County, Slovenia.

AIM: To test how the presence of peripheral arterial disease predicted mortality of middle-aged and elderly residents of Metlika county, a rural area in southeastern Slovenia. METHODS: In 1987, we interviewed and examined a representative cohort of 646 subjects aged 45-80 years at inclusion without overt coronary or cerebrovascular disease, for cardiovascular risk factors and measured the ankle-brachial pressure index (ABPI). Peripheral arterial disease was defined as ABPI<0.90. The subjects were followed up 15 years or until death. All-cause mortality and cardiovascular mortality were assessed and compared between subjects with and without peripheral arterial disease in a multivariate model. RESULTS: There were 580 subjects with normal ABPI and 66 subjects with peripheral arterial disease, among which 49 were asymptomatic and 17 had intermittent claudication. Because subjects with peripheral arterial disease were on average 10 years older than those without peripheral arterial disease, the mere presence of peripheral arterial disease was not an independent predictor of mortality. However, there was a significant interaction of peripheral arterial disease with age, with a more pronounced adverse prognostic effect of peripheral arterial disease in younger than in older age groups. For a 55-year-old subject with peripheral arterial disease, the hazard ratio of dying from any cause in the follow-up period was 2.44 (95% confidence interval [CI], 1.15-4.96) in comparison to an age-matched subject without peripheral arterial disease, but at 75 years of age, the hazard ratio decreased to only 0.71 (95% CI, 0.46-1.09). For cardiovascular mortality, the hazard ratio in the presence of peripheral arterial disease was 6.05 (95% CI, 1.87-16.27) at 55 years and 0.92 (95% CI, 0.54-1.52) at 75 years. Among patients with peripheral arterial disease, each decrement of ABPI at inclusion by 0.10 significantly increased the cardiovascular mortality after 15 years by 30% (P = 0.038). CONCLUSION: Peripheral arterial disease, even asymptomatic, is an important predictor of adverse cardiovascular prognosis in relatively young patients. Reduced ABPI is a strong, independent predictor of cardiovascular mortality in all patients with peripheral arterial disease.

Aged↗
PubMed2004

Methyl-methacrylate bone cement surface does not promote platelet aggregation or plasma coagulation in vitro.

Leakage of viscous bone cement into venous blood possibly resulting in pulmonary embolism may occur during percutaneous vertebroplasty. Our aim was to study if bone cement surface or cement liquid component could induce platelet aggregation or plasma coagulation in vitro. Two types of commonly used methyl-methacrylate bone cement, Palacos (Heraeus Kulzer, Germany) and Vertebroplastic (DePuy, Acro Med, England), were smeared on thin glass slides that were inserted over the bottom of cuvettes immediately or after 24 h, and platelet aggregation was recorded over 10 min. Bone cement liquid component, containing methyl-methacrylate monomer and N,N-dimethyl-p-toluidine, was tested in 2% and 4% final concentration. Partial thromboplastin time (PTT) was determined by the hook method in the presence of bone cement-smeared glass slides or 6% bone cement liquid. Both types of bone cement, either fresh or aged, did not promote platelet aggregation, whereas collagen-coated glass slides induced substantial platelet aggregation (65 +/- 37%). On the other hand, bone cement liquids reduced platelet aggregation induced by collagen solution to an average of less than 15% (p < 0.01). Bone cement, fresh or aged, had no effect on PTT, but bone cement liquids significantly prolonged PTT: median and 1st-3rd interquartile range 149 (96-171) s for Vertebroplastic and 132 (99-194) s for Palacos, p = 0.03 for both comparisons with normal pool plasma without additives that had PTT of 69 (62-71) s. We conclude that the surface of fresh or aged bone cement is not thrombogenic in vitro. The bone cement liquid inhibits platelet aggregation and plasma clotting in relatively high concentrations that cannot be expected in vivo.

Blood Coagulation↗
PubMed2004

Turbulent axially directed flow of plasma containing rt-PA promotes thrombolysis of non-occlusive whole blood clots in vitro.

The rate of thrombolysis markedly decreases after a thrombosed vessel is partly recanalized and the remaining clot poses serious risk for rethrombosis. We studied in vitro how thrombolysis depends on penetration of plasma containing thrombolytic agents - 0.2 micro g/ml rt-PA or 250 IU/ml streptokinase (SK) - and the magnetic resonance contrast agent Gd-DTPA (at 1 mmol/l) into non-occlusive clots under conditions of fast (turbulent) or slow (laminar) axially directed flow. Cylindrical non-retracted (fresh) or retracted (aged) whole blood clots were pierced lengthways and connected to a perfusion system. Dynamical spin-echo MRI was used for measuring the penetration of labeled plasma into clots and for assessing the remaining clot size. In both types of clots fast flow enhanced the penetration of Gd-DTPA-labeled plasma into clots in comparison to slow flow. In non-retracted clots, lysis with rt-PA and to a lesser extent also lysis with SK followed the path of plasma penetration into clots. After 40 minutes of fast axially directed flow rt-PA resulted in almost complete lysis and SK left only about a third of the clot undissolved, whereas with slow flow lysis was much slower (undissolved clot: 86 +/- 5 % with rt-PA and 95 +/- 1 % with SK). In retracted clots, substantial lysis was possible only with rt-PA and rapid flow (53 +/- 28% of the clot undissolved after 60 min), whereas the use of SK or slow flow precluded meaningful lysis. We conclude that rapid (turbulent) axially directed flow of plasma along non-occlusive blood clots causes forceful exchange of serum inside the clot with outer plasma which enhances both fibrin-specific and non-fibrin-specific lysis of fresh clots. Dissolution of non-occlusive retracted (aged) clots occurs only under fibrin-specific conditions combined with adequate transport of rt-PA into clots.

Blood Coagulation↗
PubMed2002

D-dimer, other markers of haemostasis activation and soluble adhesion molecules in patients with different clinical probabilities of deep vein thrombosis.

Two automated turbidimetric D-dimer assays (BC D-dimer Plus, Dade Behring, Marburg, Germany and Auto-Dimer, Biopool, Umeå, Sweden) were compared to two enzyme-linked immunosorbent assays (ELISAs) (Enzygnost D-dimer micro, Dade Behring and Asserachrome D-dimer, Diagnostica Stago, Asnières, France) and two rapid D-dimer assays (SimpliRed, Agen Biomedical, Brisbane, Australia and Minutex, Biopool) in out-patients with suspected deep vein thrombosis (DVT). In addition, the performance of prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), and soluble adhesion molecules VCAM-1 and P-selectin for DVT diagnosis was assessed. One hundred and thirty-five consecutive out-patients with suspected DVT of the lower limb were included, and in 52 (39%), DVT was confirmed by compression ultrasound. All D-dimer assays investigated reliably excluded DVT in those patients without DVT irrespective of their pre-test clinical probability of DVT. One D-dimer ELISA (Dade Behring) gave the highest area under the receiver operating characteristic (ROC) curve compared to other assays, and therefore, this was the most accurate assay in differentiating patients with from patients without DVT. The diagnostic performance of one automated turbidimetric assay (Auto Dimer, Biopool) was similar to ELISA and its convenience close to rapid latex agglutination assays. Most patients with a high pre-test clinical probability of DVT had positive D-dimer regardless of the presence or absence of DVT, which decreased the specificity of the tests and made D-dimer determination less useful for this group of patients. Because the diagnostic accuracy [sensitivity, specificity, negative (NPV) and positive predictive value (PPV)] of F1+2, TAT, VCAM-1 and P-selectin was inferior to D-dimer assay, these assays could not substitute or supplement D-dimer testing in diagnosis of DVT. Levels of VCAM-1 and P-selectin were increased in patients with DVT and should therefore be investigated further to clarify their role in DVT.

Adult↗
PubMed2002

In vivo release of tissue-type plasminogen activator antigen from the human brachial artery.

The rate of secretion of t-PA from vascular endothelial cells has been proposed as a good marker of endothelial function. Our aim was to measure the rate of in vivo t-PA antigen release from the human brachial artery and not from the combined vascular pool of the upper extremity. In 10 healthy male volunteers, we have occluded the forearm by a sphygmomanometer cuff for 5-7 min in order to reduce the blood flow in the brachial artery. Arterial blood samples were taken from the cubital artery above the occlusion and from the contralateral artery that served as the control. The arterial t-PA antigen concentrations were significantly higher after forearm occlusion than in the non-occluded contralateral arteries: median 3.3 (range between first and third quartile 2.1-3.6) vs. 2.5 (2.0-3.2) ng/ml, p=0.03. The PAI-1 antigen concentrations did not change significantly: 6.9 (2.3-18.6) ng/ml in the contralateral artery vs. 5.4 (1.8-8.0) ng/ml after occlusion, p=0.09. The average forward blood flow in the distal 15 cm of the brachial artery that was measured by duplex ultrasound decreased from 107 (97-118) ml/min at baseline to 25 ml/min (19-33) ml/min during occlusion. The release rate of circulating t-PA antigen was calculated as the product of the increment in arterial t-PA concentration and the average plasma flow in the arterial segment of interest with a volume of 2 ml. The median release rate of t-PA antigen under conditions of reduced blood flow in the brachial artery was 3.3 (1.1-11.5) ng/min. We conclude that the secretion of t-PA antigen from arterial endothelium of healthy subjects is substantial, whereas the arterial wall is not an important source of PAI-1 in vivo.

Adult↗
PubMed2002

Magnetic resonance imaging of arterial thrombi and its possible correlation to fibrinolytic treament.

For 13 patients with subacute and 4 patients with chronic occlusion, magnetic resonance imaging (MRI) of occlusive arterial thrombi in the superficial femoral artery were performed in vivo. The patients with subacute occlusion were treated with catheter-directed thrombolysis. The frequency of MR signal intensity and its distribution in thrombi were studied for 11 successfully and 2 unsuccessfully treated patients and patients with chronic occlusion. Intra-arterial thrombi were MRI inhomogenous in all of the patients, but the MR signals from lysable and chronic thrombi were significantly different than those from nonlysable ones. The MRI of occlusive arterial thrombi is probably usable to predict the therapeutic outcome of thrombolytic treatment.

Adult↗
PubMedDate not supplied

Microcirculation disturbances in patients with venous ulcer before and after healing as assessed by laser Doppler flux-metry.

BACKGROUND: We studied whether a characteristic pattern of laser Doppler flux (LDF) could be identified in perimalleolar skin of patients with venous ulcer before and after ulcer healing. METHODS: Nine subjects with venous ulcer that healed after conservative treatment in 1-6 months and nine healthy persons were included in the study. Microcirculation investigations of laser Doppler flux (LDF) were carried out before and after ulcer healing at rest, upon arterial occlusion, during thermal stimulation and during experimental venous hypertension. RESULTS: Resting LDF expressed as median and range (in arbitrary perfusion units) was significantly higher in patients with venous ulcer in comparison to healthy subjects: 60.6 (40.2-156.5) vs. 9.2 (6.5-19.5), p=0.008. During thermal stimulation and during postischemic reactive hyperemia, absolute values of LDF were slightly but significantly higher in patients with venous ulcer than in healthy subjects, but indices of hyperemic reactivity were very low in patients (median postischemic LDF increase to 101.8 vs. 450.0% in healthy controls, p=0.008; and thermally induced LDF increase to 125.5 vs. 881.5% in healthy controls, p=0.008. Experimental venous hypertension (cuff pressure 40 and 70 mmHg, respectively) led to an equally pronounced relative reduction of LDF in healthy persons as in patients with venous ulcer before and after ulcer healing, but the absolute values of flow remained about six to seven times higher in patients when compared to healthy subjects. Hyperemic reactivity and venoarteriolar response did not change after ulcer healing. CONCLUSIONS: Elevated basal LDF and preserved maximal LDF during reactive hyperemia were found in perimalleolar skin of patients with venous ulcers that eventually healed. The relative venoarteriolar response was preserved in spite of elevated absolute values of LDF during experimental venous hypertension. These hemodynamic characteristics remained unchanged after epithelialization of venous ulcers.

Adult↗
PubMedDate not supplied

Blood clot dissolution dynamics simulation during thrombolytic therapy.

Nonocclusive blood clots only partially fill blood vessels and together with the adjacent vessel wall form a channel through which blood flows at usually much higher velocities than in normal vessels. Our aim was to find a theoretical explanation for the experimentally observed fact that fast flowing blood through the channel has a large effect on the increase of the clot dissolution rate compared to the dissolution rate in the absence of flow. Blood flow through the channel increases transport of dissolution agents to the clot and also exerts large forces to the surface of the clot along the channel. Proposed is a model for clot dissolution which assumes that the clot dissolution rate is proportional to the forces of flowing blood to the surface of the clot multiplied by the average blood velocity. The model has been verified by fitting to experimental magnetic resonance imaging data obtained by dynamical magnetic resonance microscopy of clots dissolved by recombinant tissue plasminogen activator in an artificial blood flow system.

Algorithms↗