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ABSTRACT: The number of patients receiving oral anticoagulant therapy has increased markedly in recent years, with the consequence that monitoring must be decentralized. The aim of this study was to provide reference values for the quality of care in patients receiving oral anticoagulants at large specialized Spanish centers for use in future comparative analyses.
The records of 20,347 outpatients who were receiving oral anticoagulants between January and December 2003 at four large Spanish centers were assessed. Databases at the four hospitals were searched for severe adverse events.
In total, 211,987 regular check-ups were carried out, 72.7% of which gave international normalized ratios (INRs) within the range 2-4. Overall, 2369 hemorrhagic events were observed, 190 (8%) of which were severe, with 20 deaths (0.1 per 100 patient-years). In addition, there were 299 thromboembolic events, with 11 deaths (0.05 per 100 patient-years). The frequency of these events was greater in patients with a cardiac prosthesis, who required more intense anticoagulation. The incidence of death with different diagnoses was also greater in anticoagulated patients with a cardiac prosthesis, and the highest probability of death (1 in 3) was associated with episodes of cerebral hemorrhage. The incidence of hemorrhage increased as the INR increased. In contrast, thrombotic events occurred principally when the INR was below 2, and were not observed with INRs over 6.
The incidence of adverse events in patients receiving oral anticoagulant therapy at large Spanish centers was similar to that observed in other European countries.
Revista Espa de Cardiologia 01/2008; 60(12):1226-32. · 2.53 Impact Factor
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ABSTRACT: Platelet activation needs a high energy demand which is supplied by the degradation of glucose into lactate. Platelet response to agonists in patients with primary thrombocythemia is defective. We studied the production of lactate by the platelets of patients with this disease and defective platelet aggregation.
Ten patients suffering from primary thrombocythemia and ten controls were included in this study. The lactate generation was measured in resting and thrombin activated platelets in absence or presence of glucose.
Resting platelets incubated for 30 min in phosphate-buffered saline (PBS) generated the same amount of lactate in patients (44.6+/-21.6 micromol/10(11) cells) and controls (41.0+/-17.3 micromol/10(11) cells). Addition of glucose led to similar increases in lactate formation by platelets in patients (82.2+/-26.4 micromol/10(11) cells) and controls (88.1+/-34.5 micromol/10(11) cells). The addition of thrombin in absence of glucose did not modify the lactate formation respective to PBS. Finally, the incubation of platelets with both glucose and thrombin caused further increases in the generation of lactate in both groups, patients (236.9+/-83.9 micromol/10(11) cells) and controls (228.6+/-63.5 micromol/10(11) cells) without differences between them. The production of lactate in both groups was also similar when platelets were incubated for 10 min or 20 min with both thrombin and glucose. However at 5 min, platelets of patients generated more lactate (97.8+/-23.7 micromol/10(11) cells) than controls (66.5+/-38.7 micromol/10(11) cells, p<0.05).
These results suggest that thrombin is able to induce an initial hyperactivity of those pathways involved in the platelet energy production of patients with primary thrombocythemia.
Thrombosis Research 02/2006; 118(3):335-9. · 2.44 Impact Factor
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ABSTRACT: We evaluated the influence of aging, gender and indications of anticoagulant therapy on acenocoumarol requirements in 1845 patients from 30 to 99 years old receiving acenocoumarol therapy who were monitored in our hospital outpatient anticoagulation clinic from March 1993 through September 1999. The patients were stratified in seven age groups, comprising older than 80 years and the five decades between 30 years and 80 years. We found a progressive decrease in the acenocoumarol requirements from 30 years to 80 years (rho=-0.98), which was estimated as 2.7 mg/week per decade (11.5% per decade). This decrease was not the consequence of a different range of anticoagulation or differences in body weight. We did not find correlation between the decrease of acenocoumarol requirements and different biochemical parameters including, creatinine, calcium and alanine aminotransferase. We detected a progressive decrease in levels of serum total proteins but changes in this parameter did not correlate with the amount of acenocoumarol requirements. The dose of acenocoumarol (mg/week per patient) of those patients suffering from venous thromboembolism were higher than the remainder of the patients (18.4 +/- 9.3 versus 14.5 +/- 7.8, P <0.0001). This finding was also detected, after stratifying the patients by decades, from 60 years to 80 years. In conclusion, requirements of acenocoumarol decrease with aging; this decrease represents an important amount from 30 years to 80 years and it should be kept in mind to choose the initial dose of acenocoumarol. Patients with venous thromboembolism required a higher dose of acenocoumarol.
Blood Coagulation and Fibrinolysis 11/2004; 15(8):673-6. · 1.24 Impact Factor
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ABSTRACT: Pulmonary embolism (PE) is a potentially fatal and frequent complication of deep venous thrombosis, and the most reliable techniques for the diagnosis of PE are not universally available and have other limitations.
To determine the efficacy of 4 different fibrinolysis system parameters, namely, tissue plasminogen activator (tPA), tissue plasminogen activator inhibitor type 1 (PAI-1), plasmin-antiplasmin complexes (PAP), and D-dimer, in the diagnosis of acute PE.
A 350-bed university hospital serving an area with 280,000 inhabitants.
Sixty-six consecutive outpatients with clinically suspected PE. The diagnosis of PE was based on ventilation-perfusion (V/Q) lung scan in combination with clinical assessment, lower limb study, and (when required) pulmonary angiography.
At the moment of clinical suspicion, a sample of venous blood was obtained to measure levels of tPA, PAI-1, PAP, and D-dimer using an enzyme-linked immunosorbent assay method.
Twenty-seven patients (41%) were classified as PE positive (high clinical probability and V/Q lung scan [n = 12], nondiagnostic V/Q lung scan and high clinical probability [n = 1], inconclusive V/Q lung scan and positive lower limb examination for deep venous thrombosis [n = 11], and positive pulmonary angiography [n = 3]), and 39 patients (59%) were classified PE negative. The sensitivity/negative predictive value for tPA, using a cutoff of 8.5 ng/mL, and PAI-1, using a cutoff of 15 ng/mL, were 100%/100% and 100%/100%, respectively. A tPA level lower than 8.5 ng/mL occurred in 13 (19.7%; all PE negative) of 66 patients with suspected PE, and PAI-1 levels were lower than 15 ng/mL in 9 (13.6%; all PE negative) of 66 patients with suspected PE. The D-dimer, using a cutoff of 500 ng/mL, showed a sensitivity and negative predictive value of 92.6% and 87.5%, respectively.
Our data indicate that tPA and PAI-1 levels are potentially useful in ruling out PE, although tPA seems to be the better parameter. The sensitivity levels and negative predictive values for the rapid enzyme-linked immunosorbent assay for D-dimer used in this investigation were low compared with previous studies using the same test.
Archives of pathology & laboratory medicine 04/2003; 127(3):310-5. · 2.58 Impact Factor
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ABSTRACT: Platelets of patients with uremia develop a defective platelet function and have a decreased production of thromboxane B2 (TxB2). Activated platelets generate thromboxane from free arachidonate that is previously released from the membrane phospholipids (PLs) by phospholipases. Phospholipase A2 (PLA2) release up to 70% of the arachidonate in normal platelets, and to date, the activity of this enzyme in uremia is unknown. This work studied the PLA2 activity in the platelets of nine uremic patients and nine healthy volunteers. Washed platelets were labelled with [(14)C]arachidonic acid and activated with calcium ionophore A-23187 (4 microgr/ml). Lipids were resolved by TLC and identified by autoradiography. The distribution of [(14)C]arachidonic acid in the five major platelet phospholipids was found to be normal. Uremic platelets released more radioactivity than normal platelets (19.0 +/- 5.2% versus 11.3 +/- 1.6%, P = 0.001). The production of both, radioactive thromboxane B2 and hydroxyheptadecatrienoic acid was normal (2.6 +/- 1.2% and 3.5 +/- 1.6% of total radioactivity respectively), but the formation of the lipoxygenase metabolite hydroxyeicosatetraenoic acid was increased with respect to the controls (12.9 +/- 4.6% vs 7.0 +/- 1.3% of total radioactivity, P = 0002). In conclusion, platelets of patients with uremia have an increased activity of phospholipase A2 and produce increased amounts of hydroxyeicosatetraenoic acid, an inhibitor of the platelet function.
Platelets 12/2002; 13(7):415-8. · 1.85 Impact Factor
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ABSTRACT: Red cell phospholipids (PLs) were assessed in 11 patients with essential thrombocythemia and 5 patients with polycythemia vera. Platelet and plasma PLs were also determined in 10 of these patients, and the results were compared with studies performed in 16 healthy volunteers. The amount of platelet PLs in patients was similar to controls (556 ± 90 nmol/109cells, versus 481 ± 91 nmol/109cells), as was the percentage of the main specimens of these compounds, including phosphatidylserine (11.1 ± 0.8%), which is relevant for platelet procoagulant activity. We did not find differences between red cell PLs of patients (300 ± 60 nmol/109cells), versus controls (289 ± 71 nmol/109cells), and the sphingomyelin/phosphatidylcholine ratio in these cells was the same in both groups (0.75 ± 0.1). Finally, we did not detect any alteration in the amount of plasma PLs specimens.
European Journal Of Haematology 03/1993; 50(4):234 - 236. · 2.61 Impact Factor
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ABSTRACT: An increased activity of phospholipase A2 has been observed in the plasma of patients with uremia. This enzyme converts phosphatidylcholine to lysophosphatidylcholine (LPC), an inhibitor of platelet aggregation. We measured the levels of plasma phospholipids including LPC, and platelet aggregation in 7 patients with uremia. Platelet response to agonists was defective, mainly with collagen (p < 0.001). The patients’ levels of LPC in plasma were similar to those of controls (109.7 ± 41.6 vs. 80.4 ± 16.8 nmol/ml) and did not correlate with the platelet response to adenosine diphosphate (r = -0.51). The amount of phosphatidylcholine was increased with respect to normal plasma (1,041.0 ± 201.8 vs. 760.8 ± 142.7 nmol/ml, p < 0.01), while the levels of other phospholipids were normal. These results do not suggest a participation of plasma LPC in the genesis of the platelet defect observed in patients with uremia.
American Journal of Nephrology. 08/1970; 16(5):409-411.
