Clasificación y tratamiento de la embolia pulmonar aguda / Classification and treatment of acute pulmonary embolism

El empleo de escalas clínicas, ecocardiografía, angiografía torácica computarizada, biomarcadores y electrocardiograma permite clasificar la embolia pulmonar aguda en masiva, submasiva y de bajo riesgo con el objetivo de poder administrar al paciente el tratamiento adecuado. En ausencia de contraindicaciones deben tratarse inicialmente con heparinas de bajo peso molecular, fondaparinux o heparinas no fraccionadas. La trombólisis es el tratamiento de elección en la embolia pulmonar masiva al tener un riesgo aceptable de complicaciones hemorrágicas. La trombectomía percutánea y la embolectomía quirúrgica son tratamientos efectivos en la embolia masiva o submasiva con disfunción ventricular derecha. A los pacientes que presenten episodios embólicos recurrentes, a pesar de recibir una anticoagulación adecuada, se les debe colocar un filtro en la vena cava inferior. Debe realizarse un ecocardiograma con suero salino agitado previamente a su administración intravenosa para descartar o confirmar un foramen oval persistente y, por tanto, una embolia paradójica (AU)

The use of clinical scales, echocardiography, computed tomography scans, biomarkers and electrocardiography, allows the classification of the acute pulmonary embolism to be classified into, massive, submassive, and low-risk in order to provide patients with a more appropriate treatment. In the absence of contraindications they should be initially treated with low molecular weight heparins, fondaparinux, or unfractionated heparins. Thrombolysis is the treatment of choice for massive pulmonary embolism with an acceptable risk of haemorrhagic complications. Percutaneous thrombectomy and surgical embolectomy are effective treatments in massive or submassive pulmonary embolism with right ventricular dysfunction. An inferior vena cava filter must be installed in patients who have recurrent episodes despite receiving suitable anticoagulation. An echocardiogram with saline serum infusion (that must be mixed prior to the intravenous administration), rules out or confirms the presence of a patent foramen ovale and therefore, a paradoxical embolism (AU)

Usefulness of thrombophilia testing in venous thromboembolic disease: findings from the RIETE registry.

BACKGROUND: Information on thrombophilia risk factors for patients with upper extremity deep vein thrombosis (UEDVT) is limited. The genetic, acquired, and coagulation risk factors of an acute episode of lower EDVT (LEDVT) or UEDVT, either isolated or associated with pulmonary embolism (PE), were studied. MATERIALS AND METHODS: A total of 4503 patients participated in a thrombophilia study. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated. RESULTS: Mean age of the participants was 55 ± 19 years. The risk of LEDVT or UEDVT, isolated or associated with PE, was calculated according to thrombophilia factors. We found association between LEDVT and factor V Leiden ([FVL]; OR: 1.8; 95% CI 1.4-2.4) and resistance to activated protein C ([APC-R]; OR: 1.6; 95% CI 1.1-2.4). The LEDVT + PE presented an association with PTG20210A (OR: 1.5; 95% CI 1.1-2.1). No association was found between the thrombophilic defects studied and UEDVT or UEDVT + PE. CONCLUSIONS: Both FVL and APC-R carriers had the risk of developing LEDVT. The PTG20210A carriers had the risk of developing LEDVT + PE. No thrombophilic defects studied presented risk factors for UEDVT or UEDVT + PE.

Effects of eprosartan on mitochondrial membrane potential and H2O2 levels in leucocytes in hypertension.

We investigated whether circulating leucocytes from hypertensive patients exhibit more spontaneous, stimulated hydrogen peroxide (H2O2) production and greater mitochondrial membrane potential (Deltapsi) than those from normotensive individuals. We also investigated the effects of oral treatment with the angiotensin II (AT II) type 1 receptor blocker eprosartan (600 mg day(-1)) on these markers of oxidative stress. In 25 hypertensive patients and 28 healthy volunteers, spontaneous H2O2 formation was measured by flow cytometry after preincubation of buffy coat-leucocytes from fresh peripheral venous blood at 37 degrees C with 2',7' dichlorofluorescein. Stimulation of H2O2 formation by circulating leucocytes was elicited by the addition of tert-butylhydroperoxide (tBHP). Deltapsi was determined by flow cytometry after the addition of tetramethylrhodamine methyl ester (TMRM). Compared with healthy individuals, lymphocytes from hypertensive patients exhibited higher Deltapsi (12.28+/-3.20 vs 16.25+/-2.88 arbitrary fluorescence units (AFU), respectively; P<0.001) and greater spontaneous H2O2 production (4.75+/-5.15 vs 8.98+/-9.97 AFU, respectively; P<0.05). tBHP stimulation was associated with higher H2O2 levels in circulating leucocytes in patients with uncorrected hypertension than in normotensive individuals. H2O2 overproduction was corrected by eprosartan treatment. These results suggest that oxidative stress could be important in the pathogenesis of hypertension. Furthermore, measurement of leucocyte oxidant activities may be useful for the evaluation of oxidative stress, which may be reduced with the use of antihypertensive drugs. Our results demonstrate that treatment of hypertension with eprosartan normalizes blood pressure and corrects oxidative disturbances, suggesting that leucocytes could be a target for this drug.

Papel de la atorvastatina en la prevención del ictus. ¿Puede estar relacionado con su acción sobre la activación plaquetaria? Consideraciones basadas en nuestra propia experiencia / Role of atorvastatin in the prevention of stroke. Can it be related with its action on platelets activation? Considerations based on our own experience

Está bien establecido que la hipertensión arterial es el principal factor de riesgo de ictus y que los pacientes hipertensos presentan frecuentemente otros factores asociados de riesgo vascular, como una mayor activación plaquetaria. Nuestro grupo de trabajo ha comunicado que determinados fármacos hipotensores, además de normalizar las cifras tensionales, disminuyen dicha hiperactivación plaquetaria, lo que supone un beneficioso efecto añadido, dado el papel que las plaquetas juegan en el proceso aterotrombótico. Actualmente no se ha establecido claramente si la hipercolesterolemia tiene algún papel en el ictus, pero, sin embargo, numerosos autores han demostrado que la administración de estatinas, que son potentes fármacos utilizados en el tratamiento de la hipercolesterolemia, produce una reducción significativa en la incidencia de ictus. Esta observación se ha atribuido a diversos efectos pleiotrópicos de las estatinas. Dado que nuestro grupo de trabajo ha descrito el efecto normalizador de la atorvastatina sobre la activación de las plaquetas, parece razonable especular que las estatinas reducen la incidencia de ictus a través de su efecto sobre la hiperactivación plaquetaria. Sin embargo, la confirmación de este probable mecanismo de acción requiere la realización de estudios clínicos más amplios

It is well known that arterial hypertension is the main stroke risk factor and hypertensive patients frequently have other vascular risk factors, such as high platelet activation. Our work group has reported that some hypotensive drugs not only normalize blood pressure values but decrease platelet hyperactivity, which is supposed to be an added beneficial factor as the platelets play an important role in atherothrombotic process. Currently, it has not been clearly established if hypercholesterolemia plays a role in stroke. However, many authors have demonstrated that administration of statins, a potent drug used in the hypercholesterolemia treatment, produces a significant reduction in the stroke incidents. This observation is attributed to different statin pleiotropic effects. Since our group has described the normalization of the platelet activation with atorvastatin, it seems reasonable to think that statins decrease stroke incidents due to their effect on platelet hyperactivation. However, the confirmation of the possible mechanism action requires a more extensive clinical study

Effect of a modified fibrate (Biniwas Retard) on hemorheological alterations in hyperlipemic patients.

The effect of a binifibrate (Biniwas Retard, Wasserman) on the plasma lipids and hemorheological profile of 30 primary hyperlipemic patients was studied. Our results indicate that the patients under study had evident rheological alterations as well as the expected lipid alterations. Treatment with Biniwas (2 x 550 mg/day) for six months not only substantially improved the alterations in the lipid balance but also tended to normalize the patients' hemorheological alterations, and there was a statistically significant correlation between the two effects. Apart from the decrease in plasma viscosity (1.20 +/- 0.05 vs 1.29 +/- 0.07 mPa.s, p < 0.001), the most noteworthy effects of Biniwas treatment were the decrease in red blood cell aggregability (8.7 +/- 1.2 vs 9.3 +/- 1.1, p < 0.05) and increased deformability (55 +/- 3 vs 47 +/- 5%, p < 0.001). Both changes may be due to modifications in the lipid composition of the erythrocyte membrane due to cell-plasma lipid exchange.

The effect of long-term treatment with hypotensive drugs on blood viscosity and erythrocyte deformability in patients with essential arterial hypertension.

This study examined ninety-six patients with essential arterial hypertension (WHO grade I-II) who had been under treatment for a period of at least one year before participating in the study. When the study began the patients received no drug treatment for one month. At the end of this washout period their basal situation was evaluated and drug treatment was begun (26 patients on calcium antagonists, 39 on beta-blockers and 31 on angiotensin converting enzyme inhibitors). The patients were evaluated again after one and two years of uninterrupted treatment with the chosen medication. The results obtained indicate that in a basal situation hypertensive patients have higher blood viscosity and erythrocyte rigidity values than the control group. Regardless of the drug treatment used, the patients experienced during the study a progressive deterioration of their hemorheological situation consisting of an increase in red blood cell rigidity and increased blood viscosity. These results indicate the importance of evaluating the hemorheological parameters of hypertensive patients and suggest that it may be advisable to include in their treatment some kind of medication that prevents progressive rheological deterioration.

Hemorheological profile in patients with cardiovascular risk factors.

In order to find out whether hemorheological alterations precede the atherosclerotic lesions and could constitute an atherothrombotic risk factor, we studied the hemorheological profile in 150 healthy normotensive offspring whose parents were diagnosed as having essential hypertension WHO I-II grade and in another group of 40 children with familial hypercholesterolemia (FH) but without vascular atherosclerosis lesions, whose parents also suffer from FH. In offspring of hypertensive individuals, a significant increase in the fibrinogen level with respect to the control group was found both in males and females. In addition, only the female offspring showed a higher leucocyte count. FH children showed increased erythrocyte aggregation and increased plasma viscosity with respect to the control group. The fact that the rheological alterations appear prior to the development of the vascular lesion suggests that they could play a role in the pathogenesis of the atherosclerotic process.

Hemorheological alterations in mild essential hypertension.

Blood rheological properties were studied in 21 patients suffering from essential hypertension (EHT), degree I-II according to WHO criteria. These patients were diagnosed "de novo". The whole blood filterability (WBF), blood viscosity (BV) at 230 s-1 and 23 s-1, red cell deformability (FI), erythrocyte aggregation in autologous (MEA) and normal plasma (MEAc), fibrinogen (Fbg) and hematocrit (Ht) have been evaluated. In the hypertensive patients we have found decreased WBF, greater BV and FI in comparison with the control group (p less than 0.001). Likewise, MEA and Fbg were increased, though the differences were less significant (p less than 0.01). The evaluation of Ht did not show any differences between the two groups. The results suggest that in the newly diagnosed EHT, clear hemorheological alterations occur, both in plasma and in the erythrocytes, which could play a role in the pathogenesis of the aforementioned disease.

[The blood rheology of diuretics]. / Hemorreología de los diuréticos.

We have studied a group of 33 (27 female and 6 male) patients suffering pure essential arterial hypertension, with a mean age of 54.06 years, and who received a daily monodose of chlortalidone. Arterial pressure, blood viscosity at different shearing levels, as well as those parameters capable of modifying this viscosity were determined at days 0, 30, 60, 90, and 180 of treatment. Similarly, blood viscosity in this group of patients on day 0 is compared to a normotense control group. We observed a statistically significant (p less than 0.05) increase in blood viscosity in the hypertense group at day 0 when compared to the control group. No significant changes due to treatment could be observed in blood viscosity or any of the parameters studied. However, there was a significant decrease (p less than 0.0001) in arterial blood viscosity. "Chronic" treatment of essential hypertense patients have an inherent increase in blood viscosity. "Chronic" treatment of essential arterial hypertension with diuretics (chlortalidone) does not modify the hematocrit nor other biochemical parameters studies, nor blood viscosity. Treatment normalises blood pressure levels, but it does not "primarily" hemodynamically prevent ischemic events at the microcirculatory level.