"Aspirin - resistance"? A few critical considerations on definition, terminology, diagnosis, clinical value, natural course of atherosclerotic disease, and therapeutic consequences.

Based upon various platelet function tests and the fact that patients experience vascular events despite taking acetylsalicylic acid (ASA or aspirin), it has been suggested that patients may become resistant to the action of this pharmacological compound. However, the term "aspirin resistance" was created almost two decades ago but is still not defined. Platelet function tests are not standardized, providing conflicting information and cut-off values are arbitrarily set. Interest comparison reveals low agreement. Even point of care tests have been introduced before appropriate validation. Inflammation may activate platelets, co-medication(s) may interfere significantly with aspirin action on platelets. Platelet function and Cox-inhibition are only some of the effects of aspirin on haemostatic regulation. One single test is not reliable to identify an altered response. Therefore, it may be more appropriate to speak about "treatment failure" to aspirin therapy than using the term "aspirin resistance". There is no evidence based justification from either the laboratory or the clinical point of view for platelet function testing in patients taking aspirin as well as from an economic standpoint. Until evidence based data from controlled studies will be available the term "aspirin resistance" should not be further used. A more robust monitoring of factors resulting in cardiovascular events such as inflammation is recommended.

The Vienna protocol and perspectives in radionuclide therapy.

The Vienna protocol for [153]Sm-EDTMP-therapy is based on the experience of the last two decades. Repeated treatments at a low dose are applied by several authors in order to achieve the maximum therapeutic effect with the lowest haematological toxicity. Significant benefits on pain palliation and some regression are documented. In contrast to earlier claims, [153]Sm-EDTMP treatment should be started as soon as more than 1 bone lesion appears in bone scintigraphy and/or bone pain becomes evident. Prospective randomized controlled studies, however, are urgently warranted in order to assess benefits beyond bone pain palliation on an evidence base. The combination with chemotherapy as well as radiotherapy may further improve the clinical results. Further research should be directed to identify underlying mechanisms of response and predictors of benefit and to elaborate an improved therapeutic schedule for further enhancing the response rate.

[Complications during exercise testing]. / Komplikationen bei der Ergometrie.

Exercise electrocardiogram forms the basis for diagnosis of ischemia in coronary heart disease. Blood pressure behavior, physical fitness, training heart rate and possible cardiac arrhythmias can additionally be assessed using bicycle ergometry or treadmill testing. When the indications for and contraindications to exercise testing (either bicycle ergometry or treadmill testing) are closely observed, serious complications are rare. However, it is important that the treating physician is aware of and able to recognize possible complications. The present article discusses possible cardiovascular complications and their incidence.

Natriuretic peptides levels are related to HDL-cholesterol with no influence on endothelium dependent vasodilatation.

BACKGROUND: The natriuretic peptides, Brain Natriuretic Peptide (BNP), C-type Natriuretic Peptide (CNP), are mediators of cardiovascular homeostasis. The impairment of arterial ability to vasodilate, also known as endothelial dysfunction, represents the first stage of atherosclerotic damage and may be assessed as brachial flow mediated vasodilation (FMV) in human. Generally an altered brachial FMV is documented in association to several cardiovascular risk factors as hypercholesterolemia. Aim of the study was to evaluate the behaviour of BNP and CNP in hyperlipemia and the potential relationship to FMV. PATIENTS AND METHODS: Forty-four hyperlipemic patients (LDL-cholesterol > 130 mg/dl and/or triglycerides > 150, age 35-60 y) of both genders and 20 normolipemic patients, matched for age and sex were investigated. RESULTS: Patients had lower values of brachial FMV in comparison to controls (3.9 +/- 3.5 vs 7.5 +/- 0.5%, p < 0.005), no differences were observed in BNP (4.6 +/- 4.6 vs 5.9 +/- 3.4 ng/mL, p = n.s) and CNP (4.1 +/- 5.8 vs 5.7 +/- 3.3 ng/mL, p = n.s). Univariate analysis showed a positive correlation between BNP and HDL-cholesterol values (r = 0.36, p = 0.001). In the multivariate analysis, LDL-cholesterol (beta = -0.57), HDL-cholesterol (beta = 0.26) and brachial artery diameter (beta = -0.33) were predictors of brachial FMV. The only predictive variable for CNP was HDL-cholesterol (beta = 0.37). CONCLUSIONS: The present study suggested that natriuretic peptides, BNP and CNP, are not altered in patients affected by hypercholesterolemia. Nevertheless, the levels of HDL-cholesterol are strictly related to the values of CNP. This observation, in humans, adds another mechanism to the vascular control exerted by HDL.

Platelet function after single [153Sm]EDTMP therapy in prostate cancer.

AIM: Aim of the study was to assess whether [153Sm] EDTMP therapy at a low-dose is associated with platelet activation. METHODS: In 29 patients suffering from metastatic prostate cancer platelet count and various platelet function parameters have been monitored for 2 months after a single (the first) application of 1.1 GBq mCi [153Sm]EDTMP. RESULTS: After 3 days insignificant signs of platelet activation (increase in malondialdehyde, adenosine diphosphate-induced platelet aggregation, decreased platelet sensitivity) occur, normalizing rapidly. At the nadir of platelet count (3-4 weeks) platelet aggregation response in non-count adjusted samples is somewhat lower, while activity per cell (count adjusted samples) is unchanged. Platelet proteins do not change at all. Insignificant activation of platelet function at day 3 is interpreted as an indicator of mild oxidation injury, late aggregation response changes in non-adjusted samples seem only to reflect temporarily decreased number of circulating platelets. Samarium-153-EDTMP therapy at doses (1.1 GBq) used in the Vienna-protocol is not associated with a significantly altered functional behavior of platelets. CONCLUSIONS: We conclude that a single dose of 1.1 GBq 153Sm-EDTMP does not significantly affect in vivo and ex vivo platelet function.

Modification of low-density lipoprotein during radiolabeling with 99mTc using three labeling methods.

AIM: The mechanisms of native low-density lipoprotein (LDL) uptake by monocytes and macrophages via the specific cholesterol down-regulated LDL-receptor differs form the mechanism responsible for the unregulated scavenging of the modified, for example, oxidized LDL, by the atherosclerotic plaques and foam cells. For this reason, we investigated if the 99mTc-labeled LDL stands for the native or modified molecule. The influence of the LDL sampling methods, isolation, preparation and radiolabeling of lipoproteins on structure modification and the subsequent imaging behavior has as yet not been addressed in detail. METHODS: Herein we present data on the effects of 99mTc labeling on some oxidation relevant parameters of LDL, such as the lag-time, thiobarbituric acid reactive substances (TBARS), relative electrophoretic mobility (REM), baseline dienes (BD), lipid peroxides (POX), free amino-groups (NH2-groups) and free sulphydryl-groups (SH-groups). Three methods of 99mTc labeling were compared: dithionite method (1), borohydride method (2) and ascorbic acid method (3). Data for oxidation parameters are expressed as a percent of freshly isolated native LDL (% native LDL) or as a percent of LDL treated with the labeling buffers and reagents, but in absence of the radioisotope (% control LDL). RESULTS: The levels of BD were most influenced by methods 2 and 3, and remained almost unchanged when the method 1 was used. The lag-time of 99mTc-LDL produced by method 2 doubled but it was decreased by 23% when the method 3 was employed. No change in the lag-time compared to the native LDL was observed with the method 1. The TBARS levels were 3-5 fold higher than in native LDL when methods 1 and 2 were used, but 33% lower in products made by the method 3. The number of thiol groups increased 3 fold in method 1, was only slightly elevated in method 3, but reduced in method 2 compared to native LDL. NH2-groups were increased with all three labeling procedures, but this increase was not considered significant. REM was altered only in products obtained by methods 1 (1.5x increase) and by method 2 (1.25x increase). No fragmentation of Apo B using sodium dodecyl sulfate polyacrylamide gel (SDS-PAGE) electrophoresis was observed by 99mTc-LDL produced in any of the METHODS: The increase of lipid peroxide generation was observed only when the method 2 was used. CONCLUSIONS: Of the three tested methods, we found all of them to render LDL oxidatively modified to some extent. Therefore, it appears that the native-LDL imaging with 99mTc-labeled LDL is impossible. Only the ascorbic acid method 3 appears to offer some protection and exerts antioxidant effects.

Radionuclide vascular imaging and characterization of human metabolic endothelial surface lining.

Atherosclerotic vascular disease is the leading cause of death in the Western world. Early diagnostic non-invasive imaging is thus of key interest. Despite a large number of successful attempts in experimental conditions, radionuclide vascular imaging in human has not been very successful. Why is that? Experimental lesions are well defined and homogenous with respect to age, size, intensity and structure. Morphological and biochemical evaluations after radionuclide imaging demonstrate excellent correlation in experimental animals. Human lesions, in contrast, are extremely heterogeneous. Certain aspects, such as lesion monitoring (platelets, low-density lipoprotein) do work. Targeting specific antigens in atherosclerotic lesions with a variety of different antibodies, however, has not succeeded. If we learn to better understand functional imaging information vascular imaging data eventually are better than widely considered as a consequence of a lacking comparative standard for the functional activity of the vascular wall. More basic experimental information is required to improve application and optimize information. Stem cell research is the next upcoming approach to give nuclear medicine a chance to demonstrate its clinical value in a rapidly developing new discipline.

Troglitazone inhibits long-term glycation and oxidation of low-density lipoprotein.

Troglitazone (T) is a member of a new class of antidiabetic drugs termed thiazolidinediones (TZDs), which has previously been used as an anti-diabetic agent. In this study we investigated the influence of T, a ligand for PPAR-gamma receptor, on copper-catalyzed or cell-mediated oxidation of native, glycated, and glycoxidated low-density lipoprotein (LDL). A dose-dependent inhibition of copper-mediated low-density lipoprotein-oxidation, as monitored by the formation of oxidation-specific fluorescence, was observed for both native and glycated low-density lipoprotein. At the concentration of 20 microg/mL the inhibition amounted from 14.7% to 64.7% by all low-density lipoprotein forms. For glycated low-density lipoprotein we obtained the highest oxidation rate, but the most pronounced inhibition by T was found for glycoxidated low-density lipoprotein (goLDL). Inhibitory effects of T were also investigated by measurement of relative electrophoretic mobility (REM) in the concentration range of 0 to 20 microg/mL. The inhibition of 4h oxidation of native low-density lipoprotein was found in the entire concentration range, but significance was seen at 10 microg/mL. The long-term glycation and glycoxidation of low-density lipoprotein as measured by 5-hydroxymethyl-2-furaldehyde (5-HMF) formation and binding of fructosamine was found to be inhibited by T. In endothelial cell-mediated oxidation of low-density lipoprotein cytotoxicity of T in the concentration range of 0 to 160 microg/mL during 2 to 24 h oxidation was investigated. In the non-cytotoxic concentration range of 5 to 20 microg/mL, a significantly reduced liberation of isoprostane 8-epi-PGF2alpha during 24 h cell-mediated oxidation of low-density lipoprotein and its modifications was found. This inhibitory action of T was most significant in the case of goLDL and amounted to approximately 20% to 60% inhibition at 5 to 20 microg/mL T, respectively. In the concentration range of 40 to 160 microg/mL, however, T showed an increasing cytotoxic action, as evidenced by loss of cell adhesion, loss of cellular protein, morphological changes, and cell disintegration as well as by strongly enhanced troglitazone-mediated isoprostane 8-IP liberation (fivefold to sixfold). T may be used as a model to explore the thiazolidinediones' mechanism on oxidation in a more general aspect for treatment for T2DM, because T is not clinically available.

Should lidocaine be avoided for local anesthesia in radiation synovectomy?

AIM: Leakage is of major concern when performing radiation synovectomy. Although post-treatment immobilization was provided, extra-articular leakage of radioactivity has occasionally been observed in patients receiving local anesthesia in the course of radiation synovectomy. This study was performed to uncover any unfavourable effect of lidocaine on stability of (166)Ho-FHMA (ferrum hydroxide macroaggregate). METHODS: The radiopharmaceutical was investigated in bovine serum albumin (BSA) solutions (5, 10 mg/ml) at pH 6, 7 and 8. Furthermore, the tracer was incubated for 0, 2, 24, 48 and 120 hours in synovial fluid. In both series the influence of lidocaine-HCl 2% (500, 1000 microl) has been evaluated. RESULTS: In BSA test solutions, amount of lidocaine added [df(2), F=7.82, p-level: 0.00] and pH [df(2), F=7.82, p-level: 0.00] significantly influenced in vitro stability of (166)Ho labeled FHMA (n=72). This finding was confirmed in synovial fluid [df(2), F=3.82, p-level: 0.03] (n=60). CONCLUSION: In an experimental design mimicking normal and inflammatory conditions in the joint, addition of a few milliliters of lidocaine-HCl followed by a shift towards lower pH-values in synovial fluid may endanger stability of the carrier-tracer complex (166)Ho-FHMA and thereby enhance extra-articular leakage.

(Iso) Prostaglandins in saliva indicate oxidation injury after radioiodine therapy.

UNLABELLED: As salivary glands concentrate radioiodine the radiation injury associated with 131I-therapy may result in sialoadenitis and xerostoma leading to a lasting impaired quality of life. Recently we reported about prostaglandin concentration changes as biochemical markers for radiation injury. Isoprostanes, a new family of prostaglandin-like compounds, have been demonstrated to be reliable markers for oxidation injury in vivo. PATIENTS AND METHODS: In this study we examined the levels of 8-epi-PGF2alpha, the major member of the isoprostane family in 24 patients undergoing 1311 treatment in different doses for hyperthyroidism and differentiated thyroid cancer. 6 healthy sex and age-matched volunteers were monitored in parallel. Saliva(iso)prostaglandins were determined before 131I treatment, as well as 1, 3, 7, 14, 21, and 28 days, and 2, 3, and 6 months after therapy. RESULTS: 8-epi-PGF2alpha showed a significant 1311 dose-dependent temporary increase. The alterations were comparable in all investigated patients and significantly higher in cigarette smokers. TXB2 and 6-oxo-PGF, showed a dose-dependent increase too. TXB2 was higher in cigarette smokers and 6-oxo-PGF1alpha lower as compared to non-smokers. CONCLUSION: These results clearly demonstrate a dose- and time-dependent tissue (TXB2, 6-oxo-PGF1alpha) and oxidation in-jury (8-epi-PGF2alpha) after 131I-therapy in the salivary glands.

(Iso) Prostaglandins in saliva indicate oxidation injury after radioiodine therapy / (Iso) Prostaglandinas en saliva indican daño oxidativo después de terapia con radioyodo

As salivary glands concentrate radioiodine the radiation injury associated with 131I-therapy may result in sialoadenitis and xerostoma leading to a lasting impaired quality of life. Recently we reported about prostaglandin concentration changes as biochemical markers for radiation injury. Isoprostanes, a new family of prostaglandin-like compounds, have been demonstrated to be reliable markers for oxidation injury in vivo. Patients and methods: In this study we examined the levels of 8-epi-PGF2, the major member of the isoprostane family in 24 patients undergoing 131I treatment in different doses for hyperthyroidism and differentiated thyroid cancer. 6 healthy sex and age-matched volunteers were monitored in parallel. Saliva (iso)prostaglandins were determined before 131I treatment, as well as 1, 3, 7, 14, 21, and 28 days, and 2, 3, and 6 months after therapy. Results: 8-epi-PGF2 showed a significant 131I dose-dependent temporary increase. The alterations were comparable in all investigated patients and significantly higher in cigarette smokers. TXB2 and 6-oxo-PGF1 showed a dose-dependent increase too. TXB2 was higher in cigarette smokers and 6-oxo-PGF1 lower as compared to non-smokers. Conclusion: These results clearly demonstrate a dose- an time-dependent tissue (TXB2, 6-oxo-PGF1) and oxidation injury (8-epi-PGF2) after 131I-therapy in the salivary glands (AU)

Ya que las glándulas salivares concentran radioyodo, el daño de la radiación asociado a la terapia con 131I puede dar lugar a sialoadenitis y xerostoma, conduciendo a una calidad de vida dañada de forma duradera. Recientemente, hemos informado sobre cambios en la concentración de prostaglandina como marcadores bioquímicos para daño después de radiación. Se ha demostrado que los isoprostanos, una nueva familia del compuestos del tipo prostaglandina, son marcadores fiables para daño oxidativo in vivo. Pacientes y métodos: En este estudio, exploramos los niveles de 8-epi-PGF2, el miembro más importante de la familia de isoprostanos, en 24 pacientes recibiendo tratamiento 131I con dosis diferentes para hipertiroidismo y cáncer de tiroides diferenciados. Fueron monitorizados en paralelo 6 voluntarios sanos pareados por edad y sexo. Se determinaron (iso) prostaglandinas en saliva antes del tratamiento de 131I, así como 1, 3, 7, 14, 21 y 28 días y 2, 3, y 6 meses después del tratamiento. Resultados: 8-epi-PGF2 demostraron un aumento temporal significativo dependiendo de la dosis de 131I. Las alteraciones en todos los pacientes investigados fueron comparables y significativamente más altas en los que fumaban. TXB2 y 6-oxo-PGF1 demostraron también un aumento dependiente de la dosis. TXB2 fue más alto en los que fumaban y 6-oxo-PGF1 más bajo al compararlo con no-fumadores. Conclusión: Estos resultados demostraron claramente un daño tisular tiempo y dosis dependiente (TXB2, 6-oxo-PGF1) y daño oxidativo (8-epi-PGF2) después de terapia con 131I en las glándulas salivares (AU)

Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscular problems.

AIMS: Muscular problems are the major group of side-effects during statin treatment. They are known to occur much more frequently during and after exercise. METHODS AND RESULTS: For the last 8 years we have monitored 22 professional athletes in whom, because of familial hypercholesterolaemia, treatment with different statins was attempted. Only six out of the 22 finally tolerated at least one member of this family of drugs. In three of these six the first statin prescribed allowed training performance without any limitation. Changing the drug demonstrated that only two tolerated all the four or five statins examined (atorvastatin, fluvastatin, lovastatin, pravastatin, simvastatin). Cerivastatin was not among the statins prescribed. CONCLUSIONS: These findings indicate that in top sports performers only about 20% tolerate statin treatment without side-effects. Clinical decision making as to lipid lowering therapy thus becomes a critical issue in this small subgroup of patients.

Modification of low-density lipoprotein by different radioiodination methods.

Scintigraphic imaging of radiolabeled low-density lipoproteins (LDL) is an interesting tool for the understanding of its role in pathomechanism of atherosclerosis. Metabolism of native LDL shows quite different pattern and kinetics as compared to that of modified LDL which is not mediated by classical LDL-receptor and accumulates in atherosclerotic lesions to form lipid-laden foam cells. Therefore we were interested whether radiolabelling of LDL induces structural modifications. We performed the iodine labeling of LDL for scintigraphic imaging of atherosclerosis by three different methods: chloramine-T (A), iodine monochloride (B) and iodogen (C). The highest radiolabelling yield of (125)I was obtained by the iodogen method (75.44+/-13.52%) and the lowest (49.01+/-12.74%) by iodine monochloride. Chloramine T showed a labeling yield of 62.82+/-6.17%. The stability of the tracer was very high with all the methods, persisting up to 6 h (98.83+/-1.2% - 91.38+/-4.7%, 15 min vs 6 h after labeling). For the first time we not only investigated the influence of radiolabelling on relative electrophoretic mobility (REM), but also various oxidation parameters such as baseline dienes (BD), thiobarbituric acid reactive substances (TBARS), endogenous peroxides (POX) and oxidation resistance in the copper-mediated oxidation system (expressed as lag-time) were measured. Furthermore, oxidation- derived fragmentation of the lipoproteins was examined with SDS-PAGE electrophoresis. Data are expressed as % change compared to native LDL before radiolabeling. BD were reduced by 32% using the method (A), but increased by 33% and 47% with the monochloride (B) and iodogen method (C), respectively. The effect on lag-time was comparable for all the three methods, ranging from 25 to 36% reduction in lag-time. TBARS were strongly increased 5-7 fold by all the methods. REM was changed by all three methods. While by methods A and C we have found a moderate increase in REM by 1.75 and 2.0 fold, respectively, and no fragmentation of Apo B was observed, in contrast by method B a dramatic 4.5 fold increase in REM was found. SDS-PAGE-electrophoresis showed strong fragmentation of the apoB only for method B. We conclude, that iodine labeling of LDL induces significant modification of the molecule. Once modified, LDL no longer reflects the native molecule, exhibiting altered functional properties. Using radiolabeled LDL this fact should be considered.

[Radiation doses deriving from patients treated with (166)Ho-ferric hydroxide]. / Strahlenexposition in der Umgebung von Patienten bei Radiosynoviorthese mit (166)Ho-Eisenhydroxid.

AIM: To estimate radiation doses deriving from patients treated with (166)Ho ferric hydroxide. METHODS: For radiation synoviorthesis about 900 +/- 100 MBq (166)Ho ferric hydroxide was injected into the knee joint of 16 patients. To estimate the radiation exposure of persons in the neighbourhood of the patients measurements of the dose rates were performed at 0.5 m, 1 m and 2 m distance of the treated joint 10 min after tracer injection. Measurements were carried out with and without radiation protection devices of the syringe. RESULTS: The initial values of the dose rate were 11.9 micro Sv/h at 0.5 m, 3.5 micro Sv/h at 1 m and 1 micro Sv/h at 2 m distance, respectively. The whole body doses were 2.9 micro Sv for the physician and 4.6 micro Sv for the technologist. The finger doses for the technologist and the physician were ranging from 65 to 111 micro Sv. After discharge at home other persons might receive 118 micro Sv. CONCLUSION: Our results, under very strict assumptions, clearly demonstrate that the calculated radiation exposure to medical and non medical personnel is well below the maximum annual dose limit. The use of any additional radiation protection device as syringe shielding does not significantly lower radiation exposure.

Effects of fenofibrate on endothelial function and cell adhesion molecules during post-prandial lipemia in hypertriglyceridemia.

BACKGROUND: Fasting and post-prandial hypertriglyceridemia have been associated with endothelial dysfunction. OBJECTIVE: To investigate the effects of a 3-month treatment with fenofibrate (200 mg daily) on endothelial reactivity and inflammatory state in hypertriglyceridemic patients at fast and after an oral fat load. METHODS: Brachial flow-mediated vasodilation (FMV) and the circulating levels of intercellular adhesion molecule (ICAM) and vascular cellular adhesion molecule (VCAM) were determined in 10 hypertriglyceridemic patients. RESULTS: Before treatment, post-prandial phase was characterized by an increase in triglycerides (3.7 +/- 1 mmol/L at baseline vs. 4.2 +/- 1, 6.5 +/- 1, 6.6 +/- 2, and 5.3 +/- 2 mmol/L after 2, 4, 6, and 8 h), a decrease in FMV (4.3 +/- 2% at baseline vs. 2.8 +/- 1, 2.2 +/- 1, and 1.3 +/- 1% after 2, 4, and 6 h), and an increase in ICAM and VCAM. After fenofibrate there was a significant reduction in fasting triglycerides (3.7 +/- 1.3 vs. 2.1 +/- 0.8 mmol/L), ICAM (480 +/- 113 vs. 269 +/- 65 ng/mL) and VCAM (1821 +/- 570 vs. 1104 +/- 376 ng/mL), and an increase in FMV (4.3 +/- 2 vs. 7.1 +/- 2%). Post-prandially triglycerides increased (2.1 +/- 1 at baseline vs. 2.4 +/- 2 and 3.6 +/- 1 mmol/L after 4 and 6 h), FMV decreased (7.1 +/- 2 at baseline vs. 5.8 +/- 2, 5.5 +/- 2, 5.9 +/- 2, 6.4 +/- 2% after 2, 4, 6, and 8 h), and there was an increase of ICAM and VCAM. Before therapy post-prandial changes in FMV had an inverse correlation with the changes in triglycerides (r = -0.34; P < 0.05) and ICAM (r = -0.66; P < 0.001). CONCLUSIONS: The transient endothelial dysfunction observed in hypertriglyceridemic subjects during post-prandial lipemia is mediated by post-prandial triglyceride increase and by the activation of inflammatory response. The anti-inflammatory activity of fenofibrate may represent an additional mechanism of its favorable action on the endothelial function during fasting and the post-prandial phase.

Daily prickly pear consumption improves platelet function.

Prickly pear is traditionally used by Pima Indians as a dietary nutrient against diabetes mellitus. We examined the effect of daily consumption of 250 g in 8 healthy volunteers and 8 patients with mild familial heterozygous hypercholesterolemia on various parameters of platelet function. Beside its action on lipids and lipoproteins, prickly pear consumption significantly reduced the platelet proteins (platelet factor 4 and beta-thromboglobulin), ADP-induced platelet aggregation and improved platelet sensitivity (against PGI2 and PGE1) in volunteers as well as in patients. Also plasma 11-DH-TXB2 and the WU-test showed a significant improvement in both patients and volunteers. In contrast, collagen-induced platelet aggregation and the number of circulating endothelial cells showed a significant response in patients only. No influence of prickly pear ingestion on peripheral platelet count was monitored. The dietary run-in period did not influence any of the parameters of haemostasis examined. No sex difference was seen. Prickly pear may induce at least part of its beneficial actions on the cardiovascular system via decreasing platelet activity and thereby improving haemostatic balance.