Inhibition of Platelet Aggregation by Contrast Media

Gafter, Uzi; Creter, D; Zevin, D; Catz, Rama; Djaldetti, Meir

doi:10.1148/132.2.341

Cited by 20 publications

(8 citation statements)

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“…This general observation parallels several previously published reports suggesting inhibition of platelet aggregation by various RCM [3,4,[6][7][8]111. An inhibitory effect of similar magnitude was noted for RCM concentrations of 1, 2.5, 5 and 7.5 percent by volume.…”

Section: Aggregation Kineticssupporting

confidence: 91%

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Radiographic contrast agents and platelet function: A quenched‐flow study

Taylor

Angello

Ayers

et al. 1991

Cathet. Cardiovasc. Diagn.

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Radiographic contrast media (RCM) may alter platelet behavior at concentrations achieved during cardiac angiography. We used quenched-flow aggregometry coupled to single-particle counting to study the influence of RCM on the kinetics of platelet aggregation (less than 5.0 sec) induced by adenosine diphosphate (ADP, 2.86 microM). At a concentration in platelet-rich plasma (PRP) of 5 per cent RCM by volume, platelet aggregation was inhibited by diatrizoate, iopamidol and ioxaglate either directly or following incubation of each contrast agent with PRP for 20 minutes. Diatrizoate inhibited more than did iopamidol or ioxaglate (56 +/- 6, versus 39 +/- 3 and 40 +/- 9 per cent respectively; P less than 0.003, p less than 0.009, n = 20 normal subjects). A small reduction (about 16 per cent) in aggregation velocity occurred within 5 seconds of exposure of PRP to all 3 RCM and the onset time (t) or lag period before aggregation begins was significantly prolonged by diatrizoate (p less than 0.03). The RCM vehicles alone (iodinated moiety removed, osmolality readjusted) had no effect on the ADP-induced aggregation. Platelet counts fell significantly after incubation with diatrizoate (12%; p = 0.04). Our data therefore show that early platelet aggregation was inhibited by 3 commonly-used ionic and nonionic contrast agents. Inhibition was apparently caused by the iodinated contrast molecule, began within seconds of platelet-RCM contact and was independent of vehicle composition. Since diatrizoate inhibited aggregation more than iopamidol or ioxaglate, its use may be of additional value during angiographic procedures in clinical situations involving enhanced platelet activation.

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Section: Aggregation Kineticssupporting

confidence: 91%

“…Subsequent studies [5,6] have suggested inhibition of aggregation appearing within 1 1/2 to 3 min. of RCM exposure, but whether the ex vivo effect is persistent [3,4] or more transient (returning to normal within 15 min [6], is controversial. We did not study aggregation kinetics for platelet-RCM exposure times exceeding 20 min.…”

Section: Time Course Of Effectsmentioning

confidence: 99%

Radiographic contrast agents and platelet function: A quenched‐flow study

Taylor

Angello

Ayers

et al. 1991

Cathet. Cardiovasc. Diagn.

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“…It is interesting to note that the only previous study to suggest that non-ionic contrast media cause platelet aggregation used heparin as an anticoagulant, which, like hirudin, maintains plasma divalent cation concentrations at a physiological level (Hay & Bull, 1995). Other studies in which citrate was used as anticoagulant suggest that contrast media inhibit platelet aggregation (Gafter et al, 1979;Dawson et al, 1986;Taylor et al, 1991;Carr et al, 1995;Tamura et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…Some reports suggest that non-ionic low-osmolar contrast media can cause degranulation (Chronos et al, 1993;Hardeman et al, 1994;Van Beek et al, 1994;Albanese et al, 1995;Koza et al, 1995;Grabowski et al, 1995;Corot et al, 1996;Hay & Bull, 1995), which, through release of aggregating agents stored in intracellular granules, would be expected to be associated with platelet aggregation. However, the situation is confused by other reports that suggest that some contrast media inhibit platelet aggregation (Gafter et al, 1979;Dawson et al, 1986;Taylor et al, 1991;Carr et al, 1995;Tamura et al, 1995). In only one in vitro study has there been any indication that platelet aggregation can occur as a direct consequence of adding a contrast agent to blood (Hay & Bull, 1995).…”

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confidence: 98%

Differential effects of three radiographic contrast media on platelet aggregation and degranulation: implications for clinical practice?

et al. 1998

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Summary.We have determined the effects of three radiographic contrast media on platelet aggregation and degranulation in vitro. Aggregation was measured as loss of single platelets, and degranulation was measured as P-selectin expression using flow cytometry. Iopamidol added to hirudinized blood induced aggregation directly and also potentiated that induced by weak platelet agonists such as adenosine diphosphate (ADP). Iodixanol also potentiated platelet aggregation, but ioxaglate inhibited it. Iopamidol also caused marked platelet degranulation. The pro-aggregatory effect of iopamidol was evident in non-anticoagulated blood as well as in hirudinized blood, but not in citrated blood. In platelet-rich plasma (PRP) prepared from hirudinized blood neither iopamidol nor iodixanol directly induced platelet aggregation, but they rendered platelets hypersensitive to ADP. ADP antagonists inhibited the platelet aggregation and degranulation induced by iopamidol in whole blood, whereas aspirin, an inhibitor of thromborane A 2 synthesis, did not. These data are consistent with clinical reports of increased thromboembolic risk with non-ionic low-osmolar media, and raise concerns about the routine use of these contrast media during diagnostic and interventional arteriographic procedures. Routine use of citrate in previous experiments may have masked a pro-aggregatory effect of some contrast media.

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“…Diatrizoate contrast media have been found to inhibit human platelet aggregation after incubation with platelet-rich plasma (Gafter et al, 1979;Goldstone, 1974;Shapiro et al, 1977;Zir et al, 1974) and after in vivo use (Gafter et al, 1979;Shapiro et al, 1977;Zir et al, 1974). Shapiro et al (1977) found a prolonged template bleeding time in 3 of 13 patients after cardiac angiography with 210-560 ml of Renografin 76.…”

Section: Introductionmentioning

confidence: 99%

The effect of radiographic contrast agents on bleeding time and platelet aggregation

Verdirame

Davis

Phillips

1984

Clinical Cardiology

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Summary:The purpose of this study was to determine whether the use of relatively small amounts of radiographic contrast agents may impair hemostasis. Before and after injection of contrast agents, we measured the template bleeding time, platelet count in whole blood and platelet-rich plasma, platelet aggregation induced by epinephrine and adenosine diphosphate (ADP). and percent disaggregation of ADP-induced platelet aggregates in platelet-rich plasma of 18 patients. Ten patients received 50-100 ml of sodium iothalamate (66.8%) for intravenous urography and 8 patients received 125-200 ml of a combination of meglumine diatrizoate (66%) and sodium diatrizoate (10%) for coronary angiography and left ventriculography. Neither group demonstrated a statistically significant mean difference (p >0.05) for any parameter measured before and after administration of the contrast agents. However, 2 pa- tients who received diatrizoate had lengthening of their bleeding times to greater than twice the baseline value without any change in in vitro platelet aggregation. Physicians should be aware of this potential cause of bleeding which could be of particular danger to patients undergoing cardiopulmonary bypass with its inherent hemostatic defects.

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Inhibition of Platelet Aggregation by Contrast Media

Cited by 20 publications

References 0 publications

Radiographic contrast agents and platelet function: A quenched‐flow study

Radiographic contrast agents and platelet function: A quenched‐flow study

Differential effects of three radiographic contrast media on platelet aggregation and degranulation: implications for clinical practice?

The effect of radiographic contrast agents on bleeding time and platelet aggregation

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