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Coagulation status and platelet function in patients with myocardial infarction with non-obstructive coronary arteries (cohort study)
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Abstract
Background
Some studies have found no difference in hemostasis between these groups, others have reported increased prothrombotic activity in patients with MINOCA.
Purpose
To study platelet function and coagulation status in patients with MINOCA.
Methods
The study included 42 patients with NSTEMI, divided into two groups: the MINOCA group (24 patients) and the MI-CAD group (18 patients). Platelet aggregation following activation was assessed using Solar AP2110 and LASCA aggregometers. Furthermore, platelet functional activity and calcium signaling were assessed using flow cytometry. Global coagulation function was also assessed using thrombodynamics analysis.
Results
Evaluation of platelet aggregation using aggregometry, revealed significantly worse aggregation in MINOCA patients compared to MI-CAD patients when ADP was used for platelet stimulation and vice versa when collagen was used. Furthermore, MI-CAD patients showed a noticeable decrease in the formation of aggregates compared to MINOCA patients using light scattering amplitude parameter. This applied both to the formation of large aggregates according to the Solar 2110 aggregometer data, and to the formation of small aggregates according to the LASCA aggregometer data. The aggregates were less stable in both groups, compared to healthy volunteers according to the irreversibility index in the aggregometry test when stimulated with different concentrations of ADP and TRAP-6. Using flow cytometry according to the platelet function testing protocol, it was revealed that in both groups, compared to healthy volunteers, the platelet size after activation was significantly increased, while the platelet granularity (SSC) was reduced, both at rest and during activation. The number of procoagulant phosphatidylserine-positive platelets was significantly reduced, and the release of dense granules after activation was reduced. All these parameters together indicate a reduced platelet response to activation in both groups. The calcium signaling test revealed a reduction of calcium release in response to ADP in the MINOCA group compared to the MI-CAD group. When assessing the coagulation status, both according to the data from routine coagulation parameters and results of the "Thrombodynamics" test, no significant differences between the groups, as well as deviations from the norm, were noted.
Conclusion
According to most test results, platelet function did not differ significantly between the two groups; however, some tests showed lower platelet activity in the MINOCA group compared to the MI-CAD group. No difference was found in coagulation function, with both groups showing a normal coagulation profile. This data, along with platelet function indicators, suggests the phenotype of "exhausted" platelets in patients with MINOCA, reflecting sub-activation in the bloodstream and a reduction in normal platelet function.Figure 1.LTA. Maximum Aggregation. Figure 2.LTA. Aggregation rate.
Title: Coagulation status and platelet function in patients with myocardial infarction with non-obstructive coronary arteries (cohort study)
Description:
Abstract
Background
Some studies have found no difference in hemostasis between these groups, others have reported increased prothrombotic activity in patients with MINOCA.
Purpose
To study platelet function and coagulation status in patients with MINOCA.
Methods
The study included 42 patients with NSTEMI, divided into two groups: the MINOCA group (24 patients) and the MI-CAD group (18 patients).
Platelet aggregation following activation was assessed using Solar AP2110 and LASCA aggregometers.
Furthermore, platelet functional activity and calcium signaling were assessed using flow cytometry.
Global coagulation function was also assessed using thrombodynamics analysis.
Results
Evaluation of platelet aggregation using aggregometry, revealed significantly worse aggregation in MINOCA patients compared to MI-CAD patients when ADP was used for platelet stimulation and vice versa when collagen was used.
Furthermore, MI-CAD patients showed a noticeable decrease in the formation of aggregates compared to MINOCA patients using light scattering amplitude parameter.
This applied both to the formation of large aggregates according to the Solar 2110 aggregometer data, and to the formation of small aggregates according to the LASCA aggregometer data.
The aggregates were less stable in both groups, compared to healthy volunteers according to the irreversibility index in the aggregometry test when stimulated with different concentrations of ADP and TRAP-6.
Using flow cytometry according to the platelet function testing protocol, it was revealed that in both groups, compared to healthy volunteers, the platelet size after activation was significantly increased, while the platelet granularity (SSC) was reduced, both at rest and during activation.
The number of procoagulant phosphatidylserine-positive platelets was significantly reduced, and the release of dense granules after activation was reduced.
All these parameters together indicate a reduced platelet response to activation in both groups.
The calcium signaling test revealed a reduction of calcium release in response to ADP in the MINOCA group compared to the MI-CAD group.
When assessing the coagulation status, both according to the data from routine coagulation parameters and results of the "Thrombodynamics" test, no significant differences between the groups, as well as deviations from the norm, were noted.
Conclusion
According to most test results, platelet function did not differ significantly between the two groups; however, some tests showed lower platelet activity in the MINOCA group compared to the MI-CAD group.
No difference was found in coagulation function, with both groups showing a normal coagulation profile.
This data, along with platelet function indicators, suggests the phenotype of "exhausted" platelets in patients with MINOCA, reflecting sub-activation in the bloodstream and a reduction in normal platelet function.
Figure 1.
LTA.
Maximum Aggregation.
Figure 2.
LTA.
Aggregation rate.
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