4.1 Experimental results
The normal reference value ranges of the in vitro coagulation dynamic detection sensing system prepared in this paper for different kits are shown in Fig. 4.
Test results of healthy group are presented in Fig. 5
For patients in patient group 1, their blood samples collected at 0, 6, 12, 18 and 24 h were analyzed using the nor-channel of the in vitro coagulation dynamic detection sensing system to obtain the ACT values. Then, the values at corresponding time points were compared with those in healthy group. As a result, there were not significant differences in the results (P > 0.05).
For patients in patient group 1, their blood samples collected at 0, 6, 12, 18 and 24 h were analyzed using the nor-channel of the in vitro coagulation dynamic detection sensing system to obtain the CR values. Then, the values at corresponding time points were compared with those in healthy group. The results revealed no significant differences in the results (P > 0.05).
For patients in patient group 1, their blood samples collected at 0, 6, 12, 18 and 24 h were analyzed using the nor-channel of the in vitro coagulation dynamic detection sensing system to obtain the PF values. Later, the values at corresponding time points were compared with those in healthy group. The results suggested no significant differences in the results (P > 0.05).
Non-channel test results of patient group 1 at different time points are exhibited in Fig. 9–11.
The blood samples collected from patient group 1 at 0, 6, 12, 18 and 24 h were analyzed by the non-channel of the in vitro coagulation dynamic detection sensing system to obtain ACT value. Then, the values at corresponding time points were compared with those in healthy group. As a result, there was significant difference in ACT value at 0 h compared with control group (P < 0.05), while no significant differences were observed in ACT value at other time points (P > 0.05).
The blood samples collected from patient group 1 at 0, 6, 12, 18 and 24 h were analyzed by the non-channel of the in vitro coagulation dynamic detection sensing system to obtain CR value. Thereafter, the values at corresponding time points were compared with those in healthy group. As a result, there were significant differences in CR value at 0 and 24 h compared with control group (P < 0.05), while no significant differences were observed in CR value at other time points (P > 0.05).
The blood samples collected from patient group 1 at 0, 6, 12, 18 and 24 h were analyzed by the non-channel of the in vitro coagulation dynamic detection sensing system to obtain PF value. Thereafter, the values at corresponding time points were compared with those in healthy group. As a result, there was no significant difference in PF value at 0 h compared with control group (P > 0.05), whereas significant differences were observed in PF value at the remaining time points (P < 0.05).
2)Nor-channel test results of patient group 2 at different time points are exhibited in Fig. 12–14.
For patients in patient group 2, their blood samples collected at 0, 6, 12, 18 and 24 h were analyzed using the nor-channel of the in vitro coagulation dynamic detection sensing system to obtain the ACT values. Later, the values at corresponding time points were compared with those in healthy group. As a result, there were not significant differences in the results (P > 0.05).
For patients in patient group 2, their blood samples collected at 0, 6, 12, 18 and 24 h were analyzed using the nor-channel of the in vitro coagulation dynamic detection sensing system to obtain the CR values. Then, the values at corresponding time points were compared with those in healthy group. The results revealed no significant differences in the results (P > 0.05).
For patients in patient group 2, their blood samples collected at 0, 6, 12, 18 and 24 h were analyzed using the nor-channel of the in vitro coagulation dynamic detection sensing system to obtain the PF values. Later, the values at corresponding time points were compared with those in healthy group. The results suggested no significant differences in the results (P > 0.05).
Non-channel test results of patient group 2 at different time points are exhibited in Fig. 15–17.
For patients in patient group 2, their blood samples collected at 0, 6, 12, 18 and 24 h were analyzed using the non-channel of the in vitro coagulation dynamic detection sensing system to obtain the ACT values. Later, the values at corresponding time points were compared with those in healthy group. As a result, there was significant difference in ACT value at 24 h compared with control group (P < 0.05), while no significant differences were observed in ACT value at other time points (P > 0.05).
The blood samples collected from patient group 2 at 0, 6, 12, 18 and 24 h were analyzed by the non-channel of the in vitro coagulation dynamic detection sensing system to obtain CR value. Thereafter, the values at corresponding time points were compared with those in healthy group. As a result, there were significant differences in CR value at 0 and 24 h compared with control group (P < 0.05), while no significant differences were observed in CR value at other time points (P > 0.05).
The blood samples collected from patient group 2 at 0, 6, 12, 18 and 24 h were analyzed by the non-channel of the in vitro coagulation dynamic detection sensing system to obtain PF value. Later, the values at corresponding time points were compared with those in healthy group. The results revealed significant differences in PF value at all time points (P < 0.05).
Changes in the values of diverse parameters of patient groups 1 and 2 before and after administration are presented in Fig. 18–21.
4.2 Evaluation and analysis
For patient group 1, the values of diverse nor-channel parameters at corresponding time points were compared with the normal values. For ACT, it was observed from the test results that, the ACT values obtained by the non-channel of the in vitro coagulation dynamic detection sensing system before and after administration at diverse time points showed a shortening trend, but there was no significant difference when comparing them with normal values (P > 0.05). These results suggested that, long-term oral administration of aspirin (100 mg/day) was necessary for patients with coronary atherosclerosis, which greatly suppressed the platelet activation pathway, further demonstrating that ACT values were maintained within the normal range even in the presence of exogenous coagulation pathway. With regard to CR, the reduction at 0 h revealed no significant difference (P = 0.089), while the values at other time points significantly decreased, indicating that the exogenous coagulation pathway was involved during the coagulation activation process after oral administration of aspirin, which promoted the increased contents of fibrin in blood. Such result suggested that oral administration of aspirin reduced the fibrin content produced by the endogenous coagulation pathway, but more healthy subjects should be enrolled into the control group to compare whether excessive antiplatelet activity existed in such result. In terms of PF, the PF values obtained by the non-channel of the in vitro coagulation dynamic detection sensing system displayed a decreasing trend at each time point. The PF values at corresponding time points were compared with the normal values, and there was no significant difference in the results (P > 0.05), indicating that long-term oral administration of aspirin (100 mg/day) led to certain changes in platelet function of patients with coronary atherosclerosis activated by the exogenous coagulation pathway at each time point. But such as variation range was within the normal level, further demonstrating that the current dose for patients was suitable, with no need for adjustment [8].
The values of diverse non-channel parameters in patient group 1 at corresponding time points were compared with the normal values. The kit used in the non-channel was the ordinary coagulation dry kit with no addition of glass beads; as a result, there was only blood coagulation shear force. For ACT, in patients taking aspirin for a long time, aspirin partially suppressed the activation of the platelet pathway, but the postoperative coagulation function was active, and ACT values were significantly shortened (P = 0.027). Such result sufficiently demonstrated that the daily dose of aspirin no longer satisfied the postoperative needs of patients, and it was necessary to appropriately increase the drug dose. At 6 h after oral administration of aspirin, the ACT values were slightly higher than those before administration and showed a shortening trend compared with the normal value. With regard to CR: the changes in CR value at 0 and 24 h were significantly different (Ps < 0.05), while those at the other time points showed no significant difference (P > 0.05). As revealed by such result, oral administration of aspirin at daily dose suppressed platelet activation for a short time in patients with coronary atherosclerosis, which indicated the insufficient routine dose and further suggested the importance of drug dose. As for PF, the PF value at 0 h was at normal level, but with the increase in drug dose, the PF values at the remaining time points significantly decreased. However, it was no enough to analyze the risk of postoperative bleeding from this indicator alone, and the conclusions should be drawn based on clinical results [9].
The values of diverse nor-channel parameters in patient group 1 at corresponding time points were compared with values in healthy group. The results suggested that, the ACT and CR values obtained by the nor-channel of the in vitro coagulation dynamic detection sensing system showed a decreasing trend at each time point. Compared with before administration, the values after administration were extended. However, there were no significant differences in the values at corresponding time points when compared with those from healthy group (P > 0.05). As suggested by these results, for patients with coronary atherosclerosis, oral administration of aspirin (100 mg/day) slightly extended ACT at each time point after administration, and the levels of fibrin produced by this pathway decreased accordingly. After oral administration, the PF values obtained by the nor-channel of the in vitro coagulation dynamic detection sensing system showed a decreasing trend at each time point. Values at corresponding time points were compared with those from healthy group, and all results were significantly different (P < 0.05). Based on this result, for patients with coronary atherosclerosis, oral administration of aspirin (100 mg/day) reduced platelet activation via the exogenous coagulation pathway at each time point, but such variation range was normal, and no significant decrease was observed [10].
The values of diverse nor-channel parameters in patient group 1 at corresponding time points were compared with values in healthy group. In patient group 1, the ACT values of blood samples collected at 0, 6, 12, 18 and 24 h were analyzed by the analyzer and compared with values in the healthy group. The results suggested that the ACT value at 0 h displayed significant difference (P < 0.05), while those at the other time points did not show significant differences (P > 0.05). Thereafter, CR values were compared with those in healthy group. The results indicated that changes in CR value at 0 and 24 h exhibited significant differences (P < 0.05), while those at other time points revealed no significant difference (P > 0.05). Further, PF values were compared with those in healthy group, and it was found that changes in PF values were significantly different except for that at 0 h (P < 0.05). According to the above results, in the absence of exogenous coagulation mechanism, the comparisons of diverse non-channel parameters in patients with those in healthy group after increasing the oral administration dose demonstrated the presence or absence of excessive antiplatelet activity, and the parameter range might be determined if there was excessive antiplatelet activity [11].
The values of diverse nor-channel parameters in patient group 2 at corresponding time points were compared with values in healthy group. As for ACT, for patients with the initial diagnosis of coronary atherosclerosis who never received antiplatelet drug therapy, a certain amount of platelets were activated in their blood. The ACT value at 0 h obtained by the nor-channel of the in vitro coagulation dynamic detection sensing system was apparently shortened compared with normal value. But after administration of antiplatelet drug aspirin, the ACT values within 6 h were extended, and the efficacy of aspirin was preliminarily manifested at this moment. But the ACT values were still lower than the normal values, and there were no significant differences (P > 0.05). Subsequently, with the metabolism in the patient body, the ACT value at 12 h was shortened, suggesting the efficacy of aspirin was gradually weakened. The ACT values were higher than those before administration, but they were still shortened compared with the normal values. This phenomenon indicated that the dose of oral aspirin might be enhanced in the patients, but more healthy subjects should be enrolled for comparison to examine whether excessive antiplatelet activity existed in such result. For CR, its value at 0 h obtained by the nor-channel of the in vitro coagulation dynamic detection sensing system was apparently higher than that of the normal value (P = 0.687). This result demonstrated that oral administration of aspirin notably reduced the fibrin content produced by the endogenous coagulation pathway; therefore, the fibrin content produced by that pathway was higher than the normal value. The CR value detected at 6 h was still higher than the normal value, but it showed an apparently decreasing trend, with no significant difference (P = 0.126). Based on the above result, after oral administration of aspirin, the fibrin content in blood produced by the exogenous coagulation pathway was higher than the normal value; afterwards, with the metabolism in patient body, the CR value detected at 12 h was higher than the normal value (P = 0.256). This indicated that oral administration of aspirin alone no longer thoroughly suppressed the platelet activation function, and there was a risk of ischemia. Consequently, the anticoagulant drug should be increased or replaced to assist in treatment. With regard to PF, the changes in PF values at all time points were not significantly different. This might be mainly explained by the following three reasons based on clinical analysis. First of all, the sample size set to evaluate the anticoagulant drug efficacy by the new in vitro coagulation dynamic detection sensing technique was small, which was insufficient to reflect the overall variation trend of each parameter. Secondly, although the ACT and CR values showed corresponding variation trends after oral administration of aspirin, they were limited to reflect the activated platelet time parameter, but not attained the ideal requirement of suppressing platelet activation. According to the coagulation mechanism, thrombin was the most potent activation pathway to activate platelet function during the entire coagulation process. Nonetheless, it was analyzed that platelets began to be activated by thrombin before the measurement of PF values, and PF values showed an increasing trend, yet this was not the truth. Therefore, the aspirin efficacy should be further analyzed when such condition occurs during interventional treatment.
In patient group 2, the values of diverse non-channel parameters at corresponding time points were compared with the normal values. The kit used in the non-channel was the ordinary coagulation dry kit with no addition of glass beads; as a result, there was only blood coagulation shear force. For ACT, in patients who never took antiplatelet drug, there was a certain amount of activated platelets in the blood. From the perspective of data, the ACT value at 0 h was apparently shortened compared with normal value (P = 0.000). At 6–18 h, the ACT values showed an increasing trend because of drug action after admission, but they were significantly different from the normal values. At 24 h, with drug metabolism, the platelet function gradually decreased, and the ACT value showed a decreasing trend (P = 0.011). Based on the above results, it was speculated that for patients with initial diagnosis of coronary atherosclerosis who received oral administration of aspirin at 100 mg/day after admission, the ACT was slightly extended, but was not at the normal level. With regard to CR, CR showed a similar variation trend to ACT. In the absence of any inducer, the CR values in patients with initial diagnosis of coronary atherosclerosis at 0 h were apparently higher than the normal value (P = 0.000), exhibiting certain endogenous coagulation function. After oral administration of antiplatelet drug aspirin at a certain dose, the CR values at 6–18 h slightly decreased but were higher than the normal level. With the drug metabolism, the platelet activation at 24 h showed a decreasing trend. Thus, it was further speculated that, the drug dose should be increased to maximally reduce platelet aggregation and prevent sudden disorders like thrombosis. In terms of PF, the PF values in patients before and after oral administration of aspirin were higher than the normal value, which were opposite to the expected results. Combined with clinical analysis, such results might be explained by two aspects. First of all, the sample size in this experiment was small, which did not objectively reflect the overall variation trend. Secondly, for patients with coronary atherosclerosis, the platelet function in blood decreased, and the PF value increased before and after administration because platelets were activated, suggesting that it might be necessary to increase the drug dose or replace the drug.
In patient group 2, the values of diverse nor-channel parameters at corresponding time points were compared with the values in healthy group. Compared with values at 0 h, the ACT values at 6, 12, 18 and 24 h (namely, after oral administration of aspirin in patients with coronary atherosclerosis) elevated, while the CR values decreased, and the differences were all statistically significant (P < 0.05). The above findings suggested that the exogenous coagulation pathway was involved in the coagulation mechanism. As analyzed previously, this pathway extended the ACT and reduced fibrin content, but the PF value showed an increasing trend. After analysis, platelets begun to be activated by thrombin before the measurement of PF values, so the measured PF values showed an increasing trend, but this was not the truth. Therefore, the aspirin efficacy should be further analyzed when such condition occurs during the interventional treatment. In addition, the changes in PF value might be related to the platelet activation by thrombin.
The values of diverse non-channel parameters in patient group 2 at corresponding time points were compared with those in healthy group. The blood samples collected from patients in patient group 2 at 0, 6, 12, 18 and 24 h were analyzed by the analyzer. According to our results, the ACT value at 24 h showed significant difference, while those at other time points did not show any significant difference (P > 0.05). With regard to CR, there were significant differences at 0 and 24 h (P < 0.05), while those at other time points did not show any significant difference (P > 0.05). Moreover, changes in PF values at all time points were significantly different (P < 0.05). The dry coagulation kit without any inducer was used in this experiment; therefore, our results truly reflected the change process after the drug acted on the blood, thus reflecting the antiplatelet drug efficacy, which might provide reference for platelet functional evaluation and guide clinical treatment.