Abstract
Introduction
Patients with coronary artery disease (CAD) have prothrombotic changes compared with healthy individuals. Regular exercise reduces cardiovascular mortality in patients with stable CAD. However, the underlying mechanism for the beneficial effect is unknown. We investigated whether regular exercise would inhibit platelet aggregation and thrombin generation and increase fibrinolysis in patients with CAD.
Materials and methods Patients with CAD were randomised 1:1 to a supervised high-intensity exercise training programme or standard care for 12 weeks. Blood samples were obtained at baseline and after 6 and 12 weeks. Platelet aggregation was evaluated with the Multiplate Analyser, thrombin generation using the calibrated automated thrombogram and fibrinolysis employing a clot lysis assay.
Results A total of 169 stable patients with CAD were randomised, and 142 patients (67±9 years, 83% males) completed the study; 64 in the exercise group and 78 in the standard care group. All but one patients received single antiplatelet therapy. From baseline to 12 weeks postintervention (Δ), no significant between-group differences were found in adenosine diphosphate-induced platelet aggregation (Δ−15 aggregation units (AU), AU×min, 95% CI −70 to 40 in the exercise group and Δ−26 AU×min, 95% CI −77 to 26 in the standard care group, p=0.44); endogenous thrombin potential (medians: Δ−5%, 95% CI −12 to 3 in the exercise group and Δ−6%, 95% CI −13 to 1 in the standard care group, p=0.26); nor in 50% clot lysis time (medians: Δ−9%, 95% CI −23 to 7 in the exercise group and Δ−17%, 95% CI −29 to −3 in the standard care group, p=0.60).
Conclusions Twelve weeks of high-intensity whole-body endurance exercise did not affect platelet aggregation, thrombin generation or fibrinolysis in patients with stable CAD.
Patients with coronary artery disease (CAD) have prothrombotic changes compared with healthy individuals. Regular exercise reduces cardiovascular mortality in patients with stable CAD. However, the underlying mechanism for the beneficial effect is unknown. We investigated whether regular exercise would inhibit platelet aggregation and thrombin generation and increase fibrinolysis in patients with CAD.
Materials and methods Patients with CAD were randomised 1:1 to a supervised high-intensity exercise training programme or standard care for 12 weeks. Blood samples were obtained at baseline and after 6 and 12 weeks. Platelet aggregation was evaluated with the Multiplate Analyser, thrombin generation using the calibrated automated thrombogram and fibrinolysis employing a clot lysis assay.
Results A total of 169 stable patients with CAD were randomised, and 142 patients (67±9 years, 83% males) completed the study; 64 in the exercise group and 78 in the standard care group. All but one patients received single antiplatelet therapy. From baseline to 12 weeks postintervention (Δ), no significant between-group differences were found in adenosine diphosphate-induced platelet aggregation (Δ−15 aggregation units (AU), AU×min, 95% CI −70 to 40 in the exercise group and Δ−26 AU×min, 95% CI −77 to 26 in the standard care group, p=0.44); endogenous thrombin potential (medians: Δ−5%, 95% CI −12 to 3 in the exercise group and Δ−6%, 95% CI −13 to 1 in the standard care group, p=0.26); nor in 50% clot lysis time (medians: Δ−9%, 95% CI −23 to 7 in the exercise group and Δ−17%, 95% CI −29 to −3 in the standard care group, p=0.60).
Conclusions Twelve weeks of high-intensity whole-body endurance exercise did not affect platelet aggregation, thrombin generation or fibrinolysis in patients with stable CAD.
Original language | English |
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Article number | e002127 |
Number of pages | 10 |
Journal | Open Heart |
Volume | 9 |
Publication status | Published - 25 Nov 2022 |
Keywords
- high intensity exercise
- Coronary artery disease