Key result
In vitro treatment of blood from post-stroke patients with aspirin resistance using dipyridamole decreased PAR-1 receptor expression by 22-26% and annexin V binding by 28-31%.
Why the study?
Does in vitro dipyridamole decrease protease-activated receptor and annexin-V binding on platelets of post-stroke patients with aspirin resistance?
Population
20 post-stroke patients with aspirin resistance (AR)
Design
Preclinical
Authors
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Suggests mechanistic role for dipyridamole in aspirin-resistant stroke; hypothesis-generating and requires clinical validation.
Does in vitro dipyridamole decrease protease-activated receptor and annexin-V binding on platelets of post-stroke patients with aspirin resistance?
p-value: p=0.021, 0.024, 0.031, 0.02
In vitro dipyridamole decreases PAR-1 receptor expression and annexin V binding on platelets from post-stroke patients with aspirin resistance, suggesting a mechanistic basis for its clinical benefit.
Serebruany et al. (2005) studied Poststroke patients with aspirin nonresponsiveness (n=20). Dipyridamole was evaluated on Expression of intact PAR-1 receptor and annexin V binding (p=0.021, 0.024, 0.031, 0.02). In vitro treatment of blood from post-stroke patients with aspirin resistance using dipyridamole decreased PAR-1 receptor expression by 22-26% and annexin V binding by 28-31%.
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