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postulated that RBCs are able to modulate PLT aggregability and recruitment by enhancing α(IIb)β(3) integrin receptor activation and P-selectin expression on PLTs (182)
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Pathologically, HCM is characterized by enhanced L-type calcium channel (LTCC) activity [35], leading to intracellular calcium overload and an increased risk of arrhythmic sudden death [36,37]
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