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Brief low-workload myocardial ischemia induces protection against exercise-related increase of platelet reactivity in patients with coronary artery disease
  1. Giancarla Scalone,
  2. Ilaria Coviello,
  3. Lucy Barone,
  4. Chiara Pisanello,
  5. Alfonso Sestito,
  6. Gaetano A Lanza*,
  7. Filippo Crea
  1. 1 Università Cattolica del Sacro Cuore, Roma, Italy
  1. Correspondence to: , ; g.a.lanza{at}rm.unicatt.it

Abstract

Objective: In patients with acute myocardial infarction, pre-infarction angina is associated with smaller infarct size, probably mainly through myocardial protection induced by ischemic preconditioning (IPC). However, in models of recurrent thrombosis myocardial ischemia also improves arterial patency. We investigated whether myocardial ischemia has any effect on platelet function in patients with CAD.

Patients and design: Twenty patients with low workload myocardial ischemia underwent, in a randomized cross-over study, 2 treadmill exercise stress tests (ESTs) in 2 separate days: 1) a single maximal EST (EST-1), and 2) a maximal EST (EST-2) performed 45 minutes after a low-workload EST stopped at 1 mm ST depression (p-EST). Platelet reactivity was evaluated by measuring the closure time (CT) in response to ADP/collagen by the PFA-100 method, and monocyte–platelet aggregate (MPA) formation and CD41 platelet expression, with and without ADP stimulation, by flow cytometry.

Results: Compared to resting values, CT decreased at peak EST-1 (p<0.001) but not at peak EST-2. MPA after ADP stimulation increased more significantly at peak EST-1 compared to peak EST-2 (p<0.001). Repetition in 7 patients of the pEST/EST-2 protocol after intravenous administration of the adenosine antagonist theophylline showed prevention of the effects of p-EST on exercise induced platelet reactivity.

Conclusions: A short episode of myocardial ischemia induces protection against exercise induced increase of platelet reactivity. Our data also suggest a role for adenosine in this phenomenon.

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