Acute coronary syndrome is associated with platelet hyperactivity, which in its persistent form, promotes recurrent thrombotic events. Complex cardiac rehabilitation after acute coronary syndrome improves clinical outcome; however, its effect on platelet hyperactivity is unknown.Design and methods
We enrolled 84 acute coronary syndrome patients on dual antiplatelet therapy, who underwent a new complex cardiac rehabilitation programme (NovaCord physiotherapy, lifestyle counselling, strict diet, stress management and regular coaching) and 51 control acute coronary syndrome patients with traditional cardiac rehabilitation. Platelet functionality was determined at enrolment and at three months follow-up by aggregometry, serum platelet-derived growth factor levels, total- and platelet-derived microvesicle counts (PMV; CD41a+/CD61+, CD62P+).Results
Platelet aggregation parameters and platelet-derived growth factor levels were significantly decreased in the complex cardiac rehabilitation group at three months (1 µg/ml collagen, median (interquartile range): 22 (10–45) vs 14 (7.5–25.5)%, p = 0.0015; 2 µg/ml collagen: 36 (22–60) vs 26.5 (16–37)%, p = 0.0019; 1.25 µM adenosine-diphosphate: 4.5 (1–10) vs 1 (0–3)%, p = 0.0006; 5 µM adenosine-diphosphate: 27 (16–38) vs 22 (12–31)%, p = 0.0078; epinephrine: 33 (15–57) vs 27 (12–43)%, p = 0.01; platelet-derived growth factor: 434.6 (256.0–622.7) vs 224.8 (148.5–374.1) pg/ml, p = 0.0001). In contrast, these changes were absent or did not reach statistical significance in the traditional cardiac rehabilitation group. Platelet–derived microvesicle counts were significantly decreased in both groups, while total microvesicle count was significantly reduced only in the complex cardiac rehabilitation group (median (interquartile range): 3945.5 (2138–5661) vs 1739 (780–2303) count/µl; p = 0.0001).Conclusions
Platelet hyperactivity three months after acute coronary syndrome significantly decreased in patients undergoing complex cardiac rehabilitation. Besides dual antiplatelet therapy, effective management and comprehensive control of cardiovascular risk factors might represent a new, non-pharmacological approach to influence platelet functionality.