Microvascular obstruction seems to predict poor outcome in patients undergoing elective
percutaneous coronary intervention (PCI), but the underlying mechanism is still unclear. We analyzed whether serum
thromboxane B2, a stable metabolite of
thromboxane A2, may be implicated in post-PCI microvascular obstruction.
METHODS AND RESULTS: We enrolled 91 patients (74 males, 66±10 years) on chronic low-dose
aspirin therapy (
aspirin, 100 mg daily) scheduled for elective PCI and randomly assigned to receive
aspirin reload (325 mg orally, n=46) or no reload (control group, n=45) ≥1 hour before elective PCI. Serum levels of
thromboxane B2, reperfusion indexes (corrected Thrombolysis In
Myocardial Infarction frame count and myocardial blush grade), and serum cardiac
troponin I were assessed before and after PCI. Serum
thromboxane B2 significantly increased after 120 minutes (P=0.0447) from PCI in control but not in
aspirin reload group. After PCI, both groups showed a statistically significant reduction in corrected Thrombolysis In
Myocardial Infarction frame count more evident in
aspirin reload group (P=0.0023). Moreover, after PCI, 61% of patients allocated to
aspirin reload and only 32% of patients allocated to control group reached normal microcirculatory reperfusion (myocardial blush grade=3); patients with myocardial blush grade=3 exhibited lower values of serum
thromboxane B2 compared with those with myocardial blush grade <3 (P=0.05). Periprocedural cardiac
troponin I significantly increased (F=3.64; P=0.01334) and correlated with serum
thromboxane B2 (ρ=0.31; P=0.0413) in control but not in
aspirin reload group. In addition, left ventricular ejection fraction significantly increased after PCI only in the
aspirin reload group (P=0.0005).
CONCLUSIONS:
Aspirin loading dose before elective PCI improves myocardial reperfusion and injury indexes, suggesting a possible role of platelet
thromboxane A2 in microvascular occlusion.
CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01374698.