Myocardial Infarction-3 Flow After Streptokinase
Background: The initial white cell counts in patients with acute myocardial infarction (AMI) may reflect the stage of AMI evolution, and may also be related to the efficacy of thrombolytic agents in recanalizing occluded epicardial arteries.
Methods: In 312 patients with a first AMI, we divided the initial white cell counts into quartiles and investigated their relationship with the time to treatment and the incidence of Thrombolysis In Myocardial Infarction (TIMI)-3 flow at 90 minutes after commencement of streptokinase.
Results: A longer time from symptom onset to treatment was independently associated with a higher neutrophil count and a lower non-neutrophil count. These times were 2.6, 2.9, and 3.8 hours, respectively, in the lowest, combined second and third (ie, middle), and highest neutrophil quartiles (P = .003), and 4.3, 3, and 1.9 hours, respectively, in the lowest, combined middle, and highest non-neutrophil quartiles (P < .0001).
TIMI-3 flow was achieved in 44% of the lowest total white cell quartile, 41% of the combined middle quartile, and 60% of the highest quartile (P = .05). The corresponding figures were 47%, 49%, and 46% (P = .657) for the neutrophil quartiles, and 32%, 46%, and 68% for the non-neutrophil quartiles (P = .001). On multivariable analysis, the incidence of TIMI-3 flow was independently and positively associated with the initial non-neutrophil count. Patients with non-neutrophil counts in the highest quartile had a higher incidence of TIMI-3 flow than those in the lowest quartile (odds ratio 2.86, 95% CI 1.32-6.23, P = .008).
Conclusions: A longer time from symptom onset to thrombolysis for AMI is associated with a higher neutrophil count and a lower non-neutrophil count at presentation. A higher neutrophil count is not associated with worse epicardial blood flow at 90 minutes after streptokinase, and a higher non-neutrophil count predicts a greater likelihood of achieving TIMI-3 flow.

A high initial white blood cell count commonly occurs in patients presenting with acute myocardial infarction (AMI) and is associated with poorer early outcomes. There are two possible mechanisms. First, a high initial white cell count may be a manifestation of the inflammatory response to a more evolved AMI at the time of presentation, which in itself has an adverse prognosis. Second, the white cell count may be related to the efficacy of thrombolytic agents in recanalizing occluded infarct-related arteries.

White blood cells play an important role in thrombosis. In laboratory studies, leucocyte accumulation and fibrin deposition in thrombi are dependent on P-selectin, which mediates adhesion of monocytes and platelets, leading to tissue factor release from monocytes and the initiation of coagulation. Platelet-neutrophil interactions may also perpetuate coagulation.

In 975 patients pooled from the Thrombolysis In Myocardial Infarction (TIMI)-10 A and B trials who were treated with either tissue plasminogen activator (TPA) or its deriative, tenecteplase, a higher initial white cell count was associated with impaired epicardial coronary flow on 60- to 90-minute angiography. However, the relationships between differential white cell counts and early coronary flow were not analyzed in TIMI-10.

We studied patients with a first AMI in the Hirulog Early Reperfusion/Occlusion (HERO-1) trial to investigate whether the initial total and differential (neutrophil and non-neutrophil) white cell counts were associated with 1) impaired epicardial coronary flow at 90 minutes after administration of streptokinase, and 2) the stage of AMI evolution as measured by the time from symptom onset to treatment and initial electrocardiographic changes.