Comparison of usefulness of C-reactive protein versus white blood cell count to predict outcome after primary percutaneous coronary intervention for ST elevation myocardial infarction.

White blood cell (WBC) count and high-sensitive C-reactive protein (hs-CRP) are both used as markers of inflammation and prognosis after an ST elevation myocardial infarction (STEMI), but it is unknown whether they have independent prognostic value. We investigated the association and independent prognostic importance of WBC and hs-CRP after STEMI. In this subanalysis of the On-TIME trial, in 490 of 507 (97%) patients, either WBC count or CRP, and in 362 (71%) patients, both WBC count and CRP, were measured on admission before primary percutaneous coronary intervention. There was no significant correlation between WBC count and CRP (R = 0.080). Higher levels of CRP were associated with a reinfarction or death within 1 year (mean hs-CRP 14.2 +/- 20.4 vs 6.1 +/- 14.2, p = 0.006), but CRP was not associated with enzymatic infarct size (lactate dehydrogenase, LDHQ48) or left ventricular ejection fraction. A higher baseline WBC count was associated with larger LDHQ48 and lower left ventricular ejection fraction but not with 1-year reinfarction or death. In conclusion, although both WBC count and CRP are markers of inflammation and predictors of outcome after STEMI, we did not find a correlation between baseline WBC count and CRP levels in patients treated with primary percutaneous coronary intervention for STEMI. The mechanisms by which WBC counts predict outcome were related to myocardial infarct size whereas CRP were not.

Platelet microaggregation inhibition in patients with acute myocardial infarction pretreated with tirofiban and relationship with angiographic and clinical outcome.

BACKGROUND: The relationship between the level of platelet aggregation inhibition in patients with acute myocardial infarction and their clinical outcome is unknown. METHODS: In patients with acute myocardial infarction included in the On-TIME trial and transferred to the primary percutaneous coronary intervention (PCI) center of Zwolle, who were pretreated with tirofiban on top of acetylsalicylic acid and heparin, platelet microaggregation inhibition was assessed on admission and immediately after PCI, using the Sysmex K4500 (Sysmex Corp, Kobe, Japan) platelet microaggregation measurement. The level of platelet microaggregation inhibition was compared with angiographic and clinical outcome. Patients were randomized to early prehospital initiation of tirofiban or to initiation in the catheterization laboratory. Therefore, the effect of tirofiban on platelet microaggregation inhibition could additionally be determined by measuring baseline platelet microaggregation also at entrance into the hospital. RESULTS: In 412 (89%) of 463 patients, platelet microaggregation inhibition was measured after receiving tirofiban. There was no difference between the 4 quartiles of the level of platelet microaggregation inhibition with regard to distal embolization, TIMI-3 flow and blush grade 3 after PCI, mean corrected TIMI frame count, ejection fraction, enzymatic infarct size, and percentage ST-segment resolution (P values .91, .97, .46, .94, .73, .33, and .72, respectively). The baseline platelet microaggregation inhibition in patients treated with tirofiban was 38% +/- 25% (mean +/- SD), and in the patients treated with placebo, 14% +/- 22% (P < .001). CONCLUSIONS: We found no correlation between the level of platelet microaggregation inhibition after tirofiban and outcome, whereas only a modest increase in platelet microaggregation inhibition was observed after a commonly used dose of tirofiban.

Incidence and predictors of subacute thrombosis in patients undergoing primary angioplasty for an acute myocardial infarction.

Subacute thrombosis (SAT) is a major concern in patients undergoing percutaneous coronary intervention (PCI). So far, only little data has been available on characteristics and outcome of patients with SAT after primary PCI for ST elevation myocardial infarction (STEMI). From 1997-2001, 1,548 unselected consecutive patients underwent primary PCI for STEMI as part of a randomized controlled trial stenting vs. balloon angioplasty. All patients received acetylsalicylic acid (500 mg i.v.) and heparin (5,000 IU) before the procedure. After stenting, all patients received ticlopidine 250 mg daily (before July 1999) or clopidogrel 75 mg daily (after July 1999) for one month. Five percent of patients received glycoprotein IIb/IIIa blockers. We prospectively recorded incidence and characteristics of patients with SAT during one year follow-up. SAT occurred in 4.1% (63/1548) and reinfarction in 6.0% of patients. The incidence of SAT did not change over time (1997: 8/175[4.6%],1998: 8/325 [2.5%],1999: 13/358 [3.6%], 2000: 22/426 [5.2%], 2001: 12/264 [4.5%]). SAT occurred in 39/63(62%) patients during hospital stay. The incidence did not differ between patients after ticlopidine 23/681 (3.4%) or clopidogrel 40/867 (4.6%, p = 0.222). Univariate predictors of SAT were: patients with an LAD stenosis (5.4% vs. 2.9%, p = 0.016), with Killip class >1 at presentation (8.6% vs. 3.7%, p = 0.007) and in patients who received a stent (5.1% vs. 2.7%, p = 0.022). After multivariate analysis, Killip class >1 on admission was the only independent predictor of SAT(OR 2.26, 95% CI 1.14-4.47, p = 0.019). SAT was associated with a higher mortality at long-term follow-up (15% vs. 7%, p = 0.026). In a prospectively recorded, unselected consecutive series of patients undergoing PCI for STEMI, SAT occurred in 4.1% of patients at one-year follow-up. Signs of heart failure on admission, anterior myocardial infarction and stenting were predictors of SAT.