Effect of Using the HEART Score in Patients With Chest Pain in the Emergency Department: A Stepped-Wedge, Cluster Randomized Trial.

BACKGROUND: The HEART (History, Electrocardiogram, Age, Risk factors, and initial Troponin) score is an easy-to-apply instrument to stratify patients with chest pain according to their short-term risk for major adverse cardiac events (MACEs), but its effect on daily practice is unknown. OBJECTIVE: To measure the effect of use of the HEART score on patient outcomes and use of health care resources. DESIGN: Stepped-wedge, cluster randomized trial. (ClinicalTrials.gov: NCT01756846). SETTING: Emergency departments in 9 Dutch hospitals. PATIENTS: Unselected patients with chest pain presenting at emergency departments in 2013 and 2014. INTERVENTION: All hospitals started with usual care. Every 6 weeks, 1 hospital was randomly assigned to switch to "HEART care," during which physicians calculated the HEART score to guide patient management. MEASUREMENTS: For safety, a noninferiority margin of a 3.0% absolute increase in MACEs within 6 weeks was set. Other outcomes included use of health care resources, quality of life, and cost-effectiveness. RESULTS: A total of 3648 patients were included (1827 receiving usual care and 1821 receiving HEART care). Six-week incidence of MACEs during HEART care was 1.3% lower than during usual care (upper limit of the 1-sided 95% CI, 2.1% [within the noninferiority margin of 3.0%]). In low-risk patients, incidence of MACEs was 2.0% (95% CI, 1.2% to 3.3%). No statistically significant differences in early discharge, readmissions, recurrent emergency department visits, outpatient visits, or visits to general practitioners were observed. LIMITATION: Physicians were hesitant to refrain from admission and diagnostic tests in patients classified as low risk by the HEART score. CONCLUSION: Using the HEART score during initial assessment of patients with chest pain is safe, but the effect on health care resources is limited, possibly due to nonadherence to management recommendations. PRIMARY FUNDING SOURCE: Netherlands Organisation for Health Research and Development.

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.

Impact of failed mechanical reperfusion in patients with acute myocardial infarction treated with primary angioplasty.

Percutaneous coronary intervention is not successful in all patients whose acute myocardial infarction is controlled with primary angioplasty, and, after an initial successful procedure, reperfusion is not always sustained due to subacute (stent) thrombosis. In a studied population that had acute myocardial infarction, failed mechanical reperfusion occurred in 108 patients (6.9%). Killip's class >I at admission, a left anterior descending artery as the infarct-related vessel, or a preprocedural Thrombolysis In Myocardial Infarction grade 0 or 1 flow was an independent predictor of failed reperfusion. Outcome after successful early and sustained mechanical reperfusion is excellent. Failure of the initial procedure and reocclusion of the infarct-related vessel are important determinants of adverse outcome.

Achieved platelet aggregation inhibition after different antiplatelet regimens during percutaneous coronary intervention for ST-segment elevation myocardial infarction.

OBJECTIVES: To evaluate the extent of platelet aggregation inhibition in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI), treated with different antiplatelet agents and dosages. BACKGROUND: The extent of platelet aggregation inhibition is an independent predictor of major cardiac events after elective PCI. In STEMI patients undergoing PCI, routine dose of antiplatelet agents may be associated with less effective platelet aggregation inhibition. METHODS: Patients were treated with clopidogrel before angiography and randomized to abciximab, tirofiban, high-dose tirofiban, or no glycoprotein (GP) IIb/IIIa inhibitor; GP IIb/IIIa inhibitor bolus, followed by maintenance infusion, was administered after angiography, but before PCI. Platelet aggregation inhibition was assessed before angiography, immediately after PCI, and 1 and 6 h afterwards. RESULTS: The total study population consisted of 112 patients. Platelet aggregation inhibition was variable for individuals and suboptimal for all agents, particularly in the periprocedural period. Only with high-dose tirofiban, mean periprocedural platelet aggregation inhibition exceeded 80%. Angiographic parameters after PCI were not different between the groups. No relationship was found between the level of platelet aggregation and parameters of PCI success (Thrombolysis In Myocardial Infarction frame count and myocardial blush grade), after combining the data from all four groups studied. CONCLUSIONS: Platelet aggregation inhibition in STEMI patients undergoing PCI, treated with antiplatelet agents, is variable and suboptimal for all agents and dosages studied. Only with high-dose tirofiban, mean periprocedural platelet aggregation inhibition exceeded 80%. However, no relationship of platelet aggregation inhibition and angiographic outcome was found in this patient cohort.