In the subgroup of ST -segment-elevation myocardial infarction the IRR was 1.00, 95% CI 0.98 to 1.03, while for non-ST-segment-elevation myocardial infarction, the IRR was 1.08, 95% CI 1.05 to 1.10.
A total of 100 patients presenting with stable angina or non-ST segment elevation myocardial infarction and an indication to perform FFR between Jan 2016 and Oct 2016 were included. vFFR was calculated based on the aortic root pressure along with two angiographic projections and validated against pressure wire-derived FFR.
In the ACCOAST (A Comparison of Prasugrel at PCI or Time of Diagnosis of Non-ST Elevation Myocardial Infarction) trial, the prasugrel pre-treatment strategy versus placebo was associated with excess bleeding complications and no improved ischemic outcome in non-ST-segment elevation myocardial infarction (MI).
We identified patients in the Atherosclerosis Risk in Communities Surveillance Study admitted with chest pain and an initially elevated cardiac troponin I, who presented within 12 hours of symptom onset and were classified with non-ST-segment elevation myocardial infarction.
Prognostic value of neutrophil gelatinase-associated lipocalin and glycosylated hemoglobin for non-ST-segment elevation myocardial infarction patients with single concomitant chronic total occlusion following primary percutaneous coronary intervention: A prospective observational study.
Comparison of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers in patients with diabetes mellitus and non-ST-segment elevation myocardial infarction who underwent successful percutaneous coronary intervention.
Prognostic impact of prepercutaneous coronary intervention TIMI flow in patients with ST-segment and non-ST-segment elevation myocardial infarction: Results from the FAST-MI 2010 registry.
Comparison of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers in patients with diabetes mellitus and non-ST-segment elevation myocardial infarction who underwent successful percutaneous coronary intervention.
Findings were similar for ST-segment elevation myocardial infarction (ATE coefficient: 0.30; 95% CI: -0.98 to 1.58; p = 0.637) and non-ST-segment elevation myocardial infarction (ATE coefficient: -0.07; 95% CI: -0.68 to 0.54; p = 0.819).
ST-segment elevation myocardial infarction exhibited a higher CRP concentration than without elevation (non-ST-segment elevation myocardial infarction) and patients with unstable angina (21.81, 17.10, and 5.91 mg/L; p < 0.01).
Occurrence of new episodes of unstable angina, non-ST-segment elevation myocardial infarction and STE myocardial infarction over the years was recorded and compared between subjects not carrying and carrying C2238/ANP-minor allele.
Compared with the controls, circulating AhR expression was found to be significantly increased in patients with CAD and its subtypes including ST-segment and non-ST-segment elevation myocardial infarction, and stable and unstable angina pectoris.
Elevated plasma level of pentraxin-3 predicts in-hospital and 30-day clinical outcomes in patients with non-ST-segment elevation myocardial infarction who have undergone percutaneous coronary intervention.
Whether the CYP2C19 genotype has the potential to influence clinical choice of these drugs prior to PCI for individuals with unstable angina or non-ST segment elevation myocardial infarction is currently uncertain.