Primary PCI is still beneficial later than 24 hours after STEMI

Background: The impact of a mechanical reperfusion strategy beyond a 24-hour cut-off is still unsettled. Optimal management for these patients remains uncertain. Purpose: We sought to investigate the effect of delayed primary percutaneus coronary intervention (p-PCI) – 24 to 48 hours after symptom onset-for patients with ST-segment elevation myocardial infarction (STEMI) not undergoing timely reperfusion therapy. Methods: We conducted a cohort study of 1822 STEMI first-day survivors who were admitted with a diagnosis of STEMI, but did not receive any mechanical or pharmacological reperfusion therapy within 24 hours from symptom onset. We used multivariable logistic regression combined to landmark analysis to evaluate the effect of delayed p-PCI on in-hospital mortality and incidence of severe left ventricular dysfunction (LVD; ejection fraction<40%) at discharge. Patients who had routine medical treatment (RMT) and never received PCI served as controls. Data were adjusted for patient characteristics, concurrent medications and baseline risk status. Results: Patients undergoing delayed p-PCI had lower unadjusted in-hospital mortality (1.0% versus 6.2%, p<0.001) and incidence of severe LVD (19.6% versus 26.6%, p<0.05) than patients receiving RMT. Benefit of PCI remained significantly associated with mortality (OR: 0.32; 95% CI: 0.12–0.87) and LVD (OR:0.53; 95% CI: 0.33–0.87) after adjustment for baseline characteristics and concomitant medications. Benefit was greatest in the highest TIMI risk index patients where delayed p-PCI was associated with both a considerably lower risk of death (12.8% versus 2.5%; p<0.001) and a significant (p=0.04) reduction in the incidence of severe LVD (31.2% versus 23.1%). Conclusions: Patients not undergoing timely reperfusion therapy should be offered p-PCI on a liberal basis up to 48 hours from symptom onset

Gender differences on short term outcomes after contemporary percutaneous coronary intervention

Purpose: Conflicting information exists on sex-based differences in outcomes after percutaneous coronary intervention (PCI). In addition, previous data may not be reflective of the entire general clinical population, as most studies were post-hoc analyses of clinical trials with inherent possibility of a differential attrition rate in the pre-randomization phase by sex. Methods: We investigated the relationship between sex and the risks of shortclinical outcomes after PCI in current practice, using data on 13259 acute coronary syndromes (ACS) consecutive patients from January 2010 to January 2015. Patients treated in a conservative manner or with CABG were excluded, leaving a final study population of 7792 patients who underwent PCI (28.7% were women). Cox proportional hazards regression model was adjusted to covariates significantly different between groups in univariate analysis. The primary endpoint was 30-days mortality; the secondary endpoint was the composite of cardiovascular mortality, stent thrombosis, stroke or major bleeding; the tertiary endpoint was left ventricular dysfunction (LVD) defined as an LV ejection fraction <40% at echocardiography Results: Women were older (mean age: 65.5 vs. 59.7 years, p<0.001), had higher rates of diabetes (30.9% vs. 22.0%, p<0.001), hypertension (77.8% vs. 65.6%, p<0.001), cerebrovascular disease (4.7% vs. 3.3%, p=0.003) and higher rates of Killip class ≥2 (25.1% vs. 19.6%, p<0.001), but lower rates of smoking (30.3% vs. 45.3%, p<0.001) than male patients. Unadjusted mortality was significantly higher in women than men (7.1% vs. 4.4%, p<0.001), as well as the overall the rates of the secondary endpoint (10.5% vs. 7.1%, p<0.001). No differences were observed in the unadjusted rates of the tertiary endpoint (19.1% vs. 21.2%, p=0.16). After multivariable adjustment, female sex was no longer associated with a higher risk of death (HR: 1.13, 95% CI: 0.87–1.48) and higher risk of secondary endpoint (HR: 1.18, 95% CI: 0.97–1.45). On the contrary female sex was associated with lower risk of LVD (adjusted HR: 0.73, 95% CI: 0.60–0.89). These sex-specific findings for outcomes were consistent across patient subgroups using bare metal stents (HR: 1.25, 95% CI: 0.88–1.77) or drug-eluting stents (HR: 1.13, 95% CI: 0.78–1.62). Conclusions: In our cohort, among patients undergoing contemporary PCI, no differences in short-terms major cardiovascular outcomes were observed between women and men. Women undergoing PCI has a lower risk of LVD than men. There was no association between sex and stent type on short-term outcomes

Effect of pre-procedural antiplatelet and anticoagulant therapy on myocardial no-reflow following percutaneus coronary intervention

Background: No-reflow occurring during percutaneus coronary intervention (PCI) has been associated with poor in-hospital outcomes. Purpose: The objectives of this study were to evaluate the incidence of no-reflow as independent predictor of adverse events and to assess whether baseline preprocedural treatment options may affect clinical outcomes. Methods: Data were derived from the International Survey of Acute Coronary Syndromes in Transitional Countries (NCT01218776) registry, a prospective survey of patients presenting with ACS over a 5-year period (January 2010 to January 2015). We prospectively collected data from 5997 patients undergoing PCI, identifying those with no-reflow, and analyzed their treatments and clinical outcomes. No-reflow was defined as post-PCI TIMI flow grade 0–1, in the absence of post-procedural significant (≥25%) residual stenosis, abrupt vessel closure, dissection, perforation, thrombus of the original target lesion, or epicardial spasm. The outcome measure was in-hospital mortality. Results: No-reflow was identified in 128 of 5997 patients who have undergone PCI (2.1%). On multivariate analysis, patients with no-reflow were more likely to be older (≥75 years; OR: 2.78; 95% CI: 1.15–6.71) and to have ST-elevation myocardial infarction (OR: 3.67; 95% CI: 1.57–8.56). No-reflow was highly predictive of in-hospital mortality (17.2% vs. 4.2%, P<0.001) and remained a significant independent predictor of death after adjustment for demographic and clinical variables (OR: 4.78; 95% CI: 2.7- 8.3). Multivariable regression analysis was also performed to identify independent relationship between pre-procedural treatment regimens and no-reflow phenomenon. A 600 mg loading dose of clopidogrel, showed a strong inverse predictive value in terms of post-PCI TIMI flow and no-reflow phenomenon (OR: 0.58; 95% CI: 0.35–0.95). Similarly, unfractioned heparin was associated with a reduction in the likehood of no-reflow (OR: 0.62; 95% CI: 0.41–0.94). Aspirin, enoxaparin, 300 mg loading dose of clopidogrel, did not significantly impact the occurrence of the no-reflow. Conclusions: No-reflow is a strong independent predictor of in-hospital mortality. Pre-procedural administration of 600 mg loading dose of clopidogrel and/or unfractioned heparin is associated with reduced incidence of no-reflo