Background The Acute Coronary Treatment and Intervention Outcomes Network (ACTION) Registry-Get With The Guidelines (GWTG) AMI mortality model and risk score (ACTION) were introduced in 2011 to predict in-hospital mortality. In 2016 score was updated to enable a more accurate assessment, but, up-to-date, external validation in direct comparison was not performed. Purpose We aimed to externally validate and compare the prognostic value of original and updated ACTION score for in-hospital and one-year mortality. Method From a prospective electronic registry of a high-volume catheterization laboratory in a period from January 2009 to December 2017, a total of 5615 consecutive patients who underwent pPCI were available for analysis. For each patient, original (O-) and updated (U-) ACTION scores were calculated using required clinical and angiographic characteristics. In-hospital and one-year mortality (follow-up available for 91%) were assessed. Calibration and discrimination of the three risk models were evaluated by the Hosmer-Lemeshow (H-L) goodness-of-fit test and C-statistic, respectively. Results Mortality rates for in-hospital and one-year mortality were 4.2% and 9.6%, respectively. Both scores showed good model calibration as assessed by the H-L test and very good discriminative power for in-hospital and one-year mortality as assessed by C-statistics (Table 1 & Figure 1). Net reclassification index (NRI=1.06) showed that 48% of patients with in-hospital event and 58% without event, had their risk recalculated with U-ACTION with Integrated Discrimination Improvement slope 9.1% higher than in first model. Table 1 Risk score H-L H-L p value AUC 95% CI p value AUC 95% CI Significant p value O-ACTION 9.4 0.3 0.829 0.819 to 0.839 p<0.0001 0.781 0.769 to 0.792 p<0.0001 U-ACTION 10.9 0.2 0.918 0.911 to 0.925 0.838 0.827 to 0.848 Figure 1 Conclusion Updated ACTION score enables better prediction of in-hospital and one-year mortality in patients undergoing pPCI for acute myocardial infarction, thus it can be used preferentially over the original ACTION score for assessment of short and long-term mortality risks of this population.
Aims Previous studies indicated that a chronic total occlusion (CTO) in a non-infarct-related artery is linked to higher mortality mainly in the acute setting in patients with ST-elevation myocardial infarction (STEMI). Our aim was to assess the temporal distribution of mortality risk associated with non-culprit CTO over years after STEMI. Methods and results The study included 8679 STEMI patients treated with primary percutaneous coronary intervention (PCI). Kaplan–Meier cumulative mortality curves for non-culprit CTO vs. no CTO were compared with log-rank test, with landmarks set at 30 days and 1 year. Adjusted Cox regression models were constructed to assess the impact of non-culprit CTO on mortality over different time intervals. Tests for interaction were pre-specified between non-culprit CTO and acute heart failure and left ventricular ejection fraction. The primary outcome variable was all-cause mortality, and the median follow-up was 5 years. Non-culprit CTO was present in 11.6% of patients (n = 1010). Presence of a CTO was associated with increased early [30-day adjusted hazard ratio (HR) 1.91, 95% confidence interval (CI) 1.54–2.36; P < 0.001] and late mortality (5-year adjusted HR 1.66, 95% CI 1.42–1.95; P < 0.001). Landmark analyses revealed an annual two-fold increase in mortality in patients with vs. without a CTO after the first year of follow-up. The observed pattern of mortality increase over time was independent of acute or chronic LV impairment. Conclusions Non-culprit CTO is independently associated with mortality over 5 years after primary PCI for STEMI, with a constant annual two-fold increase in the risk of death beyond the first year of follow-up.
Background Previous studies have indicated that patients with non-anterior ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) have a more favorable prognosis compared with anterior STEMI, especially in the short term. Purpose Our aim was to identify predictors of increased 30-day mortality in patients with non-anterior STEMI undergoing primary PCI. Methods This analysis included 8188 patients referred to primary PCI during 2009–2017, from a prospective electronic registry of a high-volume catheterization laboratory, for whom 30-day follow-up was available. Non-anterior infarction was defined as presence of ST-segment elevation in inferior and/or lateral ECG leads or true posterior MI. Multivariable Cox regression was used to assess the mortality risk at 30 days. Results 59.4% (n=4863) of the included patients presented with a non-anterior STEMI. Mortality rate was significantly lower in patients with non-anterior vs. anterior STEMI (4.2% vs. 8.3%, p<0.001). Older age (> median of 61, HR 2.2, p=0.002), baseline renal failure (eGFR <60, HR 4.0, p<0.001), Killip class ≥2 (HR 3.8, p<0.001), previous stroke (HR 1.8, p=0.004), non-culprit chronic total occlusion (CTO, HR 2.0, p<0.001) and final TIMI flow grade <3 in the infarct-related artery (HR 3.1, p<0.001) were independently associated with an increased risk of 30-day mortality in non-anterior STEMI. The presence of at least one of these high-risk factors was noted in 61.2% of patients with non-anterior STEMI and was associated with a significantly higher risk of 30-day mortality (HR 18.2, p<0.001), similarly to the overall risk associated with anterior STEMI (HR 22.9, p<0.001), as compared with patients with non-anterior STEMI but without any of the here identified high-risk factors (Figure). Figure 1 Conclusions Crude mortality rate was significantly lower in patients with non-anterior vs. anterior STEMI. However, the majority of non-anterior STEMI patients had at least one of the high-risk factors (older age, previous CVI, baseline renal failure, Killip class ≥2, non-culprit CTO or final TIMI flow <3), which predisposed these patients to a similar increase in short-term mortality risk as in patients with anterior STEMI.
Background Considering clinical importance of bleeding complications in patients with acute myocardial infarction (AMI), bleeding risk stratification is a key part of the management of these patients. CRUSADE, ACTION and ACUITY-HORIZONS bleeding risk scores are available for predicting in-hospital major bleeding events in patients with acute myocardial infarction. Purpose We aimed to evaluate performance of the three above mentioned risk scores for predicting in-hospital bleeding events defined according to The Bleeding Academic Research Consortium (BARC) criteria. Methods From a prospective electronic registry of a high-volume catheterization laboratory in a period from January 2009 to December 2017, a total of 6505 consecutive patients with acute myocardial infarction who underwent pPCI were included in analysis. Calibration and discrimination of the three risk models were evaluated by the Hosmer-Lemeshow (H-L) goodness-of-fit test and C-statistic, respectively. Results Overall there were 372 (5.7%) bleeding events out of which 117 (1.8%) fulfilled stage BARC 3 or higher bleeding criteria. All three scores showed good model calibration as assessed by the H-Ls test and very good discriminative power for BARC 3 of higher bleeding events detection as assessed by C-statistics (Table 1 & Figure 1): Bleeding events stage BARC 3 or higher were statistically highly related with higher in-hospital mortality (13.7% vs. 3.5%; p<0.000). Table 1 Risk score H-L H-L p AUC 95% CI p CRUSADE 11.46 0.177 0.761 0.750–0.771 vs. ACUITY = ns vs. ACTION <0.000 ACUITY-HORIZONS 10.47 0.236 0735 0.724–0.745 vs. ACTION = ns ACTION 5.74 0.677 0.701 0.698–0.712 Figure 1 Conclusions All three evaluated scores showed very good discriminative capacity for predicting BARC 3 or higher bleeding events in patients undergoing pPCI for AMI.
Background Clinical practice guidelines provide class I recommendation for the use of angiotensin-converting enzyme inhibitors (ACE-I) and beta-blockers in patients with prior myocardial infarction and left ventricular (LV) dysfunction, whereas their use in patients without LV dysfunction is considered to be a class IIa recommendation. Purpose Our aim was to comparatively assess the impact of ACE-I and/or beta-blockers on 3-year mortality in patients with or without impaired left ventricular (LV) function undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). Methods The analysis included 4425 patients admitted for primary PCI during 2009–2015 from a prospective, electronic registry of a high-volume tertiary center, who survived initial hospitalization, and for whom information on LV function and discharge medication were available. Patients were stratified according to LV systolic dysfunction, defined as LVEF <40%. Unadjusted and adjusted Cox regression models were created to investigate the impact of beta-blocker and/or ACE-I therapy on 3-year mortality. Results 22.9% (n=1013) had LV dysfunction, 23.0% (n=1017) received either an ACE-I or a beta-blocker and 72.2% received both medications at discharge (n=3197). The concurrent use of both ACE-I and beta-blockers was not different in LVEF≥40% vs. LVEF<40% (72.4% vs. 71.7%, p=0.43). The use of at least one of the guideline-recommended medications was associated with a significantly lower 3-year mortality in both patients with LVEF≥40% (18.7% if neither was used, 11.2% if either a beta-blocker or an ACE-I were used and 9.4% if both were used, p=0.001), and LVEF<40% (55.4% if neither was used, 32.5% if either a beta-blocker or an ACE-I were used and 22.9% if both were used, p<0.001) (Figure). After adjusting for significant mortality predictors including older age, diabetes, hypertension, renal failure, previous stroke, Killip class ≥2 and non-culprit chronic total occlusion (CTO), the concurrent use of both a beta-blocker and an ACE-I remained independently associated with lower 3-year mortality in both patients with LVEF<40% (HR 0.30, p<0.001) and LVEF≥40% (HR=0.41, p=0.001). The use of a single agent was independently associated with lower mortality in patients with LVEF<40% (HR 0.45, p=0.002), but not in patients with LVEF≥40% (HR 0.61, p=0.07). Conclusions Guideline-recommended use of both a beta-blocker and an ACE-I in post-MI patients was associated with a lower 3-year mortality regardless of the LV function, whereas using only one of the two agents was associated with improved prognosis only in patients with LV dysfunction, but not in patients without LV impairment.
Background Since patients with STEMI have high rate of adverse events not only during hospital stay, but also during short and long-term follow–up, appropriate risk stratification is a key part of the management of these patients following hospital discharge. CADILLAC score was derived and subsequently validated as accurate clinical tool for identifying patients with heightened risk following index event. Purpose We aimed to compare predictive value of recalculated, maximal, (M-) CADILLAC score vs. baseline (B-) CADILLAC score for long-term mortality in hospital survivors. Methods From a prospective electronic registry of a high-volume catheterization laboratory in a period from January 2009 to December 2017, a total of 5387 consecutive patients STEMI who underwent primary PCI were included in analysis. For each patient B-CADILLAC score was calculated, and for survivors, we recalculated M-CADILLAC score, incorporating changes in three variable score individual contributors (worsening of Killip class, anemia development and renal function deterioration). As in original score derivation, patients with cardiogenic shock were excluded from analysis. Discrimination of the two risk models was evaluated by the C-statistic, Net reclassification index (NRI) and Integrated Discrimination Improvement (IDI) index. Results For 111 (2.1%) patients that died in-hospital, B-CADILLAC very well predicted the event (AUC 0.87, 95% CI 0.86–0.88; p<0.0001) (Figure 1A). For hospital survivors, both evaluated scores showed good discriminative ability for long-term mortality (11.7%) but recalculated M-CADILLAC score was statistically better predictor of long-term mortality, as assessed by C-statistics (Table 1 & Figure 1B): NRI showed that 38% of patients were reclassified with M-CADILLAC with IDI slope 0.8% higher than in first model. Table 1 4723 pts (follow-up=90% pts, 41±27 months) AUC 95% CI p B-CADILLAC 0.756 0.744–0.768 p=0.018 M-CADILLAC 0.776 0.754–0.779 Figure 1 Conclusions Baseline CADILLAC score has very good predictive ability for in-hospital mortality, but recalculated, maximal CADILLAC score offers discriminative advantage in hospital survivors for prediction of long-term mortality in STEMI patients undergoing primary PCI.
Background Previous studies showed increased mortality rates in patients with ST-elevation myocardial infarction (STEMI) and a chronic total occlusion (CTO) in a non-infarct-related artery, but long-term data are scarce. Purpose Our aim was to assess all-cause mortality during 5 years follow-up in patients with a remaining nonculprit CTO after being treated with primary PCI. Methods The study included 9504 patients admitted for primary PCI during 2009–2019, with available baseline angiography, from an electronic, prospective registry of a high-volume catheterization laboratory. Kaplan Meier cumulative mortality curves for non-culprit CTO vs. no CTO were compared with the log-rank test, with landmarks set at 30 days and then annually up to 5 years follow-up. Adjusted Cox regression models were constructed to assess 30-day and 5-year mortality risk of a non-culprit CTO. Median follow-up was 1507 days. Results Nonculprit CTO was present in 13.2% of patients (n=1253). Presence of a nonculprit CTO was associated with older age (64 vs. 61, p<0.001), more frequent history of cardiovascular disease including prior MI (33% vs. 14%, p<0.001), stroke (10.3% vs. 5.9%, p<0.001) and CABG (10.5% vs. 1.5%, p<0.001), higher rates of renal failure (10.7% vs. 4.8%, p<0.001), as well as more often Killip class 2–4 on admission (29% vs. 16%, p<0.001) and a lower ejection fraction (40% vs. 47%, p<0.001). Crude mortality rates were significantly increased in patients with a nonculprit CTO vs. no CTO, at both 30 days (15.7% vs. 5.6%, p<0.001) and 5 years (54.6% vs. 27.9%, p<0.001). After adjusting for the observed baseline differences, nonculprit CTO was still associated with an elevated mortality risk at both 30-days (HR 1.5, CI95% 1.1–1.9, p=0.007) and 5 years (HR 1.6, CI95% 1.4–1.9, p<0.001). Landmark analyses showed continuously increasing risk of mortality in the presence of a nonculprit CTO, as compared with primary PCI-treated patients with no CTO (30 days to 1 year 11.4% vs. 4.9%, p<0.001; 1st to 2nd year of follow-up 6.3% vs. 3.4%, p<0.001; 2nd to 3rd year 6.2% vs. 2.8%, p<0.001; 3rd to 4th year 7.4% vs. 3.0%, p<0.001; and 4th to 5th year 5.2% vs. 3.6%, p=0.1). Conclusions Presence of a nonculprit CTO is independently associated with 5-year mortality after primary PCI. Importantly, the mortality risk increases continuously with an average annual absolute difference of 3%, in patients with a nonculprit CTO vs. those with no CTO. Nonculprit CTO vs. no CTO Funding Acknowledgement Type of funding source: None
Background Contrast induced nephropathy (CIN) has been associated with increased mortality in patients with acute myocardial infarction (AMI). However, different definitions of CIN have so far been used. Purpose We aimed to compare predictive accuracy of the 2 contemporary CIN definitions in patients with AMI undergoing primary percutaneous coronary intervention (PCI). Method From a high-volume, single-centre, prospective registry, in a period from 2009–2019, we identified 7987 pts who underwent primary PCI for AMI in whom creatinine measurements were available for analysis. CIN incidence was evaluated according to relative creatinine increases of ≥25% (CIN25) and ≥50% (CIN50) from baseline levels within 72 hours after intervention. The primary end point was in-hospital mortality. Results Overall, 1116 (13.9%), and 345 (4.3%) patients developed CIN25, CIN50, respectively. Crude in-hospital mortality rate was 3.9% (312 pts) in the overall population. Both definitions were independently associated with in-hospital mortality (CIN25 adjusted odds ratio (OR) 4.2, 95% CI 2.7–6.6; p<0.001, and CIN 50 adjusted OR 8.2, 95% CI 4.9–13.9; p<0.001). Comparison of ROC curves showed that only the addition of the CIN50 (and not CIN25) definition to the combined model of clinical predictors of in-hospital mortality, which included pre-intervention TIMI flow 0–1, cardiogenic shock on admission, baseline creatinine clearance, prior stroke, chronic occlusion of non-culprit artery, post-intervention TIMI flow 3, left ventricular ejection fraction and procedure time, improved prognostic accuracy of the model (Figure 1). Conclusion Only acute kidney injury according to the CIN50 definition, but not the CIN25 definition, offers additional prognostic information above and beyond the combination of baseline predictors of in-hospital mortality in patients with AMI undergoing primary PCI. Figure 1 Funding Acknowledgement Type of funding source: None
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