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.
a canine model with MI, with higher T2 values in the infarct. We investigated its reproducibility in the clinical setting using native T1-and T2-mapping CMR in ST-segment elevation myocardial infarction (STEMI) patients treated by primary percutaneous coronary intervention (PPCI). Methods: We included STEMI patients with CMR performed at median of 3 (2-4) days, and excluded those with late microvascular obstruction, intramyocardial haemorrhage or >75% transmural extent of infarct. One short-axis slice per patient of native T1-mapping by Modified Look-Locker Inversion sequence, T2-mapping, and late gadolinium enhancement (LGE) images were analysed. Manual ROIs were drawn in the infarcted, salvaged and remote myocardium using CVI42 (Figure 1). Results: Out of 48 STEMI patients, 15 met the inclusion criteria. Majority (13/15) were males with median age of 56 (42-67) years old. Median MI size was 19 (10-28)% of the left ventricle (%LV) and area-at-risk was 39 (31-53)%LV. T2 values in the infarcted and salvaged myocardium were higher than remote myocardium (T2infarct: 64±5ms versus T2remote: 48±3ms, P<0.001; T2salvage 62±7ms versus T2remote: 48±3ms; P<0.001). However, there was no difference between T2infarct and T2salvage (P=0.45). A similar pattern was observed with native T1 mapping (T1infarct: 1284±81ms versus T1remote: 993±49ms; P<0.001; T1salvage 1235±61ms versus T1remote: 993±49ms, P<0.001, T1infarct versus T1salvage; P=0.38). Conclusion: Native T1 and T2-mapping CMR were unable to distinguish between infarcted and salvaged myocardium in reperfused STEMI patients. LGE remains the gold standard for identifying infarcted myocardium, whereas T1 and T2-mapping remain the reference to detect oedema-based area-at-risk.
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 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 Recent large randomized studies have indicated the potential of anti-inflammatory therapies to reduce adverse cardiovascular events in patients with myocardial infarction, with the most pronounced benefit in patients with baseline elevated C-reactive protein (CRP). Purpose Our aim was to assess the association of CRP levels with 30-day and 1-year mortality in patients with acute myocardial infarction treated with primary PCI and with residual cholesterol risk. Methods The study included 1531 patients admitted for primary PCI, with the residual cholesterol risk, i.e. low-density lipoprotein cholesterol (LDL-C) levels of >1.80 mmol/l (70 mg/dl), from a prospectively kept electronic registry of a high-volume tertiary center, for whom in-hospital CRP measurements were available. Elevated CRP was defined as ≥5 mg/l (local laboratory cut off value), measured during index hospitalization. Cox regression models were constructed to assess the impact of elevated CRP on 30-day and 1-year mortality. Results 72% of the included patients with LDL-C >1.80 mmol/l had elevated in-hospital CRP (n=1107). Compared with patients with CRP levels within reference limit, elevated CRP was associated with older age (62 vs. 60, p<0.001), higher rates of diabetes (25.8% vs. 18.5%, p=0.002), renal failure (6.4% vs. 2.1%, p<0.001) and Killip class >1 at presentation (22.5% vs. 12.3%, p<0.001), as well as lower EF (44% vs. 48%, p<0.001) and lower haemoglobin on admission (13.9 g/dl vs. 14.2 g/dl, p<0.001). Crude mortality rates were increased in patients with CRP ≥5mg/l at both 30 days (6.0% vs. 2.4%, p=0.003) and 1 year (13.2% vs. 6.3%, p<0.001) (Figure). After adjusting for the observed baseline differences, CRP ≥5mg/l remained an independent predictor of mortality at 1 year (HR 1.691, 95% CI: 1.050–2.724, p=0.03), but not at 30 days (HR 1.690, 95% CI: 0.859–3.324, p=0.13). Conclusion In primary PCI-treated patients with residual cholesterol risk, elevated in-hospital CRP was independently associated with 1-year mortality. Our findings may thus suggest a potential window of opportunity, for anti-inflammatory therapies to improve outcomes beyond the acute phase. Figure 1 Funding Acknowledgement Type of funding source: None
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