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Background: Coronary microvascular dysfunction is associated with adverse prognosis after ST-segment elevation myocardial infarction (STEMI). We aimed to compare the invasive, Doppler wire-based coronary flow reserve (CFR) with the non-invasive transthoracic Doppler echocardiography (TTDE)-derived CFR, and their ability to predict infarct size. Methods: We included 36 patients with invasive Doppler wire assessment on days 3-7 after STEMI treated with primary percutaneous coronary intervention (PCI), of which TTDE-derived CFR was measured in 47 vessels (29 patients) within 6 h of the invasive Doppler. Infarct size was assessed by cardiac magnetic resonance at a median of 8 months. Results: The correlation between invasive and non-invasive CFR was modest in the overall cohort (rho 0.400, p = 0.005). It improved when only measurements in the LAD artery were considered (rho 0.554, p = 0.002), with no significant correlation in the RCA artery (rho -0.190, p = 0.435). Both invasive (AUC 0.888) and non-invasive (AUC 0.868) CFR, measured in the recanalized culprit artery, showed a good ability to predict infarct sizes ≥18% of the left ventricular mass, with the optimal cut off values of 1.85 and 1.80, respectively. Conclusions: In patients with STEMI, TTDE- and Doppler wire-derived CFR exhibit significant correlation, when measured in the LAD artery, and both have a similarly strong association with the final infarct size.
RESUMO
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.