Background: No-reflow after primary PCI in ST-elevation myocardial infarction (STEMI) reflects severe microvascular injury and may adversely affect outcomes. We evaluated the incidence, predictors, and prognostic impact of angiographic no-reflow in a cohort of 2 160 consecutive patients who underwent primary PCI for STEMI
Methods
Consecutive patients with STEMI who presented to a single center over a period of 21 years were analyzed. Patients with previous CABG and patients treated concervatively were excluded from the analysis. Baseline characteristics and, after review of all angiograms, culprit lesion characteristics as well as TIMI flow before (TIMI_Pre) and after PCI (TIMI_post) were determined. No-reflow was defined as post-procedural TIMI flow 0, I, or II. Multivariable logistic regression identified predictors of no-reflow. The association between no-reflow and in-hospital mortality was evaluated after adjustment for age, sex, culprit lesion location, any prior PCI, type of primary PCI procedure, and thrombectomy use.
Results: Among the 2 160 patients, mage was 65 (IQR 55–75) years and 27.9% of all patients were female. The infarct-related vessel was the LAD in 47.8%, RCA in 38.6%, LCX in 12.5%, and LM in 1.1%. Pre-PCI TIMI 0 flow was present in 64.4%. Final TIMI 3 flow was achieved in 83.0%. No-reflow occurred in 368 patients (17.0%; TIMI 0: 3.2%, TIMI 1: 2.9%, TIMI 2: 10.9%) No-reflow occurred in 15.4% of men vs. 21.3% of women (p = 0.0015) and in 13.3% vs. 21.6% of patients below and above the median age (65 years, p < 0.001). No reflow occurred in 38.4% of patients treated with balloon angioplasty alone as compared to 13.6% with DES and 20.1% with BMS (p < 0.001). In multivariable analysis, higher age, culprit localization in the LAD, treatment with balloon angioplasty alone, use of thrombectomy, and absence of DES were independently associated with no-reflow, whereas culprit localization in the RCA was associated with a lower risk. In-hospital mortality was 22.0% in patients with no-reflow vs 6.8% without (crude OR 3.86, 95% CI 2.84–5.25). After adjustment, no-reflow remained an independent predictor of in-hospital mortality (adjusted OR 3.23, 95% CI 2.29–4.57, p < 0.001), along with older age, LM infarction, and any prior PCI.
Conclusions: In this large real-world STEMI cohort, angiographic no-reflow occurred in 17% of patients and was associated with a three-fold higher in-hospital mortality. No-reflow therefore identifies a high-risk subset beyond established clinical and angiographic predictors and should be considered a key risk metric in primary PCI.
