Background: Whereas the efficacy and safety of intravascular lithotripsy (IVL) have been confirmed in de novo calcified coronary lesions, little is known about its utility in treating stent underexpansion. This study aimed to investigate the impact of IVL in treating stent underexpansion. Methods and Results: Consecutive patients with stent underexpansion treated with IVL entered the multicenter IVL-Dragon Registry. The procedural success (primary efficacy endpoint) was defined as a relative stent expansion >80%. Thirty days device-oriented composite endpoint (DOCE) (defined as a composite of cardiac death, target lesion revascularization, or target vessel myocardial infarction) was the secondary endpoint. A total of 62 patients were enrolled. The primary efficacy endpoint was achieved in 72.6% of patients. Both stent underexpansion 58.5% (47.5–69.7) vs. 11.4% (5.8–20.7), p < 0.001, and the stenotic area 82.6% (72.4–90.8) vs. 21.5% (11.1–37.2), p < 0.001, measured by quantitative coronary angiography improved significantly after IVL. Intravascular imaging confirmed increased stent expansion following IVL from 37.5% (16.0–66.0) to 86.0% (69.2–90.7), p < 0.001, by optical coherence tomography and from 57.0% (31.5–77.2) to 89.0% (85.0–92.0), p = 0.002, by intravascular ultrasound. Secondary endpoint occurred in one (1.6%) patient caused by cardiac death. There was no target lesion revascularization or target vessel myocardial infarction during the 30-day follow-up. Conclusions: In this real-life, largest-to-date analysis of IVL use to manage underexpanded stent, IVL proved to be an effective and safe method for facilitating stent expansion and increasing luminal gain.

Background: Data regarding the use of percutaneous coronary intervention with drug-eluting balloons (DEB) versus thin-strut drug-eluting stents (thin-DES) for treating DES in-stent restenosis in everyday clinical practice is scarce. Our goal was to evaluate the efficacy and safety profile of DEB versus thin-DES in DES in-stent restenosis. Methods: Consecutive patients with DES in-stent restenosis who underwent percutaneous coronary intervention between 2008 and 2019 entered the multicenter DEB-DRAGON Registry with a follow-up of 3 years. Patients who received DEB at the index procedure (n=557, 49.9%) were compared with those who received thin-DES (n=560, 50.1%). Results: Analysis of the unmatched cohort revealed lower rates of target lesion revascularization (9.1% versus 13.6%; hazard ratio [HR], 0.58 [95% CI, 0.41–0.83], P =0.003), target vessel revascularization (11.8% versus 16.7%; HR, 0.62 [95% CI, 0.45–0.84], P =0.003) and device-oriented composite end point, defined as a composite of cardiac death, target lesion revascularization, and target vessel myocardial infarction (12.7% versus 16.0%; HR, 0.69 [95% CI, 0.50–0.94], P =0.018) in the thin-DES group compared with the DEB group. The incidence of cardiac death, target vessel-myocardial infarction, and myocardial infarction were similar in both groups. However, after propensity score matching, there were no significant differences in target lesion revascularization (11.2% versus 11.2%; HR, 0.91 [95% CI, 0.55–1.51], P =0.707), target vessel revascularization (13.4% versus 14.2%; HR, 0.86 [95% CI, 0.55–1.36], P =0.523), and device-oriented composite end point (14.2% versus 14.2%; HR, 0.91 [95% CI, 0.58–1.42], P =0.667) between the thin-DES and DEB group, respectively. Conclusions: This analysis of a real-life registry revealed similar long-term outcomes of thin-DES and DEB in DES in-stent restenosis regarding target lesion revascularization, myocardial infarction, cardiac death, and device-oriented composite end point. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04415216.

There is a lack of studies directly comparing the effect of air pollution on acute coronary syndrome (ACS) occurrence in industrial and non-industrial areas. A comparison of association of air pollution exposure with ACS in two cohorts of industrially different areas. The study covered 6,000,000 person-years of follow-up and five pollutants between 2008 and 2017. A time series regression analysis with 7-lag was used to assess the effects air pollution on ACS. A total of 9046 patients with ACS were included in the analysis, of whom 3895 (43.06%) had ST-elevation myocardial infarction (STEMI) - 45.39% from non-industrial area, and 42.37% from industrial area; and 5151 (56.94%) had non-ST-elevation myocardial infarction (NSTEMI) - 54.61% from non-industrial area and 57.63% from industrial area. The daily concentrations of PM_2.5, PM₁₀, NO₂, SO₂, CO were higher in industrial than in non-industrial area (P < 0.001). In non-industrial area, an increase of 10 μg/m³ of NO₂ concentration (Odds Ratio (OR) = 1.126, 95%CI = 1.009-1.257; P = 0.034, lag-0) and an increase of 1 mg/m³ in CO concentration (RR = 1.055, 95%CI = 1.010-1.103; P = 0.017, lag-0) were associated with an increase in the number of hospitalization due to NSTEMI (for industrial area increase of 10 μg/m³ in NO₂ (OR = 1.062, 95%CI = 1.020-1.094; P = 0.005, lag-0), SO₂ (OR = 1.061, 95%CI = 1.010-1.116; P = 0.018, lag-4), PM₁₀ (OR = 1.010, 95%CI = 1.001-1.030; P = 0.047, lag-6). In STEMI patients in industrial area, an increased hospitalization was found to be associated with an increase of 10 μg/m³ in SO₂ (OR = 1.094, 95%CI = 1.030-1.162; P = 0.002, lag-1), PM_2.5 (OR = 1.041, 95%CI = 1.020-1.073; P < 0.001, lag-1), PM₁₀ (OR = 1.030, 95%CI = 1.010-1.051; P < 0.001, lag-1). No effects of air pollution on the number of hospitalization due to STEMI were noted from non-industrial area. The risk of air pollution-related ACS was higher in industrial over non-industrial area. The effect of NO₂ on the incidence of NSTEMI was observed in both areas. In industrial area, the effect of PMs and SO₂ on NSTEMI and STEMI were also observed. A clinical effect was more delayed in time in patients with NSTEMI, especially after exposure to PM₁₀. Chronic exposure to air pollution may underlie the differences in the short-term effect between particulate air pollution impact on the incidence of STEMI.

Background: The impact of complete revascularization (CR) on the development of heart failure (HF) in patients with acute coronary syndrome and multivessel coronary artery disease undergoing percutaneous coronary intervention remains to be elucidated. Methods and Results: Consecutive patients with acute coronary syndrome with multivessel coronary artery disease from the CORALYS (Incidence and Predictors of Heart Failure After Acute Coronary Syndrome) registry were included. Incidence of first hospitalization for HF or cardiovascular death was the primary end point. Patients were stratified according to completeness of coronary revascularization. Of 14 699 patients in the CORALYS registry, 5054 presented with multivessel disease. One thousand four hundred seventy‐three (29.2%) underwent CR, while 3581 (70.8%) did not. Over 5 years follow‐up, CR was associated with a reduced incidence of the primary end point (adjusted hazard ratio [HR], 0.66 [95% CI, 0.51–0.85]), first HF hospitalization (adjusted HR, 0.67 [95% CI, 0.49–0.90]) along with all‐cause death and cardiovascular death alone (adjusted HR, 0.74 [95% CI, 0.56–0.97] and HR, 0.56 [95% CI, 0.38–0.84], respectively). The results were consistent in the propensity‐score matching population and in inverse probability treatment weighting analysis. The benefit of CR was consistent across acute coronary syndrome presentations (HR, 0.59 [95% CI, 0.39–0.89] for ST‐segment elevation myocardial infarction and HR, 0.71 [95% CI, 0.50–0.99] for non‐ST‐elevation acute coronary syndrome) and in patients with left ventricular ejection fraction >40% (HR, 0.52 [95% CI, 0.37–0.72]), while no benefit was observed in patients with left ventricular ejection fraction ≤40% (HR, 0.77 [95% CI, 0.37–1.10], P for interaction 0.04). Conclusions: CR after acute coronary syndrome reduced the risk of first hospitalization for HF and cardiovascular death, as well as first HF hospitalization, and cardiovascular and overall death both in patients with ST‐segment elevation myocardial infarction and non‐ST‐elevation acute coronary syndrome. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT 04895176.