Background: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly used to treat cardiogenic shock. However, VA-ECMO might hamper myocardial recovery. The Impella unloads the left ventricle. The aim of this study was to evaluate if left ventricular unloading in cardiogenic shock patients treated with VA-ECMO was associated with lower mortality. Methods: Data from 686 consecutive patients with cardiogenic shock treated with VA-ECMO with or without left ventricular unloading (using an Impella) at 16 tertiary-care centers in 4 countries were collected. The association between left ventricular unloading and 30-day mortality was assessed by Cox regression models in a 1:1 propensity-score-matched cohort. Results: Left ventricular unloading was used in 337 of the 686 patients (49%). After matching, 255 patients with left ventricular unloading were compared with 255 patients without left ventricular unloading. In the matched cohort, left ventricular unloading was associated with lower 30-day mortality (hazard ratio 0.79, 95% confidence interval 0.63-0.98, p=0.03) without differences in various subgroups. Complications occurred more frequently in patients with left ventricular unloading; e.g. severe bleeding in 98 (38.4%) vs. 45 (17.9%), access-site related ischemia in 55 (21.6%) vs. 31 (12.3%), abdominal compartment in 23 (9.4%) vs. 9 (3.7%) and renal replacement therapy in 148 (58.5%) vs. 99 (39.1%). Conclusions: In this international, multicenter cohort study, left ventricular unloading was associated with lower mortality in cardiogenic shock patients treated with VA-ECMO, despite higher complication rates. These findings support use of left ventricular unloading in cardiogenic shock patients treated with VA-ECMO and call for further validation, ideally in a randomized, controlled trial.

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) has been used for refractory cardiogenic shock; however, it is associated with increased left ventricular afterload. Outcomes associated with the combination of a percutaneous left ventricular assist device (Impella) and VA-ECMO remains largely unknown. We retrospectively reviewed patients treated for refractory cardiogenic shock with VA-ECMO (2014-2016). The primary outcome was all-cause mortality within 30 days of VA-ECMO implantation. Secondary outcomes included duration of support, stroke, major bleeding, hemolysis, inotropic score, and cardiac recovery. Outcomes were compared between the VA-ECMO cohort and VA-ECMO + Impella (ECPELLA cohort). Sixty-six patients were identified: 30 ECPELLA and 36 VA-ECMO. Fifty-eight percentage of VA-ECMO patients (n = 21) had surgical venting, as compared with 100% of the ECPELLA cohort (n = 30) which had Impella (±surgical vent). Both cohorts demonstrated relatively similar baseline characteristics except for higher incidence of ST-elevation myocardial infarction (STEMI) and percutaneous coronary intervention (PCI) in the ECPELLA cohort. Thirty-day all-cause mortality was significantly lower in the ECPELLA cohort (57% vs. 78%; hazard ratio [HR] 0.51 [0.28-0.94], log rank p = 0.02), and this difference remained intact after correcting for STEMI and PCI. No difference between secondary outcomes was observed, except for the inotrope score which was greater in VA-ECMO group by day 2 (11 vs. 0; p = 0.001). In the largest US-based retrospective study, the addition of Impella to VA-ECMO for patients with refractory cardiogenic shock was associated with lower all-cause 30 day mortality, lower inotrope use, and comparable safety profiles as compared with VA-ECMO alone.

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Aims: The pathophysiology of apical ballooning syndrome (ABS) remains to be elucidated. The aim of this study was to evaluate the coronary vascular reactivity of patients who were previously diagnosed with ABS. Methods and results: A total of 228 cases of ABS were prospectively identified, and of these, 10 patients (median age 61 years ; all females) who underwent coronary vasomotion testing were included in the study. Coronary epicardial and microvascular responses to intracoronary acetylcholine (ACH; % change in diameter and % change in blood flow at doses of 10 −6 -10 −4 mol/l), nitroglycerin (200-300 mg), and adenosine (36-60 µg) were evaluated. The median change in diameter with ACH was -9.3% (IQR -36.4, 3.2) with six patients (60%) demonstrating epicardial coronary constriction. The median increase in peak coronary blood flow in response to ACH was 13.1% (IQR -18.6, 55.0). This was markedly lower than the blood flow response seen in a reference group of 211 women from our laboratory (mean age 60 years) with normal microvascular responses to ACH: 103% (IQR 75, 149). Seven (70%) patients had <50% increase in coronary blood flow indicating abnormal microvascular response to ACH. 70% had either abnormal epicardial or microvascular response to ACH. Median coronary flow reserve was abnormal at 2.2% (IQR 2.0, 3.4; normal >2.5), and 90% had at least one abnormal measure of microvascular vasomotion. Conclusion:The novel observation is that coronary microvascular dysfunction is highly prevalent in patients with ABS. Thus, chronically impaired coronary vascular reactivity, especially involving the microcirculation, may be a central feature of the pathophysiology of ABS.