Background: Venoarterial 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. This study aimed to evaluate whether left ventricular unloading in patients with cardiogenic shock 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% CI, 0.63–0.98]; P =0.03) without differences in various subgroups. Complications occurred more frequently in patients with left ventricular unloading: severe bleeding in 98 (38.4%) versus 45 (17.9%), access site–related ischemia in 55 (21.6%) versus 31 (12.3%), abdominal compartment in 23 (9.4%) versus 9 (3.7%), and renal replacement therapy in 148 (58.5%) versus 99 (39.1%). Conclusions: In this international, multicenter cohort study, left ventricular unloading was associated with lower mortality in patients with cardiogenic shock treated with VA-ECMO, despite higher complication rates. These findings support use of left ventricular unloading in patients with cardiogenic shock treated with VA-ECMO and call for further validation, ideally in a randomized, controlled trial.

The Official Journal of EuroPCR and the European Association of Percutaneous Cardiovascular Interventions (EAPCI)

Trials on intra-aortic balloon pump (IABP) use in cardiogenic shock related to acute myocardial infarction have shown disappointing results. The role of IABP in cardiogenic shock treatment remains unclear, and new (potentially more potent) mechanical circulatory supports with arguably larger device profile are emerging. A reappraisal of the physiological premises of intra-aortic counterpulsation may underpin the rationale to maintain IABP as a valuable therapeutic option for patients with acute decompensated heart failure and tissue hypoperfusion. Several pathophysiological features differ between myocardial infarction- and acute decompensated heart failure–related hypoperfusion, encompassing cardiogenic shock severity, filling status, systemic vascular resistances rise, and adaptation to chronic (if preexisting) left ventricular dysfunction. IABP combines a more substantial effect on left ventricular afterload with a modest increase in cardiac output and would therefore be most suitable in clinical scenarios characterized by a disproportionate increase in afterload without profound hemodynamic compromise. The acute decompensated heart failure syndrome is characterized by exquisite afterload-sensitivity of cardiac output and may be an ideal setting for counterpulsation. Several hemodynamic variables have been shown to predict response to IABP within this scenario, potentially guiding appropriate patient selection. Finally, acute decompensated heart failure with hypoperfusion may frequently represent an end stage in the heart failure history: IABP may provide sufficient hemodynamic support and prompt end-organ function recovery in view of more definitive heart replacement therapies while preserving ambulation when used with a transaxillary approach.

Background: Coronavirus disease 2019 (COVID-19) pandemic has led to a fast and radical transformation in social, economic, and healthcare networks. COVID-19 outbreak may thus have profound indirect consequences on clinical presentation and management of patients with ST-segment–elevation myocardial infarction (STEMI). Aim of this study was to assess clinical features of patients with STEMI during COVID-19 pandemic. Methods: This single-center, prospective study from a regional public service healthcare hub in Milan included all consecutive patients with STEMI admitted to our institute from February 21 to April 1, 2020 (during COVID-19 pandemic). These patients were compared with a historical cohort of patients admitted for STEMI during the analogous time period (February 21 to April 1) in 2018 and 2019, in terms of time from symptoms onset to hospital admission, clinical characteristics, and in-hospital outcomes. Results: A total of 26 patients were admitted for STEMI during the study period, and 7 (26.9%) of these patients tested positive for severe acute respiratory syndrome coronavirus 2. On admission, medical therapy, including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers use, was similar between cohorts. Median (interquartile range) time from symptoms onset to hospital admission was significantly longer in 2020 as compared to the historical cohort (15.0 [2.0–48.0] versus 2.0 [1.0–3.0] hours; P <0.01). A higher proportion of patients presenting with late presentation STEMI was observed in 2020 compared with the historical cohort (50.0% versus 4.8%; P <0.01). Primary percutaneous coronary intervention resulted indicated in 80.8% of patients in 2020 compared with 100% in the historical cohort ( P =0.06). In-hospital death, thromboembolism, mechanical ventilation, or hemodynamic decompensation needing inotropic or mechanical support were similar between years. Conclusions: These preliminary results from a cardiovascular regional public service healthcare hub demonstrate a significantly longer time from symptoms onset to hospital admission among patients with STEMI during COVID-19 pandemic compared with the same time period in the previous 2 years.

BACKGROUND: Patients presenting with cardiogenic shock (CS) are at risk of developing mixed shock (MS), characterized by distributive-inflammatory phenotype. However, no objective definition exists for this clinical entity. METHODS: We assessed the frequency, predictors, and prognostic relevance of MS complicating CS, based on a newly proposed objective definition. MS complicating CS was defined as an objective shock state secondary to both an ongoing cardiogenic cause and a distributive-inflammatory phenotype arising at least 12 hours after the initial CS diagnosis, as substantiated by predefined longitudinal changes in hemodynamics, clinical, and laboratory parameters. RESULTS: Among 213 consecutive patients admitted at 2 cardiac intensive care units with CS, 13 with inflammatory-distributive features at initial presentation were excluded, leading to a cohort of 200 patients hospitalized with pure CS (67±13 years, 96% Society of Cardiovascular Angiography and Interventions CS stage class C or higher). MS complicating CS occurred in 24.5% after 120 (29–216) hours from CS diagnosis. Lower systolic arterial pressure ( P =0.043), hepatic injury ( P =0.049), and suspected/definite infection ( P =0.013) at CS diagnosis were independent predictors of MS development. In-hospital mortality (53.1% versus 27.8%; P =0.002) and hospital stay (21 [13–48] versus 17 [9–27] days; P =0.018) were higher in the MS cohort. At logistic multivariable analysis, MS diagnosis (odds ratio [OR], 3.00 [95% CI, 1.39–6.63]; P _adj =0.006), age (OR, 1.06 [95% CI, 1.03–1.10] years; P _adj <0.001), admission systolic arterial pressure <100 mm Hg (OR, 2.41 [95% CI, 1.19–4.98]; P _adj =0.016), and admission serum creatinine (OR, 1.61 [95% CI, 1.19–2.26]; P _adj =0.003) conferred higher odds of in-hospital death, while early temporary mechanical circulatory support was associated with lower in-hospital death (OR, 0.36 [95% CI, 0.17–0.75]; P _adj =0.008). CONCLUSIONS: MS complicating CS, objectively defined leveraging on longitudinal changes in distributive and inflammatory features, occurs in one-fourth of patients with CS, is predicted by markers of CS severity and inflammation at CS diagnosis, and portends higher hospital mortality.