Background: Acute myocarditis (AM) is thought to be a rare cardiovascular complication of COVID-19, although minimal data are available beyond case reports. We aim to report the prevalence, baseline characteristics, in-hospital management, and outcomes for patients with COVID-19–associated AM on the basis of a retrospective cohort from 23 hospitals in the United States and Europe. Methods: A total of 112 patients with suspected AM from 56 963 hospitalized patients with COVID-19 were evaluated between February 1, 2020, and April 30, 2021. Inclusion criteria were hospitalization for COVID-19 and a diagnosis of AM on the basis of endomyocardial biopsy or increased troponin level plus typical signs of AM on cardiac magnetic resonance imaging. We identified 97 patients with possible AM, and among them, 54 patients with definite/probable AM supported by endomyocardial biopsy in 17 (31.5%) patients or magnetic resonance imaging in 50 (92.6%). We analyzed patient characteristics, treatments, and outcomes among all COVID-19–associated AM. Results: AM prevalence among hospitalized patients with COVID-19 was 2.4 per 1000 hospitalizations considering definite/probable and 4.1 per 1000 considering also possible AM. The median age of definite/probable cases was 38 years, and 38.9% were female. On admission, chest pain and dyspnea were the most frequent symptoms (55.5% and 53.7%, respectively). Thirty-one cases (57.4%) occurred in the absence of COVID-19–associated pneumonia. Twenty-one (38.9%) had a fulminant presentation requiring inotropic support or temporary mechanical circulatory support. The composite of in-hospital mortality or temporary mechanical circulatory support occurred in 20.4%. At 120 days, estimated mortality was 6.6%, 15.1% in patients with associated pneumonia versus 0% in patients without pneumonia ( P =0.044). During hospitalization, left ventricular ejection fraction, assessed by echocardiography, improved from a median of 40% on admission to 55% at discharge (n=47; P <0.0001) similarly in patients with or without pneumonia. Corticosteroids were frequently administered (55.5%). Conclusions: AM occurrence is estimated between 2.4 and 4.1 out of 1000 patients hospitalized for COVID-19. The majority of AM occurs in the absence of pneumonia and is often complicated by hemodynamic instability. AM is a rare complication in patients hospitalized for COVID-19, with an outcome that differs on the basis of the presence of concomitant pneumonia.

Background: Inflammation is a key factor of myocardial damage in reperfused ST-segment–elevation myocardial infarction. We hypothesized that colchicine, a potent anti-inflammatory agent, may reduce infarct size (IS) and left ventricular (LV) remodeling at the acute phase of ST-segment–elevation myocardial infarction. Methods: In this double-blind multicenter trial, we randomly assigned patients admitted for a first episode of ST-segment–elevation myocardial infarction referred for primary percutaneous coronary intervention to receive oral colchicine (2-mg loading dose followed by 0.5 mg twice a day) or matching placebo from admission to day 5. The primary efficacy outcome was IS determined by cardiac magnetic resonance imaging at 5 days. The relative LV end-diastolic volume change at 3 months and IS at 3 months assessed by cardiac magnetic resonance imaging were among the secondary outcomes. Results: We enrolled 192 patients, 101 in the colchicine group and 91 in the control group. At 5 days, the gadolinium enhancement–defined IS did not differ between the colchicine and placebo groups with a mean of 26 interquartile range (IQR) [16–44] versus 28.4 IQR [14–40] g of LV mass, respectively ( P =0.87). At 3 months follow-up, there was no significant difference in LV remodeling between the colchicine and placebo groups with a +2.4% (IQR, –8.3% to 11.1%) versus –1.1% (IQR, –8.0% to 9.9%) change in LV end-diastolic volume ( P =0.49). Infarct size at 3 months was also not significantly different between the colchicine and placebo groups (17 IQR [10–28] versus 18 IQR [10–27] g of LV mass, respectively; P =0.92). The incidence of gastrointestinal adverse events during the treatment period was greater with colchicine than with placebo (34% versus 11%, respectively; P =0.0002). Conclusions: In this randomized, placebo-controlled trial, oral administration of high-dose colchicine at the time of reperfusion and for 5 days did not reduce IS assessed by cardiac magnetic resonance imaging. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03156816.

Background Soluble vascular cell adhesion molecule‐1 (sVCAM‐1) is a biomarker of endothelial activation and inflammation. There is still controversy as to whether it can predict clinical outcome after ST‐elevation myocardial infarction (STEMI). Our aim was to assess the sVCAM‐1 kinetics and to evaluate its prognostic predictive value. Method We prospectively enrolled 251 consecutive STEMI patients who underwent coronary revascularization in our university hospital. Blood samples were collected at admission, 4, 24, 48 h and 1 month after admission. sVCAM‐1 serum level was assessed using ELISA assay. All patients had cardiac magnetic resonance imaging at 1‐month for infarct size (IS) and left ventricular ejection fraction (LVEF) assessment. Clinical outcomes were recorded over 12 months after STEMI. Results sVCAM‐1 levels significantly increased from admission up to 1 month and were significantly correlated with IS, LVEF, and LV end‐systolic and diastolic volume. (H48 area under curve (AUC) ≥ H48 median) were associated with an increased risk of adverse clinical events during the 12‐month follow‐up period with a hazard ratio (HR) = 2.6 (95% confidence interval [CI] of ratio = 1.2–5.6, p = .02). The ability of H48 AUC for sVCAM‐1 to discriminate between patients with or without the composite endpoint was evaluated using receiver operating characteristics with an AUC at 0.67 (0.57–0.78, p = .004). This ability was significantly superior to H48 AUC creatine kinase (p = .03). Conclusions In STEMI patients, high sVCAM‐1 levels are associated with a poor clinical outcome. sVCAM‐1 is an early postmyocardial infarction biomarker and might be an interesting target for the development of future therapeutic strategies.

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Background and Aim of the Study Acute cardiovascular failure remains a leading cause of death in severe poisonings. Veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO) has been increasingly used as a rescue therapeutic option for those cases refractory to optimal conventional treatment. We sought to evaluate the outcomes after VA‐ECMO used for drug intoxications in a single‐center experience. Methods We performed an observational analysis of our prospective institutional database. The primary endpoint was survival to hospital discharge. Results Between January 2007 and December 2020, 32 patients (mean age: 45.4 ± 15.8 years; 62.5% female) received VA‐ECMO for drug intoxication‐induced refractory cardiogenic shock (n = 25) or cardiac arrest (n = 7). Seven (21.8%) patients developed lower limb ischemia during VA‐ECMO support. Twenty‐six (81.2%) patients were successfully weaned after a mean VA‐ECMO support of 2.9 ± 1.3 days. One (3.1%) patient died after VA‐ECMO weaning for multiorgan failure and survival to hospital discharge was 78.1% (n = 25). In‐hospital survivors were discharged from hospital with a good neurological status. Survival to hospital discharge was not statistically different according to sex (male = 75.0% vs. female = 80.0%; p = .535), type of intoxication (single drug = 81.8% vs. multiple drugs = 76.1%; p = .544) and location of VA‐ECMO implantation (within our center = 75% vs. peripheral hospital using our Mobile Unit of Mechanical Circulatory Support = 100%; p = .352). Survival to hospital discharge was significantly lower in patients receiving VA‐ECMO during on‐going cardiopulmonary resuscitation (42.8% vs. 88.0%; p = .026). Conclusions VA‐ECMO appears to be a feasible therapeutic option with a satisfactory survival rate and acceptable complications rate in poisonings complicated by refractory cardiogenic shock or cardiac arrest.

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