Aim We sought to describe the contemporary annual incidence of cardiogenic shock (CS) following acute myocardial infarction (AMICS), the proportion of patients developing CS following ST‐elevation myocardial infarction (STEMI), and other temporal changes in AMICS in Denmark between 2010 and 2017. Methods and results Medical records of patients suspected of having AMICS during 2010–2017 were reviewed to identify consecutive patients with AMICS in a cohort corresponding to two‐thirds of the Danish population. Due to changes in recruitment area over the study period, population‐based incidence could only be calculated from 2012 to 2017. A total of 1716 patients with AMICS were identified and an increase in the annual incidence was observed, from a nadir 65.3 per million person‐years in 2013 to 80.0 per million person‐years in 2017 (P‐value for trend < 0.001). This trend corresponded to an increase in patients with non‐STEMI and a decrease in patients developing CS after STEMI (10.0–6.6%, P‐value for trend < 0.001) Also, mean arterial blood pressure at the time of AMICS was lower (63 ± 11 mmHg to 61 ± 13 mmHg, P‐value for trend = 0.001) and the frequency of patients with left ventricular ejection fraction ≤ 30% increased (61.8%–71.4%, P‐value for trend = 0.004). The annual 30‐day mortality during the study period remained unchanged at about 50%. Conclusion The incidence rate of AMICS increased in the Danish population between 2012 and 2017. Fewer patients with STEMI developed CS, and haemodynamic severity of CS increased during the study period; however, survival rates remained unchanged.

In this study, 10% of patients admitted with suspected STEMI for acute coronary angiography presented with or developed CS. Most were in shock on admission. Irrespective of the timing of shock, mortality was high.

Background: After resuscitation from out-of-hospital cardiac arrest, mean arterial pressure below 65 mm Hg is avoided with vasopressors. A higher blood-pressure target could potentially improve outcome. The aim of this pilot trial was to investigate the effect of a higher mean arterial pressure target on biomarkers of organ injury. Methods: This was a single-centre, double-blind trial of 50 consecutive, comatose out-of-hospital cardiac arrest patients randomly assigned in a 1:1 ratio to a mean arterial pressure target of 65 mm Hg (MAP65) or 72 mm Hg (MAP72). Modified blood pressure modules with a –10% offset were used, enabling a double-blind study design. End-points were biomarkers of organ injury including markers of endothelial integrity (soluble trombomodulin) brain damage (neuron-specific enolase) and renal function (estimated glomerular filtration rate). Results: Mean arterial pressure was significantly higher in MAP72 with a mean difference of 5 mm Hg ( pgroup=0.03). After 48 h, soluble trombomodulin (median (interquartile range)) was 8.2 (6.7–12.9) ng/ml and 8.3 (6.0–10.8) ng/ml ( p=0.29), neuron-specific enolase was 20 (13–31 μg/l) and 18 (13–44 μg/l) p=0.79) and estimated glomerular filtration rate (mean (±standard deviation)) was 61±19 ml/min/1.73m2 and 48±22 ml/min/1.73 m2 ( p=0.08) for the MAP72 and MAP65 groups, respectively. Renal replacement therapy was needed in eight patients (31%) in MAP65 and three patients (13%) in MAP72 ( p=0.14). Conclusions: Double-blind allocation to different mean arterial pressure targets is feasible in comatose out-of-hospital cardiac arrest patients. A mean arterial pressure target of 72 mm Hg compared to 65 mm Hg did not result in improved biomarkers of organ injury. We observed a trend towards preserved renal function in the MAP72 group.

BACKGROUNDThe appropriate oxygenation target for mechanical ventilation in comatose survivors of out-of-hospital cardiac arrest is unknown. METHODSIn this randomized trial with a 2-by-2 factorial design, we randomly assigned comatose adults with out-of-hospital cardiac arrest in a 1:1 ratio to either a restrictive oxygen target of a partial pressure of arterial oxygen (Pao 2 ) of 9 to 10 kPa (68 to 75 mm Hg) or a liberal oxygen target of a Pao 2 of 13 to 14 kPa (98 to 105 mm Hg); patients were also assigned to one of two blood-pressure targets (reported separately). The primary outcome was a composite of death from any cause or hospital discharge with severe disability or coma (Cerebral Performance Category [CPC] of 3 or 4; categories range from 1 to 5, with higher values indicating more severe disability), whichever occurred first within 90 days after randomization. Secondary outcomes were neuron-specific enolase levels at 48 hours, death from any cause, the score on the Montreal Cognitive Assessment (ranging from 0 to 30, with higher scores indicating better cognitive ability), the score on the modified Rankin scale (ranging from 0 to 6, with higher scores indicating greater disability), and the CPC at 90 days. RESULTSA total of 789 patients underwent randomization. A primary-outcome event occurred in 126 of 394 patients (32.0%) in the restrictive-target group and in 134 of 395 patients (33.9%) in the liberal-target group (hazard ratio, 0.95; 95% confidence interval, 0.75 to 1.21; P = 0.69). At 90 days, death had occurred in 113 patients (28.7%) in the restrictive-target group and in 123 (31.1%) in the liberal-target group. On the CPC, the median category was 1 in the two groups; on the modified Rankin scale, the median score was 2 in the restrictive-target group and 1 in the liberaltarget group; and on the Montreal Cognitive Assessment, the median score was 27 in the two groups. At 48 hours, the median neuron-specific enolase level was 17 μg per liter in the restrictive-target group and 18 μg per liter in the liberaltarget group. The incidence of adverse events was similar in the two groups. CONCLUSIONSTargeting of a restrictive or liberal oxygenation strategy in comatose patients after resuscitation for cardiac arrest resulted in a similar incidence of death or severe disability or coma. (Funded by the Novo Nordisk Foundation; BOX ClinicalTrials .gov number, NCT03141099.

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Aims: The diagnosis of cardiogenic shock depends on clinical signs of poor perfusion and low blood pressure. Lactate concentration will increase with poor tissue perfusion, and it has prognostic value in cardiogenic shock patients. We sought to assess the prognostic value of lactate concentration in subjects admitted with suspected ST-elevation myocardial infarction (STEMI). Methods and Results: In 2,094 (93%) out of 2,247 consecutive suspected STEMI-subjects, lactate concentration was measured on admission. The prognostic value of lactate concentration on 30-day mortality was assessed in addition to clinical signs of peripheral hypoperfusion, systolic blood pressure (sBP), and left ventricular ejection fraction (LVEF) in multivariable models. Lactate concentration added prognostic information beyond signs of peripheral hypoperfusion, sBP, and LVEF, and was independently associated with 30-day mortality (hazard ratio [95% confidence interval] 1.11 [1.07–1.14], P < 0.0001). Lactate also provided predictive information on 30-day mortality to the combination of signs of peripheral hypoperfusion, sBP, and LVEF (area under the receiver-operating characteristics curve = 0.88 vs. 0.83, P < 0.0001). Conclusions: In conclusion, admission lactate concentration in suspected STEMI-subjects contains prognostic information on 30-day mortality when added to variables used in cardiogenic shock-definition. We recommend lactate measurement in STEMI-subjects, especially when signs of compromised hemodynamics are present.

In patients with severe psoriasis treatment with biologic therapy was associated with improved PASI and amelioration of myocardial dysfunction.