Cardiogenic shock (CS) is the most life-threatening manifestation of acute heart failure. Its complexity and high in-hospital mortality may justify the need for invasive monitoring with a pulmonary artery catheter (PAC). Patients with CS included in the CardShock Study, an observational, prospective, multicenter, European registry, were analyzed, aiming to describe the real-world use of PAC, evaluate its impact on 30-day mortality, and the ability of different hemodynamic parameters to predict outcomes. Pulmonary artery catheter was used in 82 (37.4%) of the 219 patients. Cardiogenic shock patients who managed with a PAC received more frequently treatment with inotropes and vasopressors, mechanical ventilation, renal replacement therapy, and mechanical assist devices (P < .01). Overall 30-day mortality was 36.5%. Pulmonary artery catheter use did not affect mortality even after propensity score matching analysis (hazard ratio = 1.17 [0.59-2.32], P = .66). Cardiac index, cardiac power index (CPI), and stroke volume index (SVI) showed the highest areas under the curve for 30-day mortality (ranging from 0.752-0.803) and allowed for a significant net reclassification improvement of 0.467 (0.083-1.180), 0.700 (0.185-1.282), 0.683 (0.168-1.141), respectively, when added to the CardShock risk score. In our contemporary cohort of CS, over one-third of patients were managed with a PAC. Pulmonary artery catheter use was associated with a more aggressive treatment strategy. Nevertheless, PAC use was not associated with 30-day mortality. Cardiac index, CPI, and SVI were the strongest 30-day mortality predictors on top of the previously validated CardShock risk score.

Cardiogenic shock (CS) is a cardiac emergency often leading to multiple organ failure and death. Assessing organ dysfunction and appropriate risk stratification are central for the optimal management of these patients. The purpose of this study was to assess the prevalence of abnormal liver function tests (LFTs), as well as early changes of LFTs and their impact on outcome in CS. We measured LFTs in 178 patients in CS from serial blood samples taken at 0 hours, 12 hours, and 24 hours. The associations of LFT abnormalities and their early changes with all-cause 90-day mortality were estimated using Fisher's exact test and Cox proportional hazards regression analysis. Baseline alanine aminotransferase (ALT) was abnormal in 58% of the patients, more frequently in nonsurvivors. Abnormalities in other LFTs analyzed (alkaline phosphatase, gamma-glutamyl transferase, and total bilirubin) were not associated with short-term mortality. An increase in ALT of >20% within 24 hours (ΔALT>+20%) was observed in 24% of patients. ΔALT>+20% was associated with a more than 2-fold increase in mortality compared with those with stable or decreasing ALT (70% and 28%, p +20% was associated with increased 90-day mortality independent of other known risk factors. In conclusion, an increase in ALT in the initial phase was seen in 1/4 of patients in CS and was independently associated with 90-day mortality. This finding suggests that serial ALT measurements should be incorporated in the clinical assessment of patients in CS.

Background: Coronary microvascular dysfunction (CMD) has been proposed as a key mechanism in Takotsubo syndrome (TTS). The non-hyperaemic angiography-derived index of microcirculatory resistance (NH-IMRangio) has been validated as a pressure-wire-free tool for the assessment of coronary microvasculature. We aimed to study the presence of CMD in TTS patients and its association with levels of cardiac biomarkers and systolic dysfunction patterns. Methods: We recruited 181 consecutive patients admitted for TTS who underwent cardiac angiography at a tertiary center from January 2014 to January 2021. CMD was defined as an NH-IMRangio ≥ 25. Plasma levels of NT-proBNP, high-sensitive cardiac troponin T (hs-cTnT) and the left ventricular ejection fraction (LVEF) by echocardiography were measured at admission. Results: Mean age was 75.3 years, 83% were women and median LVEF was 45%. All patients presented CMD (NH-IMRangio ≥ 25) in at least one epicardial coronary artery. The left anterior descending artery (LAD) showed higher median NH-IMRangio values than left circumflex (LCx) and right coronary arteries (RCA) (44.6 vs. 31.3 vs. 36.1, respectively; p < 0.001). NH-IMRangio values differed among ventricular contractility patterns in the LAD and RCA (p = 0.0152 and 0.0189, respectively) with the highest values in the mid-ventricular + apical and mid-ventricular + basal patterns. NT-proBNP levels, but not high-sensitive cardiac troponin T (hs-cTnT), were correlated with both the degree and the extent of CMD in patients with TTS. Lower LVEF was also associated with higher NH-IMRangio values. Conclusions: CMD is highly prevalent in patients admitted for TTS and is associated with both a higher degree of systolic dysfunction and higher BNP levels, but not troponin.

Using proteomics, we previously found that serum levels of glycosylated (Glyc) forms of apolipoprotein J (ApoJ), a cytoprotective and anti-oxidant protein, decrease in the early phase of acute myocardial infarction (AMI). We aimed to investigate: (i) ApoJ-Glyc intracellular distribution and secretion during ischaemia; (ii) the early changes in circulating ApoJ-Glyc during AMI; and (iii) associations between ApoJ-Glyc and residual ischaemic risk post-AMI. Glycosylated apolipoprotein J was investigated in: (i) cells from different organ/tissue origin; (ii) a pig model of AMI; (iii) de novo AMI patients (n = 38) at admission within the first 6 h of chest pain onset and without troponin T elevation at presentation (early AMI); (iv) ST-elevation myocardial infarction patients (n = 212) who were followed up for 6 months; and (v) a control group without any overt cardiovascular disease (n = 144). Inducing simulated ischaemia in isolated cardiac cells resulted in an increased intracellular accumulation of non-glycosylated ApoJ forms. A significant decrease in ApoJ-Glyc circulating levels was seen 15 min after ischaemia onset in pigs. Glycosylated apolipoprotein J levels showed a 45% decrease in early AMI patients compared with non-ischaemic patients (P < 0.0001), discriminating the presence of the ischaemic event (area under the curve: 0.934; P < 0.0001). ST-elevation myocardial infarction patients with lower ApoJ-Glyc levels at admission showed a higher rate of recurrent ischaemic events and mortality after 6-month follow-up (P = 0.008). These results indicate that ischaemia induces an intracellular accumulation of non-glycosylated ApoJ and a reduction in ApoJ-Glyc secretion. Glycosylated apolipoprotein J circulating levels are reduced very early after ischaemia onset. Its continuous decrease indicates a worsening in the evolution of the cardiac event, likely identifying patients with sustained ischaemia after AMI. Glycosylated apolipoprotein J as a novel marker of ischaemia. Under ischaemic conditions there is a decrease in the secretion of glycosylated apolipoprotein J. The quantification of specific glycosylated apolipoprotein J variants with a novel immunoassay discriminates the presence of a cardiac ischaemic event, indicating that glycosylated apolipoprotein J could be a novel marker of cardiac ischaemia.