CANCARE RESEARCH
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An automated research-discovery feed. Summaries are based on published abstracts and are not clinical recommendations.
Effects of inhaled nitric oxide during mechanical circulatory support: a prospective pilot study.
Clinical takeaway Inhaled nitric oxide was temporally associated with an early reduction in pulmonary artery pressure during Impella-based support. This pilot does not establish clinical benefit or a causal haemodynamic effect.
Summary & abstract
Study summary
This prospective single-centre pilot evaluated inhaled nitric oxide in adults with cardiogenic shock receiving Impella or ECPELLA support; 11 patients were enrolled and 10 analysed. The primary endpoint was change in mean pulmonary artery pressure at 30 minutes, which decreased from 19.0 to 16.5 mmHg (P=0.004). The baseline-to-24-hour difference was not significant, and no clear improvement in systemic haemodynamic indices was observed. Lactate decreased, but without a control group this temporal change could not be attributed directly to inhaled nitric oxide.
Study limitation: Only 10 patients were analysed at one centre without a control group, limiting causal interpretation and generalisability.
Published abstract
Among patients with cardiogenic shock receiving Impella-based mechanical circulatory support, pulmonary vascular load and right ventricular dysfunction may affect left ventricular preload and device flow. Prospective data on the acute hemodynamic effects of inhaled nitric oxide (iNO) in this setting are limited. We evaluated short-term hemodynamic changes after iNO initiation in patients receiving Impella or Impella combined with veno-arterial extracorporeal membrane oxygenation (ECPELLA) support. We conducted a prospective single-center pilot study of adult patients receiving Impella or ECPELLA support who were treated with iNO. iNO was initiated at 20 ppm after initial circulatory resuscitation once pulmonary artery pulse pressure could be reliably assessed. Hemodynamic variables were recorded immediately before iNO initiation (T0) and 30 min (T1) and 24 h (T2) after initiation. The primary endpoint was the change in mean pulmonary artery pressure (mPAP) from T0 to T1. We enrolled 11 patients, and 10 were analyzed. mPAP decreased from 19.0 (14.8-20.3) mmHg at T0 to 16.5 (12.8-19.3) mmHg at T1 (P = 0.004). The T0-T2 difference was not significant. Lactate levels decreased, but this temporal change could not be attributed directly to iNO without a control group. Methemoglobin levels increased slightly at T2 without clinical methemoglobinemia. iNO was temporally associated with an early reduction in mPAP in patients receiving Impella-based support, without clear improvement in systemic hemodynamic indices. These hypothesis-generating findings require confirmation in larger controlled studies.
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Clinical significance of elevated body temperature without infection following removal of VA-ECMO.
Clinical takeaway Temperature elevation after VA-ECMO removal was common but did not distinguish overall mortality in this cohort. The association between larger temperature rises and mortality within the elevated-temperature subgroup is exploratory.
Summary & abstract
Study summary
This retrospective study evaluated 163 cardiogenic shock patients without evidence of infection undergoing VA-ECMO removal. Temperature reached at least 38.0°C within 24 hours in 58.9%, accompanied by lower systolic blood pressure and systemic vascular resistance and higher lactate. All-cause mortality was 30.2% with versus 29.9% without elevated temperature (log-rank p=0.983). Among patients with elevated temperature, a greater temperature rise, particularly at least 1.1°C, was associated with higher all-cause mortality (HR 1.968, 95% CI 1.096–3.535); the abstract did not specify the mortality follow-up duration.
Study limitation: The retrospective design limits causal interpretation, and the subgroup association requires confirmation; mortality follow-up duration was not reported.
Published abstract
BACKGROUND: Previous studies have reported elevated body temperature following the removal of veno-arterial extracorporeal membrane oxygenation (VA-ECMO). However, the clinical implications of elevated body temperature after the removal of VA-ECMO remain unknown. OBJECTIVES: To characterize elevated body temperature after VA-ECMO removal in patients with cardiogenic shock (CS). METHODS: We retrospectively evaluated 163 CS patients undergoing VA-ECMO removal. All patients did not exhibit any evidence of infection. Blood temperature was continuously monitored using a Swan-Ganz catheter. Elevated body temperature was defined as a maximum body temperature ≥38.0 °C within 24 h after VA-ECMO removal. All-cause mortality was compared between patients with and without elevated body temperature. RESULTS: Elevated body temperature was observed in 58.9% (96/163) of study subjects. Patients with elevated body temperature had higher C-reactive protein (CRP) levels (11.1 ± 8.6 vs. 8.5 ± 6.1 mg/dL, p = 0.027), accompanied by reductions in systolic blood pressure and systemic vascular resistance, and increased lactate levels. CRP levels independently predicted elevated body temperature (OR=1.050, 95%CI=1.003-1.100, p = 0.037). All-cause mortality did not differ between the two groups (30.2%vs. 29.9%, log-rank p = 0.983). However, among patients with elevated body temperature, an increase in body temperature, especially ≥1.1 °C, was associated with higher all-cause mortality (HR=1.968, 95%CI=1.096-3.535, p = 0.023). CONCLUSIONS: In CS patients requiring VA-ECMO, body temperature elevated in 58.9% patients after the removal of VA-ECMO. In those with elevated body temperature, a greater rise in body temperature was associated with higher mortality, suggesting body temperature as a potential signature to stratify risks of mortality in CS patients without any infectious signs.
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Antithrombotic strategies and outcomes in acute myocardial infarction-related cardiogenic shock requiring short-term mechanical circulatory support.
Clinical takeaway This cohort highlights frequent early major bleeding alongside substantial mortality in infarct-related shock requiring mechanical support. It does not establish which antithrombotic strategy offers the best balance of bleeding and ischemic outcomes.
Summary & abstract
Study summary
This retrospective, single-center study included 71 patients with acute myocardial infarction-related cardiogenic shock receiving short-term mechanical circulatory support after PCI. In-hospital mortality was 56%, while the composite of ischemic events and all-cause mortality during shock occurred in 42%. Triple therapy use decreased from 79% at support initiation to 39% by day 7. Ischemic events occurred in 8%, with no recurrent myocardial infarction or stent thrombosis observed. Major bleeding occurred in 32%, typically within 48 hours, and was more frequent among patients receiving VA-ECMO.
Study limitation: The small, retrospective, single-center cohort and absence of reported adjusted regimen comparisons limit causal interpretation.
Published abstract
BACKGROUND: Cardiogenic shock following acute myocardial infarction (AMI-CS) is associated with high mortality. Short-term mechanical circulatory support (ST-MCS) is frequently used after percutaneous coronary intervention (PCI) to stabilize hemodynamics. However, balancing anticoagulation (AC) and antiplatelet therapy in this setting poses substantial bleeding risk. OBJECTIVES: This study aimed to evaluate real-world antithrombotic strategies and associated ischemic and hemorrhagic complications in AMI-CS patients receiving ST-MCS. METHODS: This retrospective, single-center study included all consecutive AMI-CS patients who underwent PCI and required ST-MCS between January 2017 and October 2024. AC and antiplatelet regimens were recorded from ST-MCS initiation until shock resolution. Ischemic and hemorrhagic events during this period were analyzed. The primary composite clinical endpoint was major adverse cardiovascular events (MACE), defined as a composite of ischemic events and all-cause mortality occurring during the period of cardiogenic shock. RESULTS: Among 71 patients with AMI-CS who underwent PCI and required ST-MCS (mean age 62 ± 13 years, 69% male), in-hospital mortality was 56%, and MACE occurred in 42%. At ST-MCS initiation, 79% received triple therapy, decreasing to 39% by Day 7. Ischemic events were infrequent (8%) and mainly cerebrovascular. No cases of recurrent myocardial infarction or stent thrombosis were observed. Major bleeding (BARC ≥ 3) occurred in 32% of patients, typically within the first 48 h, and was more frequent in those supported with VA-ECMO. CONCLUSION: In AMI-CS patients requiring ST-MCS, ischemic events were uncommon, whereas major bleeding was frequent and occurred early. These findings underscore the need for individualized antithrombotic strategies in this high-risk population.
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Microcirculatory Hemodynamic Changes on Full Support Microaxial Flow Pump in Cardiogenic Shock.
Clinical takeaway Full-support microaxial pump use was associated with improved microcirculatory measures, particularly when baseline perfusion was impaired. These exploratory physiological findings do not establish a device-specific benefit.
Summary & abstract
Study summary
This prospective, single-arm observational study assessed serial sublingual microcirculation in 18 patients with cardiogenic shock undergoing Impella 5.5 placement. Immediately on support, microvascular flow index (p = 0.004) and proportion of perfused vessels (p = 0.003) improved, including after adjustment for vasoactive-inotropic score. Changes in microvascular heterogeneity index (p = 0.055) and perfused vessel density (p = 0.067) did not reach statistical significance. Improvements were greatest among patients with impaired baseline microcirculation; no systemic haemodynamic marker was sufficient to ensure adequate microcirculatory perfusion.
Study limitation: The small, single-arm study cannot separate device effects from overall clinical improvement, and its endpoints are physiological rather than patient-centred.
Published abstract
Impaired microcirculation predicts mortality in cardiogenic shock independent of systemic hemodynamics, yet current treatment strategies focus primarily on restoring macrocirculatory markers. We studied whether full-support microaxial flow pump (mAFP) therapy improves sublingual microcirculation in cardiogenic shock. A prospective, single-arm, observational study of serial sublingual microcirculation imaging via incident darkfield handheld videomicroscopy was performed in 18 cardiogenic shock patients undergoing Impella 5.5 (mAFP) placement. Microvascular flow index (MFI), microvascular heterogeneity index (MHI), proportion of perfused vessels (PPV), and perfused vessel density (PVD) were measured. Eighteen patients were enrolled. Microvascular flow index (p = 0.004), MHI (p = 0.055), PPV (p = 0.003), and PVD (p = 0.067) improved immediately on support, including when adjusted for vasoactive-inotropic score. Improvement in MFI, MHI, PPV, or PVD was most pronounced in those with impaired baseline microcirculatory hemodynamics (all p < 0.05), whereas those with preserved baseline values demonstrated no change. Improved agreement between systemic and microcirculatory hemodynamics was observed in association with mAFP support, and none experienced worsening microcirculatory function. These exploratory findings suggest full-support mAFPs may improve impaired microcirculation during cardiogenic shock, although device-specific effects cannot be isolated from overall clinical improvement; validation in larger studies is warranted. Although agreement between systemic and microcirculatory hemodynamic markers improved, no macrohemodynamic marker proved sufficient to ensure adequate microcirculatory perfusion.
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Physiological Effects and Clinical Limitations of Impella-Bridge Strategy for Post-Infarction Ventricular Septal Rupture.
Clinical takeaway This small series documents achievement of scheduled repair in most patients, alongside improving haemodynamic measures but worsening SOFA-defined organ dysfunction. It does not establish comparative benefit for an Impella-bridge strategy.
Summary & abstract
Study summary
This retrospective study evaluated 10 consecutive patients with post-infarction ventricular septal rupture managed with Impella support; median age was 74 years. Four patients also received veno-arterial extracorporeal life support, and one underwent Impella upgrade. Scheduled repair was achieved in nine patients (90%), with a median interval from Impella initiation to repair of 8 (7, 10) days. Pulmonary artery and central venous pressures, B-type natriuretic peptide, and lactate decreased before repair, while non-CNS SOFA scores increased. Organ support requirements and device-related complications were also observed during bridging.
Study limitation: The retrospective, 10-patient series lacked a comparator, limiting causal interpretation and assessment of comparative clinical outcomes.
Published abstract
BACKGROUND: Post-infarction ventricular septal rupture (VSR) remains a life-threatening mechanical complication of acute myocardial infarction. We evaluated the feasibility of an Impella-bridge strategy for scheduled VSR repair. METHODS: We retrospectively analyzed 10 consecutive patients with post-infarction VSR who were transferred to our institution and managed with Impella support. Outcomes included achievement of scheduled repair and serial changes in hemodynamic parameters and organ dysfunction during the bridging period. RESULTS: The median age was 74 years. All patients received Impella 2.5 or CP support after transfer; veno-arterial extracorporeal life support was added in four patients, and Impella support was upgraded in one patient. The median duration from Impella initiation to VSR repair was 8 (7, 10) days. Scheduled repair was achieved in nine patients (90%). Mean pulmonary artery pressure, central venous pressure, plasma B-type natriuretic peptide levels, and lactate decreased over time before repair, whereas non-CNS SOFA scores increased during bridging. CONCLUSIONS: In patients with post-infarction VSR, an Impella-bridge strategy may help achieve scheduled VSR repair with improved hemodynamic stabilization; however, SOFA-defined abnormalities, organ support requirements, and device-related complications were observed during the bridging period. Further studies are needed to define patient selection, management strategies, and the optimal timing of repair for this strategy.
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Forty-Eight Hour Lactate Normalization Predicts Favorable Neurologic Recovery and Survival in Venoarterial ECMO for Cardiogenic Shock.
Clinical takeaway Lactate normalization at 48 hours was associated with better neurologic discharge outcomes and 12-month survival during VA-ECMO. These findings support prognostic relevance, not a causal benefit of targeting lactate normalization.
Summary & abstract
Study summary
A retrospective multicenter registry analysis included 662 patients with cardiogenic shock who remained on VA-ECMO for at least 48 hours. Patients with 48-hour lactate below 2.0 mmol/L had more favorable neurologic discharge, defined as Cerebral Performance Category 1–2, than those with persistent elevation (71.4% versus 41.9%). Normalization remained independently associated with favorable neurologic discharge (odds ratio 3.12, 95% confidence interval 2.21–4.41). It was also associated with lower all-cause mortality at 12 months (hazard ratio 0.49, 95% confidence interval 0.38–0.64).
Study limitation: Retrospective analysis restricted to patients remaining on ECMO for at least 48 hours; baseline severity differences leave potential residual confounding.
Published abstract
Extracorporeal membrane oxygenation (ECMO) for cardiogenic shock (CS) is associated with high mortality and poor neurological outcomes. Dynamic assessment of metabolic recovery, reflected by lactate normalization, may offer additional prognostic value compared with static severity indices. We retrospectively analyzed 662 consecutive patients from the multicenter RESCUE II registry who remained on venoarterial ECMO for at least 48 hours. Patients were stratified by 48 hour lactate level: 48 hour lactate normalization group (< 2.0 mmol/L, n = 371) and persistent lactate elevation group (≥ 2.0 mmol/L, n = 291). The primary outcome was favorable neurologic discharge (FND), defined as discharge with a Cerebral Performance Category score of 1 or 2. The persistent lactate elevation group had a higher SOFA score (9.8 ± 3.2 vs. 8.5 ± 3.4, p < 0.001) and initial serum lactate (7.9 ± 4.8 mmol/L vs. 6.0 ± 4.3 mmol/L, p < 0.001). Lactate normalization was associated with a higher rate of FND (71.4% vs. 41.9%, p < 0.001), remained an independent predictor of FND (odds ratio [OR]: 3.12, 95% confidence interval [CI]: 2.21-4.41, p < 0.001), and was associated with lower risks of all-cause death (hazard ratio [HR]: 0.49, 95% CI: 0.38-0.64, p < 0.001) at 12 months. In conclusion, lactate normalization within 48 hours of ECMO initiation is associated with favorable neurologic status and 12 month survival.
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Enhanced Early Risk Stratification in Cardiogenic Shock Using Machine Learning: A Hierarchical Clustering Analysis.
Clinical takeaway Early clinical phenotypes may provide additional mortality stratification within SCAI stages in cardiogenic shock. These retrospective findings support further validation, not established clinical use.
Summary & abstract
Study summary
This multicenter retrospective registry included 2,906 adults with cardiogenic shock admitted to ICUs between 2016 and 2022. Hierarchical clustering was applied independently to clinical variables from ICU days 1, 2, and 3. Day-1 Cardiac, Cardio-Renal, and Cardio-Metabolic phenotypes had reported mortality of 15%, 27%, and 55%, respectively. Similar phenotypes persisted through days 2 and 3, and phenotype classification enhanced mortality stratification within each SCAI stage across the first three ICU days. The authors concluded that prospective validation is required before clinical implementation.
Study limitation: The retrospective design limits inference; the abstract does not specify the mortality timepoint or quantify incremental predictive performance.
Published abstract
BACKGROUND: Cardiogenic shock (CS) exhibits marked clinical heterogeneity, limiting the performance of conventional risk stratification tools like the Society for Cardiovascular Angiography and Interventions (SCAI) staging system. Machine learning (ML) has identified reproducible CS phenotypes that improve risk prediction, but their temporal consistency across the progression of shock remains incompletely described. OBJECTIVES: The purpose of this study was to evaluate the temporal evolution of ML-derived CS phenotypes across the first 3 intensive care unit (ICU) days and determine whether phenotype trajectories enhance mortality stratification beyond SCAI staging. METHODS: In a multicenter retrospective registry of 2,906 adults with CS admitted to ICUs between 2016 and 2022, hierarchical agglomerative clustering was applied independently to clinical variables on ICU days 1, 2, and 3. RESULTS: On day 1, 3 phenotypes emerged: Cardiac (younger, acute myocardial infarction-predominant, preserved renal function; 15% mortality), Cardio-Renal (older, non-acute myocardial infarction-predominant, isolated renal extracardiac impairment, predominantly SCAI A and B on admission; 27% mortality), and Cardio-Metabolic (severe renal and tissue malperfusion, predominantly SCAI D and E on admission; 55% mortality). Similar phenotypes persisted on day 2 and day 3. These ML-derived phenotypes enhanced mortality stratification within each SCAI stage across days 1 to 3. CONCLUSIONS: Hierarchical clustering reproduced previously identified CS phenotypes that were consistent across the first 3 days of ICU stay, providing an enhanced framework for early risk stratification. Prospective validation is required for clinical implementation.
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Sex Differences in Vasopressor De-escalation With Arginine Vasopressin in Mixed Cardiogenic-Vasodilatory Shock Under VA-ECMO.
Clinical takeaway Sex was associated with vasopressor de-escalation after vasopressin initiation in this VA-ECMO cohort. These hypothesis-generating findings do not establish sex-specific treatment effects or a survival benefit.
Summary & abstract
Study summary
A multicentre retrospective cohort assessed sex differences in vasopressor de-escalation after arginine vasopressin initiation in 193 patients with cardiogenic shock supported by VA-ECMO. Successful de-escalation at 48 hours, defined as norepinephrine equivalent dose below 0.25 µg/kg/min, occurred in 32% of women versus 49% of men (p=0.023). Male sex was independently associated with success (adjusted odds ratio 2.08, 95% confidence interval 1.07–4.15). In subgroup findings, excess failure risk was confined to postmenopausal women aged 55 years or older (adjusted odds ratio 2.75, 95% confidence interval 1.32–5.93).
Study limitation: Retrospective associations remain vulnerable to confounding; the menopause subgroup is exploratory, and vasopressor de-escalation is a surrogate endpoint.
Published abstract
BACKGROUNDS: Women with cardiogenic shock (CS) under VA-ECMO face excess mortality, yet the pharmacological basis of this disparity remains poorly understood. Arginine vasopressin (AVP) is increasingly used as a non-adrenergic vasopressor in this setting, but whether sex modifies the hemodynamic response to AVP is unknown. METHODS: In this multicenter retrospective cohort of VA-ECMO-supported CS patients, we assessed whether sex was independently associated with successful vasopressor de-escalation at 48 hours (norepinephrine equivalent dose [NEE] <0.25 µg/kg/min) after AVP initiation. Multivariable logistic regression and linear mixed-effects models were used to evaluate sex differences in treatment response and NEE trajectories over time. RESULTS: Among 193 eligible patients, 32% of women achieved successful de-escalation versus 49% of men (p = 0.023). Male sex was independently associated with treatment success (aOR 2.08, 95% CI 1.07-4.15, p = 0.033). A significant sex-by-time interaction was observed in NEE trajectories (p = 0.041), with divergence emerging at 48 hours (NEE 0.24 vs. 0.01 µg/kg/min, p = 0.008). The excess failure risk was confined to postmenopausal women aged ≥55 years (aOR 2.75, 95% CI 1.32-5.93, p = 0.008). CONCLUSION: Female sex, particularly in a postmenopausal context, was independently associated with impaired vasopressor de-escalation following AVP in CS on VA-ECMO. These hypothesis-generating findings suggest that hormonal status may modulate vascular responsiveness to AVP and support the need for prospective studies incorporating hormonal profiling.
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Development and Validation of an Adult Medical Urgency Score for US Donor Heart Allocation.
Clinical takeaway The score improved short-term risk stratification and simulated prioritization of higher-risk transplant candidates. Whether implementation improves patient outcomes remains unestablished.
Summary & abstract
Study summary
This US registry study developed and validated a heart transplant urgency score estimating 6-week mortality without transplant in adult candidates. The score incorporated five laboratory values and four therapeutic devices, including mechanical circulatory support. In test data, mean discrimination was higher than the current six-status system (AUC 0.807 versus 0.693). In allocation simulations, observed 6-week transplant-censored mortality among first-ranked candidates was 15.7% (95% CI, 13.9%-17.6%) with score-based allocation versus 11.2% (95% CI, 10.1%-12.5%) under the current system, indicating prioritization of higher-risk candidates rather than a demonstrated survival benefit.
Study limitation: Registry-based prediction and simulated allocation do not establish the effects of implementing this policy on survival.
Published abstract
IMPORTANCE: One in 5 heart transplant candidates in the US die or are delisted without transplant. Donor hearts are currently allocated by a 6-status therapy-based system criticized for limited risk stratification and susceptibility to gaming. OBJECTIVE: To develop a new heart allocation policy based on an objective medical urgency score that ranks candidates based on the interaction between physiology and mechanical circulatory support. DESIGN, SETTING, AND PARTICIPANTS: Registry-based observational study using data from the US organ transplant system. All adult (aged ≥18 years) heart transplant candidates from January 2019 to August 2025 were included, split into training (2019-2023), validation (2023-2024), and test (2024-2025) datasets. MAIN OUTCOMES AND MEASURES: A marginal structural model of 6-week mortality without transplant was estimated (the US Candidate Risk Score [US-CRS]). Eight models were compared in held-out data by weighted time-dependent area under the curve (AUC) and calibration by status. Finally, US-CRS was converted into an allocation policy and a match-run simulation of waitlist reordering was performed compared with the current 6-status system. RESULTS: Adult heart transplant candidates were partitioned into consecutive training (n = 21 859), validation (n = 7897), and test (n = 8256) datasets (mean [SD] age, 53 [13] years; 74% male). The chosen US-CRS model included 5 laboratory values and 4 therapeutic devices (durable left ventricular assist device, intra-aortic balloon pump, microaxial flow pump, and advanced mechanical circulatory support). In test-set cross-sections of candidates actively waiting on the same calendar date, US-CRS had similar or significantly higher time-dependent AUC than the current 6-status system (mean AUC, 0.807 vs 0.693, respectively) and acceptable calibration by status, especially for candidates who received their status by exception. In match-run analysis (n = 45 530 donor hearts), a US-CRS-based system led to 67% of transplant recipients moving down in rank order and increased observed 6-week transplant-censored mortality for the first candidate on the match run from 11.2% (95% CI, 10.1%-12.5%) under the current system to 15.7% (95% CI, 13.9%-17.6%) under the US-CRS-based system. CONCLUSIONS AND RELEVANCE: In this registry-based study of US heart transplant candidates, a US-CRS-based allocation system prioritized sicker candidates with higher mortality without transplant compared with the current medical urgency statuses.
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Clinical Validation of the Nursing Diagnosis "Risk for Shock" in Patients with Acute Myocardial Infarction Admitted to the ICU.
Clinical takeaway These findings identify bedside indicators associated with cardiogenic shock in ICU patients with myocardial infarction. They do not establish prospective prediction of deterioration or improved outcomes from indicator-guided monitoring.
Summary & abstract
Study summary
This Brazilian retrospective case-control study evaluated nursing indicators in 116 adult ICU patients with acute myocardial infarction, including 58 with cardiogenic shock and 58 without. Unstable blood pressure had 85.0% sensitivity (95% CI 76.2–93.8) and 83.6% specificity (95% CI 74.4–92.8) for distinguishing the groups. In adjusted analysis, unstable blood pressure was associated with shock (adjusted odds ratio 7.80; 95% CI 3.10–19.60), alongside hypoxia, hypoxemia, and inadequate fluid volume. Thermal and hemorrhagic indicators were no longer significant after adjustment.
Study limitation: The single-centre retrospective case-control design does not establish whether these indicators preceded shock or predict future deterioration.
Published abstract
ObjectiveTo clinically validate the nursing diagnosis "Risk for shock" in patients with acute myocardial infarction (AMI) admitted to an Intensive Care Unit (ICU).MethodA retrospective case-control study conducted at a high-complexity university hospital in Brazil. The sample consisted of 116 medical records of adult patients with AMI, equally distributed between the case group (with cardiogenic shock; n = 58) and the control group (without cardiogenic shock; n = 58). Diagnostic accuracy measures (sensitivity, specificity, predictive values, and likelihood ratios) were calculated, and multivariate binary logistic regression using the Stepwise Forward method was applied to identify independent predictors and control for confounders.ResultsIn the accuracy analysis, the indicator "Unstable blood pressure" showed the best clinical balance, with a sensitivity of 85.0% (95% CI: 76.2-93.8) and a specificity of 83.6% (95% CI: 74.4-92.8). "Hyperthermia" and "Inadequate fluid volume" showed the highest individual specificities (90.1% and 80.3%, respectively). After adjusting the logistic regression model (Nagelkerke R2 = 0.614; Hosmer-Lemeshow p = 0.782), only four factors remained significant as independent predictors of the outcome: unstable blood pressure (aOR = 7.80; 95% CI: 3.10-19.60; p < 0.001), hypoxia (aOR = 3.70; 95% CI: 1.50-9.20; p = 0.006), hypoxemia (aOR = 2.90; 95% CI: 1.40-6.10; p = 0.004), and inadequate fluid volume (aOR = 2.10; 95% CI: 1.00-4.50; p = 0.048). Thermal and hemorrhagic indicators lost significance after adjustment.ConclusionThe study clinically validated the diagnosis and confirmed a robust predictive model composed of four indicators. Prioritizing the monitoring of these risk factors enables critical care nurses to anticipate hemodynamic collapse, support targeted care protocols, and optimize multiprofessional decision-making at the bedside.
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Acute Effects of Impella 5.5 on Biventricular Filling and Pressure-Volume Area in Patients With Heart Failure Associated Cardiogenic Shock.
Clinical takeaway This small study documents acute haemodynamic changes after Impella 5.5 activation in refractory heart failure-associated shock. These physiological findings do not establish patient-centred benefit.
Summary & abstract
Study summary
Nine patients with medically refractory decompensated heart failure-associated cardiogenic shock underwent Impella 5.5 placement with invasive biventricular pressure-volume assessment. Acutely after activation, cardiac output increased from 3.4 ± 0.5 to 5.0 ± 0.7 L/min versus baseline (p = 0.0011). Left ventricular end-diastolic pressure decreased from 24.1 ± 6.7 to 16.8 ± 5.4 mm Hg (p = 0.0027), alongside reductions in end-diastolic volume and pressure-volume area. Right ventricular end-diastolic and end-systolic pressures and pressure-volume area also decreased, suggesting acute biventricular physiological effects of left ventricular unloading.
Study limitation: Only nine patients were studied using acute before-and-after measurements, without a separate control group or reported patient-centred outcomes.
Published abstract
Use of Impella 5.5 in patients with decompensated heart failure-associated cardiogenic shock (ADHF-CS) is increasing as a bridge to advanced therapies. The effects of maximal trans-valvular unloading on biventricular filling and pressure-volume area (PVA) in ADHF-CS are poorly understood. Nine patients with medically refractory ADHF-CS underwent Impella 5.5 placement with simultaneous invasive arterial, venous, and biventricular pressure-volume loop analysis. Acutely after Impella 5.5 activation, cardiac output (3.4 ± 0.5 vs. 5.0 ± 0.7 L/min, p = 0.0011), diastolic (67.2 ± 8.0 vs. 80.7 ± 9.7 mm Hg, p = 0.0044) and mean arterial pressures (77.9 ± 7.1 vs. 86.9 ± 10.4 mm Hg, p = 0.029) increased, compared to baseline. Left ventricular end-diastolic pressure (24.1 ± 6.7 vs. 16.8 ± 5.4 mm Hg, p = 0.0027), volume (262.1 ± 103.9 vs. 231.5 ± 104.3 ml, p = 0.0036), and PVA (21,913 ± 7,055 vs. 18,357 ± 7,758 mmHg·ml, p = 0.013) decreased. Right ventricular end-diastolic (12.4 ± 4.6 vs. 9.1 ± 3.8 mm Hg, p = 3.8E-5) and end-systolic pressure (42.1 ± 11.9 vs. 34.4 ± 11.1 mm Hg, p = 0.030) and PVA (6,303 ± 3,851 vs. 4,437 ± 2,473 mm Hg·ml, p = 0.027) also decreased. These findings suggest that maximal left ventricular unloading can acutely reduce biventricular filling pressures and PVA in patients with ADHF-CS.
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Neurologic complications in venoarterial versus venovenous extracorporeal membrane oxygenation: A propensity score-matched retrospective cohort study.
Clinical takeaway VA ECMO recipients had greater observed ischemic and hypoxic-ischemic neurologic burden than matched VV recipients. These associations do not establish that ECMO configuration caused the differences.
Summary & abstract
Study summary
This retrospective TriNetX study compared 30-day neurologic outcomes in adults receiving VA versus VV ECMO during 2015–2024, with 6,944 patients per group after propensity matching. Cerebral infarction occurred in 7.04% versus 5.13%, respectively (OR 1.40, 95% CI 1.22–1.61). VA ECMO was also associated with higher odds of seizures, hypoxic-ischemic encephalopathy and brain death; hemorrhagic stroke showed no statistically clear difference (OR 0.83, 95% CI 0.66–1.04). The authors emphasized that hypoxic-ischemic endpoints could not be separated from the indication for VA support and reflected burden rather than modality effect.
Study limitation: Retrospective propensity matching cannot separate hypoxic-ischemic outcomes from the indication for VA support or establish a causal modality effect.
Published abstract
BACKGROUND: Neurologic complications are among the most devastating events associated with extracorporeal membrane oxygenation (ECMO), yet propensity-balanced comparisons of mode-specific neurologic risk between venoarterial (VA) and venovenous (VV) configurations remain limited. OBJECTIVES: To compare the 30-day incidence of five discrete neurologic outcomes: ischemic stroke, hemorrhagic stroke, seizures, hypoxic-ischemic encephalopathy (HIE), and brain death, between adult VA and VV ECMO patients. METHODS: In this retrospective cohort study using the TriNetX federated network, adults undergoing VA or VV ECMO (2015-2024) were identified by ICD-10-PCS codes and 1:1 propensity score matched on demographics, comorbidities, and antithrombotic exposures. Odds ratios (OR), risk ratios, and hazard ratios (HR) with 95% confidence intervals (CI) were estimated within 30 days; multivariable Cox regression was performed for each outcome. RESULTS: After matching (6944 per cohort), VA ECMO was associated with higher 30-day rates of cerebral infarction (7.04%vs 5.13%; OR 1.40, 95% CI 1.22-1.61), seizures (OR 1.15, 1.002-1.324), HIE (OR 2.17, 1.82-2.58), and brain death (OR 2.63, 1.67-4.14). Hemorrhagic stroke did not differ (OR 0.83, 0.66-1.04). Cox models concordantly showed higher hazard for all outcomes except hemorrhagic stroke (brain death adjusted HR 2.37, 1.58-3.57); heparin exposure was associated with lower hazard of cerebral infarction and HIE. CONCLUSION: VA ECMO was associated with higher 30-day ischemic and hypoxic-ischemic neurologic risk than VV ECMO, while hemorrhagic risk did not differ. The hypoxic-ischemic endpoints are not separable from the indication for VA support and reflect burden rather than modality effect. These findings motivate prospective evaluation of mode-specific neurologic surveillance.
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