Impella malrotation affects left ventricle unloading in cardiogenic shock patients.

AIMS: Impella malrotation-inlet orientation away from the left ventricular (LV) apex with normal console waveforms and proper device depth-is commonly observed and possibly associated worse haemodynamics. This study aimed to characterize the haemodynamic consequences of Impella malrotation in cardiogenic shock (CS) patients. METHODS AND RESULTS: We included 100 CS patients (60 ± 12 years; 79.0% males) with available echocardiography during Impella support and pulmonary artery catheter assessment before and during (at 48 h) Impella support. Impella malrotation was identified in 36%. At 48 h, malrotation patients had higher pulmonary artery wedge pressure (PAWP, 16.0 ± 8.2 vs. 13.0 ± 4.6 mmHg; P = 0.033), higher systolic pulmonary artery pressure (PAP, 35.0 ± 11.3 vs. 29.5 ± 9.0 mmHg; P = 0.015), higher diastolic-PAP (19.3 ± 8.1 vs. 15.1 ± 6.1 mmHg; P = 0.007), higher mean-PAP (25.7 ± 9.1 vs. 20.8 ± 6.8 mmHg; P = 0.005), higher right atrial pressure (10.3 ± 4.8 vs. 7.7 ± 4.3 mmHg; P = 0.009), higher pulmonary vascular resistance index (4.78 ± 2.75 vs. 3.49 ± 1.94 WUm2; P = 0.020) and higher pulmonary artery elastance (0.91 ± 0.60 vs. 0.67 ± 0.40 mmHg/mL; P = 0.045). Serum lactate at 48 h was higher in malrotation patients (6.63 ± 6.25 vs. 3.60 ± 4.21 mmol/L; P = 0.004). Malrotation patients presented larger LVEDD during support (52 ± 10 vs. 46 ± 11 mm; P = 0.006), higher rates of aortic regurgitation (AR, 86 vs. 56%; P = 0.004) and higher increase in AR severity (+0.94 ± 0.92 vs. + 0.46 ± 0.95; P = 0.016). No significant differences were found in major adverse outcomes. CONCLUSIONS: In CS patients, Impella malrotation is associated with suboptimal unloading of the LV, worse pulmonary haemodynamics and worse indexes of right ventricular afterload.

Haptoglobin Administration for Intravascular Hemolysis: A Systematic Review.

INTRODUCTION: Exogenous haptoglobin administration may enhance plasma-free hemoglobin (pfHb) clearance during hemolysis and reduce its end-organ damage: we systematically reviewed and summarized available evidence on the use of haptoglobin as a treatment for hemolysis of any cause. METHODS: We included studies describing haptoglobin administration as treatment or prevention of hemolysis-related complications. Only studies with a control group reporting at least one of the outcomes of interest were included in the quantitative synthesis. Primary outcome was the change in pfHb concentration 1 h after haptoglobin infusion. RESULTS: Among 573 articles, 13 studies were included in the review (677 patients, 52.8% received haptoglobin). Median initial haptoglobin intravenous bolus was 4,000 (2,000, 4,000) IU. Haptoglobin was associated with lower pfHb 1 h (SMD -11.28; 95% CI: -15.80 to -6.75; p < 0.001) and 24 h (SMD -2.65; 95% CI: -4.73 to -0.57; p = 0.001) after infusion. There was no difference in all-cause mortality between haptoglobin-treated patients and control group (OR 1.41; 95% CI: 0.49-4.95; p = 0.520). Haptoglobin was associated with a lower incidence of acute kidney injury (OR 0.64; 95% CI: 0.44-0.93; p = 0.020). No adverse events or side effects associated with haptoglobin use were reported. CONCLUSIONS: Haptoglobin administration has been used in patients with hemolysis from any cause to treat or prevent hemolysis-associated adverse events. Haptoglobin may reduce levels of pfHb and preserve kidney function without increase in adverse events.

Mixed Shock Complicating Cardiogenic Shock: Frequency, Predictors, and Clinical Outcomes.

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]; Padj=0.006), age (OR, 1.06 [95% CI, 1.03-1.10] years; Padj<0.001), admission systolic arterial pressure <100 mm Hg (OR, 2.41 [95% CI, 1.19-4.98]; Padj=0.016), and admission serum creatinine (OR, 1.61 [95% CI, 1.19-2.26]; Padj=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]; Padj=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.

Pulmonary artery elastance as a predictor of hospital mortality in heart failure cardiogenic shock.

AIMS: The initial bundle of cares strongly affects haemodynamics and outcomes in acute decompensated heart failure cardiogenic shock (ADHF-CS). We sought to characterize whether 24 h haemodynamic profiling provides superior prognostic information as compared with admission assessment and which haemodynamic parameters best predict in-hospital death. METHODS AND RESULTS: All patients with ADHF-CS and with available admission and 24 h invasive haemodynamic assessment from two academic institutions were considered for this study. The primary endpoint was in-hospital death. Regression analyses were run to identify relevant predictors of study outcome. We included 127 ADHF-CS patients [65 (inter-quartile range 52-72) years, 25.2% female]. Overall, in-hospital mortality occurred in 26.8%. Non-survivors were older, with greater CS severity. Among admission variables, age [odds ratio (OR) = 1.06; 95% confidence interval (CI): 1.02-1.11; Padj = 0.005] and CPIRAP (OR = 0.62 for 0.1 increment; 95% CI: 0.39-0.95; Padj = 0.034) were found significantly associated with in-hospital death. Among 24 h haemodynamic univariate predictors of in-hospital death, pulmonary elastance (PaE) was the strongest (area under the curve of 0.77; 95% CI: 0.68-0.86). PaE (OR = 5.98; 95% CI: 2.29-17.48; Padj < 0.001), pulmonary artery pulsatility index (PAPi, OR = 0.77; 95% CI: 0.62-0.92; Padj = 0.013) and age (OR = 1.06; 95% CI: 1.02-1.11; Padj = 0.010) were independently associated with in-hospital death. Best cut-off for PaE was 0.85 mmHg/mL and for PAPi was 2.95; cohort phenotyping based on these PaE and PAPi thresholds further increased in-hospital death risk stratification; patients with 24 h high PaE and low PAPi exhibited the highest in-hospital mortality (56.2%). CONCLUSIONS: Pulmonary artery elastance has been found to be the most powerful 24 h haemodynamic predictor of in-hospital death in patients with ADHF-CS. Age, 24 h PaE, and PAPi are independently associated with hospital mortality. PaE captures ventricular (RV) afterload mismatch and PAPi provides a metric of RV adaptation, thus their combination generates four distinct haemodynamic phenotypes, enhancing in-hospital death risk stratification.

Cat Scratch Endocarditis.

We reported a case of blood culture-negative infective endocarditis on a native valve, where the clinical presentation was exclusively related to extensive cerebral ischemia secondary to multiple systemic septic cardioembolic events. The cause was ascribed to subacute Bartonella henselae infection, presumably transmitted by cat scratch, documented by positive serologic findings.

A simplified echocardiographic formula to estimate cardiac index in the intensive care unit.

BACKGROUND AND AIM: Measurement of cardiac index (CI) is crucial in the hemodynamic assessment of critically ill patients in the intensive care unit (ICU). The most reliable trans-thoracic echocardiography (TTE) technique for CI estimation is the left ventricular outflow tract (LVOT) Doppler method that requires, among other parameters, the LVOT cross-sectional area (CSA) measurement. However, inherent and practical disadvantages, mostly related to the ICU setting, hamper LVOT-CSA assessment. In this study, we aimed to validate a simplified formula, leveraging on LVOT-velocity time integral (VTI) and heart rate (HR) only, for non-invasive estimation of CI in ICU patients. METHODS AND RESULTS: We prospectively enrolled 50 consecutive patients admitted to our ICU requiring pulmonary artery catheterization (PAC) over a one-year period. For each patient we measured the CI by PAC (CIPAC) and TTE. The latter was obtained both with the "traditional formula" (traditional CITTE), requiring LVOT-CSA assessment, and our new "simplified formula" (simplified CITTE). The correlation between the simplified CITTE and CIPAC was strong (r = 0.81) and resulted significantly greater than the traditional CITTE and CIPAC correlation (r = 0.70; p < 0.05 for Pearson r coefficients comparison). Both TTE-based CI showed an acceptable agreement (+0.19 ± 0.48 L/min/m2 for simplified CITTE and - 0.18 ± 0.58 L/min/m2 for traditional CITTE) with the reference CIPAC. CONCLUSION: In this study, we validated a practical approach, leveraging on TTE LVOT-VTI and HR only, for non-invasive estimation of CI in ICU patients.