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• W4387321344 abstract "This study investigates the prognostic impact of known decreased ratio of tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP) and TAPSE in patients with cardiogenic shock (CS). In patients with pulmonary artery hypertension and in critically ill patients, decreased TAPSE and TAPSE/PASP ratio are known to be negative predictors. However, studies regarding the prognostic impact in patients with CS are limited. Consecutive patients with CS from June 2019 to May 2021 treated at a single center were included. Medical history including echocardiographic parameters such as TAPSE and PASP was documented for each patient. The primary endpoint was all-cause mortality at 30 days. Statistical analyses included univariable t test, Spearman's correlation, C-statistics, Kaplan–Meier analyses, and Cox proportional regression analyses. A total of 90 patients with CS and measurement of TAPSE and TAPSE/PASP ratio were included. TAPSE and TAPSE/PASP ratio measured several months before intensive care unit admission were both able to predict 30-day survival in CS patients, and were both lower in 30-day nonsurvivors. TAPSE/PASP ratio <0.4 mm/mmHg (log-rank p = 0.006) and TAPSE <18 mm (log-rank p = 0.004) were associated with increased risk of 30-day all-cause mortality. After multivariable adjustment, TAPSE/PASP ratio <0.4 mm/mmHg was not able to predict 30-day all-cause mortality, whereas TAPSE <18 mm was still significantly associated with the primary endpoint (hazard ratio 2.336, confidence interval 1.067 to 5.115, p = 0.034). In consecutive patients presenting with CS, compared to TAPSE alone, previously determined TAPSE/PASP ratio did not improve risk prediction for 30-day all-cause mortality. This study investigates the prognostic impact of known decreased ratio of tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP) and TAPSE in patients with cardiogenic shock (CS). In patients with pulmonary artery hypertension and in critically ill patients, decreased TAPSE and TAPSE/PASP ratio are known to be negative predictors. However, studies regarding the prognostic impact in patients with CS are limited. Consecutive patients with CS from June 2019 to May 2021 treated at a single center were included. Medical history including echocardiographic parameters such as TAPSE and PASP was documented for each patient. The primary endpoint was all-cause mortality at 30 days. Statistical analyses included univariable t test, Spearman's correlation, C-statistics, Kaplan–Meier analyses, and Cox proportional regression analyses. A total of 90 patients with CS and measurement of TAPSE and TAPSE/PASP ratio were included. TAPSE and TAPSE/PASP ratio measured several months before intensive care unit admission were both able to predict 30-day survival in CS patients, and were both lower in 30-day nonsurvivors. TAPSE/PASP ratio <0.4 mm/mmHg (log-rank p = 0.006) and TAPSE <18 mm (log-rank p = 0.004) were associated with increased risk of 30-day all-cause mortality. After multivariable adjustment, TAPSE/PASP ratio <0.4 mm/mmHg was not able to predict 30-day all-cause mortality, whereas TAPSE <18 mm was still significantly associated with the primary endpoint (hazard ratio 2.336, confidence interval 1.067 to 5.115, p = 0.034). In consecutive patients presenting with CS, compared to TAPSE alone, previously determined TAPSE/PASP ratio did not improve risk prediction for 30-day all-cause mortality. Cardiogenic shock (CS) is a life-threatening heart condition in which the cardiac output is too low to guarantee end-organ perfusion. Survival of patients with CS is still poor with high mortality rates, and revascularization of the coronary arteries remains the only evidence-based strategy for improving outcomes in patients with CS.1Thiele H Akin I Sandri M Fuernau G de Waha S Meyer-Saraei R Nordbeck P Geisler T Landmesser U Skurk C Fach A Lapp H Piek JJ Noc M Goslar T Felix SB Maier LS Stepinska J Oldroyd K Serpytis P Montalescot G Barthelemy O Huber K Windecker S Savonitto S Torremante P Vrints C Schneider S Desch S Zeymer U CULPRIT-SHOCK InvestigatorsPCI strategies in patients with acute myocardial infarction and cardiogenic shock.N Engl J Med. 2017; 377: 2419-2432Crossref PubMed Scopus (637) Google Scholar, 2Thiele H Ohman EM de Waha-Thiele S Zeymer U Desch S Management of cardiogenic shock complicating myocardial infarction: an update 2019.Eur Heart J. 2019; 40: 2671-2683Crossref PubMed Scopus (316) Google Scholar, 3Aissaoui N Puymirat E Tabone X Charbonnier B Schiele F Lefèvre T Durand E Blanchard D Simon T Cambou JP Danchin N Improved outcome of cardiogenic shock at the acute stage of myocardial infarction: a report from the USIK 1995, USIC 2000, and FAST-MI French nationwide registries.Eur Heart J. 2012; 33: 2535-2543Crossref PubMed Scopus (185) Google Scholar Right ventricular function is crucial in CS.4Kapur NK Esposito ML Bader Y Morine KJ Kiernan MS Pham DT Burkhoff D Mechanical circulatory support devices for acute right ventricular failure.Circulation. 2017; 136: 314-326Crossref PubMed Scopus (188) Google Scholar,5Lala A Guo Y Xu J Esposito M Morine K Karas R Katz SD Hochman JS Burkhoff D Kapur NK Right ventricular dysfunction in acute myocardial infarction complicated by cardiogenic shock: a hemodynamic analysis of the should we emergently revascularize occluded coronaries for cardiogenic shock (SHOCK) trial and registry.J Card Fail. 2018; 24: 148-156Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar Severely increased pulmonary artery pressure can lead to heterometric adjustment, resulting in right ventricle–pulmonary artery uncoupling with increased filling pressures and dilatation of the right ventricle.6Tello K Wan J Dalmer A Vanderpool R Ghofrani HA Naeije R Roller F Mohajerani E Seeger W Herberg U Sommer N Gall H Richter MJ Validation of the tricuspid annular plane systolic excursion/systolic pulmonary artery pressure ratio for the assessment of right ventricular-arterial coupling in severe pulmonary hypertension.Circ Cardiovasc Imaging. 2019; 12e009047Google Scholar,7Vonk Noordegraaf A Westerhof BE Westerhof N The relationship between the right ventricle and its load in pulmonary hypertension.J Am Coll Cardiol. 2017; 69: 236-243Crossref PubMed Scopus (436) Google Scholar It has been shown that the tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP) ratio (TAPSE/PASP) is a noninvasively determined parameter representing right ventricle–pulmonary artery uncoupling in patients with pulmonary arterial hypertension, and a marker of long-term mortality in this population and in patients with heart failure.6Tello K Wan J Dalmer A Vanderpool R Ghofrani HA Naeije R Roller F Mohajerani E Seeger W Herberg U Sommer N Gall H Richter MJ Validation of the tricuspid annular plane systolic excursion/systolic pulmonary artery pressure ratio for the assessment of right ventricular-arterial coupling in severe pulmonary hypertension.Circ Cardiovasc Imaging. 2019; 12e009047Google Scholar,8Schmeisser A Rauwolf T Groscheck T Kropf S Luani B Tanev I Hansen M Meißler S Steendijk P Braun-Dullaeus RC Pressure-volume loop validation of TAPSE/PASP for right ventricular arterial coupling in heart failure with pulmonary hypertension.Eur Heart J Cardiovasc Imaging. 2021; 22: 168-176Crossref PubMed Scopus (33) Google Scholar, 9Guazzi M Bandera F Pelissero G Castelvecchio S Menicanti L Ghio S Temporelli PL Arena R Tricuspid annular plane systolic excursion and pulmonary arterial systolic pressure relationship in heart failure: an index of right ventricular contractile function and prognosis.Am J Physiol Heart Circ Physiol. 2013; 305: H1373-H1381Crossref PubMed Scopus (392) Google Scholar, 10Santas E De la Espriella R Chorro FJ Palau P Miñana G Heredia R Amiguet M Merenciano H Sanchis J Lupón J Bayés-Genís A Núñez J Right ventricular dysfunction staging system for mortality risk stratification in heart failure with preserved ejection fraction.J Clin Med. 2020; 9: 831Crossref Google Scholar, 11Gorter TM van Veldhuisen DJ Voors AA Hummel YM Lam CSP Berger RMF van Melle JP Hoendermis ES Right ventricular-vascular coupling in heart failure with preserved ejection fraction and pre- vs. post-capillary pulmonary hypertension.Eur Heart J Cardiovasc Imaging. 2018; 19: 425-432Crossref PubMed Scopus (88) Google Scholar, 12Deaconu S Deaconu A Scarlatescu A Petre I Onciul S Vijiiac A Zamfir D Marascu G Iorgulescu C Radu AD Bogdan S Vatasescu R Ratio between right ventricular longitudinal strain and pulmonary arterial systolic pressure: novel prognostic parameter in patients undergoing cardiac resynchronization therapy.J Clin Med. 2021; 10: 2442Crossref Scopus (7) Google Scholar Reduced TAPSE has been associated with increased short- and long-term mortality in patients presenting with ST-segment elevation myocardial infarction (STEMI) and CS.13Radwan H Hussein EM Refaat H Short- and long-term prognostic value of right ventricular function in patients with first acute ST elevation myocardial infarction treated by primary angioplasty.Echocardiography. 2021; 38: 249-260Crossref PubMed Scopus (5) Google Scholar,14Engström AE Vis MM Bouma BJ van den Brink RB Baan Jr, J Claessen BE Kikkert WJ Sjauw KD Meuwissen M Koch KT de Winter RJ Tijssen JG Piek JJ Henriques JP Right ventricular dysfunction is an independent predictor for mortality in ST-elevation myocardial infarction patients presenting with cardiogenic shock on admission.Eur J Heart Fail. 2010; 12: 276-282Crossref PubMed Scopus (61) Google Scholar Therefore, the present study comparetively investigates the prognostic role of previous measured TAPSE/PASP ratio and TAPSE regarding the risk prediction in patients presenting with CS. This study prospectively included all consecutive patients presenting with CS on admission to the internal intensive care unit (ICU) at the University Medical Centre Mannheim, Germany, from June 2019 to May 2021. All relevant clinical data related to the index event were documented using the electronic hospital information system and the IntelliSpace Critical Care and Anesthesia information system (Philips GmbH Market DACH, Hamburg, Germany) implemented on the ICU, organizing patient data, including admission documents, vital signs, laboratory values, treatment data, and consult notes. Presence of CS, important laboratory data, ICU-related scores, hemodynamic measurements, and ventilation parameters were assessed on the day of admission and on days 2, 3, 4, and 8 thereafter, respectively. Other documented data included baseline characteristics, medical history, length of index hospital stay, data derived from imaging diagnostics, and pharmacologic therapies. Documentation of source data was performed by intensivists and ICU nurses during routine clinical care. The present study was derived from an analysis of the Cardiogenic Shock Registry Mannheim (CARESMA), representing a prospective single-center registry including consecutive patients admitted for acute CS to the internal medicine ICU of the University Medical Centre Mannheim, Germany (ClinicalTrials.gov identifier: NCT02982473). The registry was established according to the principles of the Declaration of Helsinki and was approved by the Medical Ethics Committee II of the Medical Faculty Mannheim, Heidelberg University, Germany. For the present study, all consecutive patients with CS and echocardiographically assessed TAPSE and PASP were included. Risk stratification was performed according to the TAPSE and TAPSE/PASP ratio documented before the day of admission. Patients without previous documentation of TAPSE and PASP before the day of admission and patients with out-of-hospital cardiac arrest without return of spontaneous circulation before admission to the ICU were excluded. No further exclusion criteria were applied. The final cohort comprised 90 patients. Diagnosis of CS was determined according to the current recommendations of the Association for Acute CardioVascular Care of the European Society of Cardiology.15Zeymer U Bueno H Granger CB Hochman J Huber K Lettino M Price S Schiele F Tubaro M Vranckx P Zahger D Thiele H Acute cardiovascular Care Association position statement for the diagnosis and treatment of patients with acute myocardial infarction complicated by cardiogenic shock: A document of the Acute Cardiovascular Care Association of the European Society of Cardiology.Eur Heart J Acute Cardiovasc Care. 2020; 9: 183-197PubMed Google Scholar Accordingly, CS was defined by hypotension (systolic blood pressure <90 mm Hg) for >30 minutes despite adequate filling status or need for vasopressor or inotropic therapy to achieve systolic blood pressure >90 mm Hg. Additionally, signs of end-organ hypoperfusion must be present, such as oliguria with urine output <30 ml/h, altered mental status, cold clammy skin, and increased lactate >2 mmol/L. Cardiac tamponade and pulmonary embolism were classified as CS despite the obstructive mechanism of shock because existing recommendations and guidelines on acute heart failure and CS classify these entities as potential underlying causes for CS.16Ponikowski P Voors AA Anker SD Bueno H Cleland JG Coats AJ Falk V González-Juanatey JR Harjola VP Jankowska EA Jessup M Linde C Nihoyannopoulos P Parissis JT Pieske B Riley JP Rosano GM Ruilope LM Ruschitzka F Rutten FH van der Meer P Authors/Task Force Members; Document Reviewers2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.Eur J Heart Fail. 2016; 18: 891-975Crossref PubMed Google Scholar, 17McDonagh TA Metra M Adamo M Gardner RS Baumbach A Böhm M Burri H Butler J Čelutkienė J Chioncel O Cleland JGF Coats AJS Crespo-Leiro MG Farmakis D Gilard M Heymans S Hoes AW Jaarsma T Jankowska EA Lainscak M Lam CSP Lyon AR McMurray JJV Mebazaa A Mindham R Muneretto C Francesco Piepoli M Price S Rosano GMC Ruschitzka F Kathrine Skibelund A ESC Scientific Document Group2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.Eur Heart J. 2021; 42: 3599-3726Crossref PubMed Scopus (4018) Google Scholar, 18van Diepen S Katz JN Albert NM Henry TD Jacobs AK Kapur NK Kilic A Menon V Ohman EM Sweitzer NK Thiele H Washam JB Cohen MG American Heart Association Council on Clinical Cardiology, Council on Cardiovascular and Stroke Nursing, Council on Quality of Care and Outcomes Research, and Mission: LifelineContemporary management of cardiogenic shock: a scientific statement from the American Heart Association.Circulation. 2017; 136: e232-e268Crossref PubMed Scopus (956) Google Scholar, 19Yancy CW Jessup M Bozkurt B Butler J Jr Casey DE Drazner MH Fonarow GC Geraci SA Horwich T Januzzi JL Johnson MR Kasper EK Levy WC Masoudi FA McBride PE McMurray JJ Mitchell JE Peterson PN Riegel B Sam F Stevenson LW Tang WH Tsai EJ Wilkoff BL American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.J Am Coll Cardiol. 2013; 62: e147-e239Crossref PubMed Scopus (4988) Google Scholar Aortic dissection was defined as CS when aortic valve regurgitation was the leading cause for hemodynamic instability.17McDonagh TA Metra M Adamo M Gardner RS Baumbach A Böhm M Burri H Butler J Čelutkienė J Chioncel O Cleland JGF Coats AJS Crespo-Leiro MG Farmakis D Gilard M Heymans S Hoes AW Jaarsma T Jankowska EA Lainscak M Lam CSP Lyon AR McMurray JJV Mebazaa A Mindham R Muneretto C Francesco Piepoli M Price S Rosano GMC Ruschitzka F Kathrine Skibelund A ESC Scientific Document Group2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.Eur Heart J. 2021; 42: 3599-3726Crossref PubMed Scopus (4018) Google Scholar Arrhythmic causes of CS comprised supraventricular arrhythmias such as atrial fibrillation or flutter, atrial tachycardia and ventricular tachycardia including ventricular fibrillation. TAPSE and PASP were determined in cardiological practice (n = 25) or in the outpatient sector of our institution (n = 48). Furthermore, in 17 cases, the last echocardiography was performed in the inpatient setting before the patients were transferred to the ICU. Transthoracic echocardiographic images were analyzed regarding the assessment of the right ventricle as recommended by the expert consensus document of the European Association of Cardiovascular Imaging.20Galderisi M Cosyns B Edvardsen T Cardim N Delgado V Di Salvo G Donal E Sade LE Ernande L Garbi M Grapsa J Hagendorff A Kamp O Magne J Santoro C Stefanidis A Lancellotti P Popescu B Habib G 2016–2018 EACVI Scientific Documents CommitteeStandardization of adult transthoracic echocardiography reporting in agreement with recent chamber quantification, diastolic function, and heart valve disease recommendations: an expert consensus document of the European Association of Cardiovascular Imaging.Eur Heart J Cardiovasc Imaging. 2017; 18: 1301-1310Crossref PubMed Scopus (369) Google Scholar For the statistical analyses, solely the latest measurement of TAPSE and PASP was included. The median time from echocardiography to ICU admission was 236 days (interquartile range from 118 days to 405 days). All-cause mortality at 30 days was documented using the electronic hospital information system and by directly contacting state resident registration offices (“bureau of mortality statistics”). Identification of patients was verified through name, surname, day of birth, and registered living address. No patient was lost to follow-up with regard to all-cause mortality at 30 days. An overview of the inclusion and exclusion criteria is included in Supplementary Figure 1. Quantitative data is presented as mean ± SEM, median and interquartile range, and ranges depending on the distribution of the data. They were compared using the Student t test for normally distributed data or the Mann–Whitney U test for nonparametric data. Deviations from a Gaussian distribution were tested by the Kolmogorov–Smirnov test. Qualitative data are presented as absolute and relative frequencies and were compared using the chi-square test or Fisher's exact test, as appropriate. Box plots for TAPSE and TAPSE/PASP were created for the comparisons of survivors and nonsurvivors. C-statistics were applied with calculation of receiver operating characteristic curves and the corresponding areas under the curve within the entire cohort to assess the discriminative performance for 30-day all-cause mortality and determine cut-off values for TAPSE and TAPSE/PASP. Furthermore, logistic regression with Hosmer–Lemeshow testing was performed to compare TAPSE and TAPSE/PASP on their accuracy in predicting 30-day survival. Moreover, the Akaike information criterion (AIC) and the Brier score were determined. Kaplan–Meier analyses according to TAPSE <18 mm and TAPSE/PASP <0.4 mm/mmHg were performed within the entire study cohort. Univariable hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox regression. Thereafter, multivariable Cox regression models were developed using the “Enter” option, considering solely clinically relevant variables. Results of all statistical tests were considered significant with p ≤0.05. IBM SPSS Statistics, Version 25.0 (IBM Corp., Armonk, New York) and RStudio, Version 2022.07.0 (Posit PBC, Boston, Massachusetts) were used for statistics. As presented in Table 1, baseline characteristics including measured parameters on admission and medical history were evenly distributed between the survivor and nonsurvivor groups. Solely the respiratory rate (19/min vs 22/min, p = 0.034) and history of stroke (26.8% vs 10.2%, p = 0.040) differed between the groups. Systolic blood pressure on admission was equally low and exceeded 90 mm Hg in both groups as patients were already on vasopressors or dobutamine on admission. Cardiovascular risk factors and medication on admission were not significantly different between survivors and nonsurvivors.Table 1Baseline characteristics of the entire cohort stratified by survival of 30-day follow upAll patients (n=90)Survivor (n=41)Non-survivor (n=49)p valueAge, median; (IQR)78(65-83)79(64-83)76(66-83)0.676Male sex, n (%)49(54.4)23(56.1)26(53.1)0.773Body mass index, kg/m2 (median,(IQR))26.7(24.2-31.2)27.0(24.9-31.2)26.6(24.2-32.4)0.618Parameters on admission, (median, (IQR)) Body temperature (°C)36.3(35.6-36.7)36.4(36.0-36.7)36.2(35.2-36.7)0.221 Heart rate (bpm)83(66-109)82(65-109)83(68-110)0.184 Systolic blood pressure (mmHg)100(84-123)104(85-125)98(79-124)0.343 Respiratory rate (breaths/min)21(16-27)19(15-26)22(18-29)0.034Cardiovascular risk factors, n (%) Arterial hypertension78(86.7)37(90.2)41(83.7)0.361 Diabetes mellitus50(55.6)24(58.5)26(53.1)0.603 Hyperlipidemia57(63.3)25(61.0)32(65.3)0.671 Smoking38(42.2)16(39.0)22(44.9)0.574Prior medical history, n (%) Coronary artery disease52(57.8)32(65.3)20(48.8)0.188 Congestive heart failure69(76.7)32(78.0)37(75.5)0.777 Atrial fibrillation46(51.1)22(53.7)24(49.0)0.658 Chronic kidney disease60(66.7)25(61.0)35(71.4)0.295 Stroke16(17.8)11(26.8)5(10.2)0.040 COPD24(26.7)7(17.1)17(34.7)0.060 Liver cirrhosis4(4.4)2(4.9)2(4.1)0.855Medication on admission, n (%) ACE-inhibitor39(43.3)18(43.9)21(42.9)0.921 ARB24(26.7)11(26.8)13(26.5)0.975 Beta-blocker64(71.1)30(73.2)34(69.4)0.683 ARNI3(3.3)2(4.9)1(2.0)0.455 Aldosterone antagonist25(27.8)10(24.4)15(30.6)0.512 Diuretics63(70.0)28(68.3)35(71.4)0.746 ASA35(38.9)17(41.5)18(36.7)0.647 P2Y12-inhibitor11(12.2)6(14.6)5(10.2)0.523 Statin57(63.3)28(68.3)29(59.2)0.372ACE = angiotensin-converting enzyme; ARB = angiotensin receptor blockers; ARNI = angiotensin receptor neprilysin inhibitor; ASA = acetylsalicylic acid; COPD = chronic obstructive pulmonary disease; CS = cardiogenic shock; INR = international normalized ratio; IQR = interquartile range; MRA = mineralocorticoid receptor antagonist; TR = tricuspid regurgitation.Level of significance p<0.05. Open table in a new tab ACE = angiotensin-converting enzyme; ARB = angiotensin receptor blockers; ARNI = angiotensin receptor neprilysin inhibitor; ASA = acetylsalicylic acid; COPD = chronic obstructive pulmonary disease; CS = cardiogenic shock; INR = international normalized ratio; IQR = interquartile range; MRA = mineralocorticoid receptor antagonist; TR = tricuspid regurgitation. Level of significance p<0.05. As outlined in Table 2, compared with survivors, patients not surviving the 30-days of follow-up were more likely to have had an out-of-hospital or in-hospital cardiac arrest (7.3% vs 26.5% and 7.3% vs 20.04%, respectively, p = 0.005), and had a significantly longer time to return of spontaneous circulation (9 vs 27 minutes, p = 0.016). Furthermore, nonsurvivors more often needed mechanical ventilation (26.8% vs 52.1%, p = 0.016), with longer duration of invasive ventilation (1 vs 2 days, p = 0.038). Causes of CS did not differ between the 2 groups, whereas CS severity according to the Society for Cardiovascular Angiography & Interventions classification differed with more patient at stage E in the nonsurvivors (14.6% vs 46.9%, p = 0.009). Consequently, nonsurvivors were more often on norepinephrine (46.3% vs 79.6%, p = 0.001) with higher median dosage of norepinephrine prescribed on admission (0.0 vs 0.2 µg/kg/min, p = 0.001), lower pH values (7.34 vs 7.25, p = 0.012) and higher lactate levels (2.5 vs 4.6 mmol/L, p = 0.001). Furthermore, creatinine (1.54 vs 1.88 mg/100 ml, p = 0.020), white blood cells (10.68 × 106/ml vs 15.67 × 106/ml, p = 0.005), d-dimer (2.17 vs 11.21 mg/L, p = 0.018), and procalcitonin levels (0.29 vs 0.5 ng/ml, p = 0.034) were higher in nonsurvivors. Regarding cardiac biomarkers, nonsurvivors showed significantly higher levels of troponin I (0.252 vs 0.717 µg/L, p = 0.048), whereas amino-terminal brain natriuretic peptide (NT-proBNP) did not differ between both groups.Table 2Shock-related data, follow-up data and endpointsAll patients (n=90)Survivor (n=41)Non-survivor (n=49)p valueCause of CS, n (%) Acute myocardial infarction25(27.8)11(26.8)14(28.6) Arrhythmic9(10.0)7(17.1)2(4.1) ADHF39(43.3)15(36.6)24(49.0) Pulmonary embolism5(5.6)1(2.4)4(8.2)0.080 Valvular heart disease7(7.8)5(12.2)2(4.1) Cardiomyopathy2(2.2)0(0.0)2(4.1) Pericardial tamponade2(2.2)2(4.9)0(0.0) Aortic dissection1(1.1)0(0.0)1(2.0)SCAI Classification of CS, n (%) Stage A0(0.0)0(0.0)0(0.0)0.009 Stage B1(1.1)1(2.4)0(0.0) Stage C50(55.6)29(70.7)21(42.9) Stage D10(11.1)5(12.2)5(10.2) Stage E29(32.2)6(14.6)23(46.9)Transthoracic echocardiography on admission LVEF >55%, (n, %)13(15.1)8(20.0)5(10.9) LVEF 54-41%, (n, %)10(11.6)6(15.0)4(8.7) LVEF 40-30%, (n, %)16(18.6)9(22.5)7(15.2)0.261 LVEF <30%, (n, %)47(54.7)17(42.5)30(65.2) LVEF not documented, (n, %)4(4.4)1(2.4)3(6.1) Inferior vena cava, cm (median, (IQR))2.0(1.7–2.4)1.9(1.6–2.4)2.1(1.8–2.4)0.428 TAPSE, mm (median, (IQR))14.0(11.0–16.8)13.9(10.5–19.5)14.0(10.8–15.0)0.696Cardiopulmonary resuscitation OHCA, n (%)16(17.8)3(7.3)13(26.5)0.005 IHCA, n (%)13(14.4)3(7.3)10(20.4) Shockable rhythm, n (%)79(88.8)38(92.7)41(85.4)0.279 Non-shockable rhythm, n (%)10(11.2)3(7.3)7(14.6) ROSC, min (median, IQR)14(10–30)9(7–13)27(10–38)0.016Respiratory status Mechanical ventilation, n (%)36(40.4)11(26.8)25(52.1)0.016 Duration of mechanical ventilation, days, (mean, (IQR))1(0–4)1(0–3)2(1–4)0.038 PaO2/FiO2 ratio, (median, (IQR))191(130–354)263(153–364)149(108–321)0.076Coronary status Coronary angiography, n (%)34(37.8)17(41.5)17(34.7)0.435 Time from CS onset to coronary angiography, min (median, IQR)158(79–488)131(84–212)250(79–1374)0.602 Patients with culprit lesion, n (%)17(18.9)6(14.6)11(22.4)0.890Multiple organ support during ICU Norepinephrine on admission, n (%)58(64)19(46.3)39(79.6)0.001 Norepinephrine on admission,µg/kg/min (median, (IQR))0.1(0.0–0.2)0.0(0.0–0.1)0.2(0.1–0.6)0.001 Cumulative dose of dobutamine, mg/kg (median, (IQR))7(2–13)12(2–14)5(1–12)0.621 Levosimendan, n (%)22(24.4)6(14.6)16(32.7)0.048 Mechanical circulatory assist device, n (%)4(4.4)0(0.0)4(8.2)0.061Baseline laboratory values, (median, (IQR)) pH7.30(7.19–7.38)7.34(7.28–7.39)7.25(7.15–7.38)0.012 Lactate (mmol/l)3.2(1.7–6.0)2.5(1.4–3.9)4.6(2.4–10.7)0.001 Potassium (mmol/l)4.5(4.1–5.3)4.4(3.9–5.2)4.5(4.1–5.4)0.536 Creatinine (mg/dl)1.73(1.36–3.27)1.54(1.06–2.62)1.88(1.49–4.18)0.020 Hemoglobin (g/dl)11.3(9.3–13.0)10.7(9.3–12.4)11.6(9.1–13.6)0.537WBC (106/ml)14.46(10.10–18.47)10.68(8.26–16.59)15.67(12.26–21.27)0.005 Platelets (106/ml)221(165–288)224(156–318)217(184–266)0.816 INR1.20(1.10–1.50)1.17(1.08–1.55)1.25(1.12–1.50)0.156 D-dimer (mg/l)5.09(1.71–13.76)2.17(1.48–7.50)11.21(2.67–23.03)0.018 AST (U/l)56(27–168)50(28–112)69(27–459)0.370 ALT (U/l)48(24–98)32(24–76)60(26–368)0.099 Bilirubin (mg/dl)0.71(0.44–1.01)0.64(0.41–0.92)0.81(0.49–1.37)0.369 Troponin I (µg/l)0.441(0.093–2.666)0.252(0.061–1.379)0.717(0.193–3.791)0.048 NT-pro BNP (pg/ml)10282(2954–15074)8299(2603–15349)1148(4311–14262)0.481 Procalcitonin (ng/ml)0.34(0.21–0.99)0.29(0.13–0.40)0.50(0.28–1.94)0.034 CRP (mg/l)28(9–61)27(8–71)29(9–61)0.981Follow up data, n (%) ICU time, days (median, (IQR))3(2–6)4(2–6)3(1–6)0.142 Death ICU, n (%)51(56.7)3(7.3)48(98.0)0.001ALT = alanine aminotransferase; APACHE II = acute physiology and chronic health evaluation II; AST = aspartate aminotransferase; CRP = C-reactive Protein; DIC = disseminated intravascular coagulation; GFR = glomerular filtration rate; ICU = intensive care unit; INR = international normalized ratio; IQR = interquartile range; NT-pro BNP = N-terminal pro-B-type natriuretic peptide; SARS-CoV-2 = severe acute respiratory syndrome coronavirus type 2; SOFA = sepsis-related organ failure assessment score; WBC, white blood cells.Level of significance p<0.05. Bold type indicates statistical significance. Open table in a new tab ALT = alanine aminotransferase; APACHE II = acute physiology and chronic health evaluation II; AST = aspartate aminotransferase; CRP = C-reactive Protein; DIC = disseminated intravascular coagulation; GFR = glomerular filtration rate; ICU = intensive care unit; INR = international normalized ratio; IQR = interquartile range; NT-pro BNP = N-terminal pro-B-type natriuretic peptide; SARS-CoV-2 = severe acute respiratory syndrome coronavirus type 2; SOFA = sepsis-related organ failure assessment score; WBC, white blood cells. Level of significance p<0.05. Bold type indicates statistical significance. Table 3 outlines the correlation of TAPSE and TAPSE/PASP ratio with clinical and laboratory data on day 1. TAPSE inversely correlated with body mass index (r = −0.421, p = 0.012), diameter of the inferior vena cava (r = −0.407, p = 0.029), Acute Physiology score (r = −0.356, p = 0.033), APACHE (Acute Physiology and Chronic Health Evaluation) II score (r = −0.348, p = 0.038), and length of ICU stay (r = −0.363, p = 0.030). TAPSE/PASP ratio inversely correlated with cardiac troponin I (r = −0.251, p = 0.049), NT-proBNP levels (r = −0.355, p = 0.024), and echocardiographic parameters such as left ventricular ejection fraction (LVEF) (r = −0.255, p = 0.037) and the degree of tricuspid regurgitation (r = −0.622, p = 0.001). In contrast, TAPSE/PASP ratio correlated directly with albumin levels (r = 0.243, p = 0.035).Table 3Univariable correlations of TAPSE and TAPSE / PASP measured prior to ICU admission with laboratory and clinical parameters in all patients (n = 90) at day 1TAPSETAPSE/PASPrp valuerp valueAge−0.1340.437−0.1460.171BMI−0.4210." @default.
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• W4387321344 title "Outcome of Patients With Cardiogenic Shock and Previous Right Ventricular Impairment Represented by Decreased Tricuspid Annular Plane Systolic Excursion and Tricuspid Annular Plane Systolic Excursion to Pulmonary Artery Systolic Pressure Ratio" @default.
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