BACKGROUND:The admission systolic blood pressure (SBP) recorded at the emergency department is typically elevated and tends to decrease, while various degrees of blood pressure variability (BPV) remain. Whether admission SBP or mean SBP and BPV from resting beat-to-beat measurements are better associated with short-term outcome remains unknown. METHODS:We conducted a prospective study, including adults acutely admitted to the emergency department at a larger Danish tertiary care Hospital in Copenhagen, Denmark from 2019 to 2023. We measured blood pressure (BP) at admission and beat-to-beat BP and BPV during 10-minute rest. We defined BPV as the standard deviation from the mean of the beat-to-beat SBP measurements. Primary outcome was defined as 3-month all-cause mortality or readmission, and secondary outcome as 3-month cardiovascular mortality or readmission for cardiovascular disease. RESULTS:Among 951 patients included, mean age was 64 (standard deviation; 17) with 44% women. During 3-month follow-up, 284 (30%) patients met a primary outcome and 69 (7,2%) a secondary outcome. In adjusted Cox models, admission SBP, but neither mean SBP or BPV, was significantly associated with primary outcome [hazard ratio 0.971, 95% confidence interval (CI) 0.948-0.995, P  = 0.017] for each 5 mmHg increase in SBP. When exploring both extremes of upper and lower quartiles, BPV greater than 10 mmHg was associated with increased cardiovascular events (hazard ratio 2.019, 95% CI 1.142-3.569, P  = 0.016). CONCLUSION:In this study, low admission SBP was associated with all-cause readmissions and mortality, while BPV above 10 mmHg was associated with 3-month risk of cardiovascular events.

AIMS:Current guidelines recommend serial echocardiography at minimum 1-2-year intervals for monitoring patients with non-severe aortic valve stenosis (AS), which is costly and often clinically inconsequential. We aimed to develop and test whether the biomarker-based ASGARD (Aortic valve Stenosis Guarded by Amplified Risk Determination) risk score can guide the timing of echocardiograms in asymptomatic patients with non-severe AS. METHODS AND RESULTS:The development cohort comprised 1093 of 1589 (69%) asymptomatic patients with mild-to-moderate AS who remained event-free one year after inclusion into the SEAS trial. Cox regression landmark analyses with a 2-year follow-up identified the model (ASGARD) with the lowest Akaike information criterion for association to AS-related composite outcome (heart failure hospitalization, aortic valve replacement, or cardiovascular death). Fine-Gray analyses provided cumulative event rates by ASGARD score quartiles. The ASGARD score was internally validated in the remaining 496 patients (31%) from the SEAS cohort and externally in 71 asymptomatic outpatients with non-severe AS from six Copenhagen hospitals. The ASGARD score comprises updated measurements of heart rate and age- and sex-adjusted N-terminal pro-brain natriuretic peptide upon transaortic maximal velocity (Vmax) from the previous year. The ASGARD score had high predictive accuracy across all cohorts (external validation: area under the curve: 0.74 [95% CI, 0.62-0.86]), and similar to an updated Vmax measurement. An ASGARD score ≤ 50% was associated with AS-related event rates ≤ 5% for a minimum of 15 months. CONCLUSION:The ASGARD score could provide a personalized and safe surveillance alternative to routinely planned echocardiograms, so physicians can prioritize echocardiograms for high-risk patients.

Abstract Background Inflammation plays a pivotal role in the pathogenesis of aortic valve stenosis (AS) through cytokine-mediated valve calcification. Studies of explanted valves found associations of an elevated pro-inflammatory cytokine, Interleukin 6 (IL-6), with increased postoperative mortality. However, limited knowledge exists regarding the prognostic value of elevated circulating IL-6 in asymptomatic patients with nonsevere AS. Purpose To investigate the hypothesis that elevated plasma IL-6 concentration ≥7 pg/mL (above the upper limit of normal 95th percentile) correlates with more severe AS and a higher risk of adverse outcomes in asymptomatic patients with nonsevere AS. Methods We analyzed data of 1574 asymptomatic patients who had mild-to-moderate AS, preserved systolic and kidney function, no overt cardiovascular diseases, and an event-free follow-up one year after enrollment in the randomized Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial. We ascertained the correlation of year-0 and year-1 IL-6 levels with echocardiographic AS severity, defined as moderate-severe AS in the presence of ≥2 measurements at year-0: aortic valve area <1 cm², mean pressure gradient ≥40 mmHg, maximal transaortic velocity ≥4 m/s, and velocity ratio <0.25. Multivariable regression examined correlations between IL-6 at year-0 and clinical variables. Cox proportional hazard models and competing risk analyses examined associations of elevated IL-6 at year-1 and 4-year risk of the primary composite endpoint of major cardiovascular events (MACE) comprising the first event of cardiovascular death, aortic valve replacement, hospitalization with heart failure, myocardial infarction, percutaneous coronary intervention, coronary artery bypass graft, or ischemic stroke. Results At year-0, among 1574 patients with a mean (SD) age of 67.5 (9.7) years, 629 (40.0%) were women, 263 (16.7%) had moderate-severe AS, and 194 (12.3%) had elevated IL-6. The median relative IL-6 change from year-0 to year-1 was 1.0 (IQR, 0.8-1.4) across AS-severity groups (P=0.12) (Figure 1). In adjusted models, IL-6 at year-0 did not correlate with AS-severity (P=0.30). In mild AS, an elevated IL-6 at year-1 was associated with an increased 4-year MACE risk (HR 1.40; 95% CI, 1.02-1.92; p=0.04) in adjusted Cox regression analyses (Figure 2A). In sensitivity analyses, the annual IL-6 increase >50% combined with normal IL-6 was associated with an increased 4-year MACE-risk of HR 1.48 (95% CI, 1.10-2.00; P=0.009) in patients with mild AS and 1.82 (95% CI, 0.68-1.74; P=0.73) in patients with moderate-severe AS (all P for interaction>0.25) (Figure 2C-D). Conclusion In asymptomatic patients with nonsevere AS, circulating IL-6 remains stable within the reference range in 7 out of 8 patients during a 1-year follow-up, regardless of AS severity. An elevated IL-6 was associated with a 1.4-fold increased 4-year MACE-risk in patients with mild AS, suggesting its possible role as an early risk marker.Figure 1Figure 2

Abstract Background The recommended standard monitoring of patients with non-severe aortic valve stenosis (AS) involves echocardiography surveillance at 1-2 year intervals. Since many of these costly routine echocardiograms yield no clinical consequences during a prolonged watchful waiting period, we propose to replace them with a risk stratification approach. Purpose The primary aim was to validate the ability of ASGARD risk score to a) identify low-risk AS patients who do not need new echocardiography for safe monitoring, and b) estimate optimal follow-up intervals. Methods We have developed the ASGARD risk score using data from 1196/1739 (69%) asymptomatic AS-patients with mild-to-moderate AS who were enrolled in the randomized, multicentre Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial. The primary outcome was a composite of AS-related outcomes, aortic valve replacement, or hospitalization with heart failure during a clinically relevant 2-year follow-up. From multivariable Cox proportional hazards regression analyses, we chose the best prognostic model with the lowest Akaike information criterion (AIC) values and p-values <0.05. The risk score included five predictors: age, sex, systolic blood pressure, N-terminal pro-brain natriuretic peptide (NT-proBNP), and last year's measurement of transaortic maximal velocity (Vmax). Kaplan-Meier plot visualized event rates stratified by quartiles of risk score. We validated the ASGARD risk score in an internal validation cohort of 543 patients (31% hold-out from SEAS-population) and an external validation cohort of 69 asymptomatic out-clinic patients with Vmax ≤4 m/s from six hospitals from capital city. Results Patients from the external validation cohort significantly differed from those in the development cohort in terms of higher age (mean [SD], 71.7 [8.5] vs. 67.4 [9.8] years, p<0.001), less prevalent left ventricular hypertrophy (13.0% vs. 37.5%, p<0.001), and higher event-rates (12.5 [95% CI, 7.6-20.8] vs. 4.5 [3.7-5.4] events per 100 patient-years of follow-up, p<0.001). The ASGARD risk score showed consistent predictive performance across the validation cohorts (external validation: area under the curve: 0.82 [95% CI, 0.73-0.91]; calibration-in-the-large, p=0.24; calibration slope, p=0.15; Brier score, 0.18). The score performed just as well or better than a new Vmax measurement (Figure 1A-1B). In the three upper ASGARD score quartiles, 95% of patients had less than 5% risk of AVR or heart failure until 7.5, 16.5, and 22.5 months, respectively (Figure 1C). Conclusion Without a new echocardiogram, the ASGARD risk score identifies patients at low risk for AS-related events among asymptomatic patients with non-severe AS. The ASGARD risk score also estimates the safe watchful-waiting period of 6, 15, 21, and 24 months for the four ASGARD risk score quartiles in decreasing order.Figure 1

Abstract Background Routine echocardiography of asymptomatic patients with non-severe aortic valve stenosis (AS) mainly focuses on the valve condition at 1-2 year intervals but has limited ability to predict the risk of other cardiovascular comorbidities. Thus, there is a compelling need to replace routine echocardiography for low-risk patients with more individualized cardiovascular surveillance for a safe period. Aim First, to develop and validate separate risk stratification models for AS-related events (AVE) and major cardiovascular events (MCE) to identify low-risk AS patients who can safely postpone routine echocardiography replaced by tailored risk stratification and adequate risk factor management. Second, to estimate optimal follow-up intervals according to risk stratification for each outcome. Methods We analyzed serial measurements from 69% of 1579 patients with mild-to-moderate AS who were asymptomatic and event-free one year after inclusion in the randomized, multicenter Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial. We developed two ASGARD risk scores using multivariable Cox proportional hazard regression analyses, designed as landmark analyses starting at year-1 and with a clinically relevant 2-year follow-up. The ASGARD scores estimated the risk of AVE (composite of aortic valve replacement or hospitalization with heart failure) and MCE (composite of myocardial infarction, percutaneous coronary intervention, coronary artery bypass graft, stroke, and all-cause mortality). We estimated the prognostic models with backward elimination, selecting the lowest Akaike information criterion values and p<0.05. There were 7 predictors for AVE and 6 for MCE among current demographic, electrocardiograms, laboratory data, and echocardiographic measures one year earlier (baseline) (Figures 1A, 2A). We defined optimal follow-up for risk score quartiles at rates ≤5% visualized on Kaplan-Meier plots. We assessed model performance in 31% of patients held out for internal validation. Results ASGARD development models for both AVE and MCE risk demonstrated overall consistent predictive performance in the internal validation cohort, as evidenced by c-statistics, calibration-in-the-large, calibration slope, Brier score, and goodness-of-fit (all p>0.05) (Figure 1B-C, 2B-C). ASGARD predicted AVE risk similar to a new Vmax measurement (area under the curve [95% CI], 0.82 [0.78-0.87] vs. 0.85 [0.82-0.89) (Figure 1B), and MCE risk better than Framingham cardiovascular risk score (0.76 [0.70-0.82] vs. 0.68 [0.62-0.75]) (Figure 2B). The one-year event rates were ≤5% for the 2 lowest risk score quartiles (Figure 1D, 2D). Conclusion The ASGARD risk scores show promise for long-term, individualized cardiovascular surveillance of low-risk patients with non-severe AS without unnecessary echocardiography. Further studies are warranted for external model validation, continuous optimization, and exploring the potential for implementation in clinical practice.Figure 1Figure 2

Background High-sensitivity Troponin T (hsTnT), a biomarker of cardiomyocyte overload and injury, relates to aortic valve replacement (AVR) and mortality in severe aortic stenosis (AS). However, its prognostic value remains unknown in asymptomatic patients with AS. We aimed to investigate if an hsTnT level >14 pg/mL (above upper limit of normal 99th percentile) is associated with echocardiographic AS-severity, subsequent AVR, ischaemic coronary events (ICE), and mortality in asymptomatic patients with non-severe AS. Methods In this post-hoc sub-analysis of the multicentre, randomised, double-blind, placebo-controlled SEAS trial (ClinicalTrials.gov, NCT00092677), we included asymptomatic patients with mild to moderate-severe AS. We ascertained baseline and 1-year hsTnT concentrations and examined the association between baseline levels and the risk of the primary composite endpoint, defined as the first event of all-cause mortality, isolated AVR (without coronary artery bypass grafting (CABG)), or ICE. Multivariable regressions and competing risk analyses examined associations of hsTnT level >14 pg/mL with clinical correlates and 5-year risk of the primary endpoint. Findings Between January 6, 2003, and March 4, 2004, a total of 1873 patients were enrolled in the SEAS trial, and 1739 patients were included in this post-hoc sub-analysis. Patients had a mean (SD) age of 67.5 (9.7) years, 61.0% (1061) were men, 17.4% (302) had moderate-severe AS, and 26.0% (453) had hsTnT level >14 pg/mL. The median hsTnT difference from baseline to 1-year was 0.8 pg/mL (IQR, -0.4 to 2.3). In adjusted linear regression, log(hsTnT) did not correlate with echocardiographic AS severity (p = 0.36). In multivariable Cox regression, a hsTnT level >14 pg/mL vs. hsTnT =14 pg/mL was associated with an increased risk of the primary composite endpoint (HR, 1.41; 95% CI, 1.18-1.70; p = 0.0002). In a competing risk model of first of the individual components of the primary endpoint, a hsTnT level >14 pg/mL was associated with ICE risk (HR 1.71; 95% CI, 1.23-2.38; p = 0.0013), but not with isolated AVR (p = 0.064) or all-cause mortality (p = 0.49) as the first event. Interpretation hsTnT level is within the reference range (=14 pg/mL) in 3 out of 4 non-ischaemic patients with asymptomatic mild-to-moderate AS and remains stable during a 1-year follow-up regardless of AS-severity. An hsTnT level >14 pg/mL was mainly associated with subsequent ICE, which suggest that hsTnT concentration is primarily a risk marker of subclinical coronary atherosclerotic disease. Funding Merck & Co., Inc., the Schering-Plough Corporation, the Interreg IVA program, Roche Diagnostics Ltd., and Gangstedfonden. Open access publication fee funding provided by prof. Olav W. Nielsen and Department of Cardiology, Bispebjerg University Hospital, Denmark.

IMPORTANCE:Recent studies have questioned the presumed low-risk status of patients with asymptomatic nonsevere aortic stenosis (AS). Whether annual N-terminal pro-brain natriuretic peptide (NT-proBNP) measurements are useful for risk assessment is unknown.OBJECTIVE:To assess the association of annual NT-proBNP measurements with clinical outcomes in patients with nonsevere AS.DESIGN, SETTING, AND PARTICIPANTS:Analysis of annual NT-proBNP concentrations in the multicenter, double-blind Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) randomized clinical trial was performed. SEAS was conducted from January 6, 2003, to April 1, 2008. Blood samples were analyzed in 2016, and data analysis was performed from February 10 to October 10, 2021. SEAS included 1873 patients with asymptomatic AS not requiring statin therapy with transaortic maximal flow velocity from 2.5 to 4.0 m/s and preserved ejection fraction. This substudy included 1644 patients (87.8%) with available blood samples at baseline and year 1.EXPOSURES:Increased age- and sex-adjusted NT-proBNP concentrations at year 1 and a 1.5-fold or greater relative NT-proBNP concentration change from baseline to year 1. Moderate AS was defined as baseline maximal flow velocity greater than or equal to 3.0 m/s.MAIN OUTCOMES AND MEASURES:Aortic valve events (AVEs), which are a composite of aortic valve replacement, cardiovascular death, or incident heart failure due to AS progression, were noted. Landmark analyses from year 1 examined the association of NT-proBNP concentrations with outcomes.RESULTS:Among 1644 patients, 996 were men (60.6%); mean (SD) age was 67.5 (9.7) years. Adjusted NT-proBNP concentrations were within the reference range (normal) in 1228 of 1594 patients (77.0%) with NT-proBNP values available at baseline and in 1164 of 1644 patients (70.8%) at year 1. During the next 2 years of follow-up, the AVE rates per 100 patient-years for normal vs increased adjusted NT-proBNP levels at year 1 were 1.39 (95% CI, 0.86-2.23) vs 7.05 (95% CI, 4.60-10.81) for patients with mild AS (P < .01), and 10.38 (95% CI, 8.56-12.59) vs 26.20 (95% CI, 22.03-31.15) for those with moderate AS (P < .01). Corresponding all-cause mortality rates were 1.05 (95% CI, 0.61-1.81) vs 4.17 (95% CI, 2.42-7.19) for patients with mild AS (P < .01), and 1.60 (95% CI, 0.99-2.57) vs 4.78 (95% CI, 3.32-6.87) for those with moderate AS (P < .01). In multivariable Cox proportional hazards regression models, the combination of a 1-year increased adjusted NT-proBNP level and 1.5-fold or greater NT-proBNP level change from baseline was associated with the highest AVE rates in both patients with mild AS (hazard ratio, 8.12; 95% CI, 3.53-18.66; P < .001) and those with moderate AS (hazard ratio, 4.05; 95% CI, 2.84-5.77; P < .001).CONCLUSIONS AND RELEVANCE:The findings of this study suggest that normal NT-proBNP concentrations at 1-year follow-up are associated with low AVE and all-cause mortality rates in patients with asymptomatic nonsevere AS. Conversely, an increased 1-year NT-proBNP level combined with a 50% or greater increase from baseline may be associated with high AVE rates.TRIAL REGISTRATION:ClinicalTrials.gov Identifier: NCT00092677.

Abstract Background High-sensitive cardiac Troponin T (hsTnT) is the most frequently used biomarker for the detection of cardiomyocyte injury. Severe aortic stenosis (AS) leads to an increased left ventricular load, with the potential of myocardial injury reflected by increased TnT levels. However, there is a lack of studies showing the prevalence and prognostic role of elevated hsTnT in patients with asymptomatic AS. Purpose To examine the association between the hsTnT levels and AS severity in asymptomatic AS patients. We hypothesized that patients with more severe AS will have elevated hsTnT levels and that hsTnT levels are associated with a higher risk for aortic valve events (AVE) and all-cause mortality (ACM). Methods We performed a post-hoc analysis in 1739 asymptomatic patients with mild to moderate-severe AS, enrolled in the randomized, double-blinded SEAS-study (Simvastatin and Ezetimibe in Aortic Stenosis). All patients had available hsTnT blood samples measured at baseline (Year 0) and Year 1. We defined moderate to severe (mod-severe) AS as a transaortic maximal outflow velocity (Vmax)>3.5 m/s combined with aortic valve area (AVA)<1.0 cm2, otherwise non-severe AS. An hsTnT>14 ng/L was high according to assay (Roche, Elecsys Troponin T hs on cobas e 601). Linear multivariable regression model examined the association of hsTnT levels to clinical and echocardiographic variables. Cox multivariable regression model evaluated competing risks and hazard ratios (HR) of outcomes while adjusting for relevant variables, including a Framingham 10-years risk score of cardiovascular diseases. The competing risks were either ACM or AVE, i.e. the first of AVR, cardiovascular death and heart failure due to AS progression. Results At baseline, hsTnT was high in 26% (453/1739) patients; 25% (380/1529) in non-severe and 35% (73/210) in mod-severe AS. Relative TnT change over one year was 17% (mean 1.17, SD 1.01); 15% in non-severe vs. 32% in mod-severe AS, and neither associated to AS severity, hsTnT at baseline or lipid-lowering treatment. In multivariable linear regression analysis, there were significant correlations between hsTnT at baseline and age, male gender, creatinine, left ventricular mass index and BMI (all p<0.001, R-square=0.42), but not with AS severity. In multivariable Cox regression analyses, a high hsTnT at baseline was associated with AVE 1.61 [95% CI 1.29–1.99]. In contrast, hsTnT at baseline was not associated to all-cause mortality (see figure). Conclusions In asymptomatic AS patients without severe AS, high-sensitive Troponin T is not associated with AS severity in cross-sectional analyses, and its levels do not change substantially during one year of follow-up. However, patients with hsTnT >14 ng/l had a sixty percent higher independent risk of subsequent aortic valve events. Multivariable Cox regression Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Acknowledgements: Main sponsor (SEAS): MSD Singapore Company, LLC, partnership between Merck & Co. Inc. and Schering-Plough Corporation. Blood analysis sponsor: Roche

Background: The Osborn or J-wave, an upright deflection of the J-point on the electrocardiogram (ECG), is often observed during severe hypothermia. A possible relation between Osborn waves (OW) and increased risk of ventricular arrhythmia has been reported. We sought to determine whether the level of targeted temperature management (TTM) following out-of-hospital cardiac arrest (OHCA) affects the prevalence of OW and to assess the associations between OW and risk of ventricular arrhythmia and death. Methods and results: The present study is part of the TTM-trial ECG-substudy (including OHCA-patients randomized to TTM at 33 degrees C vs. 36 degrees C from 24 of 36 sites). Serial 12-lead ECGs from 680 (94%) patients were analysed and stratified by OW at predefined time-points (0, 4, 28, 36, 72-h after admission). On admission, the overall prevalence of OW was 16%, increasing to 32% at target temperature, with higher prevalence in the 33 degrees C-group (40% vs. 23%, p < 0.0001). No difference in prevalence was found between the 33 degrees C- and 36 degrees C-groups on admission (18% vs. 14%, p = .11) or after rewarming (13% vs. 10%, p = .44). OW were not associated with increased risk of ventricular arrhythmia (Odds ratio = 0.78 (0.51-1.20), p = .26), but associated with significantly lower 180-day mortality as compared to no OW (38% vs. 52%, p(log-rank) = 0.001) in univariable analyses only. Conclusion: OW are frequent during TTM, particularly in patients treated with 33 degrees C. OW are not associated with increased risk of ventricular arrhythmia, and may be considered a benign physiological phenomenon, associated with lower mortality in univariable analyses.

Background: Mortality in ST-elevation myocardial infarction (STEMI) patients developing cardiogenic shock (CS) during hospitalization is high. Catecholamines, ischemia, and inflammation (parameters present in CS) affect the endothelium. We hypothesized that plasma level of biomarkers reflecting endothelial damage would be associated with CS and mortality. Methods: In 96% of 1467 consecutive patients with suspected STEMI, biomarkers reflecting endothelial cell( soluble thrombomodulin, sTM) and glycocalyx-(syndecan-1) damage were measured on admission. Patients were stratified by CS development or not. CS-Patients were substratified by CS on admission (admission-CS), CS developed in the catheterization laboratory (cath. lab.-CS), or late CS. Results: STEMI patients with admission-CS (n = 85) and cath. lab.-CS (n = 25) had higher levels of sTM and syndecan-1 compared with no-CS patients (n = 1,299). Late CS-patients (n = 58) had higher levels of sTM (median (25th; 75th percentile) 8.8 (7.0; 11.6) vs. 7.4 (6.0; 9.0) ng/mL, P = 0.0004) but not Syndecan-1 (P = 0.26) compared with no-CS patients. sTM was, however, not independently associated with late CS development (OR (95% CI) 1.07 (0.99-1.16), P = 0.09). Patients with the highest level of sTM and syndecan-1 had the highest 30-day mortality (Plogrank< 0.0001). However, neither sTM nor Syndecan-1 was independently associated with 30-day mortality (HR (95% CI) sTM: 1.06 (0.996-1.12), P = 0.07; Syndecan-1: 1.04 (0.99-1.08), P = 0.12). Conclusion: Patients with suspected STEMI patients and admission-CS/cath. lab.-CS had elevated admission levels of sTM and Syndecan-1comparedwith noCSpatients. Patients developing lateCShad higher sTMplasma concentrationcompared with patients without shock. However, the biomarker levels were not independently associated with late CS and mortality.

Introduction: Patients with ST-segment elevation myocardial infarction (STEMI) and cardiogenic shock (CS) are a critical collective in clinical routine.There are only few "real-world" data on intervention of multivessel disease in the acute setting of CS.Methods: The Bremen-STEMI-Register (BSR) is a prospective, monocentric registry investigating all patients with STEMI from a large region in Northwest-Germany (approx. 1 mio.inhabitants) since 2006.Based on this dataset, the present analysis focuses on PCI strategies of patients with CS and multivessel disease.Outcomes of patients with PCI of the culprit lesion only were compared to patients with multivessel PCI.Results: Out of a total number of 7090 patients with STEMI, 856 patients (12%) presented with CS.In 585 cases multivessel disease was diagnosed.A culprit lesion only PCI was performed in 448 patients (77%), 53 patients (9%) had multivessel PCI.The amount of multivessel PCIs increased over the years (2006: 0% vs. 2015: 12.4%, p=0.002).Both groups (culprit only PCI vs. multivessel PCI) did not show any significant difference with respect to age, sex and hemodynamic parameters, however, patients with multivessel PCI were more likely to suffer from severe myocardial infarctions, measured by maximum creatine kinase (p=0.03) and received more often an intraaortic balloon counterpulsation (IABP) (p=0.03)compared to patients with culprit lesion only PCI.Regarding outcomes there was no significant difference in the occurrence of an acute kidney failure post PCI (culprit only PCI 21% vs. multivessel PCI: 23%, p=0.6); no significant difference in the frequency of in-hospital mortality (38% vs. 43%, p=0.5) and one-year mortality (52% vs. 47%, p=0.4) was observed.Conclusion: Only a minority of patients received a multivessel PCI during the acute setting of CS with an increasing trend towards an immediate treatment of multiple significant coronary stenosis over the last years.Even though patients with multivessel PCI suffered from more severe myocardial infarctions, the appearance of acute kidney failure as well as mortality was comparable in both groups.