2232Circulating levels of ST2 are associated with myocardial injury, left ventricular function and future adverse clinical events in patients with ST-elevation myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Shetelig ◽  
T Ueland ◽  
S Limalanathan ◽  
P Hoffmann ◽  
P Aukrust ◽  
...  

Abstract Background Soluble ST2, a member of the IL-1 receptor family, seems to be associated with adverse outcome in acute myocardial infarction and heart failure (HF), and is suggested to be involved in left ventricular (LV) remodelling. Purpose To elucidate a possible role of ST2 in LV injury, remodelling and prognosis in ST-elevation myocardial infarction (STEMI) patients. The main objectives of the study were to investigate whether circulating ST2 levels were associated with infarct size, LV function, adverse remodeling and clinical outcome in a cohort of patients with STEMI. Methods 270 patients with clinically stable first-time STEMI treated with primary percutaneous coronary intervention (PCI) were included. Blood samples were drawn before and immediately after the PCI procedure, at day 1 (median 18.3 hours after PCI) and after 4 months. Cardiac magnetic resonance (CMR) was performed in the acute phase and after 4 months. Clinical events and all-cause mortality were registered during 12 months' and 70 months' follow-up, respectively. A composite endpoint was defined as death, MI, unscheduled revascularisation >3 months after the index infarction, rehospitalisation for HF or stroke. Associations between ST2 and CMR parameters and clinical events were evaluated with linear regression and logistic regression, respectively. Results There was a significant increase in ST2 levels from the PCI procedure to day 1 with a subsequent decline from day 1 to 4 months in the POSTEMI cohort. Patients with high ST2 levels (>median) at all sampling points during hospitalisation had significantly larger infarct size, lower myocardial salvage, lower LVEF, larger increase in EDV and higher frequency of MVO. After adjustment for relevant clinical variables, peak CRP and peak troponin T, ST2 measured at day 1 remained associated with infarct size (β 2.0 per SD of ST2, p<0.001) and LVEF (β −1.8 per SD of ST2, p=0.02) at 4 months. High levels of ST2 measured at day 1 (>75th percentile) were associated with increased risk of having an adverse clinical event during the first year and with long-term all-cause mortality (Figure). High levels of ST2 measured in a stable phase 4 months after STEMI were also associated with an increased risk of all-cause mortality (Figure). Figure 1 Conclusions High levels of ST2 in STEMI patients were associated with large infarct size, impaired recovery of LV function, and adverse clinical outcome in patients with STEMI. ST2 measured 4 months after STEMI remained associated with all-cause mortality.

2016 ◽  
Vol 6 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Yacov Shacham ◽  
Amir Gal-Oz ◽  
Jeremy Ben-Shoshan ◽  
Gad Keren ◽  
Yaron Arbel

Background: Only limited data is present regarding the incidence and prognostic implications of acute kidney injury (AKI) in ST elevation myocardial infarction (STEMI) patients with preserved left ventricular (LV) function in the primary percutaneous coronary intervention (PCI) era. Methods: We conducted a retrospective study of 842 consecutive STEMI patients with preserved LV function (ejection fraction ≥50%, assessed by echocardiography) who underwent primary PCI between January 2008 and January 2015. AKI was defined as an increase of ≥0.3 mg/dl in serum creatinine within 48 h following admission. Patients were assessed for all-cause mortality up to 5 years. Results: Fifty-two patients (6.2%) developed AKI. Patients with AKI were older, had impaired baseline renal function, and presented more often with heart failure throughout their hospitalization. Patients with AKI had a higher 5-year all-cause mortality (13.4 vs. 2.4%, p < 0.001). Compared to patients with no AKI, the adjusted hazard ratio for all-cause mortality was 2.64 (95% CI 1.25-5.56, p = 0.01). Conclusions: Among STEMI patients with preserved LV function undergoing primary PCI, AKI is associated with a higher long-term mortality.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nicole L Bonfig ◽  
Chase R Soukup ◽  
Ross F Garberich ◽  
Sarah J Davidson ◽  
Rose M Peterson ◽  
...  

Introduction: The development of microvascular obstruction (MVO) in the setting of ST-Elevation Myocardial Infarction (STEMI) is a powerful predictor of reduced left-ventricular (LV) function, adverse LV remodeling and increased mortality. Although MVO is associated with increasing infarct size and ischemic duration, additional causes of MVO have not been clearly identified. Although MVO may arise from intravascular obstruction from embolization of thrombus, it may also arise from compression of the microvasculature due to increased myocardial edema and extravascular compressive forces. Hypothesis: Because left-ventricular hypertrophy (LVH) is associated with increased extravascular compressive forces, we hypothesized that patients with greater LV mass may be more susceptible to the development of MVO during STEMI. Methods: We measured MVO in 385 patients (59.4 + 12.3 years; 77% male) admitted to our Institution with STEMI who underwent cardiac MRI for measurement of LV function and infarct size following successful primary PCI. A total of 219 patients (57%) had MVO on cardiac MRI measured 1-3 days following PCI of which 172 patients had paired measurements of LV mass. Results: Patients with MVO (13.7 + 13.9 grams) had significantly greater infarct size (54 vs. 31 g; p < 0.001) and LV mass (151 vs 140 g; p<0.01) but reduced LVEF (43.1 vs. 47.8%) despite having similar ischemic times. Among patients with MVO, there was a linear increase in MVO with increasing LV mass (Figure). Conclusions: MVO increases with increasing LV mass and may contribute to the known adverse effects of LVH in STEMI.


2021 ◽  
Vol 10 (23) ◽  
pp. 5677
Author(s):  
Mohammad A. Almesned ◽  
Femke M. Prins ◽  
Erik Lipšic ◽  
Margery A. Connelly ◽  
Erwin Garcia ◽  
...  

The gut metabolite trimethylamine N-oxide (TMAO) at admission has a prognostic value in ST-elevation myocardial infarction (STEMI) patients. However, its sequential changes and relationship with long-term infarct-related outcomes after primary percutaneous coronary intervention (PCI) remain elusive. We delineated the temporal course of TMAO and its relationship with infarct size and left ventricular ejection fraction (LVEF) post-PCI, adjusting for the estimated glomerular filtration rate (eGFR). We measured TMAO levels at admission, 24 h and 4 months post-PCI in 379 STEMI patients. Infarct size and LVEF were determined by cardiac magnetic resonance 4 months after PCI. TMAO levels decreased from admission (4.13 ± 4.37 μM) to 24 h (3.41 ± 5.84 μM, p = 0.001) and increased from 24 h to 4 months (3.70 ± 3.86 μM, p = 0.026). Higher TMAO values at 24 h were correlated to smaller infarct sizes (rho = −0.16, p = 0.024). Larger declines between admission and 4 months suggestively correlated with smaller infarct size, and larger TMAO increases between 24 h and 4 months were associated with larger infarct size (rho = −0.19, p = 0.008 and rho = −0.18, p = 0.019, respectively). Upon eGFR stratification using 90 mL/min/1.73 m2 as a cut-off, significant associations between TMAO and infarct size were only noted in subjects with impaired renal function. In conclusion, TMAO levels in post-PCI STEMI patients are prone to fluctuations, and these fluctuations could be prognostic for infarct size, particularly in patients with impaired renal function.


Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000852 ◽  
Author(s):  
Artin Entezarjou ◽  
Moman Aladdin Mohammad ◽  
Pontus Andell ◽  
Sasha Koul

BackgroundST-elevation myocardial infarction (STEMI) occurs as a result of rupture of an atherosclerotic plaque in the coronary arteries. Limited data exist regarding the impact of culprit coronary vessel on hard clinical event rates. This study investigated the impact of culprit vessel on outcomes after primary percutaneous coronary intervention (PCI) of STEMI.MethodsA total of 29 832 previously cardiac healthy patients who underwent primary PCI between 2003 and 2014 were prospectively included from the Swedish Coronary Angiography and Angioplasty Registry and the Registry of Information and Knowledge about Swedish Heart Intensive care Admissions. Patients were stratified into three groups based on culprit vessel (right coronary artery (RCA), left anterior descending artery (LAD) and left circumflex artery (LCx)). The primary outcome was 1-year mortality. The secondary outcomes included 30-day and 5-year mortality, as well as heart failure, stroke, bleeding and myocardial reinfarction at 30 days, 1 year and 5 years. Univariable and multivariable analyses were done using Cox regression models.ResultsOne-year analyses revealed that LAD infarctions had the highest increased risk of death, heart failure and stroke compared with RCA infarctions, which had the lowest risk. Sensitivity analyses revealed that reduced left ventricular ejection fraction on discharge partially explained this increased relative risk in mortality. Furthermore, landmark analyses revealed that culprit vessel had no significant influence on 1-year mortality if a patient survived 30 days after myocardial infarction. Subgroup analyses revealed female sex and multivessel disease (MVD) as significant high-risk groups with respect to 1-year mortality.ConclusionsLAD and LCx infarctions had a relatively higher adjusted mortality rate compared with RCA infarctions, with LAD infarctions in particular being associated with an increased risk of heart failure, stroke and death. Culprit vessel had limited influence on mortality after 1 month. High-risk patient groups include LAD infarctions in women or with concomitant MVD.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Marie Sophie L de Koning ◽  
B. D Westenbrink ◽  
Solmaz Assa ◽  
Dirk J van Veldhuisen ◽  
Robin P Dullaart ◽  
...  

Background: Circulating ketone bodies (KB) are increased in patients with heart failure, corresponding with increased utilization of KB as a cardiac fuel. Whether circulating KB are increased in patients presenting with ST-elevation myocardial infarction (STEMI) and whether this is associated with infarct size is unknown. Methods: KB were measured in 379 non-diabetic participants of the Glycometabolic Intervention as Adjunct to Primary Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction (GIPS) III trial (Clinicaltrial.gov Identifier: NCT01217307). Non-fasting plasma concentrations of the KB beta-hydroxybutyrate, acetoacetate, acetone were measured at presentation, 24 hours and 4 months after STEMI presentation using nuclear magnetic resonance spectroscopy. Associations of circulating KB with myocardial infarct size and left ventricular ejection fraction (both detected with MRI at 4 months after STEMI) were determined using multivariable linear regression analyses. Results: Circulating KB were higher at baseline (total KB 520 [315-997](median [IQR], μmol/L), compared to 206 [174-246] at 24 hours and 166 [143-201] at 4 months ( P <0.001 for all)). KB at 24 hours were positively associated with enzymatic infarct size, HbA1C and beta-blocker use. KB at 24 hours were independently associated with MRI outcomes at 4 months. Higher KB was associated with larger myocardial infarct size (total KB: standardized β=0.17, 95%-confidence interval (CI) (0.04-0.31), P =0.012) and lower ejection fraction (standardized β=-0.15, 95%-CI (-0.29- -0.009), P =0.037). Conclusion: Circulating KB are increased in patients with STEMI and are independently associated with myocardial infarct size and left ventricular function after 4 months of follow-up. The increase in circulating KB may reflect maladaptive changes of myocardial metabolism during the acute phase.


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