Relationship Between Infarct Artery, Myocardial Injury, and Outcomes After Primary Percutaneous Coronary Intervention in ST-Segment-Elevation Myocardial Infarction.

BACKGROUND: The extent to which infarct artery impacts the extent of myocardial injury and outcomes in patients with ST-segment-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention is uncertain. METHODS AND RESULTS: We performed a pooled analysis using individual patient data from 7 randomized STEMI trials in which myocardial injury within 30 days after primary percutaneous coronary intervention was assessed in 1774 patients by cardiac magnetic resonance (n=1318) or technetium-99m sestamibi single-photon emission computed tomography (n=456). Clinical follow-up was performed at a median duration of 351 days (interquartile range, 184-368 days). Infarct size and outcomes were assessed in anterior (infarct vessel=left anterior descending) versus nonanterior (non-left anterior descending) STEMI. Median infarct size (percentage left ventricular myocardial mass) was larger in patients with anterior compared with nonanterior STEMI (19.7% [interquartile range, 9.4%-31.7%] versus 12.6% [interquartile range, 5.1%-20.5%]; P<0.001). Patients with anterior compared with nonanterior STEMI were at higher risk for 1-year all-cause mortality (6.2% versus 3.6%; adjusted hazard ratio [HR], 1.66 [95% CI, 1.02-2.69]; P=0.04) and heart failure hospitalization (4.4% versus 2.6%; adjusted HR, 1.96 [95% CI, 1.15-3.36]; P=0.01). Infarct size was a predictor of subsequent all-cause mortality or heart failure hospitalization in anterior STEMI (adjusted HR per 1% increase, 1.05 [95% CI, 1.03-1.07]; P<0.001), but not in nonanterior STEMI (adjusted HR, 1.02 [95% CI, 0.99-1.05]; P=0.19). The P value for this interaction was 0.04. CONCLUSIONS: Anterior STEMI was associated with substantially greater myonecrosis after primary percutaneous coronary intervention compared with nonanterior STEMI, contributing in large part to the worse prognosis in patients with anterior infarction.

Senescent CD4+ T-Cell Phenotypes and Inflammatory Milieu in the Coronary and Systemic Circulation in ST-Elevation Myocardial Infarction: An Exploratory Study.

INTRODUCTION: In ST-elevation myocardial infarction (STEMI), inflammation is pivotal, with early senescent CD4+CD28null cells implicated in its pathogenesis. However, the functional phenotype of these cells within the coronary circulation remains unclear. METHODS: We examined CD4+ cell subpopulations in blood samples from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of seven healthy controls. RESULTS: Our findings revealed reduced CD4+ cell counts in STEMI patients compared to controls (1,998, 1,275-3,268 vs. 4,278, 3,595-4,449), alongside an increased proportion of CD4+ cells lacking CD28 expression (20.1 vs. 6.1%). These CD4+CD28null cells in STEMI predominantly exhibited a Th1 phenotype (47.8% vs. 6.6%). Intriguingly, no significant differences were detected in CD4+CD28null cells between coronary sinus and vena cava, and cytokine levels in these compartments remained similar. CONCLUSION: CD4+CD28null cells are increased in STEMI, mainly polarized toward a Th1 phenotype, and distributed equally between the different vascular beds.

Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction.

Pericardial fluid (PF) has been suggested as a reservoir of molecular targets that can be modulated for efficient repair after myocardial infarction (MI). Here, we set out to address the content of this biofluid after MI, namely in terms of microRNAs (miRs) that are important modulators of the cardiac pathological response. PF was collected during coronary artery bypass grafting (CABG) from two MI cohorts, patients with non-ST-segment elevation MI (NSTEMI) and patients with ST-segment elevation MI (STEMI), and a control group composed of patients with stable angina and without previous history of MI. The PF miR content was analyzed by small RNA sequencing, and its biological effect was assessed on human cardiac fibroblasts. PF accumulates fibrotic and inflammatory molecules in STEMI patients, namely causing the soluble suppression of tumorigenicity 2 (ST-2), which inversely correlates with the left ventricle ejection fraction. Although the PF of the three patient groups induce similar levels of fibroblast-to-myofibroblast activation in vitro, RNA sequencing revealed that PF from STEMI patients is particularly enriched not only in pro-fibrotic miRs but also anti-fibrotic miRs. Among those, miR-22-3p was herein found to inhibit TGF-ß-induced human cardiac fibroblast activation in vitro. PF constitutes an attractive source for screening diagnostic/prognostic miRs and for unveiling novel therapeutic targets in cardiac fibrosis.

Excessive accumulation of epicardial adipose tissue promotes microvascular obstruction formation after myocardial ischemia/reperfusion through modulating macrophages polarization.

BACKGROUND: Owing to its unique location and multifaceted metabolic functions, epicardial adipose tissue (EAT) is gradually emerging as a new metabolic target for coronary artery disease risk stratification. Microvascular obstruction (MVO) has been recognized as an independent risk factor for unfavorable prognosis in acute myocardial infarction patients. However, the concrete role of EAT in the pathogenesis of MVO formation in individuals with ST-segment elevation myocardial infarction (STEMI) remains unclear. The objective of the study is to evaluate the correlation between EAT accumulation and MVO formation measured by cardiac magnetic resonance (CMR) in STEMI patients and clarify the underlying mechanisms involved in this relationship. METHODS: Firstly, we utilized CMR technique to explore the association of EAT distribution and quantity with MVO formation in patients with STEMI. Then we utilized a mouse model with EAT depletion to explore how EAT affected MVO formation under the circumstances of myocardial ischemia/reperfusion (I/R) injury. We further investigated the immunomodulatory effect of EAT on macrophages through co-culture experiments. Finally, we searched for new therapeutic strategies targeting EAT to prevent MVO formation. RESULTS: The increase of left atrioventricular EAT mass index was independently associated with MVO formation. We also found that increased circulating levels of DPP4 and high DPP4 activity seemed to be associated with EAT increase. EAT accumulation acted as a pro-inflammatory mediator boosting the transition of macrophages towards inflammatory phenotype in myocardial I/R injury through secreting inflammatory EVs. Furthermore, our study declared the potential therapeutic effects of GLP-1 receptor agonist and GLP-1/GLP-2 receptor dual agonist for MVO prevention were at least partially ascribed to its impact on EAT modulation. CONCLUSIONS: Our work for the first time demonstrated that excessive accumulation of EAT promoted MVO formation by promoting the polarization state of cardiac macrophages towards an inflammatory phenotype. Furthermore, this study identified a very promising therapeutic strategy, GLP-1/GLP-2 receptor dual agonist, targeting EAT for MVO prevention following myocardial I/R injury.

Comprehensive characterization of cardiac contraction for improved post-infarction risk assessment.

This study aims at identifying risk-related patterns of left ventricular contraction dynamics via novel volume transient characterization. A multicenter cohort of AMI survivors (n = 1021) who underwent Cardiac Magnetic Resonance (CMR) after infarction was considered for the study. The clinical endpoint was the 12-month rate of major adverse cardiac events (MACE, n = 73), consisting of all-cause death, reinfarction, and new congestive heart failure. Cardiac function was characterized from CMR in 3 potential directions: by (1) volume temporal transients (i.e. contraction dynamics); (2) feature tracking strain analysis (i.e. bulk tissue peak contraction); and (3) 3D shape analysis (i.e. 3D contraction morphology). A fully automated pipeline was developed to extract conventional and novel artificial-intelligence-derived metrics of cardiac contraction, and their relationship with MACE was investigated. Any of the 3 proposed directions demonstrated its additional prognostic value on top of established CMR indexes, myocardial injury markers, basic characteristics, and cardiovascular risk factors (P < 0.001). The combination of these 3 directions of enhancement towards a final CMR risk model improved MACE prediction by 13% compared to clinical baseline (0.774 (0.771-0.777) vs. 0.683 (0.681-0.685) cross-validated AUC, P < 0.001). The study evidences the contribution of the novel contraction characterization, enabled by a fully automated pipeline, to post-infarction assessment.

[Predictive value of cardiac magnetic resonance imaging for adverse left ventricular remodeling after acute ST-segment elevation myocardial infarction].

OBJECTIVE: To assess the value of cardiac magnetic resonance (CMR) imaging for predicting adverse left ventricular remodeling in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: We retrospectively analyzed the clinical data and serial CMR (cine and LGE sequences) images of 86 STEMI patients within 1 week and 5 months after percutaneous coronary intervention (PCI), including 25 patients with adverse LV remodeling and 61 without adverse LV remodeling, defined as an increase of left ventricular end-systolic volume (LVESV) over 15% at the second CMR compared to the initial CMR. The CMR images were analyzed for LV volume, infarct characteristics, and global and infarct zone myocardial function. The independent predictors of adverse LV remodeling following STEMI were analyzed using univariate and multivariate Logistic regression methods. RESULTS: The initial CMR showed no significant differences in LV volume or LV ejection fraction (LVEF) between the two groups, but the infarct mass and microvascular obstructive (MVO) mass were significantly greater in adverse LV remodeling group (P < 0.05). Myocardial injury and cardiac function of the patients recovered over time in both groups. At the second CMR, the patients with adverse LV remodeling showed a significantly lower LVEF, a larger left ventricular end-systolic volume index (LVESVI) and a greater extent of infarct mass (P < 0.001) with lower global peak strains and strain rates in the radial, circumferential, and longitudinal directions (P < 0.05), infarct zone peak strains in the 3 directions, and infarct zone peak radial and circumferential strain rates (P < 0.05). The independent predictors for adverse LV remodeling following STEMI included the extent of infarct mass (AUC=0.793, 95% CI: 0.693-0.873; cut-off value: 30.67%), radial diastolic peak strain rate (AUC=0.645, 95% CI: 0.534-0.745; cut-off value: 0.58%), and RAAS inhibitor (AUC= 0.699, 95% CI: 0.590-0.793). CONCLUSION: The extent of infarct mass, peak radial diastolic strain rate, and RAAS inhibitor are independent predictors of adverse LV remodeling following STEMI.

Lipid Content Distribution and its Clinical Implication in Patients with Acute Myocardial Infarction-Plaque Erosion: Results from the Prospective OCTAMI Study.

AIMS: Plaque erosion (PE) is one of the main plaque phenotypes of acute coronary syndrome (ACS). However, the underlying plaque component and distribution have not been systematically analysed. This study aims to investigate the distribution of lipid and calcium content in culprit lesions assessed by optical coherence tomography (OCT) in patients with PE and explore its relationship with prognosis in a cohort of ST segment elevation myocardial infarction (STEMI) patients. METHODS: A prospective cohort of 576 patients with STEMI was enrolled in our study. After exclusion, 152 PE patients with clear underlying plaque components were ultimately analysed. The culprit lesion was divided into the border zone, external erosion zone and erosion site in the longitudinal view. Each pullback of the culprit lesions was assessed by 3 independent investigators frame-by-frame, and the quantity and distribution of lipid and calcium components were recorded. RESULTS: Of the 152 PE patients, lipid and calcium contents were more likely to exist in the external erosion zone than in the other regions. In particular, a high level of lipid content proximal to the erosion site was significantly associated with plaque vulnerability and a higher incidence of MACEs. CONCLUSION: This study revealed that high level of lipid content in the proximal external erosion zone was related to high-risk plaque characteristics and poor prognosis, which provided a novel method for risk stratification and precise management in patients with plaque erosion.

Exogenous Transforming Growth Factor-ß1 and Its Helminth-Derived Mimic Attenuate the Heart's Inflammatory Response to Ischemic Injury and Reduce Mature Scar Size.

Coronary reperfusion after acute ST-elevation myocardial infarction (STEMI) is standard therapy to salvage ischemic heart muscle. However, subsequent inflammatory responses within the infarct lead to further loss of viable myocardium. Transforming growth factor (TGF)-ß1 is a potent anti-inflammatory cytokine released in response to tissue injury. The aim of this study was to investigate the protective effects of TGF-ß1 after MI. In patients with STEMI, there was a significant correlation (P = 0.003) between higher circulating TGF-ß1 levels at 24 hours after MI and a reduction in infarct size after 3 months, suggesting a protective role of early increase in circulating TGF-ß1. A mouse model of cardiac ischemia reperfusion was used to demonstrate multiple benefits of exogenous TGF-ß1 delivered in the acute phase. It led to a significantly smaller infarct size (30% reduction, P = 0.025), reduced inflammatory infiltrate (28% reduction, P = 0.015), lower intracardiac expression of inflammatory cytokines IL-1ß and chemokine (C-C motif) ligand 2 (>50% reduction, P = 0.038 and 0.0004, respectively) at 24 hours, and reduced scar size at 4 weeks (21% reduction, P = 0.015) after reperfusion. Furthermore, a low-fibrogenic mimic of TGF-ß1, secreted by the helminth parasite Heligmosomoides polygyrus, had an almost identical protective effect on injured mouse hearts. Finally, genetic studies indicated that this benefit was mediated by TGF-ß signaling in the vascular endothelium.

Comprehensive review of ST-segment elevation myocardial infarction: Understanding pathophysiology, diagnostic strategies, and current treatment approaches.

ST-Segment Elevation Myocardial Infarction (STEMI) is a life-threatening medical emergency characterized by complete coronary artery occlusion, leading to myocardial ischemia and subsequent necrosis. Over the years, STEMI has remained a significant cause of morbidity and mortality worldwide, necessitating a comprehensive understanding of its pathophysiology, accurate diagnostic strategies, and effective treatment approaches. This review article aims to thoroughly analyze the current knowledge surrounding STEMI, emphasizing key aspects crucial for optimizing patient outcomes. Firstly, the pathophysiology of STEMI will be explored, elucidating the sequence of events from coronary artery plaque rupture to thrombus formation and occlusion. This section will also cover the underlying risk factors contributing to STEMI development, including atherosclerosis, hypertension, and diabetes. Secondly, the diagnostic modalities for STEMI will be critically evaluated. Traditional electrocardiography remains the cornerstone of STEMI diagnosis. Still, advancements in imaging techniques such as cardiac magnetic resonance imaging and coronary angiography have enhanced accuracy and allow for better risk stratification. Furthermore, the review will delve into the latest treatment approaches for STEMI. Prompt reperfusion therapy through primary percutaneous coronary intervention or thrombolytic therapy is essential in restoring blood flow and salvaging the jeopardized myocardium. The role of adjunctive medical treatment, including antiplatelet agents, beta-blockers, and statins, will also be discussed in post-STEMI management.

Differentiation of acute non-ST elevation myocardial infarction and acute infarct-like myocarditis by visual pattern analysis: a head-to-head comparison of different cardiac MR techniques.

OBJECTIVES: Parametric cardiac magnetic resonance (CMR) techniques have improved the diagnosis of pathologies. However, the primary tool for differentiating non-ST elevation myocardial infarction (NSTEMI) from myocarditis is still a visual assessment of conventional signal-intensity-based images. This study aimed at analyzing the ability of parametric compared to conventional techniques to visually differentiate ischemic from non-ischemic myocardial injury patterns. METHODS: Twenty NSTEMI patients, twenty infarct-like myocarditis patients, and twenty controls were examined using cine, T2-weighted CMR (T2w) and late gadolinium enhancement (LGE) imaging and T1/T2 mapping on a 1.5 T scanner. CMR images were presented in random order to two experienced fully blinded observers, who had to assign them to three categories by a visual analysis: NSTEMI, myocarditis, or healthy. RESULTS: The conventional approach (cine, T2w and LGE combined) had the best diagnostic accuracy with 92% (95%CI: 81-97) for NSTEMI and 86% (95%CI: 71-94) for myocarditis. The diagnostic accuracies using T1 maps were 88% (95%CI: 74-95) and 80% (95%CI: 62-91), 84% (95%CI: 67-93) and 74% (95%CI: 54-87) for LGE, and 83% (95%CI: 66-92) and 73% (95%CI: 53-87) for T2w. The accuracies for cine (72% (95%CI: 52-86) and 60% (95%CI: 38-78)) and T2 maps (62% (95%CI: 40-79) and 47% (95%CI: 28-68)) were significantly lower compared to the conventional approach (p < 0.001 and p < 0.0001). CONCLUSIONS: The conventional approach provided a reliable visual discrimination between NSTEMI, myocarditis, and controls. The diagnostic accuracy of a visual pattern analysis of T1 maps was not significantly inferior, whereas the diagnostic accuracy of T2 maps was not sufficient in this context. CLINICAL RELEVANCE STATEMENT: The ability of parametric compared to conventional CMR techniques to visually differentiate ischemic from non-ischemic myocardial injury patterns can avoid potentially unnecessary invasive coronary angiography and help to shorten CMR protocols and to reduce the need of gadolinium contrast agents. KEY POINTS: • A visual differentiation of ischemic from non-ischemic patterns of myocardial injury is reliably achieved by a combination of conventional CMR techniques (cine, T2-weighted and LGE imaging). • There is no significant difference in accuracies between visual pattern analysis on native T1 maps without providing quantitative values and a conventional combined approach for differentiating non-ST elevation myocardial infarction, infarct-like myocarditis, and controls. • T2 maps do not provide a sufficient diagnostic accuracy for visual pattern analysis for differentiating non-ST elevation myocardial infarction, infarct-like myocarditis, and controls.

Predictive value of total ischaemic time and T1 mapping after emergency percutaneous coronary intervention in acute ST-segment elevation myocardial infarction.

AIM: To investigate the predictive value of ischaemic time and cardiac magnetic resonance imaging (CMRI) T1 mapping in acute ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI). MATERIALS AND METHODS: A total of 127 patients with STEMI treated by primary PCI were studied. All patients underwent CMRI with native T1 and extracellular volume (ECV) measurement, 61 of whom also had 4-month follow-up data. The total ischaemic (symptom onset to balloon, S2B) time expressed in minutes was recorded. CMRI cine, T1 mapping, and late gadolinium enhancement (LGE) images were analysed to evaluate left ventricular (LV) function, T1 value, ECV, and myocardial infract (MI) scar characteristics, respectively. The correlation between S2B time and T1 mapping was evaluated. The predictive values of S2B time and T1 mapping for large final infarct size were estimated. RESULTS: The incidence of microvascular obstruction (MVO) increased with the prolongation of ischaemia time. Regardless of MVO or not, ECV in myocardial infarction (ECVMI) was significantly correlated with S2B time (r=0.61, p<0.001), while native T1 in MI (T1MI) was not (r=-0.19, p=0.029). In the 4-month follow-up, native T1MI was improved (1385.1 ± 90.4 versus 1288.6 ± 74 ms, p<0.001). Furthermore, ECVMI was independently associated with final larger infarct size (AUC = 0.89, 95% confidence interval [CI] = 0.81-0.98, p<0.001) in multivariable regression analysis. CONCLUSION: ECVMI was correlated with total ischaemic time and was an independent predictor of final larger infarct size.

Cardiac magnetic resonance shows increased adverse ventricular remodeling in younger patients after ST-segment elevation myocardial infarction.

OBJECTIVES: Young patients account for about half of ST-segment elevation myocardial infarction (STEMI) patients and display a unique risk profile compared with old patients. Whether these differences are related to disparities in ventricular remodeling remains unknown. This study aimed to evaluate age-related differences in ventricular remodeling after primary percutaneous coronary intervention (PPCI) for STEMI. METHODS: In this observational study, consecutive STEMI patients between October 2019 and March 2021 who underwent serial cardiovascular magnetic resonance at index admission (3 to 7 days) and 3 months after PPCI were enrolled. Adverse remodeling was defined as ≥ 10% enlargement in left ventricular end-diastolic volume index (LVEDVi), while reverse remodeling was defined as a decrease in left ventricular end-systolic volume index (LVESVi) of more than 10%. RESULTS: A total of 123 patients were included and grouped into young (< 60 years, n = 71) and old (≥ 60 years, n = 52) patients. Despite generally similar baseline structural and infarct characteristics, LVESVi significantly decreased only in old patients during follow-up (p = 0.034). The incidence of adverse remodeling was higher (49.3% vs 30.8%, p = 0.039), while the incidence of reverse remodeling was lower (31.0% vs 53.8%, p = 0.011) in young compared with old patients. Younger age (< 60 years) was associated with a significantly higher risk of adverse remodeling (adjusted OR 3.51, 95% CI 1.41-8.74, p = 0.007) and lower incidence of reverse remodeling (adjusted OR 0.42, 95% CI 0.18-0.97, p = 0.046). CONCLUSIONS: In STEMI patients undergoing PPCI, young patients are at a higher risk of adverse remodeling and less probably develop reverse remodeling than old patients. Equal or more attention should be paid to young patients with STEMI compared with their older counterparts. KEY POINTS: • In STEMI patients undergoing PPCI, young patients displayed unfavorable remodeling compared with old patients. • Young patients are at a higher risk of adverse remodeling and less probably develop reverse remodeling than old patients. • Equal or more attention should be paid to young patients compared with their older counterparts.

Pathophysiology of LV Remodeling Following STEMI: A Longitudinal Diffusion Tensor CMR Study.

BACKGROUND: Adverse LV remodeling post-ST-segment elevation myocardial infarction (STEMI) is associated with a poor prognosis, but the underlying mechanisms are not fully understood. Diffusion tensor (DT)-cardiac magnetic resonance (CMR) allows in vivo characterization of myocardial architecture and provides unique mechanistic insight into pathophysiologic changes following myocardial infarction. OBJECTIVES: This study evaluated the potential associations between DT-CMR performed soon after STEMI and long-term adverse left ventricular (LV) remodeling following STEMI. METHODS: A total of 100 patients with STEMI underwent CMR at 5 days and 12 months post-reperfusion. The protocol included DT-CMR for assessing fractional anisotropy (FA), secondary eigenvector angle (E2A) and helix angle (HA), cine imaging for assessing LV volumes, and late gadolinium enhancement for calculating infarct and microvascular obstruction size. Adverse remodeling was defined as a 20% increase in LV end-diastolic volume at 12 months. RESULTS: A total of 32 patients experienced adverse remodeling at 12 months. Compared with patients without adverse remodeling, they had lower FA (0.23 ± 0.03 vs 0.27 ± 0.04; P < 0.001), lower E2A (37 ± 6° vs 51 ± 7°; P < 0.001), and, on HA maps, a lower proportion of myocytes with right-handed orientation (RHM) (8% ± 5% vs 17% ± 9%; P < 0.001) in their acutely infarcted myocardium. On multivariable logistic regression analysis, infarct FA (odds ratio [OR]: <0.01; P = 0.014) and E2A (OR: 0.77; P = 0.001) were independent predictors of adverse LV remodeling after adjusting for left ventricular ejection fraction (LVEF) and infarct size. There were no significant changes in infarct FA, E2A, or RHM between the 2 scans. CONCLUSIONS: Extensive cardiomyocyte disorganization (evidenced by low FA), acute loss of sheetlet angularity (evidenced by low E2A), and a greater loss of organization among cardiomyocytes with RHM, corresponding to the subendocardium, can be detected within 5 days post-STEMI. These changes persist post-injury, and low FA and E2A are independently associated with long-term adverse remodeling.

Cardiac MRI Left Atrial Strain Associated With New-Onset Atrial Fibrillation in Patients With ST-Segment Elevation Myocardial Infarction.

BACKGROUND: Left atrial (LA) strain is associated with structural remodeling of the LA. Whether there is an association between LA strain obtained by cardiac magnetic resonance imaging (MRI) and new-onset atrial fibrillation (AF) after ST-segment elevation myocardial infarction (STEMI) is unclear. PURPOSE: To investigate the relationship between LA strain and new-onset AF after STEMI. STUDY TYPE: Retrospective. POPULATION: Three hundred and seventy-nine STEMI patients were enrolled, of which 26 had new-onset AF. FIELD STRENGTH/SEQUENCE: 3.0 T, balanced turbo field echo sequence. ASSESSMENT: Patients were divided into w/o AF group and new-onset AF group. Cardiac MRI images were analyzed using cardiovascular imaging software CVI 42 (Circle Cardiovascular Imaging, Canada). An automatic tracing algorithm was applied to obtain strain values. The reservoir strain, conduit strain, and booster strain were included in model 1, model 2, and model 3, respectively. STATISTICAL TESTS: Student's t-test, Mann-Whiney U test, and chi-square test were performed. Variables with a P ≤ 0.05 were incorporated into the logistic regression analysis. Area under curve of receiver operating characteristic was used to assess the ability of LA strain to identify new-onset AF. Bayesian information criterion, Akaike information criterion, and C-index were used to make comparisons between three models. P < 0.05 was considered statistically significant. RESULTS: Three models were used to assess LA strain identification ability for new-onset AF. After including multiple factors, right coronary artery (RCA), LVEF, and reservoir strain were still risk factors for new-onset AF in model 1. In model 2, age, RCA, LVEF, and conduit strain were still risk factors for new-onset AF. In model 3, RCA, LVEF, LVEDVi, and booster strain were still risk factors for new-onset AF. Model 2 has a stronger identification ability than others. DATA CONCLUSION: LA strain associated with new-onset AF after STEMI. The model including conduit strain was the best-fit one. LEVEL OF EVIDENCE: 4 TECHNICAL EFFICACY: Stage 3.

Cardiac magnetic resonance feature tracking global and segmental strain in acute and chronic ST-elevation myocardial infarction.

Strain is an important imaging parameter to determine myocardial deformation. This study sought to 1) assess changes in left ventricular strain and ejection fraction (LVEF) from acute to chronic ST-elevation myocardial infarction (STEMI) and 2) analyze strain as a predictor of late gadolinium enhancement (LGE). 32 patients with STEMI and 18 controls prospectively underwent cardiac magnetic resonance imaging. Patients were scanned 8 [Formula: see text] 5 days and six months after infarction (± 1.4 months). Feature tracking was performed and LVEF was calculated. LGE was determined visually and quantitatively on short-axis images and myocardial segments were grouped according to the LGE pattern (negative, non-transmural and transmural). Global strain was impaired in patients compared to controls, but improved within six months after STEMI (longitudinal strain from -14 ± 4 to -16 ± 4%, p < 0.001; radial strain from 38 ± 11 to 42 ± 13%, p = 0.006; circumferential strain from -15 ± 4 to -16 ± 4%, p = 0.023). Patients with microvascular obstruction showed especially attenuated strain results. Regional strain persisted impaired in LGE-positive segments. Circumferential strain could best distinguish between LGE-negative and -positive segments (AUC 0.73- 0.77). Strain improves within six months after STEMI, but remains impaired in LGE-positive segments. Strain may serve as an imaging biomarker to analyze myocardial viability. Especially circumferential strain could predict LGE.

Two successive electrocardiograms of an old male with acute myocardial infarction: What on earth was going on?

A 68-year-old male complained of a sudden 2-h chest pain accompanied by dizziness and diaphoresis. His consciousness lost several times because of ventricular fibrillation attack. Emergent CAG showed proximal left anterior descending (LAD) occlusion, but two previous successive electrocardiograms established diagnoses of non-ST-elevation myocardial infarction (NSTEMI) and STEMI respectively, indicating that the patient had experienced acute subtotal occlusion of proximal LAD to total occlusion of the left main coronary trunk (LMT). It is vital to identify de Winter pattern associated with proximal LAD lesion in view of the potential circulatory collapse, fatal arrhythmias and sudden cardiac death from it.

Detection of Intramyocardial Iron in Patients Following ST-Elevation Myocardial Infarction Using Cardiac Diffusion Tensor Imaging.

BACKGROUND: Intramyocardial hemorrhage (IMH) following ST-elevation myocardial infarction (STEMI) is associated with poor prognosis. In cardiac magnetic resonance (MR), T2* mapping is the reference standard for detecting IMH while cardiac diffusion tensor imaging (cDTI) can characterize myocardial architecture via fractional anisotropy (FA) and mean diffusivity (MD) of water molecules. The value of cDTI in the detection of IMH is not currently known. HYPOTHESIS: cDTI can detect IMH post-STEMI. STUDY TYPE: Prospective. SUBJECTS: A total of 50 patients (20% female) scanned at 1-week (V1) and 3-month (V2) post-STEMI. FIELD STRENGTH/SEQUENCE: A 3.0 T; inversion-recovery T1-weighted-imaging, multigradient-echo T2* mapping, spin-echo cDTI. ASSESSMENT: T2* maps were analyzed to detect IMH (defined as areas with T2* < 20 msec within areas of infarction). cDTI images were co-registered to produce averaged diffusion-weighted-images (DWIs), MD, and FA maps; hypointense areas were manually planimetered for IMH quantification. STATISTICS: On averaged DWI, the presence of hypointense signal in areas matching IMH on T2* maps constituted to true-positive detection of iron. Independent samples t-tests were used to compare regional cDTI values. Results were considered statistically significant at P ≤ 0.05. RESULTS: At V1, 24 patients had IMH on T2*. On averaged DWI, all 24 patients had hypointense signal in matching areas. IMH size derived using averaged-DWI was nonsignificantly greater than from T2* (2.0 ± 1.0 cm2 vs 1.89 ± 0.96 cm2 , P = 0.69). Compared to surrounding infarcted myocardium, MD was significantly reduced (1.29 ± 0.20 × 10-3  mm2 /sec vs 1.75 ± 0.16 × 10-3  mm2 /sec) and FA was significantly increased (0.40 ± 0.07 vs 0.23 ± 0.03) within areas of IMH. By V2, all 24 patients with acute IMH continued to have hypointense signals on averaged-DWI in the affected area. T2* detected IMH in 96% of these patients. Overall, averaged-DWI had 100% sensitivity and 96% specificity for the detection of IMH. DATA CONCLUSION: This study demonstrates that the parameters MD and FA are susceptible to the paramagnetic properties of iron, enabling cDTI to detect IMH. EVIDENCE LEVEL: 1 TECHNICAL EFFICACY: Stage 2.

Associations of Infarct Size and Regional Myocardial Function Examined by Cardiac Magnetic Resonance Feature Tracking Strain Analysis with the Infarct Location in Patients with Acute ST-Segment Elevation Myocardial Infarction.

Objective To quantitatively evaluate the associations of infarct size, regional myocardial function examined by cardiac magnetic resonance feature tracking (CMR-FT) strain analysis with infarct location in patients with ST-segment elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention.Methods Cardiac magnetic resonance images were retrospectively analyzed in 95 consecutive STEMI patients with successful reperfusion. The patients were divided into the anterior wall myocardial infarction (AWMI) and nonanterior wall myocardial infarction (NAWMI) groups. Infarct characteristics were assessed by late gadolinium enhancement. Global and regional strains and associated strain rates in the radial, circumferential and longitudinal directions were assessed by CMR-FT based on standard cine images. The associations of infarct size, regional myocardial function examined by CMR-FT strain analysis with infarct location in STEMI patients were evaluated by the Spearman or Pearsonmethod. Results There were 44 patients in the AWMI group and 51 in the NAWMI group. The extent of left ventricular enhanced mass was significantly larger in patients with AWMI compared with the NAWMI group (24.47±11.89, 21.06±12.08 %LV; t=3.928, P = 0.008). In infarct zone analysis, strains in the radial, circumferential and longitudinal directions were remarkably declined in the AWMI group compared with the NAWMI group (z=-20.873, -20.918, -10.357, all P < 0.001). The volume (end-systolic volume index), total enhanced mass and extent of enhanced mass of the left ventricular were correlated best with infarct zone strain in the AWMI group (all P < 0.001). Conclusion In STEMI patients treated by percutaneous coronary intervention, myocardial damage is more extensive and regional myocardial function in the infarct zone is lower in the AWMI group compared with the NAWMI group.

Culprit site extracellular DNA and microvascular obstruction in ST-elevation myocardial infarction.

AIMS: Extracellular chromatin and deoxyribonuclease (DNase) have been identified as important players of thrombosis, inflammation, and homeostasis in a murine model. We previously demonstrated that activated neutrophils release neutrophil extracellular traps (NETs) at the culprit site in ST-elevation myocardial infarction (STEMI), which significantly contribute to extracellular chromatin burden, and are associated with larger infarcts. To understand the correlation between neutrophil activation, extracellular chromatin, and infarct size (IS), we investigated these parameters in a porcine myocardial infarction model, and at different time points and sites in a prospective STEMI trial with cardiac magnetic resonance (CMR) endpoints. METHODS AND RESULTS: In a prospective STEMI trial (NCT01777750), 101 STEMI patients were included and blood samples were obtained from first medical contact until 6 months after primary percutaneous coronary intervention (pPCI) including direct sampling from the culprit site. CMR was performed 4 ± 2 days and 6 months after pPCI. Neutrophil counts, markers of extracellular chromatin, and inflammation were measured. Double-stranded deoxyribonucleic acid (dsDNA), citrullinated histone 3, nucleosomes, myeloperoxidase, neutrophil elastase, and interleukin (IL)-6 were significantly increased, while DNase activity was significantly decreased at the culprit site in STEMI patients. High neutrophil counts and dsDNA levels at the culprit site correlated with high microvascular obstruction (MVO) and low ejection fraction (EF). High DNase activity at the culprit site correlated with low MVO and high EF. In correspondence, dsDNA correlated with IS in the porcine myocardial infarction model. In porcine infarcts, neutrophils and extracellular chromatin were detected in congested small arteries corresponding with MVO. Markers of neutrophil activation, extracellular chromatin, DNase activity and CMR measurements correlated with markers of systemic inflammation C-reactive protein and IL-6 in patients. CONCLUSIONS: NETs and extracellular chromatin are important determinants of MVO in STEMI. Rapid degradation of extracellular chromatin by DNases appears to be crucial for microvascular patency and outcome.

EpCAM and microvascular obstruction in patients with STEMI: a cardiac magnetic resonance study.

INTRODUCTION AND OBJECTIVES: Microvascular obstruction (MVO) is negatively associated with cardiac structure and worse prognosis after ST-segment elevation myocardial infarction (STEMI). Epithelial cell adhesion molecule (EpCAM), involved in epithelium adhesion, is an understudied area in the MVO setting. We aimed to determine whether EpCAM is associated with the appearance of cardiac magnetic resonance (CMR)-derived MVO and long-term systolic function in reperfused STEMI. METHODS: We prospectively included 106 patients with a first STEMI treated with percutaneous coronary intervention, quantifying serum levels of EpCAM 24hours postreperfusion. All patients underwent CMR imaging 1 week and 6 months post-STEMI. The independent correlation of EpCAM with MVO, systolic volume indices, and left ventricular ejection fraction was evaluated. RESULTS: The mean age of the sample was 59±13 years and 76% were male. Patients were dichotomized according to median EpCAM (4.48 pg/mL). At 1-week CMR, lower EpCAM was related to extensive MVO (P=.021) and larger infarct size (P=.019). At presentation, EpCAM values were significantly associated with the presence of MVO in univariate (OR, 0.58; 95%CI, 0.38-0.88; P=.011) and multivariate logistic regression models (OR, 0.55; 95%CI, 0.35-0.87; P=.010). Although MVO tends to resolve at chronic phases, decreased EpCAM was associated with worse systolic function: reduced left ventricular ejection fraction (P=.009) and higher left ventricular end-systolic volume (P=.043). CONCLUSIONS: EpCAM is associated with the occurrence of CMR-derived MVO at acute phases and long-term adverse ventricular remodeling post-STEMI.