Microvascular injury in the course of acute ST-segment-elevation myocardial infarction (STEMI) has been identified a as determinant of adverse outcomes and manifests as microvascular obstruction (MVO). MVO has long been regarded as a transient finding, vanishing within a few weeks after infarction. However, recent studies have shown that it may persist beyond the early phase, resulting in adverse remodeling. However, its clinical implications remain unclear. This study aims to evaluate the association of MVO persistence and major adverse cardiac events after STEMI.

In total, 609 patients with revascularized first-time STEMI underwent cardiac magnetic resonance imaging (CMR) at 4 days, 4 months, and 12 months after STEMI to assess MVO, infarct size, and left ventricular function. Major adverse cardiac events were defined as composite of death, reinfarction, and new congestive heart failure within a median interval of 3.2 years.

Baseline MVO was present in 365 (60%) patients and persisted in 35 (10%) patients at 4-month CMR and in 20 (5%) patients at 12-month CMR. Compared with transient MVO not present at follow-up, patients with MVO persistence ≥4 months were more likely to experience major adverse cardiac events during follow-up (29% versus 13%; P=0.016). Within patients with MVO, those with MVO persistence had lower left ventricular ejection fraction (P=0.002), larger infarcts (P=0.00001), and more frequent intramyocardial hemorrhage (P=0.001) at baseline CMR.

Persistent MVO after STEMI occurs in up to 10% of patients with baseline MVO and is linked to major adverse cardiac events. Patients with MVO persistence had larger infarcts, lower left ventricular function, and more frequent intramyocardial hemorrhage at baseline CMR. All patients with MVO persisting ≥12 months initially showed intramyocardial hemorrhage.

Microvascular obstruction (MVO) is associated with heart failure (HF) following ST-segment-elevation myocardial infarction. Angiography-derived microcirculatory resistance (AMR), a wire- and adenosine-free measure, may facilitate early assessment of microvascular function post-primary percutaneous coronary intervention. This study aimed to evaluate the ability of AMR to detect MVO and its prognostic value for predicting HF in patients with ST-segment-elevation myocardial infarction post-primary percutaneous coronary intervention.

Patients with consecutive ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention with a cardiac magnetic resonance examination 2 to 7 days post-procedure between April 2016 and February 2023 were retrospectively reviewed. AMR was computed from coronary angiography. MVO was identified and quantified via cardiac magnetic resonance. The end point was new-onset HF during follow-up.

Overall, 475 patients (aged 56.8±11.7 years; 399 men) were included. The area under the curve for AMR to detect MVO was 0.821 (95% CI, 0.782-0.859), with an optimal cutoff value of 2.7 mm Hg*s/cm. During a median follow-up of 37.3 months, 121 (25.5%) patients developed HF. AMR, whether as a continuous (per 0.5-mm Hg*s/cm increase; hazard ratio, 1.29 [95% CI, 1.10-1.52]; P=0.002) or categorical (AMR >2.7 mm Hg*s/cm; hazard ratio, 2.15 [95% CI, 1.43-3.22]; P<0.001) variable, was independently associated with HF after adjusting for traditional risk factors (age, symptom-to-balloon time, left anterior descending coronary artery, and ejection fraction) and late gadolinium enhancement-cardiac magnetic resonance parameters. AMR improved prognostication over traditional risk factors and late gadolinium enhancement-cardiac magnetic resonance parameters (net reclassification improvement, 0.533; P<0.001; integrative discrimination index, 0.023; P=0.005).

AMR showed good diagnostic performance in detecting MVO and was an independent and incremental predictor of HF in patients with ST-segment-elevation myocardial infarction post-primary percutaneous coronary intervention.

Strain assessed by cardiac magnetic resonance (CMR) is a key prognostic indicator in myocardial infarction. However, the strain characteristics and prognostic value in myocardial infarction with nonobstructive coronary arteries (MINOCA) with different causes are unclear. This study aims to describe left atrial (LA) and left ventricular strain in patients with MINOCA and evaluate their predictive value for major adverse cardiovascular events (MACEs) in "true MINOCA" cases.

This single-center retrospective study included patients suspected of myocardial infarction who completed CMR during hospitalization. CMR images were used to obtain LA and left ventricular strain via CMR feature tracking. True MINOCA was defined by evidence of ischemia or infarction on CMR. MACEs included all-cause death, recurrent myocardial infarction, stroke, heart failure, atrial fibrillation, and angina pectoris. This study included 386 patients, with a median time from admission to CMR of 4 days. LA and left ventricular strains varied by pathogenesis, with the lowest strain in patients with cardiomyopathy. For patients with true MINOCA, Cox regression showed that global longitudinal strain (hazard ratio [HR], 0.90 [95% CI, 0.82-0.99]; P=0.022) and LA reservoir strain (HR, 0.95 [95% CI, 0.91-0.99]; P=0.014) were independently associated with MACEs. Kaplan-Meier analysis indicated that patients with LA reservoir strain ≤21.25% or global longitudinal strain ≤16.4% had a significantly higher MACE risk (P<0.001). Integrating global longitudinal strain and LA reservoir strain improved MACE prediction.

LA and left ventricular strains vary among MINOCA pathogeneses. In true MINOCA patients, global longitudinal strain and LA reservoir strains independently predict MACE risk. Integrating these strains enhances MACE prediction.

URL: https://www.clinicaltrials.gov; Unique Identifier: NCT06502899.

(1) Background: There are few data on anticoagulation therapy for left ventricular (LV) thrombosis following ST-segment elevation myocardial infarction (STEMI). The aim of this study was to assess whether microvascular obstruction (MVO) extent on cardiac magnetic resonance (CMR) worsened the prognosis of patients with LV thrombosis receiving anticoagulation. (2) Methods: reperfused STEMI patients undergoing CMR were enrolled. Patients were divided into 4 groups according to MVO and LV thrombosis presence or absence. Occurrence of major adverse cardiac events (MACE) was evaluated during follow-up. (3) Results: 80 STEMI patients were enrolled. According to MVO and LV thrombosis, 4 subgroups were obtained: patients with MVO and LV thrombosis (21 patients, 26%); patients with MVO without LV thrombosis (28 patients, 35%); patients without MVO with LV thrombosis (6 patients, 8%); patients without MVO and LV thrombosis (25 patients, 31%). All patients with LV thrombosis were treated with anticoagulation therapy. The median time to the follow-up was 11 months. Twenty-two patients (27%) experienced MACE. LV thrombosis treated with anticoagulation was an independent predictor of MACE (hazard ratio, 2.828; 95% confidence interval, 1.205-6.638; p = 0.017) and was associated with a worse prognosis (p = 0.012), regardless of MVO (p = 0.852), at Kaplan-Meier. (4) Conclusions: Patients with LV thrombosis treated with anticoagulation after a reperfused STEMI have a worse prognosis than those without; however, MVO extent did not worsen prognosis.

Early prediction of microvascular obstruction (MVO) occurrence in acute myocardial infarction (AMI) patients undergoing percutaneous coronary intervention (PCI) can facilitate personalized management and improve prognosis. This study developed a prediction model for MVO occurrence using preoperative clinical data and validated its performance in a prospective cohort. A total of 504 AMI patients were included, with 406 in the exploratory cohort and 98 in the prospective cohort. Feature selection was performed using random forest recursive feature elimination (RF-RFE), identifying five key predictors: High-Sensitivity Troponin T, Neutrophil Count, Creatine Kinase-MB, Fibrinogen, and Left Ventricular Ejection Fraction. Among the models developed, logistic regression demonstrated the highest predictive performance, achieving an AUC score of 0.800 in the exploratory cohort and 0.792 in the prospective cohort. This model has been integrated into a user-friendly online platform, providing a practical tool for guiding personalized perioperative management and improving patient prognosis.

Microvascular injury in patients with ST-segment elevation myocardial infarction (STEMI) occurs in up to 50%, yet no therapeutic target exists. Inflammation contributes directly to myocardial damage in STEMI and may also cause deleteriously effects on the microcirculation. The aim of this prespecified sub-study was to determine the effect of prehospital pulse-dose glucocorticoid on the microcirculation determined by index of microvascular resistance (IMR) and its relation to inflammation. The PULSE-MI trial was a 1:1 randomized, blinded, placebo-controlled clinical trial in patients with STEMI transferred for primary percutaneous coronary intervention (PCI) investigating the cardioprotective effects of prehospital pulse-dose glucocorticoid (methylprednisolone 250 mg) compared with placebo. In this prespecified sub-study, we investigated microvascular function as IMR by thermodilution after primary PCI and inflammation defined by C-reactive protein (CRP) at 24 hours after onset of STEMI.

Of 530 patients included in the PULSE-MI trial, 295 (56%) were assessed with coronary physiology of whom 142 (48%) were treated with glucocorticoid and 153 (52%) with placebo. Baseline characteristics were overall well-balanced in both groups. The median IMR in the glucocorticoid group was 23 (interquartile range (IQR), 11-38) and 18 (IQR, 11-42) in the placebo group (p=0.49). CRP upon arrival did not differ between treatment groups (p=0.81), but CRP at 24 hours was significantly lower in the glucocorticoid group compared to placebo (p<0.001).

Prehospital glucocorticoid did not impact IMR assessed immediately after primary PCI, albeit this compound, demonstrated significant anti-inflammatory effects as determined by CRP levels at 24 hours.

http://www.

gov ; Unique Identifier: NCT05462730.

Coronary microvascular functional and structural obstructions (CMVO) after percutaneous coronary intervention (PCI) are a major cause of poor clinical outcomes in patients with acute coronary syndrome. This study aimed to noninvasively diagnose the presence of CMVO using non-contrast multiparametric cardiac magnetic resonance (CMR) in patients with acute myocardial infarction (AMI) who underwent PCI.

We retrospectively enrolled consecutive patients with AMI who underwent PCI and subsequent acute-phase CMR at our hospital. The patients were divided into two groups: those with and those without CMVO. The top five clinical and CMR parameters were extracted based on their correlation coefficients with the presence of CMVO. Receiver-operator characteristic (ROC) curves and area under the curve (AUC) were generated to compare the diagnostic performance of CMVO detection using the Top_5 clinical parameters, Top_5 CMR parameters, and CMR left ventricular (LV) volume and structure parameters. Differences in the AUC between parameters were compared using the DeLong test.

Forty-eight patients (40 men and 8 women; mean age, 66 ± 12 years) were included in the study. For CMVO detection, the ROC curves of Top_5 clinical parameters, Top_5 CMR parameters, and CMR LV volume and structure parameters demonstrated AUCs of 0.87, 1.00, and 0.72, respectively. The Top_5 CMR parameters exhibited the highest AUC, showing significant differences compared to the other groups.

Non-contrast enhanced multiparametric CMR allows the diagnosis of CMVO with high accuracy and without kidney burden and is expected to be a useful marker for risk stratification, patient management, and treatment decision-making.

Question CMVO following PCI is difficult to diagnose through coronary angiography and can lead to adverse outcomes. Findings Non-contrast enhanced multiparametric CMR imaging has the potential to accurately diagnose CMVOs and further identify their location and extent. Critical relevance Non-contrast enhanced multiparametric CMR enables accurate, noninvasive diagnosis of CMVO, and provides both organic and functional myocardial information. These findings are crucial for diverse CMVO etiologies that require individualized treatment, and may help risk stratification, patient management, and treatment decision-making.

Cardiac imaging protocols usually result in several types of acquisitions and descriptors extracted from the images. The statistical analysis of such data across a population may be challenging, and can be addressed by fusion techniques within a dimensionality reduction framework. However, directly combining different data types may lead to unfair comparisons (for heterogeneous descriptors) or over-exploitation of information (for strongly correlated modalities). In contrast, physicians progressively consider each type of data based on hierarchies derived from their experience or evidence-based recommendations, an inspiring approach for data fusion strategies. In this paper, we propose a novel methodology for hierarchical data fusion and unsupervised representation learning. It mimics the physicians' approach by progressively integrating different high-dimensional data descriptors according to a known hierarchy. We model this hierarchy with a Hierarchical Gaussian Process Latent Variable Model (GP-LVM), which links the estimated low-dimensional latent representation and high-dimensional observations at each level in the hierarchy, with additional links between consecutive levels of the hierarchy. We demonstrate the relevance of this approach on a dataset of 1726 magnetic resonance image slices from 123 patients revascularized after acute myocardial infarction (MI) (first level in the hierarchy), some of them undergoing reperfusion injury (microvascular obstruction (MVO), second level in the hierarchy). Our experiments demonstrate that our hierarchical model provides consistent data organization across levels of the hierarchy and according to physiological characteristics of the lesions. This allows more relevant statistical analysis of myocardial lesion patterns, and in particular subtle lesions such as MVO.

Timely assessment of abnormal microvascular perfusion (MVP) may improve prognosis in patients with ST-segment elevation myocardial infarction (STEMI). This study aimed to determine the clinical implications of contrast-flow quantitative flow ratio (cQFR) in evaluating abnormal MVP and subsequent outcomes among STEMI patients after successful primary percutaneous coronary intervention (PPCI).

The study population consisted of 2 independent cohorts. The diagnostic cohort was used to evaluate the correlation and diagnostic accuracy of cQFR in predicting abnormal MVP. In this cohort, MVP and cQFR of the culprit vessel (n = 186) were assessed from a prospective consecutive registry. Abnormal MVP was determined using myocardial contrast perfusion echocardiography (MCE) in the culprit vessel after PPCI. The prognostic cohort consisted of STEMI patients undergoing PPCI who were followed for a minimum of 2 years (n = 1931). The primary outcome was all-cause mortality.

In the diagnostic cohort, cQFR exhibited a moderate correlation with abnormal MVP assessed by MCE. Specificity, sensitivity, and area under the curve of post-PPCI cQFR to predict abnormal MVP were 81.6 %, 50.9 % and 0.709 (95 % confidence interval: 0.635-0.783), respectively, with the best cut-off value of 0.875. In the prognostic cohort, patients with cQFR <0.875 showed a significantly higher risk of long-term mortality compared to those with cQFR ≥0.875 (median follow-up: 52 months; mortality: 8.0 % vs. 3.8 %; p < 0.001). Cox-regression analysis revealed that cQFR < 0.875 was an independent predictor of long-term mortality (adjusted HR: 2.132; 95 % CI: 1.358-3.346; p = 0.001) after adjusting for age, gender, diabetes mellitus, hyperlipidemia, symptom to balloon time, culprit vessel.

We found that cQFR demonstrated a relatively good performance in predicting abnormal MVP in patients with STEMI after successful PPCI. A cQFR value below 0.875 is an independent predictor of both abnormal MVP and long-term mortality. (Prognostic implication of cQFR in STEMI patients; NCT04996901).

Assessing myocardial perfusion in acute myocardial infarction is important for guiding clinicians in choosing appropriate treatment strategies. Echocardiography can be used due to its direct feedback and bedside nature, but it currently faces image quality issues and an inability to differentiate coronary macro- from micro-circulation. We previously developed an imaging scheme using high frame-rate contrast-enhanced ultrasound (HFR CEUS) with higher order singular value decomposition (HOSVD) that provides dynamic perfusion and vascular flow visualization. In this study, we aim to show the ability of this technique to image perfusion deficits and investigate the potential occurrence of false-positive contrast detection.

We used a porcine model comprising occlusion and release of the left anterior descending coronary artery. During slow contrast agent infusion, the afore-mentioned imaging scheme was used to capture and process the data offline using HOSVD.

Fast and slow coronary flow was successfully differentiated, presumably representing the different compartments of the micro-circulation. Low perfusion was seen in the area that was affected, as expected by vascular occlusion. Furthermore, we also imaged coronary flow dynamics before, during and after release of the occlusion, the latter showing hyperemia as expected. A contrast agent destruction test showed that the processed images contained actual contrast signal in the cardiac phases with minimal motion. With larger tissue motion, tissue signal leaked into the contrast-enhanced images.

Our results demonstrate the feasibility of HFR CEUS with HOSVD as a viable option for assessing myocardial perfusion. Flow dynamics were resolved, which potentially helped to directly evaluate coronary flow deficits.

Disorders of glycolipid metabolism are important pathogenic factors leading to coronary artery disease, and there is no safe and effective comprehensive treatment, while acupuncture has a certain efficacy in heart disease and disorders of glycolipid metabolism. To assess the effects of acupuncture on glycolipid metabolism in patients with coronary heart disease, we conducted a systematic review and meta-analysis.

From the time of library construction to August 18, 2023, Searches were conducted in eight databases, with no language restriction. Only RCTs that included acupuncture as a sole or secondary effect on glucose-lipid metabolism in coronary heart disease were included.Our primary outcome indicators were Low-density lipoprotein cholesterol(LDL-C), Hemoglobin A1c(HbA1c). Our analyses were conducted in strict accordance with the PRISMA statement, and the researchers used the Cochrane Handbook for literature screening and data extraction, the "Risk of Bias" tool (ROB.2) for assessing risk of bias, and RevMan (version 5.3) for meta-analysis of outcome metrics, and the GRADE criteria for assessing quality of evidence. Assessing the quality of acupuncture literature using the Standards for reporting interventions in clinical trials of acupuncture.

Our analysis included 18 eligible RCTs (N = 1346 participants). For the primary outcome metrics, acupuncture combined with standard treatment was effective in reducing LDL-C (SMD =-0.56; 95 % CI, -0.75 to -0.38; P < 0.00001), and HbA1c (MD = -1.15; 95 % CI, -1.73 to -0.58; P < 0.0001). For secondary outcome measures, combination therapy improved TC (SMD = -0.97; 95 % CI, -1.44 to -0.51; P < 0.0001), TG (MD = -0.39; 95 % CI, -0.58 to -0.20; P < 0.0001), hs-CRP (MD = -0.98; 95 % CI, -1.43 to -0.52; P <0.0001), 2hPG (MD = -1.45; 95 % CI, -1.74 to -1.16; P < 0.00001), and ORR (RR, 1.27; 95 % CI, 1.19-1.36; P < 0.00001) levels more than standard therapy alone.However, the combination therapy did not prevail in lowering HDL-C (MD = 0.11; 95 % CI, 0.07-0.14; P < 0.00001) compared with standard therapy alone. Meanwhile heterogeneity analysis showed that After coronary heart disease intervention, acupuncture was able to reduce TC (SMD = -0.85; 95 % CI, -1.37 to -0.33; P = 0.001), TG (MD = -0.14; 95 % CI, -0.24 to -0.04; P = 0.004) levels, but did not dominate in lowering LDL-C.

Acupuncture effectively regulates glycolipid metabolism in coronary artery disease, serving as an adjuvant treatment. It may aid post-PCI healing via lipid metabolism regulation, but rigorous, large-scale, long-term RCTs are needed for validation.

This study aims to investigate the relationship between segmental longitudinal strain (LS) and quantitative microvascular perfusion (qMVP) in patients with ST-segment elevation myocardial infarction (STEMI), and to explore the prognostic value of the two indicators after STEMI.

The retrospective study enrolled 61 patients who underwent primary percutaneous coronary intervention (pPCI) for first STEMI. Microvascular perfusion (MVP) and qMVP were analyzed by myocardial contrast echocardiography (MCE), and segmental LS was analyzed by two-dimensional speckle tracking echocardiography (2D-STE). Myocardial wall perfusion was qualitatively assessed visually. Quantitative myocardial perfusion parameters were analyzed using an 18-segment model. The correlation between segmental LS and qMVP was assessed. The prognostic value of segmental LS and qMVP for major cardiac adverse events were evaluated.

Among the 314 segments with abnormal wall motion, 44 showed normal microvascular perfusion (nMVP), 87 showed delayed microvascular perfusion (dMVP), and 183 exhibited microvascular obstruction (MVO). Segmental LS was correlated with segmental wall motion (WM) and qMVP. At 12-month follow-up, 19 patients experienced cardiac events. NT-proBNP, regional LS (rLS), and regional qMVP (r-qMVP) were associated with cardiac events. The area under curve (AUC) of combination of rLS and r-qMVP was bigger than single indicator for identifying prognostic value (P < 0.001).

Segmental LS indices are correlated with qMVP within the infarct zone following reperfused STEMI. Both rLS and r-qMVP are sensitive to myocardial damage and provide prognostic value for clinical events after STEMI. And the combination of rLS and r-qMVP shows improved predictive ability compared to a single indicator.

Coronary microvascular dysfunction has been associated with adverse cardiovascular events following acute myocardial infarction. This study evaluates the role of the angiography-derived index of microcirculatory resistance (angio-IMR) in predicting myocardial damage in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention (PCI).

In this post hoc analysis of the CLEVER-ACS (Controlled-Level Everolimus in Acute Coronary Syndromes) trial, the associations between post-PCI angio-IMR of infarct-related coronary arteries (IRAs) and infarct size, microvascular obstruction, and left ventricular ejection fraction at 30 days as assessed by cardiac magnetic resonance were investigated. High post-PCI angio-IMR was defined as ≥40 mm Hg*s . In non-IRAs, angio-IMR was measured before IRA-PCI. A total of 52 IRAs and 94 non-IRAs of 52 patients were analyzed. Post-PCI angio-IMR was 41.5 (interquartile range [IQR], 28.5-55.7) mm Hg*s  in IRAs and pre-PCI angio-IMR was 43.7 (IQR, 31.7-54.0) mm Hg*s in non-IRAs (P=0.70). Patients with high post-PCI angio-IMR (52%) exhibited a larger myocardial infarct size (36.0 [IQR, 23.0-52.5] g versus 14.5 [IQR, 6.50-26.5] g, P<0.001) and a lower left ventricular ejection fraction (46.5% [IQR, 39.5%-49.5%] versus 55.0% [IQR, 48.0%-61.4%], P=0.002) at 30 days as compared with those with low post-PCI angio-IMR values. Post-PCI angio-IMR positively correlated with myocardial infarct size (r=0.45, P=0.001) and extent of microvascular obstruction (r=0.40, P=0.004) at 30 days. Post-PCI angio-IMR predicted myocardial infarct size (area under the curve, 0.78 [IQR, 0.65-0.92]; P=0.001) and extent of microvascular obstruction (area under the curve, 0.74 [IQR, 0.60-0.89]; P=0.009) at 30 days.

In patients with ST-segment-elevation myocardial infarction, post-PCI angio-IMR was identified as independent predictor of myocardial infarct size and extent of microvascular obstruction.

URL: https://clinicaltrials.gov; Unique Identifier: NCT01529554.

Early detection of coronary microvascular dysfunction (CMD) in ST-segment elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention (PCI), is challenging. The index of microcirculatory resistance (caIMR), derived from computational pressure-fluid dynamics (CPFD), allows practical assessment of CMD using only routine coronary angiography. However, the prognostic implications of combining caIMR with microvascular obstruction (MVO) identified through cardiac magnetic resonance (CMR) imaging are unclear. This retrospective study investigates the utility of CPFD-caIMR and CMR-derived MVO in predicting major adverse cardiovascular events (MACEs) in 292 STEMI patients who underwent primary PCI, followed by caIMR and CMR evaluations. Patients were stratified into four groups based on caIMR thresholds (≤ 40 U or > 40 U) and the presence/absence of MVO. The primary endpoint was MACEs, defined as cardiac death, recurrent myocardial infarction, target vessel revascularization, or heart failure readmission. Overall, 101/292 patient exhibited discordant caIMR and MVO results. Specifically, 103 patients had caIMR ≤ 40 U without MVO, while 88 patients showed caIMR > 40 U with MVO. Multivariate analysis identified both caIMR > 40 U and MVO as independent predictors of MACEs, with an HR of 3.572 for each unit increase in CPFD-caIMR > 40 U. Combination of CPFD-caIMR and MVO significantly enhanced predictive accuracy. CPFD-caIMR is a reliable, minimally invasive tool for identifying microvascular dysfunction. Combination with CMR-derived MVO improves risk stratification in STEMI patients following PCI, holding promise for the early identification of high-risk patients, enabling targeted and personalized management.

Ticagrelor monotherapy after 1-3 months of dual antiplatelet therapy (DAPT) has shown to be effective and safe after percutaneous coronary intervention (PCI), including in patients with an ST elevation myocardial infarction (STEMI). Direct omission of aspirin could further reduce bleeding complications and may reduce the incidence and expansion of intramyocardial haemorrhage (IMH), a frequent complication after revascularisation for a STEMI.

This multicentre open label pilot study randomises 200 STEMI patients within 24 hours after primary PCI and before the first subsequent dose of aspirin to ticagrelor monotherapy or ticagrelor plus aspirin for twelve months. As IMH is more frequently observed after an anterior STEMI, IMH and infarct size will be determined with cardiac magnetic resonance (CMR) imaging in 60 anterior STEMI patients. In this subgroup, blood samples will be analysed for biochemical outcomes.

The primary safety endpoint consists of major adverse cardiac and cerebral events, and the primary efficacy endpoint is infarct size on CMR. Secondary efficacy endpoints consist of the incidence and extent of IMH determined by CMR, and of clinical bleeding events. Other endpoints include all-cause mortality and biochemical outcomes.

The STOP-IMH pilot study compares ticagrelor monotherapy with ticagrelor plus aspirin directly after primary PCI in 200 STEMI patients. We aim to provide a signal of safety regarding ischemic events for the direct omission of aspirin after primary PCI, and to compare the infarct size by CMR between the two treatment strategies in the first week after primary PCI.

The Canadian Cardiovascular Society recently put forth a new classification of acute reperfused myocardial infarction (MI) based on stages of myocardial injury. Backed by more than 5 decades of intense investigation in the field, the key message of this new classification is that not all MIs are the same and that the type and extent of myocardial injury should be considered in diagnosing and treating MI. We review the literature with the goal of highlighting the progressive advances that enabled the synthesis of the Canadian Cardiovascular Society classification into 4 distinct stages of tissue injury. We emphasize the major breakthroughs from insights gained from experimental, translational, and clinical studies to date. We also identify current gaps in knowledge and critical research directions that need to be pursued to improve patient care and reduce post-MI complications such as chronic heart failure and malignant arrhythmias, whose risk is linked to stage and extent of myocardial injury.

Current guidelines recommend the use of glycoprotein IIb/IIIa (GpIIb/IIIa) inhibitors in patients with ST-segment elevation myocardial infarction (STEMI) only as a bail-out therapy. However, drug penetration to the jeopardised area may not be achieved due to impeded blood flow and increased microvascular resistance. Aim of our study is to investigate the impact of distal intracoronary GpIIb/IIIa inhibitor agent infusion in STEMI patients. Primary endpoints were microvascular obstruction (MVO) and infarct size.

Patients with STEMI who have high thrombus burden or slow-flow/NR phenomenon and undergoing primary percutaneous coronary intervention (pPCI) were enrolled. Tirofiban was the preferred GpIIb/IIIa inhibitor. Patients were assigned to the systemic intravenous infusion group and intracoronary infusion group in whom bolus dose of tirofiban was distally infused to the infarct related artery. MVO and size of the infarct size were assessed via cardiac MRI.

We prospectively included 75 patients and mean follow-up duration was 383 days. Baseline characteristics were similar between groups except a lower rate of diabetes in distal intracoronary infusion group (p = .006). There was no significant difference in localisation of myocardial infarction, ischaemia duration and preloading of P2Y12 inhibitor between groups. MVO (p = .048) and infarct size (p = .030) were significantly lower in distal intracoronary infusion group.

Cardiac MRI based assessment revealed that intracoronary administration of GpIIb/IIIa inhibitors distal to the culprit lesion was associated with reduced MVO and infarct size in high thrombotic risk STEMI patients undergoing pPCI.

Several methods for measuring IMR derived from angiography have been developed. AngioIMR is a novel method for the assessment of angiography-derived IMR with no requirement for a wire and hyperemia. The prognostic value of AngioIMR is unknown in STEMI patients. We aimed to provide the prognostic value of AngioIMR in patients with ST-elevation myocardial infarction (STEMI).

This study included patients with STEMI who underwent invasive coronary angiography and primary percutaneous coronary intervention (PPCI). AngioIMR was calculated using computational flow and pressure simulation immediately after PPCI. The presence of significant coronary microvascular dysfunction was defined as AngioIMR > 40. The primary outcome was a composite of all cause death or hospitalization for heart failure (MACE).

A total of 178 patients were included (65.0 ± 12.8 years on average, 74 % male gender). An AngioIMR > 40 was found in 72 patients. During a median follow-up of 2.9 (2.3-6.9) years, a primary endpoint was observed in 56 patients. By Kaplan-Meier analysis, the risk of MACE was significantly higher in patients with AngioIMR > 40 (log-rank P < 0.01). An Angio IMR > 40 was significantly associated with the occurrence of the primary endpoint in univariate (70 % vs 27 %; hazard ratio 4.519; 95 % CI: 2.550-8.009; p < 0.0001) and multivariate analysis (Hazard ratio 4.282; 95 % CI: 2.325-7.886; p < 0.0001). AngioIMR model showed incremental prognostic value compared to a model with clinical and imaging risk predictors (C-index 0.84 vs 0.79; p = 0.04).

Elevated AngioIMR showed a independent prognostic significance in STEMI patients. In addition to well-known risk factors, assessment of coronary microvascular dysfunction can be a feasible approach for early prevention and a therapeutic target in STEMI patients.

Acute coronary syndrome (ACS) patients undergoing primary percutaneous coronary intervention (PPCI) often experience the no-reflow phenomenon (NRP), characterized by reduced myocardial perfusion despite an open coronary artery. Adenosine, a potent vasodilator, is used to aid reperfusion. To elucidate underlying molecular mechanism of this phenomenon, we investigated expression of ADORA2A and ADORA2B genes, encoding adenosine receptors, in ACS patients with NRP and non-NRP.

We conducted a case-control study of 102 ACS patients undergoing PPCI, including 51 patients with NRP (TIMI flow grade 0 or 1) and 51 non-NRP patients with normal flow (TIMI flow grade 2 or 3). Gene expression was measured using Real-Time PCR.

Analysis showed significantly reduced expression of both ADORA2A and ADORA2B genes in NRP patients compared to non-NRP (p < 0.01). Furthermore, we observed a direct and moderate correlation between the two genes in NRP patients (r = 0.45, p = 0.001), whereas the correlation was stronger and more direct in non-NRP (r = 0.8, p = 0.0001).

Reduced adenosine receptor expression may contribute to the NRP in ACS patients undergoing PPCI. These findings highlighted the importance of understanding molecular mechanisms underlying this phenomenon to develop targeted therapies aimed at improving cardiac reperfusion.

Coronary atherosclerosis can lead to acute clinical events upon atherosclerotic plaque rupture (PR) or erosion and arterial thrombus formation. Identifying the effect of distinct plaque characteristics on clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) is critical for clinical therapy. Our goal was to ascertain the correlation between clinical outcome, long-term prognosis, and morphological plaque characteristics in STEMI.

The data used in this prospective cohort research came from a prior multicenter prospective cohort study (ChiCTR1800019923). One hundred and thirteen consecutive STEMI patients were involved in our cohort study. Patients with STEMI who received primary percutaneous coronary intervention (pPCI) within 24 hours of symptom onset were included in the study and divided into two groups according to plaque characteristics derived from intravascular ultrasound (IVUS): a PR group and a non-PR group. The primary outcome was the incidence of no reflow or slow flow, the secondary outcome was major adverse cardiac events (MACEs) at 1-year follow-up.

This study enrolled 113 consecutive patients with STEMI [mean age 56 (range, 49-65.5) years; males 90.27%]. Of the 113 patients, PR was found in 93 (82.3%), while non-PR was found in 20 (17.7%). The PR group had a higher rates of plaque eccentricity index (64.28%±22.69% vs. 60.08%±15.54%; P=0.045), higher rates of lipid pool-like images (62.37% vs. 30.00%; P=0.008), and higher rates of tissue prolapse (22.95% vs. 13.33%; P=0.01). Compared with that in the non-PR group, the incidence of no reflow or slow flow was higher in the PR group after pPCI (26.88% vs. 5.00%; P=0.04). Multivariable logistic regression showed that PR [odds ratio (OR) =8.188; 95% confidence interval (CI): 1.020-65.734; P=0.048] was an independent predictor of no reflow or slow flow. Survival analysis revealed no significant differences in MACE incidence between the two groups at 1-year follow-up (7.61% vs. 10.00%; P=0.66). Furthermore, 29 patients with PR were treated without stenting, most of them were free of MACEs (27/29). MACE between subgroups of stenting and non-stenting had no significant differences (7.94% vs. 6.90%; P=0.86) in the PR group.

In comparison to patients with non-PR, PR were not associated with the risk of recurrent myocardial infarction (MI), revascularization, heart failure, or cardiac death at 1-year follow-up, while associated with an increased incidence of no reflow or slow flow during pPCI. This observation would be considered while risk stratification and dealing with patients who have STEMI. Most patients with PR who were treated without stenting were MACE free. Further research should be conducted to determine whether interventional treatment without stenting is feasible for patients with STEMI and PR.

ST-elevation myocardial infarction (STEMI) remains a leading cause of morbidity and mortality in the United States. Timely reperfusion with primary percutaneous coronary intervention is associated with improved outcomes. The Society for Cardiovascular Angiography & Interventions puts forth this expert consensus document regarding best practices for cardiac catheterization laboratory team readiness, arterial access with an algorithm to help determine proper arterial access in STEMI, and diagnostic angiography. This consensus statement highlights the strengths and limitations of various diagnostic and therapeutic interventions to access and treat a patient with STEMI in the catheterization laboratory, reviews different options to manage large thrombus burden during STEMI, and reviews the management of STEMI across the spectrum of various anatomical and clinical circumstances.

Sonothrombolysis is a therapeutic application of ultrasound with ultrasound contrast for patients with ST elevation myocardial infarction (STEMI). Recent trials demonstrated that sonothrombolysis, delivered before and after primary percutaneous coronary intervention (pPCI), increases infarct vessel patency, improves microvascular flow, reduces infarct size, and improves ejection fraction. However, it is unclear whether pre-pPCI sonothrombolysis is essential for therapeutic benefit. We designed a parallel 3-arm sham-controlled randomized controlled trial to address this.

Patients presenting with first STEMI undergoing pPCI within 6 hours of symptom onset were randomized 1:1:1 into 3 arms: sonothrombolysis pre-/post-pPCI (group 1), sham pre- sonothrombolysis post-pPCI (group 2), and sham pre-/post-pPCI (group 3). Our primary end point was infarct size (percentage of left ventricular mass) assessed by cardiac magnetic resonance imaging at day 4 ± 2. Secondary end points included myocardial salvage index (MSI) and echocardiographic parameters at day 4 ± 2 and 6 months.

Our trial was ceased early due to the COVID pandemic. From 122 patients screened between September 2020 and June 2021, 51 patients (age 60, male 82%) were included postrandomization. Median sonothrombolysis took 5 minutes pre-pPCI and 15 minutes post-, without significant door-to-balloon delay. There was a trend toward reduction in median infarct size between group 1 (8% [interquartile range, 4,11]), group 2 (11% [7, 19]), or group 3 (15% [9, 22]). Similarly there was a trend toward improved MSI in group 1 (79% [64, 85]) compared to groups 2 (51% [45, 70]) and 3 (48% [37, 73]) No major adverse cardiac events occurred during hospitalization.

Pre-pPCI sonothrombolysis may be key to improving MSI in STEMI. Multicenter trials and health economic analyses are required before clinical translation.

Approximately 50% of patients with ST elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI) experience microvascular no-reflow. Pre- and post-PCI sonothrombolysis has been shown to decrease infarct size and improve left ventricular (LV) systolic function in STEMI patients receiving urgent PCI. The aim of this study was to investigate whether post-PCI sonothrombolysis alone in STEMI patients with persistent ST elevation could reduce no-reflow and infarct size.

Patients with STEMI with symptoms <12 hours who had persistent ST elevation (≤70% ST resolution) after primary PCI were randomized to sonothrombolysis or control. The primary end point was summed (Σ) ST elevation 60 minutes after study intervention. Secondary end points included infarct size, myocardial perfusion score, LV ejection fraction on cardiovascular magnetic resonance imaging at 2 months follow-up, and clinical outcome at 6-month follow-up.

Sixty-seven STEMI patients with persistent ST elevation after PCI were randomized (49 left anterior descending, 18 right coronary/left circumflex artery). No difference was observed in Σ ST elevation 60 minutes after study intervention (mean difference, 0.6 mm; 95% CI, -1.1 to 2.2, P = .50). Complete ST resolution occurred in 14 (40%) of patients treated with sonothrombolysis compared to 6 (19%) of controls (P = .16). Myocardial perfusion score index (1.5 ± 0.3 vs 1.5 ± 0.3, P = .93), infarct size (18.0% ± 10% vs 16.8% ± 11%; P = .29) and LV ejection fraction on cardiovascular magnetic resonance (46% ± 8% vs 47% ± 11% in the control group; P = .86) were comparable. Incidence of all-cause death, acute coronary syndrome, and hospital admission for heart failure at 6-month follow-up was similar between the groups (sonothrombolysis, 2; control, 5).

In STEMI patients with persistent ST elevation after PCI, post-PCI sonothrombolysis did not result in more ST resolution or smaller infarct size compared to control subjects. The incidence of the combined clinical end points was remarkably low in this high-risk patient population.

In patients with ST-segment elevation myocardial infarction (STEMI), acute inflammation is related to the extent of myocardial damage and may increase infarct size. Thus, administration of pulse-dose glucocorticoid in the very early phase of infarction may reduce infarct size.

To determine the cardioprotective effect of prehospital pulse-dose glucocorticoid in patients with STEMI.

This was a 1:1 investigator-initiated, blinded, placebo-controlled, randomized clinical trial conducted between November 14, 2022, and October 17, 2023, with last follow-up on January 17, 2024. Patients 18 years and older with less than 12 hours of acute chest pain and STEMI were included in the prehospital setting throughout the Region Zealand and Capital Region of Denmark and transferred to Rigshospitalet, Denmark.

Patients were randomly allocated to intravenous glucocorticoid (methylprednisolone, 250 mg) or placebo in the prehospital setting.

The primary outcome was final infarct size on cardiac magnetic resonance (CMR) at 3 months. The power calculation was based on an anticipated final infarct size of 13%. Secondary outcomes included CMR outcomes on acute scan and at 3 months, peak of cardiac biomarkers, clinical end points at 3 months, and adverse events.

Of 530 included patients (median [IQR] age, 65 [56-75] years; 418 male [78.9%]) with STEMI, 401 (76%) were assessed for the primary outcome, with 198 patients treated with glucocorticoid and 203 with placebo. Median final infarct size was similar in the treatment groups (glucocorticoid, 5%; IQR, 2%-11% vs placebo, 6%; IQR, 2%-13%; P = .24). Compared with placebo, the glucocorticoid group had smaller acute infarct size (odds ratio, 0.78; 95% CI, 0.61-1.00), less microvascular obstruction (relative risk ratio, 0.83; 95% CI, 0.71-0.99), and greater acute left ventricular ejection fraction (mean difference, 4.44%; 95% CI, 2.01%-6.87%). Other secondary outcomes were similar in both groups.

In patients with STEMI, treatment with prehospital pulse-dose glucocorticoid did not reduce final infarct size after 3 months. However, the trial was likely underpowered as the final infarct size was smaller than anticipated. The glucocorticoid group had improved acute parameters compared with placebo.

ClinicalTrials.gov Identifier: NCT05462730.

Early revascularization for patients with acute myocardial infarction (AMI) is of outmost importance in limiting infarct size and associated complications, as well as for improving long-term survival and outcomes. However, reperfusion itself may further damage the myocardium and increase the infarct size, a condition commonly recognized as myocardial reperfusion injury. Several strategies have been developed for limiting the associated with reperfusion myocardial damage, including hypothermia. Hypothermia has been shown to limit the degree of infarct size increase, when started before reperfusion, in several animal models. Systemic hypothermia, however, failed to show any benefit, due to adverse events and potentially insufficient myocardial cooling. Recently, the novel technique of intracoronary selective hypothermia is being tested, with preclinical and clinical results being of particular interest. Therefore, in this review, we will describe the pathophysiology of myocardial reperfusion injury and the cardioprotective mechanics of hypothermia, report the animal and clinical evidence in both systemic and selective hypothermia and discuss the potential future directions and clinical perspectives in the context of cardioprotection for myocardial reperfusion injury.

Studies assessing the treatment of refractory no-reflow in patients with ST-elevation myocardial infarction (STEMI) are limited to clinical cases and pilot studies. This study aimed to evaluate the efficacy and safety of intracoronary adrenaline administration in such patients. Ninety consecutive patients with refractory coronary no-reflow during percutaneous coronary intervention (PCI) were prospectively included after the initial failure of conventional treatment. They were randomized into 2 groups: 45 patients in Group 1 received adrenaline, and 45 patients in Group 2 (control) received conventional treatments alone. After intracoronary drug administration, the adrenaline group demonstrated significantly higher rates of coronary flow restoration in the infarct-related artery to the level of thrombolysis in myocardial infarction grade 3 (56% vs 29% [p = 0.01]) and resolution of STEMI >50% after PCI (78% vs 36% [p <0.001]). Additionally, the adrenaline group showed a lower indexed microvascular obstruction (MVO) volume compared with the control group (0.9 [0.3; 3.1] % vs 1.9 [0.6; 7.9] % [p = 0.048]). A significant improvement in ejection fraction (EF) was observed in the adrenaline group (p = 0.025). Intracoronary adrenaline administration during PCI in patients with STEMI with refractory no-reflow is more effective compared with conventional treatments. This approach improves coronary flow in the infarct-related artery, facilitates a faster resolution of STEMI, enhances EF, and reduces MVO volume. Intracoronary adrenaline administration demonstrates a comparable safety profile to conventional treatment strategies in terms of life-threatening arrhythmias occurrence. The study suggests that intracoronary adrenaline administration during PCI could be an effective treatment strategy for patients with STEMI with refractory no-reflow.

Microvascular injury immediately following reperfusion therapy in acute myocardial infarction (MI) has emerged as a driving force behind major adverse cardiovascular events in the postinfarction period. Although postmortem investigations and animal models have aided in developing early understanding of microvascular injury following reperfusion, imaging, particularly serial noninvasive imaging, has played a central role in cultivating critical knowledge of progressive damage to the myocardium from the onset of microvascular injury to months and years after in acute MI patients. This review summarizes the pathophysiological features of microvascular injury and downstream consequences, and the contributions noninvasive imaging has imparted in the development of this understanding. It also highlights the interventional trials that aim to mitigate the adverse consequences of microvascular injury based on imaging, identifies potential future directions of investigations to enable improved detection of disease, and demonstrates how imaging stands to play a major role in the development of novel therapies for improved management of acute MI patients.

The prognostic significance of various microvascular injury (MVI) patterns after ST-segment elevation myocardial infarction (STEMI) is not well known.

This study sought to investigate the prognostic implications of different MVI patterns in STEMI patients.

The authors analyzed 1,109 STEMI patients included in 3 prospective studies. Cardiac magnetic resonance (CMR) was performed 3 days (Q1-Q3: 2-5 days) after percutaneous coronary intervention (PCI) and included late gadolinium enhancement imaging for microvascular obstruction (MVO) and T2∗ mapping for intramyocardial hemorrhage (IMH). Patients were categorized into those without MVI (MVO-/IMH-), those with MVO but no IMH (MVO+/IMH-), and those with IMH (IMH+).

MVI occurred in 633 (57%) patients, of whom 274 (25%) had an MVO+/IMH- pattern and 359 (32%) had an IMH+ pattern. Infarct size was larger and ejection fraction lower in IMH+ than in MVO+/IMH- and MVO-/IMH- (infarct size: 27% vs 19% vs 18% [P < 0.001]; ejection fraction: 45% vs 50% vs 54% [P < 0.001]). During a median follow-up of 12 months (Q1-Q3: 12-35 months), a clinical outcome event occurred more frequently in IMH+ than in MVO+/IMH- and MVO-/IMH- subgroups (19.5% vs 3.6% vs 4.4%; P < 0.001). IMH+ was the sole independent MVI parameter predicting major adverse cardiovascular events (HR: 3.88; 95% CI: 1.93-7.80; P < 0.001).

MVI is associated with future adverse outcomes only in patients with a hemorrhagic phenotype (IMH+). Patients with only MVO (MVO+/IMH-) had a prognosis similar to patients without MVI (MVO-/IMH-). This highlights the independent prognostic importance of IMH in assessing and managing risk after STEMI.

Microvascular resistance reserve (MRR) can characterize coronary microvascular dysfunction (CMD); however, its prognostic impact in ST-segment elevation myocardial infarction (STEMI) patients remains undefined.

This study sought to investigate the prevalence of CMD in STEMI patients and to elucidate the prognostic performance of MRR.

This prospective cohort study enrolled 210 STEMI patients with multivessel disease who underwent successful revascularization and returned at 3 months for coronary physiology assessments with bolus thermodilution. The prevalence of CMD (MRR <3) and the association between MRR and major adverse cardiovascular and cerebrovascular events (MACCEs) at 12 months were investigated.

The median age of patients was 65 years, and 59.5% were men. At the 3-month follow-up, 56 patients (27%) had CMD (MRR <3.0). The number of MACCEs at 12 months was higher in patients with vs without CMD (48.2% vs 11.0%; P < 0.001). MRR was independently associated with 12-month MACCEs (HR: 0.45 per unit increase; 95% CI: 0.31-0.67; P < 0.001) and with stroke, heart failure, and poorer recovery in left ventricular systolic function. The areas under the receiver-operating characteristic curves for predicting MACCEs at 12 months with fractional flow reserve, coronary flow reserve (CFR), the index of microvascular resistance (IMR), and MRR were 0.609, 0.762, 0.781, and 0.743, respectively. The prognostic performance of CFR, IMR, and MRR were all comparable.

The novel parameter MRR is a prognostic marker of MACCEs in STEMI patients with a comparable performance to CFR and IMR. (Impact of TMAO Serum Levels on Hyperemic IMR in STEMI Patients [TAMIR]; NCT05406297).

Primary percutaneous coronary intervention (pPCI) has revolutionized the prognosis of ST-segment elevation myocardial infarction (STEMI) and is the gold standard treatment. As a result of its success, the number of pPCI centres has expanded worldwide. Despite decades of advancements, clinical outcomes in STEMI patients have plateaued. Out-of-hospital cardiac arrest and cardiogenic shock remain a major cause of high in-hospital mortality, whilst the growing burden of heart failure in long-term STEMI survivors presents a growing problem. Many elements aiming to optimize STEMI treatment are still subject to debate or lack sufficient evidence. This review provides an overview of the most contentious current issues in pPCI in STEMI patients, with an emphasis on unresolved questions and persistent challenges.

Despite prompt epicardial recanalization in patients presenting with ST-segment elevation myocardial infarction (STEMI), coronary microvascular obstruction and dysfunction (CMVO) is still fairly common and is associated with poor prognosis. Various pharmacological and mechanical strategies to treat CMVO have been proposed, but the positive results reported in preclinical and small proof-of-concept studies have not translated into benefits in large clinical trials conducted in the modern treatment setting of patients with STEMI. Therefore, the optimal management of these patients remains a topic of debate. In this Review, we appraise the pathophysiological mechanisms of CMVO, explore the evidence and provide future perspectives on strategies to be implemented to reduce the incidence of CMVO and improve prognosis in patients with STEMI.