Double Culprit Lesions in a Patient With ST-Segment Elevation Myocardial Infarction: Should I Stent or Should I Go?
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ABSTRACT:
SUBMITTER: Hage G
PROVIDER: S-EPMC8693337 | biostudies-literature | 2021 Dec
REPOSITORIES: biostudies-literature
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Double Culprit Lesions in a Patient With ST-Segment Elevation Myocardial Infarction: Should I Stent or Should I Go?
Hage Georges G Reibel Iphigénie I Dib Jean Claude JC Beverelli Fabrice F Allouch Philippe P Makowski Serge S Rosencher Julien J
JACC. Case reports 20211215 18
We describe the case of simultaneous acute thrombotic occlusions in 2 major coronary arteries in a young patient admitted for extensive myocardial infarction. We highlight the importance of intravascular imaging to determine the underlying putative mechanism and to optimize treatment decisions. (<b>Level of Difficulty: Intermediate.</b>). ...[more]
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Project description:Early diagnosis of acute ST-segment elevation myocardial infarction (STEMI) and early determination of the culprit vessel are associated with a better clinical outcome. We developed three deep learning (DL) models for detecting STEMIs and culprit vessels based on 12-lead electrocardiography (ECG) and compared them with conclusions of experienced doctors, including cardiologists, emergency physicians, and internists. After screening the coronary angiography (CAG) results, 883 cases (506 control and 377 STEMI) from internal and external datasets were enrolled for testing DL models. Convolutional neural network-long short-term memory (CNN-LSTM) (AUC: 0.99) performed better than CNN, LSTM, and doctors in detecting STEMI. Deep learning models (AUC: 0.96) performed similarly to experienced cardiologists and emergency physicians in discriminating the left anterior descending (LAD) artery. Regarding distinguishing RCA from LCX, DL models were comparable to doctors (AUC: 0.81). In summary, we developed ECG-based DL diagnosis systems to detect STEMI and predict culprit vessel occlusion, thus enhancing the accuracy and effectiveness of STEMI diagnosis.
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Project description:AimsPatients with ST-segment elevation myocardial infarction (STEMI) feature thrombus-rich lesions with large necrotic core, which are usually associated with delayed arterial healing and impaired stent-related outcomes. The use of bioresorbable vascular scaffolds (Absorb) has the potential to overcome these limitations owing to restoration of native vessel lumen and physiology at long term. The purpose of this randomized trial was to compare the arterial healing response at short term, as a surrogate for safety and efficacy, between the Absorb and the metallic everolimus-eluting stent (EES) in patients with STEMI.Methods and resultsABSORB-STEMI TROFI II was a multicentre, single-blind, non-inferiority, randomized controlled trial. Patients with STEMI who underwent primary percutaneous coronary intervention were randomly allocated 1:1 to treatment with the Absorb or EES. The primary endpoint was the 6-month optical frequency domain imaging healing score (HS) based on the presence of uncovered and/or malapposed stent struts and intraluminal filling defects. Main secondary endpoint included the device-oriented composite endpoint (DOCE) according to the Academic Research Consortium definition. Between 06 January 2014 and 21 September 2014, 191 patients (Absorb [n = 95] or EES [n = 96]; mean age 58.6 years old; 17.8% females) were enrolled at eight centres. At 6 months, HS was lower in the Absorb arm when compared with EES arm [1.74 (2.39) vs. 2.80 (4.44); difference (90% CI) -1.06 (-1.96, -0.16); Pnon-inferiority < 0.001]. Device-oriented composite endpoint was also comparably low between groups (1.1% Absorb vs. 0% EES). One case of definite subacute stent thrombosis occurred in the Absorb arm (1.1% vs. 0% EES; P = ns).ConclusionStenting of culprit lesions with Absorb in the setting of STEMI resulted in a nearly complete arterial healing which was comparable with that of metallic EES at 6 months. These findings provide the basis for further exploration in clinically oriented outcome trials.
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Project description:BackgroundLeukocyte-mediated inflammation is crucial in ST-segment elevation myocardial infarction (STEMI). We recently observed that neutrophil extracellular traps (NETs) are increased at the culprit site, promoting activation and differentiation of fibrocytes, cells with mesenchymal and leukocytic properties. Fibrocyte migration is mediated by monocyte chemoattractant protein (MCP)-1 and C-C chemokine receptor type 2 (CCR2). We investigated the interplay between NETs, fibrocyte function, and MCP-1 in STEMI.MethodsCulprit site and peripheral blood samples of STEMI patients were drawn during primary percutaneous coronary intervention. MCP-1 and the NET marker citrullinated histone H3 (citH3) were measured by ELISA while double-stranded DNA was stained with a fluorescent dye. The influence of MCP-1 on NET formation in vitro was assessed using isolated healthy donor neutrophils. Human coronary artery endothelial cells (hCAECs) were stimulated with isolated NETs, and MCP-1 gene expression was measured by ELISA and qPCR. CCR2 expression of culprit site and peripheral blood fibrocytes was characterized by flow cytometry. Healthy donor fibrocyte receptor expression and chemotaxis were investigated in response to stimulation with MCP-1 and NETs in vitro.ResultsNETs and concentrations of MCP-1 were increased at the culprit site of 50 consecutive STEMI patients. NET stimulation of hCAECs induced transcription of ICAM-1, IL-6, and MCP-1, and secretion of MCP-1. MCP-1 promoted NET formation of healthy donor neutrophils in vitro. An increasing MCP-1 gradient correlated with fibrocyte accumulation at the culprit site. Locally increased MCP-1 levels were negatively correlated with CCR2 expression on fibrocytes. MCP-1 and NETs induced CCR2 downregulation on fibrocytes in vitro. NETs did not function as a chemotactic stimulus for fibrocytes or monocytes and could block migration in response to MCP-1 for both cell populations.ConclusionNETs function as signaling scaffolds at the culprit site of STEMI. NETs assist MCP-1 and ICAM-1 release from culprit site coronary artery endothelial cells. MCP-1 facilitates further NETosis. Monocytes enter the culprit site along an MCP-1 gradient, to transdifferentiate into fibrocytes in the presence of NETs.
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Project description:It is assumed that platelets in diseased conditions share similar properties to platelets in healthy conditions, although this has never been examined in detail for myocardial infarction (MI). We examined platelets from patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) compared with platelets from healthy volunteers to evaluate for differences in platelet phenotype and function. Platelet activation was examined and postreceptor signal transduction pathways were assessed. Platelet-derived plasma biomarkers were evaluated by receiver operator characteristic curve analysis. Maximum platelet activation through the thromboxane receptor was greater in STEMI than in NSTEMI but less through protease-activated receptor 1. Extracellular-signal related-kinase 5 activation, which can activate platelets, was increased in platelets from subjects with STEMI and especially in platelets from patients with NSTEMI. Matrix metalloproteinase 9 (MMP9) protein content and enzymatic activity were several-fold greater in platelets with MI than in control. Mean plasma MMP9 concentration in patients with MI distinguished between STEMI and NSTEMI (area under curve [AUC] 75% [confidence interval (CI) 60-91], P = 0.006) which was superior to troponin T (AUC 66% [CI 48-85, P = 0.08), predicting STEMI with 80% sensitivity (95% CI 56-94), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P < 0.0001), and NSTEMI with 50% sensitivity (CI 27-70), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P = 0.03). Platelets from patients with STEMI and NSTEMI show differences in platelet surface receptor activation and postreceptor signal transduction, suggesting the healthy platelet phenotype in which antiplatelet agents are often evaluated in preclinical studies is different from platelets in patients with MI.
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Project description:The clinical presentation of pulmonary embolism (PE) and acute coronary syndrome can be similar. We report a case of a patient presenting with antero-septal ST-segment elevation after cardiac arrest, found to have acute-PE-mimicking ST-segment elevation myocardial infarction (STEMI), treated with aspiration thrombectomy and catheter-directed thrombolysis (CDT). A 78-year-old man was admitted with dyspnea, chest pain and tachycardia. During evaluation, cardiac arrest in pulseless electrical activity was documented. Advanced life support was started immediately. ECG post-ROSC revealed ST-segment elevation in V1-V4 and aVR. Echocardiography showed normal left ventricular function but right ventricular (RV) dilation and severe dysfunction. The patient was in shock and was promptly referred to cardiac catheterization that excluded significant CAD. Due to the discordant ECG and echocardiogram findings, acute PE was suspected, and immediate invasive pulmonary angiography revealed bilateral massive pulmonary embolism. Successful aspiration thrombectomy was performed followed by local alteplase infusion. At the end of the procedure, mPAP was reduced and blood pressure normalized allowing withdrawal of vasopressor support. Twenty-four-hour echocardiographic reassessment showed normal-sized cardiac chambers with preserved biventricular systolic function. Bedside echocardiography in patients with ST-segment elevation post-ROSC is instrumental in raising the suspicion of acute PE. In the absence of a culprit coronary lesion, prompt pulmonary angiography should be considered if immediately feasible. In these cases, CDT and aspiration in high-risk acute PE seem safe and effective in relieving obstructive shock and restoring hemodynamics.
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Project description:Acute myocardial infarction (AMI) complicated by cardiogenic shock has high mortality and remains challenging even in the revascularization era. We conducted this study to understand patients' outcomes. We retrospectively analyzed electronic medical records data from 1175 patients with AMI complicated by cardiogenic shock that developed within 3 days of admission to a multicenter medical care system between January 1, 2000, and July 31, 2018. Patients with AMI were classified into the ST-segment elevation MI (STEMI) group or the non-ST-segment elevation MI (NSTEMI) group. The short-term and 1-year mortality and adverse events after index admission were analyzed via logistic regression and a Cox proportional hazards model. When compared with NSTEMI, patients with STEMI tended to be younger (65.68 ± 14.05 years vs 70.70 ± 12.99 years, P < .001), men (73.29% vs 60.87%, P < .001), and have fewer underlying chronic diseases. Short-term mortality at index hospitalization was 14.83% in the STEMI group and 21.30% in the NSTEMI group; long-term mortality was 17.06% for the STEMI group and 24.13% for the NSTEMI group. No difference was observed between the 2 groups for patients who developed a cerebral vascular accident during the admission period. However, the major and gastrointestinal bleeding rates were higher in the STEMI group (2.66% vs 0.22%, P = .014; 3.36% vs 0.22%, P = .007, respectively). Age and respiratory failure were the most significant risk factors for short-term mortality. Revascularization may be beneficial for the short-term outcome but did not reach significance in multivariable analysis. In patients with AMI with cardiogenic shock, NSTEMI was associated with a significantly higher mortality rate in short-term results.
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Project description:Several organizations have developed guidelines for the management of ST-segment elevation myocardial infarction (STEMI). However, the optimal strategy regarding revascularization in the setting of multivessel disease, specifically with regards to culprit vessel versus complete revascularization, continues to evolve. While previous observational studies promoted culprit vessel-only intervention in patients with STEMI, recent randomized controlled trials suggest potential benefits with multivessel revascularization, either at the time of the index event or in a staged fashion, in patients without cardiogenic shock. This may be due to the known instability of non-culprit lesions in the setting of acute coronary syndrome, and the diffuse coronary processes involved. As additional literature examines culprit vessel versus multivessel revascularization strategies, clinicians continue to be tasked with determining optimal treatment plans for their patients and understanding the factors that promote selected revascularization strategies. This review summarizes and discusses observational studies, randomized control trials and current guidelines in order to evaluate optimal reperfusion strategies for patients presenting with STEMI in the setting of multivessel disease.
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Project description:BackgroundEndothelial and microvascular dysfunction are frequently found in the non-culprit territory in patients with acute myocardial infarction (AMI). We aimed to determine whether an impaired coronary physiology of the non-culprit territory impacts long-term prognosis.MethodsFISIOIAM was an observational single-center study which included patients with AMI and another coronary artery lesion in a different territory. Intracoronary physiology of the non-culprit artery was analyzed early after primary percutaneous coronary intervention of the culprit artery, using fractional flow reserve (FFR), index of microcirculatory resistance (IMR), coronary flow reserve (CFR), endothelium-dependent CFR (eCFR) and macrovascular endothelial function . Patients were followed for a composite outcome of cardiovascular death, non-fatal myocardial infarction, coronary revascularization, and hospitalization due to heart failure or unstable angina.ResultsA total of 84 patients (mean age: 62 ± 10 years) were included and functional abnormalities were detected in 93% of them. During follow-up (median of 1422 days; interquartile range, 1287-1634), 13.1% of the patients experienced at least one adverse cardiovascular event. Kaplan-Meier analysis revealed that patients with a CFR < 2 had a higher risk of events (Hazard Ratio, HR: 4.97, 95% Confidence Interval, CI, 1.32-18.75), whereas other parameters such as FFR, IMR, eCFR, and macrovascular endothelial function had no effect. A low CFR was an independent predictor of cardiovascular events, even after adjustment for age and traditional cardiovascular risk factors (adjusted HR: 6.62, 95% CI, 1.30-33.70).ConclusionsThe presence of abnormal coronary microvascular function as measured by a CFR < 2 in the non-culprit territory predicts future risk of adverse cardiovascular events.
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Project description:ImportanceRecently, the Complete vs Culprit-Only Revascularization to Treat Multivessel Disease After Early PCI (percutaneous coronary intervention) for STEMI (ST-segment elevation myocardial infarction [MI]) (COMPLETE) trial showed that angiography-guided PCI of the nonculprit lesion with the goal of complete revascularization reduced cardiovascular (CV) death or new MI compared with PCI of the culprit lesion only in STEMI. Whether complete revascularization also reduces CV mortality is uncertain. Moreover, whether the association of complete revascularization with hard clinical outcomes is consistent when fractional flow reserve (FFR)- and angiography-guided strategies are used is unknown.ObjectiveTo determine through a systematic review and meta-analysis (1) whether complete revascularization is associated with decreased CV mortality and (2) whether heterogeneity in the association occurs when FFR- and angiography-guided PCI strategies for nonculprit lesions are performed.Data sourcesA systematic search of MEDLINE, Embase, ISI Web of Science, and CENTRAL (Cochrane Central Register of Controlled Trials) from database inception to September 30, 2019, was performed. Conference proceedings were also reviewed from January 1, 2002, to September 30, 2019.Study selectionEnglish-language randomized clinical trials comparing complete revascularization vs culprit-lesion-only PCI in patients with STEMI and multivessel disease were included.Data extraction and synthesisThe combined odds ratio (OR) was calculated with the random-effects model using the Mantel-Haenszel method (sensitivity with fixed-effects model). Heterogeneity was measured using the I2 statistic. Publication bias was evaluated using the inverted funnel plot approach. Data were analyzed from October 2019 to January 2020.Main outcomes and measuresCardiovascular death and the composite of CV death or new MI.ResultsTen randomized clinical trials involving 7030 unique patients were included. The weighted mean follow-up time was 29.5 months. Complete revascularization was associated with reduced CV death compared with culprit-lesion-only PCI (80 of 3191 [2.5%] vs 106 of 3406 [3.1%]; OR, 0.69 [95% CI, 0.48-0.99]; P = .05; fixed-effects model OR, 0.74 [95% CI, 0.55-0.99]; P = .04). All-cause mortality occurred in 153 of 3426 patients (4.5%) in the complete revascularization group vs 177 of 3604 (4.9%) in the culprit-lesion-only group (OR, 0.84 [95% CI, 0.67-1.05]; P = .13; I2 = 0%). Complete revascularization was associated with a reduced composite of CV death or new MI (192 of 2616 [7.3%] vs 266 of 2586 [10.3%]; OR, 0.69 [95% CI, 0.55-0.87]; P = .001; fixed-effects model OR, 0.69 [95% CI, 0.57-0.84]; P < .001), with no heterogeneity in this outcome when complete revascularization was performed using an FFR-guided strategy (OR, 0.78 [95% CI, 0.43-1.44]) or an angiography-guided strategy (OR, 0.61 [95% CI, 0.38-0.97]; P = .52 for interaction).Conclusions and relevanceIn patients with STEMI and multivessel disease, complete revascularization was associated with a reduction in CV mortality compared with culprit-lesion-only PCI. There was no differential association with treatment between FFR- and angiography-guided strategies on major CV outcomes.
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Project description:ObjectiveTo investigate the relationship between ST-segment resolution (STR) and myocardial scar thickness after percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI).MethodsForty-two STEMI patients with single-branch coronary artery stenosis or occlusion were enrolled. ST-segment elevations were measured at emergency admission and at 24 h after PCI. Late gadolinium-enhanced cardiac magnetic resonance imaging (CMR-LGE) was performed 7 days after PCI to evaluate myocardial scars. Statistical analyses were performed to assess the utility of STR to predict the development of transmural (> 75%) or non-transmural (< 75%) myocardial scars, according to previous study.ResultsThe sensitivity and specificity of STR for predicting transmural scars were 96% and 88%, respectively, at an STR cut-off value of 40.15%. The area under the curve was 0.925. Multivariate logistic proportional hazards regression analysis disclosed that patients with STR < 40.15% had a 170.90-fold higher probability of developing transmural scars compared with patients with STR ≥ 40.15%. Pearson correlation and linear regression analyses showed STR percentage was significantly associated with myocardial scar thickness and size.ConclusionSTR < 40.15% at 24 h after PCI may provide meaningful diagnostic information regarding the extent of myocardial scarification in STEMI patients.
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