Prevalence and outcome of patients with non-ST segment elevation myocardial infarction with occluded "culprit" artery - a systemic review and meta-analysis.
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SUBMITTER: Hung CS
PROVIDER: S-EPMC5806289 | biostudies-literature | 2018 Feb
REPOSITORIES: biostudies-literature
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Prevalence and outcome of patients with non-ST segment elevation myocardial infarction with occluded "culprit" artery - a systemic review and meta-analysis.
Hung Chi-Sheng CS Chen Ying-Hsien YH Huang Ching-Chang CC Lin Mao-Shin MS Yeh Chih-Fan CF Li Hung-Yuan HY Kao Hsien-Li HL
Critical care (London, England) 20180209 1
<h4>Background</h4>The aim was to determine the prevalence and impact of an occluded "culprit" artery (OCA) in patients with non-ST segment elevation myocardial infarction (NSTEMI).<h4>Methods</h4>We searched PubMed, EMBASE, and Web of Science, with no language restrictions, up to 1 Jul. 2016. Observational cohorts or clinical trials of adult NSTEMI were eligible for inclusion to determine the prevalence if the proportion of OCA on coronary angiography was reported. Studies were further eligible ...[more]
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Project description:BACKGROUND:Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors. METHODS:IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire-based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days). RESULTS:Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0-33.0] vs. 17 [13.0-39.0] vs. 37 [21.0-63.0], P < 0.001; CFR: 1.7 [1.4-2.5] vs. 1.5 [1.1-1.8] vs. 1.4 [1.0-1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG. CONCLUSIONS:IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR. TRIAL REGISTRATION:NCT02072850. FUNDING:A British Heart Foundation Project Grant (PG/11/2/28474), the National Health Service, the Chief Scientist Office, a Scottish Funding Council Senior Fellowship, a British Heart Foundation Intermediate Fellowship (FS/12/62/29889), and a nonfinancial research agreement with Siemens Healthcare.
| S-EPMC5033815 | biostudies-literature
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:Background: Primary percutaneous coronary intervention (PCI) is the most frequently used treatment modality for patients presenting with ST elevation myocardial infarction (STEMI). Current professional society guidelines recommend culprit artery only PCI. Recent evidence suggests the potential benefit of multivessel PCI among patients with STEMI that is not complicated by cardiogenic shock. Methods: We systematically searched PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials for clinical studies of patients with STEMI, not complicated by cardiogenic shock, who underwent primary PCI between January 1966 and January 2018. We evaluated all-cause and cardiovascular mortality, reinfarction, and repeat revascularization among patients randomized to a multivessel PCI strategy compared to a culprit artery only PCI strategy. Results: Four randomized clinical trials with a total of 1,044 patients met the inclusion criteria. Five hundred and sixty-six patients underwent multivessel PCI, and 478 patients underwent culprit artery only PCI. Multivessel PCI reduced all the studied endpoints: total death, cardiac death, reinfarction, and repeat revascularization (all P values <0.05). Conclusion: To our knowledge, this is the largest metaanalysis of randomized controlled trials studying multivessel PCI vs culprit artery only PCI in STEMI patients without shock, among whom lesion severity was graded by angiography alone. We found that compared to culprit artery only PCI, the multivessel PCI strategy was beneficial in reducing all-cause and cardiovascular mortality, reinfarction, and the need for repeat revascularization.
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Project description:BackgroundApproximately 5-15% of patients with acute coronary syndrome have myocardial infarction with unobstructed coronary arteries (MINOCA). Guidelines recommend invasive assessments to identify underlying causes for MINOCA such as coronary artery spasm (CAS), spontaneous coronary dissection, or microvascular disease as well as non-invasive assessments in search of myocarditis, takotsubo syndrome, or cardiomyopathies.Case summaryA 54-year-old male patient presented with ST-segment elevation myocardial infarction (STEMI). Upon arrival, ST-segment elevation and symptoms had ceased. Emergency coronary angiography showed diffuse epicardial atherosclerosis with stenoses in the distal left anterior descending coronary artery (LAD) and second diagonal branch (D2); however, no epicardial occlusion was seen. Left ventriculography showed no clear wall motion abnormalities. Based on these findings, intracoronary acetylcholine (ACh) testing in search of CAS was performed. At 200 µg ACh intracoronary ST-segment elevation and chest pain recurred. Angiography showed occlusive epicardial spasm in the LAD and D2. Based on studies where the tendency of epicardial CAS was linked with the presence of epicardial atherosclerosis, the decision was made to perform PCI in the LAD and D2. ACh re-challenge after intracoronary nitroglycerine revealed only very mild symptoms, no demonstrable epicardial CAS, and no ST-segment elevation anymore. Cardiac enzymes reached their peak on day one [creatine kinase max 262 U/L (norm < 190 U/L), maximum of high-sensitivity troponin T 269 pg/mL (n < 14 pg/mL)].DiscussionThere is a broad spectrum of patients with STEMI without culprit lesion regarding the extent of epicardial disease. In cases with an unclear culprit lesion, other causes for the acute presentation such as CAS should be investigated in an ad hoc fashion. The interplay of epicardial atherosclerosis and CAS should receive more attention in future trials.
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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:Background Few studies have investigated optimal revascularization strategies in non-ST-segment-elevation myocardial infarction with multivessel disease. We investigated 3-year clinical outcomes according to revascularization strategy in patients with non-ST-segment-elevation myocardial infarction and multivessel disease. Methods and Results This retrospective, observational, multicenter study included patients with non-ST-segment-elevation myocardial infarction and multivessel disease without cardiogenic shock. Data were analyzed at 3 years according to the percutaneous coronary intervention strategy: culprit-only revascularization (COR), 1-stage multivessel revascularization (MVR), and multistage MVR. The primary outcome was major adverse cardiac events (MACE: a composite of all-cause death, nonfatal spontaneous myocardial infarction, or any repeat revascularization). The COR group had a higher risk of MACE than those involving other strategies (COR versus 1-stage MVR; hazard ratio, 0.65; 95% CI, 0.54-0.77; P<0.001; and COR versus multistage MVR; hazard ratio, 0.74; 95% CI, 0.57-0.97; P=0.027). There was no significant difference in the incidence of MACE between 1-stage and multistage MVR (hazard ratio, 1.14; 95% CI, 0.86-1.51; P=0.355). The results were consistent after multivariate regression, propensity score matching, inverse probability weighting, and Bayesian proportional hazards modeling. In subgroup analyses stratified by the Global Registry of Acute Coronary Events score, 1-stage MVR lowered the risk of MACE compared with multistage MVR in low-to-intermediate risk patients but not in patients at high risk. Conclusions MVR reduced 3-year MACE in patients with non-ST-segment-elevation myocardial infarction and multivessel disease compared with COR. However, 1-stage MVR was not superior to multistage MVR for reducing MACE except in low-to-intermediate risk patients.
| S-EPMC7792267 | biostudies-literature
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.
| S-EPMC7240651 | biostudies-literature
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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Project description:ImportanceChallenges to improving ST-segment elevation myocardial infarction (STEMI) care are formidable in low- to middle-income countries because of several system-level factors.ObjectiveTo examine access to reperfusion and percutaneous coronary intervention (PCI) during STEMI using a hub-and-spoke model.Design, setting, and participantsThis multicenter, prospective, observational study of a quality improvement program studied 2420 patients 20 years or older with symptoms or signs consistent with STEMI at primary care clinics, small hospitals, and PCI hospitals in the southern state of Tamil Nadu in India. Data were collected from the 4 clusters before implementation of the program (preimplementation data). We required a minimum of 12 weeks for the preimplementation data with the period extending from August 7, 2012, through January 5, 2013. The program was then implemented in a sequential manner across the 4 clusters, and data were collected in the same manner (postimplementation data) from June 12, 2013, through June 24, 2014, for a mean 32-week period.ExposuresCreation of an integrated, regional quality improvement program that linked the 35 spoke health care centers to the 4 large PCI hub hospitals and leveraged recent developments in public health insurance schemes, emergency medical services, and health information technology.Main outcomes and measuresPrimary outcomes focused on the proportion of patients undergoing reperfusion, timely reperfusion, and postfibrinolysis angiography and PCI. Secondary outcomes were in-hospital and 1-year mortality.ResultsA total of 2420 patients with STEMI (2034 men [84.0%] and 386 women [16.0%]; mean [SD] age, 54.7 [12.2] years) (898 in the preimplementation phase and 1522 in the postimplementation phase) were enrolled, with 1053 patients (43.5%) from the spoke health care centers. Missing data were common for systolic blood pressure (213 [8.8%]), heart rate (223 [9.2%]), and anterior MI location (279 [11.5%]). Overall reperfusion use and times to reperfusion were similar (795 [88.5%] vs 1372 [90.1%]; P = .21). Coronary angiography (314 [35.0%] vs 925 [60.8%]; P < .001) and PCI (265 [29.5%] vs 707 [46.5%]; P < .001) were more commonly performed during the postimplementation phase. In-hospital mortality was not different (52 [5.8%] vs 85 [5.6%]; P = .83), but 1-year mortality was lower in the postimplementation phase (134 [17.6%] vs 179 [14.2%]; P = .04), and this difference remained consistent after multivariable adjustment (adjusted odds ratio, 0.76; 95% CI, 0.58-0.98; P = .04).Conclusions and relevanceA hub-and-spoke model in South India improved STEMI care through greater use of PCI and may improve 1-year mortality. This model may serve as an example for developing STEMI systems of care in other low- to middle-income countries.
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