Different associations between left atrial size and 2.5-year clinical outcomes in patients with anterior versus non-anterior wall ST-elevation myocardial infarction.
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ABSTRACT:
SUBMITTER: Gao F
PROVIDER: S-EPMC7140218 | biostudies-literature | 2020 Apr
REPOSITORIES: biostudies-literature
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Different associations between left atrial size and 2.5-year clinical outcomes in patients with anterior versus non-anterior wall ST-elevation myocardial infarction.
Gao Fan F Huo Jianhua J She Jianqing J Bai Ling L He Hairong H Lyu Jun J Qiang Hua H
The Journal of international medical research 20200401 4
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Project description:Background Following myocardial infarction, left ventricular remodeling (LVR) is associated with heart failure and cardiac death. At the same time, left atrial (LA) remodeling (LAR) is an essential part of the outcome of a wide spectrum of cardiac conditions. The authors sought to evaluate the correlates of LAR and its relationships with LVR after myocardial infarction. Methods and Results This is a retrospective analysis of 320 of 443 patients enrolled for study of LVR after ST-elevation myocardial infarction. Left ventricular (LV) volumes, infarct size and LA volume index were assessed by cardiac magnetic resonance imaging during index hospitalization (day 6 [interquartile range, 4-8]) and after a 3-month follow-up. LAR was studied using a linear mixed model for repeated measurements. Overall, there was a decrease in LA volume index between 6 days and 3 months (43.9±10.4 mL versus 42.8±11.1 mL, P=0.003). Patients with changes in LA volume index >8% over time were older, with greater body mass index, lower LV ejection fraction, and larger infarct size. Unadjusted predictors of LAR were age older than 70 years, infarct size, anterior infarction, time to reperfusion, history of hypertension, LV end-diastolic volume, and heart failure at day 6. Independent correlates were age older than 70 years (3.24±1.33, P=0.015) and infarct size (2.16±0.72 per 10% LV, P<0.001). LA remodeling was correlated with LV remodeling (r=0.372, P<0.001), but neither LA nor LV volumes at day 6 were related to LVR or LAR, respectively. Conclusions The authors found LA changes to occur in the months after myocardial infarction, with an overall decrease in LA volumes. While LAR coincided with LVR, the correlates for LAR were age older than 70 years and larger infarct size.
| S-EPMC10111554 | biostudies-literature
Project description:RationaleIn rodents, infarct size after ischemia/reperfusion exhibits a circadian dependence on the time of coronary occlusion. It is not known if a similar circadian dependence of infarct size occurs in humans.ObjectiveTo determine if humans exhibit a circadian dependence of infarct size in the setting of ST elevation myocardial infarction (STEMI).Methods and resultsA retrospective analysis of 1031 patients with STEMI referred for primary percutaneous coronary intervention with known ischemic times between 1 and 6 hours identified 165 patients with occluded arteries on presentation without evidence of preinfarction angina or collateral blood flow. Both ischemic duration and angiographic area at risk were not dependent on time of infarct onset. We observed that the extent of infarct size measured by creatine kinase release was significantly associated with time of day onset of infarction (P<0.0001). The greatest myocardial injury occurred at 1:00 am onset of ischemia and 5:00 am onset of reperfusion, with the peak creatine kinase measured at the peak of the curve being 82% higher than that recorded at the trough. Similarly, left ventricular ejection fraction measured within 2 days of infarction was also dependent on time of onset of STEMI with the absolute left ventricular ejection fraction at peak >7% higher than at trough (43% vs 51%; P<0.03). These findings were supported by a subgroup of patients (n = 45) who underwent cardiac MRI measurements of infarct size and area-at-risk measurements.ConclusionsThe results of this study demonstrate for the first time in humans that myocardial infarct size and left ventricular function after STEMI have a circadian dependence on the time of day onset of ischemia.
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Project description:ST segment elevation myocardial infarction remains a significant contributor to morbidity and mortality worldwide, despite a declining incidence and better survival rates. It usually results from thrombotic occlusion of a coronary artery at the site of a ruptured or eroded plaque. Diagnosis is based on characteristic symptoms and electrocardiogram changes, and confirmed subsequently by raised cardiac enzymes. Prognosis is dependent on the size of the infarct, presence of collaterals and speed with which the occluded artery is reopened. Mechanical reperfusion by primary percutaneous coronary intervention is superior to fibrinolytic therapy if delivered by an experienced team in a timely fashion. Post-reperfusion care includes monitoring for complications, evaluation of left ventricular function, secondary preventive therapy and cardiac rehabilitation.
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Project description:Adverse left ventricular (LV) remodeling after acute ST-elevation myocardial infarction (STEMI) is associated with morbidity and mortality. We studied clinical, biochemical and angiographic determinants of LV end diastolic volume index (LVEDVi), end systolic volume index (LVESVi) and mass index (LVMi) as global LV remodeling parameters 4 months after STEMI, as well as end diastolic wall thickness (EDWT) and end systolic wall thickness (ESWT) of the non-infarcted myocardium, as compensatory remote LV remodeling parameters. Data was collected in 271 patients participating in the GIPS-III trial, presenting with a first STEMI. Laboratory measures were collected at baseline, 2 weeks, and 6-8 weeks. Cardiovascular magnetic resonance imaging (CMR) was performed 4 months after STEMI. Linear regression analyses were performed to determine predictors. At baseline, patients were 21% female, median age was 58 years. At 4 months, mean LV ejection fraction (LVEF) was 54 ± 9%, mean infarct size was 9.0 ± 7.9% of LVM. Strongest univariate predictors (all p < 0.001) were peak Troponin T for LVEDVi (R2 = 0.26), peak CK-MB for LVESVi (R2 = 0.41), NT-proBNP at 2 weeks for LVMi (R2 = 0.24), body surface area for EDWT (R2 = 0.32), and weight for ESWT (R2 = 0.29). After multivariable analysis, cardiac biomarkers remained the strongest predictors of LVMi, LVEDVi and LVESVi. NT-proBNP but none of the acute cardiac injury biomarkers were associated with remote LV wall thickness. Our analyses illustrate the value of cardiac specific biochemical biomarkers in predicting global LV remodeling after STEMI. We found no evidence for a hypertrophic response of the non-infarcted myocardium.
| S-EPMC5539273 | biostudies-other
Project description:Infarction of the anterior myocardial wall results in anterior ST-elevation. However, ST-deviation may also appear inferiorly and may aid in localizing the culprit lesion.
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Project description:BackgroundIn-hospital left ventricular (LV) thrombus following acute ST-elevation myocardial infarction (STEMI) has not been evaluated on a national scale and was the focus of this investigation.MethodsWe used the 2003 to 2013 Nationwide Inpatient Sample database to identify adults ≥18 years old with a principal diagnosis code of ST-elevation myocardial infarction. Patients were divided into two groups defined by the presence or absence of LV thrombus. Clinical characteristics and in-hospital outcomes were studied using relevant statistics. Multiple linear and logistic regression models were conducted to identify factors associated with LV thrombus.ResultsOf 1,035,888 STEMI patients hospitalized in the U. S from 2003 to 2013, 1982 (0.2%) developed acute in-hospital LV thrombus. Compared to no LV thrombus, patients with LV thrombus were more likely to have in-hospital complications; acute ischemic and hemorrhagic stroke, acute renal failure, gastrointestinal bleed, cardiogenic shock, in-hospital cardiac arrest and mortality. They also had longer mean length of stay and higher hospital charges. Factors associated with LV thrombus included: anterior/anterolateral STEMI, acute or chronic heart failure with reduced ejection fraction, atrial fibrillation, LV aneurysm, Left heart valvular disease, acute or chronic deep venous thrombosis/pulmonary embolism and alcohol abuse. Patients with LV thrombus were less likely to be female [AOR 0.66, 95% CI (0.51-0.84)].ConclusionThe identification of factors associated with early development of LV thrombus following STEMI, will help direct resources for specific high-risk group and prompt cost-effective therapies. Gender variability in LV thrombus development warrants further investigations.
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Project description:Angiographic microvascular resistance (AMR) serves as an effective metric for assessing coronary microvascular status. The aim of this study was to investigate the predictive value of AMR for left ventricular thrombus (LVT) in ST-segment elevation myocardial infarction. This study enrolled 401 consecutive patients with anterior STEMI who underwent primary percutaneous coronary intervention (PPCI) between May 2019 and July 2023. AMR was measured immediately after PPCI via coronary angiography. LVT was identified during hospitalization through cardiac magnetic resonance imaging (CMR) or transthoracic echocardiography (TTE). Major adverse cardiac and cerebrovascular events (MACCEs) were recorded over 36 months follow-up. The predictive value of AMR was evaluated by logistic regression and receiver operating characteristic (ROC) analysis. Kaplan-Meier analysis was performed to estimate event-free rates for MACCEs. LVT was identified in 38 out of 401 anterior STEMI patients (9.5%). After adjusting for confounders through multivariable analysis, AMR was found to be an independent predictor of LVT (odds ratio [OR] 1.240 per 0.1 mmHg·s/cm, 95% confidence interval [CI]: 1.131-1.359, P < 0.001). ROC analysis demonstrated an area under the curve (AUC) of 0.742. For LVT, AMR provided modest incremental predictive value over established risk factors (continuous net reclassification improvement, 0.826 [95% CI: 0.523-1.129]; P < 0.001). Furthermore, Kaplan-Meier analysis revealed MACCEs for anterior STEMI patients with AMR ≥ 2.82 (log-rank P < 0.001). AMR is an independent predictor of LVT in anterior STEMI, providing incremental predictive value beyond traditional risk factors, and may be utilized to identify patients at risk for LVT.
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Project description:Isolated right ventricular myocardial infarctions (MIs) are rare, especially those presenting with anterior ST-segment elevation, which is normally seen in anterior MI. This occurs if the right coronary artery is nondominant. Differentiating between them is important for clinical management. Our case demonstrates a right ventricular MI presenting as an anterior ST-segment elevation myocardial infarction. (Level of Difficulty: Intermediate).
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Project description: Not available
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Project description:The ST-elevation Myocardial Infarction (STEMI) and Non-ST-elevation Myocardial Infarction (NSTEMI) might occur because of coronary artery stenosis. The gene biomarkers apply to the clinical diagnosis and therapeutic decisions in Myocardial Infarction. The aim of this study was to introduce, enrich and estimate timely the blood gene profiles based on the high-throughput data for the molecular distinction of STEMI and NSTEMI. The text mining data (50 genes) annotated with DisGeNET data (144 genes) were merged with the GEO gene expression data (5 datasets) using R software. Then, the STEMI and NSTEMI networks were primarily created using the STRING server, and improved using the Cytoscape software. The high-score genes were enriched using the KEGG signaling pathways and Gene Ontology (GO). Furthermore, the genes were categorized to determine the NSTEMI and STEMI gene profiles. The time cut-off points were identified statistically by monitoring the gene profiles up to 30 days after Myocardial Infarction (MI). The gene heatmaps were clearly created for the STEMI (high-fold genes 69, low-fold genes 45) and NSTEMI (high-fold genes 68, low-fold genes 36). The STEMI and NSTEMI networks suggested the high-score gene profiles. Furthermore, the gene enrichment suggested the different biological conditions for STEMI and NSTEMI. The time cut-off points for the NSTEMI (4 genes) and STEMI (13 genes) gene profiles were established up to three days after Myocardial Infarction. The study showed the different pathophysiologic conditions for STEMI and NSTEMI. Furthermore, the high-score gene profiles are suggested to measure up to 3 days after MI to distinguish the STEMI and NSTEMI.
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