Admission proteinuria predicts the incidence of acute kidney injury among patients with acute ST-segment elevation myocardial infarction: a retrospective cohort study.

BACKGROUND: Proteinuria indicates renal dysfunction and is associated with the development of acute kidney injury (AKI) in several conditions, but the association between proteinuria and AKI in patients with ST-segment elevation myocardial infarction (STEMI) remains unclear. This research aims to investigate the predictive value of proteinuria for the development of AKI in STEMI patients. METHODS: A total of 2735 STEMI patients were enrolled. The present study's endpoint was AKI incidence during hospitalization. AKI is defined according to the Kidney Disease: Improving Global Outcomes criteria. We defined proteinuria, measured with a dipstick, as mild (1+) or heavy (2+ to 4+). Multivariate logistic regression and subgroup analyses were used to testify to the association between proteinuria and AKI. RESULTS: Overall, proteinuria was observed in 634 (23.2%) patients. Multivariate logistic regression analyses revealed that proteinuria [odds ratio (OR), 1.58; 95% confidence interval (CI), 1.25-2.00; P  < 0.001] was the independent predictive factor for AKI. Severe proteinuria was associated with a higher adjusted risk for AKI compared with the nonproteinuria group (mild proteinuria: OR, 1.35; 95% CI, 1.04-1.75; P  = 0.025; severe proteinuria: OR, 2.50; 95% CI, 1.70-3.68; P  < 0.001). The association was highly consistent across all studied subgroups. (all P for interaction >0.05). CONCLUSION: Admission proteinuria measured using a urine dipstick is an independent risk factor for the development of AKI in STEMI patients.

Copeptin for the differentiation of type 1 versus type 2 myocardial infarction or myocardial injury.

BACKGROUND: The rapid and reliable differentiation of myocardial infarction (MI) due to atherothrombosis (T1MI) from MI due to supply-demand mismatch (T2MI) or acute myocardial injury is of major clinical relevance due to very different treatments, but still a major unmet clinical need. This study aimed to investigate whether copeptin, a stress hormone produced in the hypothalamus, helps to differentiate between T1MI versus T2MI or injury. METHODS: In a retrospective analysis, 1271 unselected consecutive patients presenting with symptoms suggestive of MI to the emergency department were evaluated. Patients diagnosed with ST-elevation MI were excluded. All patients with elevated cardiac troponin I (cTnI) concentration possibly indicating MI were classified into T1MI, T2MI, or acute myocardial injury using detailed clinical assessment and coronary imaging. Copeptin plasma concentration was measured in a blinded fashion. A multicenter diagnostic study with central adjudication of the final diagnosis served as external validation cohort (n = 1390). RESULTS: Among 1161 patients, 154 patients had increased cTnI concentration. Of these, 78 patients (51%) were classified as T1MI and 76 (49%) as T2MI or myocardial injury. Patients with T2MI or myocardial injury had significantly higher copeptin plasma concentration between patients versus T1MI (21,4 pmol/l versus 8,1 pmol/l, p = 0,001). A multivariable regression analysis revealed that higher concentrations of copeptin and C-reactive protein, higher heart rate at presentation and lower frequency of smoking remained significantly associated with T2MI and myocardial injury. Findings were largely confirmed in the external validation cohort. CONCLUSION: In patients without ST-segment elevation, copeptin concentration was higher in T2MI and myocardial Injury versus T1MI and may help in their differential diagnosis.

[Communication interventriculaire compliquant un infarctus de myocarde antérieur : un cas de fermeture percutanée]. / Ventricular septal defect complicating anterior acute myocardial infarction : A Case of transcatheter closure.

INTRODUCTION: Post-infarction ventricular septal defect (PIVSD) is one of the most serious mechanical complications of acute myocardial infarction (AMI). Over the last decade, percutaneous closure is increasingly undertaken, with results similar to cardiac surgery. We present a case of ST-elevated anterior AMI, complicated by apical PIVSD successfully treated with transcatheter closure. CASE REPORT: An 83-year-old man was hospitalized for chest pain occurred 18 hours before, during the night time. He was an active smoker. Clinical examination revealed normal heart sounds and pulmonary bibasilar crackles. ST-segment elevation with deep T waves inversion in anterior leads were detected on the electrocardiogram. A mildly-reduced ejection fraction (40%) was found by transthoracic echocardiogram. The patient underwent emergency coronary angiography, which revealed a subocclusive stenosis of the mid left anterior descending artery with a TIMI 2 flow, treated by balloon angioplasty and drug-eluting stent. Four days after revascularization, the patient developed an acute deterioration with signs of decompensated heart failure and a new holosystolic murmur with large irradiation. Inotropic agents' administration was required to maintain a precarious hemodynamic condition. A bedside Echo revealed an apical VSD, measuring 15 × 10 mm, with left-to-right shunting, and pulmonary hypertension. The patient was scheduled for transcatheter PIVSD closure. The procedure was performed under fluoroscopic guide. Two vascular access sites were placed, femoral arterial and right internal jugular vein. Through the right internal jugular vein, a 24-mm Amplatzer atrial septal occluder on a 9 French Amplatzer TREVISIO™ intravascular delivery system was advanced via right ventricle into the PIVSD. Contrast fluoroscopy was used to assess apposition and the degree of shunt reduction before release. Echocardiographic evaluation performed 48 hours later confirmed a correct apposition of the device with insignificant residual shunt. At 6 months follow-up, he was asymptomatic, with unchanged prosthetic findings. CONCLUSION: Percutaneous closure has been emerged as a valid cost-effective alternative to surgery and should be advised. However, debate remains on the optimal preprocedural optimization, timing of repair and modality of treatment.

Incidence and outcomes of high bleeding risk patients with type 1 and type 2 myocardial infarction in a community-based cohort: Application of the Academic Research Consortium High Bleeding Risk Criteria.

BACKGROUND AND AIMS: The incidence and outcomes of high bleeding risk (HBR) patients in a community cohort according to the Academic Research Consortium (ARC) criteria is not known. We hypothesized that HBR is common and associated with worse outcomes for all-comers with myocardial infarction. METHODS: We prospectively collected all patients with cardiac troponin T > 99th percentile upper limit of normal (≥0.01 ng/mL) in Olmsted County between 2003 and 2012. Events were retrospectively classified as type 1 myocardial infarction (T1MI), type 2 myocardial infarction (T2MI), or myocardial injury. Patients were further classified as HBR based on the "ARC-HBR definition." Outcomes included all-cause mortality, cardiovascular mortality, recurrent MI, stroke, and major bleeding. RESULTS: 2419 patients were included in the final study; 1365 were classified as T1MI and 1054 as T2MI. Patients were followed for a median of 5.5 years. ARC-HBR was more common in T2MI than T1MI (73% vs 46%, p < 0.001). Among patients with T1MI, HBR was associated with higher all-cause mortality (HR 3.7, 95% CI 3.2-4.5, p < 0.001), cardiovascular mortality (4.7, 3.6-6.3, p < 0.001), recurrent MI (2.1, 1.6-2.7, p < 0.001), stroke (4.9, 2.9-8.4, p < 0.001), and major bleeding (6.5, 3.7-11.4, p < 0.001). For T2MI, HBR was similarly associated with higher all-cause mortality (HR 2.1, 95% CI 1.8-2.5, p < 0.001), cardiovascular mortality (2.7, 1.8-4.0, p < 0.001), recurrent MI (1.7, 1.1-2.6, p = 0.02) and major bleeding (HR 15.6, 3.8-63.8, p < 0.001). CONCLUSION: HBR is common among unselected patients with T1MI and T2MI and is associated with increased overall and cardiovascular mortality, recurrent cardiovascular events, and major bleeding on long-term follow up.

Stratification of acute myocardial and endothelial cell injury, salvage index and final infarct size by systematic microRNA profiling in acute ST-elevation myocardial infarction.

AIM: Acute injury and subsequent remodelling responses to ST-segment elevation myocardial infarction (STEMI) are major determinants of clinical outcome. Current imaging and plasma biomarkers provide delayed readouts of myocardial injury and recovery. Here, we sought to systematically characterize all microRNAs (miRs) released during the acute phase of STEMI and relate miR release to magnetic resonance imaging (MRI) findings to predict acute and late responses to STEMI, from a single early blood sample. METHODS AND RESULTS: miRs were quantified in blood samples obtained from patients after primary PCI (PPCI) for STEMI. Cardiac MRI (cMRI) was performed to quantify myocardial edema, infarct size and salvage index. Regression models were constructed to predict these outcomes measures, which were then tested with a validation cohort. Transcoronary miR release was quantified from paired measurements of coronary artery and coronary sinus samples. A cell culture model was used to identify endothelial cell-derived miRs.A total of 72 patients undergoing PPCI for acute STEMI underwent miR analysis and cMRI. About >200 miRs were detectable in plasma after STEMI, from which 128 miRs were selected for quantification in all patients. Known myocardial miRs demonstrated a linear correlation with troponin release, and these increased across the transcoronary gradient. We identified novel miRs associated with microvascular injury and myocardial salvage. Regression models were constructed using a training cohort, then tested in a validation cohort, and predicted myocardial oedema, infarct size and salvage index. CONCLUSION: Analysis of miR release after STEMI identifies biomarkers that predict both acute and late outcomes after STEMI. A novel miR-based biomarker score enables the estimation of area at risk, late infarct size and salvage index from a single blood sample 6 hours after PPCI, providing a simple and rapid alternative to serial cMRI characterization of STEMI outcome.

Biomarker array for prediction of acute kidney injury after percutaneous coronary intervention for patients who had acute ST segment elevation myocardial infarction.

Acute kidney injury (AKI) is a common complication after Percutaneous Coronary Intervention (PCI) for ST segment elevation myocardial infarction (STEMI) and is associated with poor outcomes. AKI is diagnosed by the dynamic change of serum Cr, but it could not predict AKI. This study aimed to evaluate a biomarker array that may fulfill this shortage. Setting: Cardiology Department, Tanta University Hospital. Design: Prospective interventional study included 280 acute STEMI patients who underwent emergency PCI. Serial samples of blood and urine were obtained at the time of admission to the hospital (T0) and PCI unit (T1) and at 12 h and 72 h (T12 and T72) after coronary revascularization to estimate levels of serum Cr, creatine phosphokinase, and heart-type fatty acid-binding protein (H-FABP) and calculation of neutrophil/lymphocyte ratio (NLR) and urinary liver-type FABP (L-FABP). AKI was diagnosed according to the recommendations of the European Renal Best Practice as the times of increased serum Cr concerning baseline level. 85 patients developed AKI. Regression analyses defined a high NLR ratio in the T0 sample as the most significant predictor for early AKI diagnosed at T1 time, while high NLR and serum H-FABP levels in T1 samples as the significant predictors for AKI defined at T12 time. However, high urinary L-FABP levels in T12 samples and high NLR are significant predictors for AKI at T72 time. Combined estimations of serum H-FABP and urinary L-FABP with the calculation of NLR could predict the oncoming AKI and discriminate its pathogenesis. The study protocol was approved by the Local Ethical Committee at Tanta Faculty of Medicine by approval number: 35327/3/22. For blindness purposes, the authors will be blinded about the laboratory results till the end of 72 h after revascularization and the clinical pathologist will be blinded about the indication for the requested investigations.

A Real-World Analysis of New-Onset Heart Failure After Anterior Wall ST-Elevation Acute Myocardial Infarction in the United States.

The 1-year incidence of heart failure (HF) after anterior wall ST-elevation acute myocardial infarction (STEMI) remains difficult to determine because of inconsistencies in reporting, definitions, and adjudication. The objective of this study was to evaluate the 1-year incidence of HF after anterior wall STEMI in a real-world data set using a variety of potential criteria and composite definitions. In a retrospective cohort study, anonymized patient data was accessed through a federated health research network (TriNetX Limited Liability Company (LLC)) of 56 US healthcare organizations (US Collaborative Network). Patients were identified based on the International Classification of Diseases, Tenth Revision criteria for anterior wall STEMI during the 10-year period from 2013 to 2022 and the absence of prespecified signs or symptoms of HF. Values for 1-year incidence were calculated as 1 minus Kaplan-Meier survival at 12 months after anterior wall STEMI. Univariate Cox proportional hazard ratio was calculated to compare risk associated with potential risk factors. The analysis utilized 5 different types of definition criteria for HF: Diagnosis codes, Signs and symptoms, Laboratory/imaging, Medications, and Composites. A total of 34,395 patients from the US Collaborative Network met eligibility criteria and were included in the analysis. The 1-year incidence of HF varied from 2% to 30% depending upon the definition criteria. Although no single criteria exceeded a 1-year incidence of 20%, a simple composite of HF diagnosis (International Classification of Diseases, Tenth Revision-I50) or use of loop diuretic produced a 1-year incidence 26.1% that was used as the benchmark outcome for evaluation of risk factors. Age ≥65 years, Black race, low-density lipoprotein ≥100 mg/100 ml, elevated hemoglobin A1c (7% to 9% and >9%), and body mass index≥35 kg/m2 were also associated with increased risk of HF. In conclusion, patients with anterior wall STEMI continue to be at high risk for new-onset HF. In the absence of structured, prospective, systematically adjudicated diagnostic criteria, composite definitions are more likely to yield accurate estimates of HF incidence.

Surgical repair of post myocardial infarction ventricular septal defect: a retrospective analysis of a single institution experience.

INTRODUCTION: Ventricular septal defect (VSD) is a mechanical complication of acute myocardial infarction (MI) with a very high mortality, despite advances in surgical and circulatory support. The tremendous hemodynamic disturbance and the severely fragile myocardium render surgical repair a great challenge. The optimal time of surgical repair with or without circulatory support is still controversial. OBJECTIVE: The aim of this study is to review our experience with early surgical repair of post-MI VSD in a single major cardiac institution in China. METHODS: From January 2013 to October 2020, 9consecutive patients presented to our emergency department with a diagnosis of post-MI VSD. Among them, 8 were male, and the mean age was 58 ± 7years. The mean VSD size was 22.5 ± 5.7 mm. In all patients, an intra-aortic balloon pump (IABP)was inserted immediately after admission to cardiac surgery service. All patients were operated at a mean of 3.3 ± 2.9 days, and 4 within 24 h of the rupture (range 1 to 9 days post-VSD). In 5 cases, the VSD was located superiorly, and 4 cases in the posterior septum. RESULTS: The overall 30-day mortality was 11% (1/9). Coronary angiography was performed in all nine patients, four with single vessel disease had coronary stents implanted, and the other five received concomitant coronary artery bypass grafting during VSD repair surgery. There was no death in all 5 patients with anterior septal perforation. One patient with posterior septal perforation died in the operating room due to bleeding from the ventriculotomy site. Three survived patients were diagnosed with a small residual defect and mild left to right shunt post-repair. However, no further intervention was required, and patients remained asymptomatic (Killip II in 1 and III in 2). CONCLUSION: In our experience, immediate insertion of IABP and hemodynamic stabilization with early surgical intervention of VSD repair and concomitant coronary revascularization provided an 89% survival rate.

Identification of acute ST-elevation myocardial infarction via remote implantable loop recorder monitor.

The indications for the use of implantable loop recorders include the evaluation of unexplained palpitations and syncope, embolic stroke of undetermined source, dizziness and lightheadedness presumed to be due to arrhythmogenic etiology, and for atrial fibrillation to guide antiarrhythmic drug therapy or catheter ablation efficacy. Long-term monitoring is especially beneficial if symptoms occur sporadically or are asymptomatic in nature. This is the first case to our knowledge of an acute ST-elevation myocardial infarction which was identified from remote monitoring of an implantable loop recorder through a device clinic.

Predictive value of CHA2 DS2 -VASc score for in-hospital prognosis of patients with acute ST-segment elevation myocardial infarction undergoing primary PCI.

BACKGROUND: This study aimed to explore the predictive value of CHA2 DS2 -VASc score for in-hospital major adverse cardiac events (MACEs) in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary artery intervention. METHODS: A total of 746 STEMI patients were divided into four groups according to CHA2 DS2 -VASc score (1, 2-3, 4-5, >5). The predictive ability of the CHA2 DS2 -VASc score for in-hospital MACE was made. Subgroup analysis was made between gender differences. RESULTS: In a multivariate logistic regression analysis model including creatinine, total cholesterol, and left ventricular ejection fraction, CHA2 DS2 -VASc score was an independent predictor of MACE as a continuous variable (adjusted odds ratio: 1.43, 95% confidence interval [CI]: 1.27-1.62, p < .001). As a category variable, using the lowest CHA2 DS2 -VASc score of 1 as a reference, CHA2 DS2 -VASc score 2-3, 4-5, >5 groups for predicting MACE was 4.62 (95% CI: 1.94-11.00, p = .001), 7.74 (95% CI: 3.18-18.89, p < .001), and 11.71 (95% CI: 4.14-33.15, p < .001). The CHA2 DS2 -VASc score was also an independent risk factor for MACE in the male group, either as a continuous variable or category variable. However, CHA2 DS2 -VASc score was not a predictor of MACE in the female group. The area under the curve value of the CHA2 DS2 -VASc score for predicting MACE was 0.661 in total patients (74.1% sensitivity and 50.4% specificity [p < .001]), 0.714 in the male group (69.4% sensitivity and 63.1% specificity [p < .001]), but there was no statistical significance in the female group. CONCLUSIONS: CHA2 DS2 -VASc score could be considered as a potential predictor of in-hospital MACE with STEMI, especially in males.

Prevalence and outcomes of type 2 myocardial infarction in patients with cancer: A retrospective analysis from the National Inpatient Sample dataset.

BACKGROUND: This study aimed to investigate the prevalence, clinical characteristics and outcomes of type 2 myocardial infarction (T2AMI) in patients with versus without cancer. METHODS: All hospitalizations with a primary discharge diagnosis of T2AMI were stratified according to cancer status (secondary diagnosis of any-cancer vs cancer-free) using data from the US National Inpatient Sample (2016-2019). The primary outcome was in-hospital all-cause mortality while secondary outcomes were in-hospital major adverse cardiovascular and cerebrovascular events (MACCE). RESULTS: Among 61,305 included hospitalizations with primary diagnosis of T2AMI, 3745 (6.1%) were associated with a diagnosis of cancer. Patients with T2AMI and cancer presented more frequently with acute respiratory failure (23.2% vs 18.1%), acute pulmonary embolism (3.7% v 1.3%), major bleeding (6.8% vs 4.1%) and renal failure (51.0% vs 46.8%), compared to patients without. On adjusted analysis, diagnosis of cancer was associated with lower odds of invasive coronary angiography (aOR 0.75, 95% CI 0.60 to 0.93, p = 0.009) but greater odds of mortality (aOR 1.95, 95% C.I. 1.26-2.99 p = 0.002). Among the different types of cancer, adjusted risk of all-cause mortality was higher in patients with colorectal (aOR 4.17 95% CI 1.68-10.32, p = 0.002), lung (aOR 3.63, 95% CI 1.83-7.18, p < 0.001) and haematologic (aOR 2.48, 95% CI 1.22-5.05, p = 0.001) cancer. CONCLUSIONS: Patients with cancer presenting with T2AMI have lower odds of management with invasive diagnostic coronary angiography and have higher rates of in-hospital all-cause death. Further studies are warranted to improve overall care and outcomes of cancer patients and cardiovascular diseases.

Impact of clinical diagnosis of myocardial infarction in patients with elevated cardiac troponin.

OBJECTIVE: Type 2 myocardial infarction (MI) and myocardial injury are common conditions associated with an adverse prognosis. Physicians experience uncertainty how to distinguish these conditions, as well as how to manage and treat them. Therefore, the objective of this study was to compare treatment and prognosis in patients with an adjudicated diagnosis of type 2 MI and myocardial injury, who were discharged with and without a clinical diagnosis of MI. DESIGN: The study consisted of two cohorts, 964 and 281 consecutive patients with elevated cardiac troponin, discharged with and without a clinical diagnosis of MI, respectively. All cases were adjudicated into MI type 1-5 or myocardial injury and followed regarding all-cause death. RESULTS: The adjudication identified 138 and 37 cases of type 2 MI, and 86 and 185 of myocardial injury, with and without a clinical MI diagnosis, respectively. In patients with type 2 MI, a clinical MI diagnosis was associated with more coronary angiography investigations (39.1% vs 5.4%, p<0.001) and an increased use of secondary prevention medications (all p<0.001). However, no difference was observed in adjusted 5-year mortality between patients with and without a clinical MI diagnosis (HR: 0.77 with 95% CI 0.43 to 1.38). The results were similar for adjudicated myocardial injury. CONCLUSION: In both type 2 MI and myocardial injury, a clinical diagnosis of MI at discharge was associated with more investigations and treatments. However, no prognostic effect of receiving a clinical MI diagnosis was observed.

Polygenic risk scores point toward potential genetic mechanisms of type 2 myocardial infarction in people with HIV.

BACKGROUND: People with human immunodeficiency virus (HIV) infection (PWH) are at higher risk of myocardial infarction (MI) than those without HIV. About half of MIs in PWH are type 2 (T2MI), resulting from mismatch between myocardial oxygen supply and demand, in contrast to type 1 MI (T1MI), which is due to primary plaque rupture or coronary thrombosis. Despite worse survival and rising incidence in the general population, evidence-based treatment recommendations for T2MI are lacking. We used polygenic risk scores (PRS) to explore genetic mechanisms of T2MI compared to T1MI in PWH. METHODS: We derived 115 PRS for MI-related traits in 9541 PWH enrolled in the Centers for AIDS Research Network of Integrated Clinical Systems cohort with adjudicated T1MI and T2MI. We applied multivariate logistic regression analyses to determine the association with T1MI and T2MI. Based on initial findings, we performed gene set enrichment analysis of the top variants composing PRS associated with T2MI. RESULTS: We found that T1MI was strongly associated with PRS for cardiovascular disease, lipid profiles, and metabolic traits. In contrast, PRS for alcohol dependence and cholecystitis, significantly enriched in energy metabolism pathways, were predictive of T2MI risk. The association remained after the adjustment for actual alcohol consumption. CONCLUSIONS: We demonstrate distinct genetic traits associated with T1MI and T2MI among PWH further highlighting their etiological differences and supporting the role of energy regulation in T2MI pathogenesis.

Contemporary in-hospital and long-term prognosis of patients with acute ST-elevation myocardial infarction depending on renal function: a retrospective analysis.

BACKGROUND: Cardiovascular disease is often associated with chronic kidney disease (CKD), resulting in an increased risk for poor outcome. We sought to determine short-term mortality and overall survival in ST-elevation myocardial infarction (STEMI) patients with different stages of CKD. METHODS: In our retrospective cohort study with health insurance claims data of the Allgemeine Ortskrankenkasse (AOK), anonymized data of all STEMI patients hospitalized between 2010 and 2017 were analyzed regarding presence and severity of concomitant CKD. RESULTS: A total of 175,187 patients had an index-hospitalisation for STEMI (without CKD: 78.6% patients, CKD stage 1: 0.8%, CKD stage 2: 4.8%, CKD stage 3: 11.7%, CKD stage 4: 2.8%, CKD stage 5: 0.7%, CKD stage 5d: 0.6%). Patients with CKD were older and had more co-morbidities than patients without CKD. With increasing CKD severity, patients received less revascularization therapies (91.2%, 85.9%, 87.0%, 81.8%, 71.7%, 76.9% and 78.6% respectively, p < 0.001). After 1 year, guideline-recommended medications were prescribed less frequently in advanced CKD (83.4%, 79.3%, 81.5%, 74.7%, 65.0%, 59.4% and 53.7%, respectively, p < 0.001). CKD stages 4, 5 and 5d as well as chronic limb threatening ischemia (CLTI) were associated with decreased overall survival [CKD stage 4: hazard ratio (HR) 1.72; 95% CI 1.66-1.78; CKD stage 5: HR 2.55; 95% CI 2.37-2.73; CKD stage 5d: 5.64; 95% CI 5.42-5.86; CLTI: 2.06; 95% CI 1.98-2.13; all p < 0.001]. CONCLUSIONS: CKD is a frequent co-morbidity in patients with STEMI and is associated with a worse prognosis especially in advanced stages. Guideline-recommended therapies in patients with STEMI and CKD are still underused.

Predictors of in-hospital heart failure in patients with acute anterior wall ST-segment elevation myocardial infarction.

BACKGROUND: Heart failure (HF) is a severe complication of acute ST-segment elevation myocardial infarction (STEMI). Its incidence is associated with myocardial infarction location, and it occurs frequently after acute anterior wall STEMI due to the larger infarct size. However, predictors of in-hospital HF in patients with acute anterior wall STEMI are inadequately defined. We aimed to determine potential predictors of HF in patients with acute anterior wall STEMI during hospitalization. METHODS: A total of 714 consecutive patients who were diagnosed with acute anterior wall STEMI and underwent primary percutaneous coronary intervention (pPCI) between January 2013 to August 2019 were enrolled retrospectively. We assigned the patients to HF and non-HF groups. The clinical parameters were subjected to univariate analysis and logistic regression analysis to obtain the independent predictors. RESULTS: Among the 714 patients enrolled in the present study (mean age 61.0 ± 13.8 years, men 80.7%), 387 (54.2%) had in-hospital HF. According to a multivariate logistic regression analysis, ventricular fibrillation (VF, OR: 5.66, 95% CI: 2.25-14.23, P < 0.001) was the most striking independent predictor of in-hospital HF. Community-acquired pneumonia (CAP, OR: 4.72, 95% CI: 2.44-9.10, P < 0.001), age (OR: 1.03, 95% CI: 1.01-1.04, P < 0.001), left ventricular ejection fraction (LVEF, OR: 0.96, 95% CI: 0.93-0.97, P < 0.001), and peak N-terminal pro-brain natriuretic peptide (NT-pro-BNP, OR: 1.06, 95% CI: 1.02-1.11, P = 0.006) were also independently associated with in-hospital HF. CONCLUSION: VF, CAP, age, LVEF, and peak NT-pro-BNP were independently associated with in-hospital HF in patients with acute anterior wall STEMI.

Acute Response in the Noninfarcted Myocardium Predicts Long-Term Major Adverse Cardiac Events After STEMI.

BACKGROUND: Acute ST-segment elevation myocardial infarction (STEMI) has effects on the myocardium beyond the immediate infarcted territory. However, pathophysiologic changes in the noninfarcted myocardium and their prognostic implications remain unclear. OBJECTIVES: The purpose of this study was to evaluate the long-term prognostic value of acute changes in both infarcted and noninfarcted myocardium post-STEMI. METHODS: Patients with acute STEMI undergoing primary percutaneous coronary intervention underwent evaluation with blood biomarkers and cardiac magnetic resonance (CMR) at 2 days and 6 months, with long-term follow-up for major adverse cardiac events (MACE). A comprehensive CMR protocol included cine, T2-weighted, T2∗, T1-mapping, and late gadolinium enhancement (LGE) imaging. Areas without LGE were defined as noninfarcted myocardium. MACE was a composite of cardiac death, sustained ventricular arrhythmia, and new-onset heart failure. RESULTS: Twenty-two of 219 patients (10%) experienced an MACE at a median of 4 years (IQR: 2.5-6.0 years); 152 patients returned for the 6-month visit. High T1 (>1250 ms) in the noninfarcted myocardium was associated with lower left ventricular ejection fraction (LVEF) (51% ± 8% vs 55% ± 9%; P = 0.002) and higher NT-pro-BNP levels (290 pg/L [IQR: 103-523 pg/L] vs 170 pg/L [IQR: 61-312 pg/L]; P = 0.008) at 6 months and a 2.5-fold (IQR: 1.03-6.20) increased risk of MACE (2.53 [IQR: 1.03-6.22]), compared with patients with normal T1 in the noninfarcted myocardium (P = 0.042). A lower T1 (<1,300 ms) in the infarcted myocardium was associated with increased MACE (3.11 [IQR: 1.19-8.13]; P = 0.020). Both noninfarct and infarct T1 were independent predictors of MACE (both P = 0.001) and significantly improved risk prediction beyond LVEF, infarct size, and microvascular obstruction (C-statistic: 0.67 ± 0.07 vs 0.76 ± 0.06, net-reclassification index: 40% [IQR: 12%-64%]; P = 0.007). CONCLUSIONS: The acute responses post-STEMI in both infarcted and noninfarcted myocardium are independent incremental predictors of long-term MACE. These insights may provide new opportunities for treatment and risk stratification in STEMI.

Contemporary incidence and predictors of left ventricular thrombus in patients with anterior acute myocardial infarction.

BACKGROUND: The incidence of left ventricular thrombus (LVT) after anterior acute myocardial infarction (AMI) has not been well established in the era of primary percutaneous coronary intervention (pPCI) and potent dual antiplatelet therapy. The objective of this study is to establish the contemporary incidence of LVT in this population, to identify their risk factors, and to examine their association with clinical outcomes. METHODS: A multicenter retrospective cohort study including AMI patients with new-onset antero-apical wall motion abnormalities treated with pPCI between 2009 and 2017 was conducted. The primary outcome was LVT during the index hospitalization. Predictors of LVT were identified using multivariate logistic regression. Net adverse clinical events (NACE), a composite of mortality, myocardial infarction, stroke or transient ischemic attack, systemic thromboembolism or BARC type 3 or 5 bleeding at 6 months were compared between the LVT and no LVT groups. RESULTS: Among the 2136 patients included, 83 (3.9%) patients developed a LVT during index hospitalization. A lower left ventricular ejection fraction (LVEF) [adjusted odds ratio (aOR) 0.97; 95% confidence intervals (CI) 0.94-0.99] and the degree of worse anterior WMA (aOR 4.34; 95% CI 2.24-8.40) were independent predictors of LVT. A NACE occurred in 5 (5.72 per 100 patient-year) patients in the LVT group and in 127 (6.71 per 100 patient-year) patients in the no LVT group at 6 months [adjusted hazard ratio (aHR): 0.87; 95% CI 0.35-2.14]. CONCLUSIONS: The risk of LVT after anterior AMI with new-onset wall motion abnormalities is low, but this complication remains present in the contemporary era of timely pPCI and potent dual antiplatelet therapy .

The relationship between CHA2DS2VASc score and left ventricular apical thrombus formation in patients with acute anterior ST segment elevation myocardial infarction.

BACKGROUND: Left ventricular apical thrombus (LVAT) formation is a well-known complication of acute anterior myocardial infarction (AMI). The CHA2DS2VASc is a scoring system that has been used to estimate the risk of thromboembolism in patients with nonvalvular atrial fibrillation. This score has also been used for other clinical conditions. The aim of this study was to investigate the relationship between CHA2DS2VASc score and development of LVAT in patients with AMI. METHOD: The study population included 378 patients (mean age: 56.5 ± 12.3 years, male: 318) presenting with AMI between January 2016 and January 2020. Primary percutaneous coronary intervention procedure was performed in all patients. Initial echocardiogram was performed within 7 days of admission. All patients were evaluated with echocardiography at 3rd, 6th and 12th months. Patients were divided into two groups according to the presence of LVAT on echocardiography. RESULTS: The incidence of the LVAT was 8.5% (n = 32) during a mean follow-up time of 233.1 ± 66.7 days. The mean CHA2DS2VASc score was notably higher in patients with LVAT compared to patients in the control group (3.1 ± 1.9 vs. 1.9 ± 1.2, p < 0.001). In Cox regression analysis, high CHA2DS2VASc score, low left ventricular ejection fraction (LVEF) and the presence of LV apical akinesis/aneurysm were the independent predictors for LVAT formation. All of these parameters were associated with higher cumulative incidence of LVAT formation in Kaplan-Meier analyses (p < 0.001 for all). CONCLUSION: High CHA2DS2VASc score, low LVEF and the presence of LV apical akinesis/aneurysm may be used for LVAT risk prediction among patients presenting with AMI.

Single arterial access closure of post-infarction ventricular septal defect: A case series.

BACKGROUND: Post-infarction ventricular septal defect (PIVSD) carries a very poor prognosis. Surgical repair offers reasonable outcomes in patients who survive the initial healing period. Percutaneous device implantation remains a potentially effective earlier alternative. METHODS AND RESULTS: From March 2018 to May 2022, 11 trans-arterial PIVSD closures were attempted in 9 patients from two centers (aged 67.2 ± 11.1 years; 77.8% male). Two patients had a second procedure. Myocardial infarction was anterior in four patients (44.5%) and inferior in five cases (55.5%). Devices were successfully implanted in all patients. There were no major immediate procedural complications. Immediate shunt grade postprocedure was significant (11.1%), minimal (77.8%), or none (11.1%). Median length of stay after the procedure was 14.8 days. Five patients (55%) survived to discharge and were followed up for a median of 605 days, during which time no additional patients died. CONCLUSION: Single arterial access for percutaneous closure of PIVSD is a good option for these extremely high-risk patients, in the era of effective large-bore arterial access closure. Mortality remains high, but patients who survive to discharge do well in the longer term.

An unusually large left ventricular thrombus complicating anterior myocardial infarction: the value of multimodality imaging.

Since the emergence of revascularisation for the treatment of myocardial infarction (MI), the incidence of left ventricular thrombus (LVT) has been declining. However, despite this, it is independently associated with increased morbidity and mortality rates. The mainstay of treatment is vitamin K antagonists, although non-vitamin K antagonists have been shown to be effective. Imaging plays an important role in the surveillance of LVT subsequent to MI. Herein, we emphasise the utility of multimodality imaging of a case of anterior MI complicated by a large LVT, and detail its management.