Revista española de cardiología (English ed.)最新文献

Introduction and objectives: In the setting of ST-segment elevation myocardial infarction (STEMI), imaging-based biomarkers could be useful for guiding oral anticoagulation to prevent cardioembolism. Our objective was to test the efficacy of intraventricular blood stasis imaging for predicting a composite primary endpoint of cardioembolic risk during the first 6 months after STEMI.

Methods: We designed a prospective clinical study, Imaging Silent Brain Infarct in Acute Myocardial Infarction (ISBITAMI), including patients with a first STEMI, an ejection fraction ≤ 45% and without atrial fibrillation to assess the performance of stasis metrics to predict cardioembolism. Patients underwent ultrasound-based stasis imaging at enrollment followed by heart and brain magnetic resonance at 1-week and 6-month visits. From the stasis maps, we calculated the average residence time, R_T, of blood inside the left ventricle and assessed its performance to predict the primary endpoint. The longitudinal strain of the 4 apical segments was quantified by speckle tracking.

Results: A total of 66 patients were assigned to the primary endpoint. Of them, 17 patients had 1 or more events: 3 strokes, 5 silent brain infarctions, and 13 mural thromboses. No systemic embolisms were observed. R_T (OR, 3.73; 95%CI, 1.75-7.9; P<.001) and apical strain (OR, 1.47; 95%CI, 1.13-1.92; P=.004) showed complementary prognostic value. The bivariate model showed a c-index=0.86 (95%CI, 0.73-0.95), a negative predictive value of 1.00 (95%CI, 0.94-1.00), and positive predictive value of 0.45 (95%CI, 0.37-0.77). The results were confirmed in a multiple imputation sensitivity analysis. Conventional ultrasound-based metrics were of limited predictive value.

Conclusions: In patients with STEMI and left ventricular systolic dysfunction in sinus rhythm, the risk of cardioembolism may be assessed by echocardiography by combining stasis and strain imaging. Registered at ClinicalTrials.gov (NCT02917213).

Introduction and objectives: Only about 1 out of every 3 patients with acute myocardial infarction (AMI) achieve low-density lipoprotein cholesterol (LDL-C) values <55mg/dL in the first year. The present study aims to evaluate the impact of early intensive therapy on lipid control after an AMI.

Methods: An independent, prospective, pragmatic, controlled, randomized, open-label, evaluator-blinded clinical trial (PROBE design) will analyze the efficacy and safety of an oral lipid-lowering triple therapy: high-potency statin+bempedoic acid (BA) 180mg+ezetimibe (EZ) 10mg versus current European-based guidelines (high-potency statin±EZ 10mg), in AMI patients. LDL-C will be determined within the first 48hours. Patients with LDL-C ≥ 115mg/dL (without previous statin therapy), ≥ 100mg/dL (with previous low-potency or high-potency statin therapy at submaximal dose), or ≥ 70mg/dL (with previous high-potency statin therapy at high dose) will be randomly assigned 1:1 between 24 and 72hours post-AMI to the BA/EZ combination or to statin±EZ, without BA. The primary endpoint is the proportion of patients reaching LDL-C <55mg/dL at 8 weeks after treatment.

Results: The results of this study will provide novel information for post-AMI LDL-C control by evaluating the usefulness of an early intensive lipid-lowering strategy based on triple oral therapy.

Conclusions: Early intensive lipid-lowering triple oral therapy vs the treatment recommended by current clinical practice guidelines could facilitate the achievement of optimal LDL-C levels in the first 2 months after AMI (a high-risk period).

Identification number: EudraCT 2021-006550-31.

Introduction and objectives: The CHA₂DS₂-VASc score, used to assess the risk of left atrial appendage thrombus (LAAT) formation in patients with atrial fibrillation (AF), has limited predictive value. Moreover, transesophageal echocardiography imaging, the gold standard diagnostic method to identify thrombi, is semi-invasive. Consequently, there is a need for alternative and noninvasive diagnostic methods for LAAT risk assessment.

Methods: Deep proteomic analysis was conducted in plasma samples from 8 patients with nonvalvular AF, divided into thrombus and control groups (4 patients in each group) based on the presence or absence of LAAT. Biomarkers associated with LAAT were validated using an enzyme-linked immunosorbent assay in a cohort of 179 patients with available clinical, transthoracic, and transesophageal echocardiography data. Predictive models were developed to assess the improvement in LAAT identification.

Results: The LAAT group had higher CHA₂DS₂-VASc scores, larger LA diameter, and lower LAA flow velocities. Deep proteomic analysis identified 30 differentially expressed proteins, including myosin light chain 4, prenylcysteine oxidase 1 (PCYOX1), and decorin as potential diagnostic biomarkers of LAAT. The model showed that PCYOX1 and decorin provided an area under the curve (AUC) of 0.970 for LAAT prediction compared with 0.672 in a model including the CHA₂DS₂-VASc score and LAA cauliflower morphology. The incremental value of proteomic biomarkers for LAAT in patients with nonvalvular AF was further confirmed with the net reclassification improvement and integrated discrimination improvement indices.

Conclusions: Protein levels of PCYOX1 and decorin improve the predictive performance for LAAT in patients with nonvalvular AF.

Introduction and objectives: Autoimmune diseases (ADs) are associated with an increased risk of developing certain cardiac arrhythmias. However, their prognostic effect in patients with cardiac arrhythmias has not been comprehensively investigated. We aimed to assess the association between ADs and prognosis in this population.

Methods: Based on a large retrospective observational cohort, this study included patients with various cardiac arrhythmias, including atrial fibrillation/atrial flutter (AFib/AF), ventricular tachycardia/ventricular fibrillation (VT/VF), and bradyarrhythmias. ADs were considered an exposure factor. The endpoint was all-cause mortality. Cox proportional hazards regression analyses were performed to calculate hazard ratios (HR) and 95% confidence intervals (95%CI) to quantify associations. Propensity score matching was used to mitigate potential confounding bias.

Results: The analysis included 14 225 patients (mean age, 73.9 ± 12.5 years, 59.2% women), of whom 4552 (32.0%) died within 1 year of discharge. After adjustment for various covariates, patients with ADs showed a higher risk of mortality in AFib/AF (HR, 1.23; 95%CI, 1.1-1.33; P < .001) and VT/VF (HR, 1.28; 95%CI, 1.02-1.60, P = .032). For bradyarrhythmias, although a potential association was observed, the trend did not reach statistical significance (HR, 1.20; 95%CI, 0.93-1.56; P = .168). The association persisted among multiple sensitivity analyses and remained consistent after adjustment for a wide range of covariates.

Conclusions: ADs were significantly associated with an increased risk of all-cause mortality in patients with cardiac arrhythmias, particularly in those with AFib/AF and VT/VF.

Introduction y objectives: Tako-tsubo syndrome (TTS) is a cardiac condition that mimics acute coronary syndrome, characterized by transient left ventricular dysfunction in the absence of culprit coronary artery stenosis. Although its etiology remains unknown, reversible microvascular dysfunction secondary to an adrenergic surge is thought to play a role. Treatment is empirical, although most patients receive beta-blockers (BB) in clinical practice. The Beta-blockers in Tako-tsubo Syndrome study (β-Tako), is an academic, multicenter, pragmatic, prospective randomized open-label trial with blinded endpoint evaluation that aims to assess the efficacy and safety of BB in patients with TTS.

Methods: The diagnosis of TTS will be confirmed by invasive coronary angiography and serial echocardiographic assessments. Two hundred patients with TTS will be randomized (1:1) to BB (n=100) or no BB (n=100). BB with alpha or nitric oxide release activity will be used in the treatment arm.

Results: The primary efficacy endpoint is the comparison of the wall motion score index by echocardiography at 7 days, analyzed by an independent core laboratory. Changes in left ventricular ejection fraction and global longitudinal strain will also be evaluated. A composite clinical endpoint (death, stroke, admission for recurrent TTS, acute coronary syndrome, heart failure, or atrial fibrillation) at 1 year will be assessed by an independent clinical events committee. Several predefined substudies will be conducted to examine clinical, imaging, biomarker, pharmacogenetic, inflammatory, messenger ribonucleic acids, and quality-of-life parameters.

Conclusions: The β-Tako trial will generate robust scientific evidence to address unmet clinical needs and inform clinical and treatment decisions in this uniquely challenging clinical entity. The study has been registered (EU-CT number: 2023-510213-25-01, ClinicalTrials.gov Identifier, NCT06509074.