Validity of MENARI plus (self-pulse assessment and clinical scoring) mobile apps for detecting atrial fibrillation in high-risk population.

Background: Even before it is clinically diagnosed, atrial fibrillation (AF) can cause a stroke. This study validates self-pulse assessment and clinical scoring (MENARI Plus) based on android apps. Objective: The aim of this study was to examine the validity of AF screening using MENARI Plus compared with an ECG recording. Methods: We collected a total of 1385 subjects from high-risk population according to CHA2DS2-VASc score ≥2, attending 8 primary care centers (PCCs) in Malang between July 2021 and December 2021. Every participant underwent self-pulse assessment, and then was evaluated for MENARI Plus Score on android Apps. These cases had been classified as low or high probability for AF (cut-off score 7). After that, electrocardiography examinations were performed and classified with AF and Sinus Rhythm group. Results: In this study, the mean age of these patients was 61.5 ± 6.9 years old. We found that 156/1385 (11%) patients had AF. There were 68/156 (43.5%) new cases of AF. The sensitivity for self-pulse palpation was 73.1% (95% CI: 68%-76%) and specificity was 68.3% (95% CI: 65%-72%). MENARI Plus had an area under the receiver operating curve (AUC) of 0.86 (95% CI: 0.82-0.89) with sensitivity per measurement occasion was (84%, 95% CI: 82%-88%) and specificity was (87.9%, 95% CI: 82%-90%). Conclusion: In this study, we found that MENARI Plus has high sensitivity and specificity for AF. It is therefore useful for ruling out AF. It may also be a useful screen that can be applied opportunistically for previously undetected AFs.

The association between vesicle-associated membrane protein - 8 A/G gene polymorphism and the risk of acute myocardial infarction / La relación entre el polimorfismo A/G del gen de la proteína de membrana asociada a vesículas-8 y el riesgo de infarto agudo de miocardio

Abstract Introduction Until now, only few studies have reported the correlation between vesicle-associated membrane protein-8 (VAMP-8) A/G gene polymorphism and acute myocardial infarction. Whereas, theoretically, VAMP-8 plays a pivotal role in the pathogenesis of acute myocardial infarction through platelet activation, secretion, and aggregation. Objective To investigate the association between VAMP-8 A/G gene polymorphism and the risk of acute myocardial infarction. Methods A cross-sectional study was carried out at Saiful Anwar General Hospital during June 2013 - May 2014. A Mae II enzyme with restriction fragment length polymorphism method was used to genotype VAMP-8 A/G gene polymorphisms in acute myocardial infarction and control groups. A multiple logistic regression test was used to analyze the association between VAMP-8 A/G gene polymorphism and the risk of acute myocardial infarction. Results A total of 35 controls and 97 acute myocardial infarction patients from our Hospital during the period were enrolled for our study. Our results found that VAMP-8 A/G gene polymorphism was not associated with the risk of acute myocardial infarction. Moreover, we also failed to confer the association between VAMP-8 A/G gene polymorphism and both smoking and hypertension among patients with acute myocardial infarction. Furthermore, in the setting of premature acute myocardial infarction, the correlation also failed to confirm. Conclusion In our population, there is no association between VAMP-8 A/G gene polymorphism and the risk of acute myocardial infarction.

Resumen Introducción Hasta la fecha, solo unos pocos estudios han reportado la correlación entre el polimorfismo A/G del gen de la proteína de membrana asociada a vesículas-8 (VAMP-8, por sus siglas en inglés) y el infarto agudo de miocardio. Si bien, en teoría, VAMP-8 juega un papel fundamental en la patogénesis del infarto agudo de miocardio a través de la activación, secreción y agregación plaquetaria. Objetivo Investigar la relación entre el polimorfismo A/G del gen VAMP-8 y el riesgo de infarto agudo de miocardio. Métodos: Se llevó a cabo un estudio transversal en Siful Anwar General Hospital entre junio del 2013 y mayo del 2014. Se utilizó la técnica de polimorfismos de longitud de fragmentos de restricción con la enzima Mae II para genotipificar los polimorfismos A/G del gen VAMP-8 en grupos de infarto agudo de miocardio y de control. Se aplicó una prueba de regresión logística múltiple para analizar la relación entre el polimorfismo A/G del gen VAMP-8 y el riesgo de infarto agudo de miocardio. Resultados Se incluyeron un total de 35 controles y 97 pacientes con infarto agudo de miocardio de nuestro Hospital durante el periodo del estudio. Nuestros resultados encontraron que el polimorfismo A/G del gen VAMP-8 no estaba relacionado con el riesgo de infarto agudo de miocardio. Por otra parte, tampoco pudimos establecer una relación entre el polimorfismo A/G del gen VAMP-8 y tanto tabaquismo como hipertensión en pacientes con infarto agudo de miocardio. Asimismo, en el contexto de infarto agudo de miocardio prematuro, tampoco se confirmó la correlación. Conclusión: En nuestra población, no existe una relación entre el polimorfismo A/G del gen VAMP-8 y el riesgo de infarto agudo de miocardio.

Aggressive beta-blocker titration in stabilized acute heart failure patients with low left ventricular ejection fraction.

OBJECTIVES: A beta-blocker should be initiated in patients with stable acute heart failure (AHF). Beta-blocker titration should be conducted after a two-week interval. The benefits of aggressive beta-blocker titration are still unclear. This study aimed to investigate the aggressive beta-blocker titration outcomes in stabilized AHF patients with low left ventricular ejection fraction (LVEF). METHODS: In this retrospective cohort study, we analysed clinical data from the heart failure (HF) registry. AHF Patients with LVEF <40% were divided into aggressive and guideline-directed beta-blocker titration groups. The composite of worsening HF, ventricular arrhythmia, and mortality during hospitalization were defined as the primary outcomes. We considered secondary outcomes as the components of primary outcomes and also the outcomes during a 90-day follow-up after hospital discharge, including HF readmission and mortality. RESULTS: The primary outcomes between both groups were not significantly different (12.3% vs 24.4%; relative risk [RR] 0.51; 95% confidence interval [CI] 0.25-1.01; p = 0.055). However, the aggressive beta-blocker titration reduced ventricular arrhythmia events (5.7% vs 17.8%; RR 0.32; 95% CI 0.12-0.84; p = 0.016). The 90-day HF readmission rate (2.6% vs 7.5%; RR 0.35; 95% CI 0.07-1.66; p = 0.179) and mortality rate (4.3% vs 5%; RR 0.87; 95% CI 0.18-4.31; p = 1.000) between both groups were not found to be significantly different. CONCLUSION: Compared to the guideline-directed beta-blocker titration, the aggressive beta-blocker titration was safe in low LVEF AHF patients who have been previously stabilized. Additionally, aggressive beta-blocker titration effectively reduced ventricular arrhythmia events.

Phospholipase A2 is an Inflammatory Predictor in Cardiovascular Diseases: Is there any Spacious Room to Prove the Causation?

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme family of phospholipase A2 produced by the inflammatory cell in atherosclerotic plaque. It is transported in the circulation, attached mainly to low-density lipoprotein-cholesterol (LDL-C). It hydrolyzes glycerophospholipids particularly fatty acids at the sn-2 position and produces numerous bioactive lipids; and leads to endothelial dysfunction, atherosclerotic plaque inflammation, and development of the necrotic core in plaques. There are two kinds of phospholipase A2, namely: secretory phospholipase A2 (sPLA2) and Lp- PLA2. They are deemed as evolving predictors of cardiovascular disease (CVD) risk in hospitaland population-based studies, including healthy subjects, acute coronary syndromes (ACS) and patients with CVD. Unfortunately, Lp-PLA2 inhibitor (darapladib) and s-PLA2 inhibitor (varespladib methyl) failed to prove to lower the risk of composite CVD mortality, myocardial infarction and stroke in those with stable CVD and ACS. Herein, we describe the explanation based on the existing data why there is still a discrepancy among them. So, it highlights the opinion that phospholipase A2 is merely the inflammatory biomarkers of CVD and playing an important role in atherosclerosis. Further, there is more spacious room to prove the causation.