Apical longitudinal strain can help predict the development of left ventricular thrombus after anterior myocardial infarction

Abstract Background: Left ventricular (LV) thrombus formation is a common complication of anterior myocardial infarction (ANT-MI). The aim of this study was to investigate the relationship between apical longitudinal strain (ALS) and LV apical thrombus after ANT-MI. Methods: The cross-sectional study included a total of 235 patients who were followed up after primary percutaneous coronary intervention performed for ANT-MI and had a reduced LV ejection fraction (LVEF) (≤40%). Of these patients, 24 were excluded from the study, and the remaining 211 patients were included in the analysis. Patients were divided into two groups based on the presence (n = 42) or absence (n = 169) of LV thrombus detected by echocardiography. ALS was measured using speckle-tracking echocardiography. Results: Thrombus was detected in 42 of 211 patients. There was no significant difference between the groups regarding age or gender. Apical strain (AS), global longitudinal strain (GLS), apical wall thickness (AWT), and EF were significantly lower in patients with LV apical thrombus when compared to those without LV apical thrombus (AS, –5.00 ± 2.30% vs. −8.54 ± 2.48%, p < 0.001; GLS, −10.6 ± 3.54% vs. −12.1 ± 2.84%, p = 0.013; AWT, 4.71 ± 1.11 vs. 6.33 ± 1.78 mm, p < 0.001; EF, 31.40 ± 4.10% vs. 37.75 ± 3.17%, p < 0.001). On univariate and multivariate analyses, aneurysm (AA), AS, and AWT were found to be independent predictors of LV apical thrombus (AA, odds ratio [OR] 4.649, p = 0.010; AS, OR 1.749, p < 0.001; AWT, OR 0.729, p = 0.042). Conclusion: ALS is highly sensitive and specific for predicting LV thrombus after ANT-MI. An early and accurate evaluation of LV thrombus may prevent embolic complications, particularly cerebrovascular events.

The Role of Beta-1 Receptor Gene Polymorphism in Beta-Blocker Therapy for Vasovagal Syncope

Background: Vasovagal syncope (VVS) is a common clinical condition involving genetic background. The role of beta-blockers in the treatment is controversial. Objective: The aim of this study was to investigate the effect of beta-1 gene polymorphism on beta-blocker therapy in patients with VVS. Methods: We included 123 patients who were diagnosed with VVS after the tilt-table test. We searched for the polymorphism Arg389Gly (rs1801253) in the beta-1 adrenoceptor gene. Results: Overall, 64 patients (52%) had Arg389Arg genotype and 59 patients (48%) had Arg389Gly genotype. The syncopal episodes of patients with Arg389Arg genotype were more frequent compared with patients having Arg389Gly genotype (total syncopal episodes [TSE], 7.9 ± 3.7 vs. 6.4 ± 3.0; p = 0.012). TSE in patients with Arg389Arg genotype decreased significantly after 18 months of beta-blocker treatment (7.9 ± 3.7 vs. 3.0 ± 1.4, p < 0.001). After 18 months of beta-blocker treatment, patients with Arg389Arg genotype had significantly fewer syncopal episodes than patients with Arg389Gly genotype (3.0 ± 1.4 vs. 6.8 ± 3.2, p < 0.001). Conclusions: Results of beta-blocker therapy in patients with Arg389Arg genotype suggest that VVS pathophysiology is a multifactorial condition, with genetic, psychological, and environmental components, and therefore, treatment selection can be based on gene polymorphism. (REV INVEST CLIN. 2020;72(5):300-7)