The left ventricular summit (LVS) is a triangular area located at the most superior portion of the left epicardial ventricular region, surrounded by the two branches of the left coronary artery: the left anterior interventricular artery and the left circumflex artery. The triangle is bounded by the apex, septal and mitral margins and base. This review aims to provide a systematic and comprehensive anatomical description and proper terminology in the LVS region that may facilitate exchanging information among anatomists and electrophysiologists, increasing knowledge of this cardiac region. We postulate that the most dominant septal perforator (not the first septal perforator) should characterize the LVS definition. Abundant epicardial adipose tissue overlying the LVS myocardium may affect arrhythmogenic processes and electrophysiological procedures within the LVS region. The LVS is divided into two clinically significant regions: accessible and inaccessible areas. Rich arterial and venous coronary vasculature and a relatively dense network of cardiac autonomic nerve fibers are present within the LVS boundaries. Although the approach to the LVS may be challenging, it can be executed indirectly using the surrounding structures. Delivery of the proper radiofrequency energy to the arrhythmia source, avoiding coronary artery damage at the same time, may be a challenge. Therefore, coronary angiography or cardiac computed tomography imaging is strongly recommended before any procedure within the LVS region. Further research on LVS morphology and physiology should increase the safety and effectiveness of invasive electrophysiological procedures performed within this region of the human heart.Published in Diagnostics:https://doi.org/10.3390/diagnostics11081423

Introduction: Little is known about reverse cardiac remodeling (CRR) under the low-dose S/V therapy. Methods: In 37 patients (mean age 64.5±17.5 years, five females) 24/26mg S/V BID was started. After one month of observation, the following CRR parameters improved: LVEDD (-∆2,9±2.6mm, p<0.01), LVESD (-∆ 2,4±2.5mm, p<0.01), LVEDV(-∆14.6±33.1ml, p=0.04), LVESV (-∆13.4±30.6ml, p=0.04), LAVI (-∆8.7±37.7ml/m2, p<0.01), and EROA (-∆ 0.09 ± 0,01cm2; p=0.03). In opposite to LVEF global longitudinal strain (GLS) changed from -6.6% to -7.9% (absolute improvement of 16%, p <0.001). Walked distance in 6-MWT ( +∆65.4 ± 75.8 m, p <0.001), and the quality of life (MLHFQ 22 vs 16 scores, p<0.01) improved. Decreasing NT-proBNP (-∆ 1,203,1±3,121,4pg/ml, p=0.03) and troponin T (-∆ 4.7±9.4pg/ml, p=0.004) were observed. Correlation between GLS and LVESV (r = -0,43, p = 0.027) was found. ROC curve analysis showed that GLS cut-off value -8% is a good predictor of clinical improvement (6MWT: AUC 0.69 p=0.04) and CRR (MRvol: AUC:0.74 p=0.01; LAVI: AUC 0.71 p=0.04). Conclusion: One-month, low-dose (24/26 mg BID) S/V therapy initiates CRR. GLS’s ability to evaluate LV function is better than LVEF’s. S/V should be started early as patients with symptomatic HFrEF and less impaired LV systolic function (GLS <-8%) are more likely to develop CRR and clinical improvement.