Purpose of Review: This review aims to synthesize current knowledge on the angiographic anatomy of the coronary sinus and its tributaries veins, with focus on venous branches other than classical ones used in cardiac resynchronization therapy. It also presents common anatomical aspects that could impact the clinical outcome. Recent Findings: Recent advancements in the electrophysiology field, like epicardial arrhythmia mapping and ablation through coronary sinus or cardiac pacing from atypical veins requires a detailed angiographic assessment of cardiac veins. There is an increased interest for the veins coursing in the left ventricular summit (LVS) area and could potentially provide a pathway to reach the LVS arrhythmogenic foci. However, there is no consensus regarding the nomenclature and classification of these veins. Summary: This review could offer a better understanding of the coronary sinus and its tributary veins distribution, dimensions and relationship with nearby structures that could help the development of new ablation and pacing tools and strategies, with higher success rates.
Background: Papillary muscles are structures integrated into the mitral valve apparatus, having both electrical and mechanical roles. The importance of the papillary muscles (PM) is mainly related to cardiac arrhythmias and mitral regurgitation. The aim of this review is to offer an overview of the anatomy and physiology of the papillary muscles, along with their involvement in cardiovascular pathologies, including arrhythmia development in various conditions and their contribution to secondary mitral regurgitation. Methods: A literature search was performed on PubMed using the following relevant keywords: papillary muscles, mitral valve, arrhythmia, anatomy, and physiology. Results: During the cardiac cycle, papillary muscles have continuous dimensional and pressure changes. On one hand, their synchrony or dyssynchrony impacts the process of mitral valve opening and closure, and on the other hand, the pressure changes can trigger electrical instability. There is increased awareness of papillary muscles as an arrhythmic source. Arrhythmias arising from PM were found in patients with or without structural heart disease, via Purkinje fibres, due to increased automaticity or triggered activity. Conclusions: Despite the interest in mitral valve physiology, there are still many unknowns in relation to the papillary muscles, especially with regard to their role in arrhythmogenesis and the pathogenesis of mitral regurgitation.
Background: Functional mitral regurgitation results from interacting mechanisms whose contributions vary between atrial and ventricular subtypes and shift within each heartbeat, producing temporal patterns static analyses cannot capture. Objectives: To identify which structural determinants predict mitral regurgitation variability beat to beat using Granger causality within vector autoregression, focusing on papillary muscle dynamics across subtypes. Methods: Frame-level echocardiographic time series from 41 patients (21 atrial, 20 ventricular; 1,959 frames) were z-score standardised within patient. Individual (lag 3) and pooled panel vector autoregression models, with supplementary full-cycle analysis across lags 1–20, tested whether LV volume, left atrial volume, papillary muscle length, and annulus diameter Granger-predict mitral regurgitation area. Results: Individual models revealed marked heterogeneity. In pooled analysis, LV volume was the strongest Granger predictor at the shortest lag (atrial p=0.011; ventricular p=0.006), while left atrial volume reached significance at longer lags (lag 6 atrial p=0.033, ventricular p=0.004). Systolic papillary muscle length was not predictive at any lag. Full-cycle analysis revealed an asymmetric subtype dissociation: papillary muscle length Granger-predicted regurgitation only in the ventricular subtype (lag 1 p<0.001) whereas regurgitation predicted papillary muscle deformation at every lag in the atrial subtype (20/20) but at none in the ventricular subtype. Cross-sectional comparisons of the four determinants did not distinguish MR severity within subtypes. Conclusions: Beat-to-beat vector autoregression and Granger modelling reveals heterogeneous, subtype-specific temporal patterns and a strong directional asymmetry between regurgitation and papillary muscle dynamics across subtypes. This disease-agnostic framework may support patient-specific temporal phenotyping of functional mitral regurgitation. Graphical
Reflex syncope (RS) is the most prevalent form of syncope, yet its pathophysiology and clinical presentation are not well understood. Despite controversy, the ‘ventricular theory’ remains the most plausible hypothesis to explain RS in susceptible patients. Certain assumptions regarding the geometry and function of the heart are essential in supporting this theory. Given these considerations, the goal of this review was to try to integrate data on heart morphology and function in a phenotype of a patient susceptible to RS. Previous research suggests that a small left ventricle and atria, in addition to a normo- or hypercontractile myocardium, predispose to more syncopal events. These findings have been confirmed in different subsets of patients, including those with small heart and chronic fatigue syndrome, highlighting common pathophysiologic pathways in these subgroups of population. Heart geometry and function seem to play a role in different treatment strategies for RS patients, including the administration of medications, pacing, and possibly cardioneural ablation. In addition, parameters related to the geometry of the heart chambers and of the electrical activation of the heart seem to have predictive value for syncope recurrence. These parameters could be included in the future and improve the accuracy of predictive models for RS.