Electromechanical reciprocity – comprising electro‐mechanical (EMC) and mechano‐electric coupling (MEC) – provides cardiac adaptation to changing physiological demands. Understanding electromechanical reciprocity and its impact on function and heterogeneity in pathological conditions – such as (drug‐induced) acquired long QT syndrome (aLQTS) – might lead to novel insights in arrhythmogenesis. Our aim is to investigate how electrical changes impact on mechanical function (EMC) and vice versa (MEC) under physiological conditions and in aLQTS. To measure regional differences in EMC and MEC in vivo, we used tissue phase mapping cardiac MRI and a 24‐lead ECG vest in healthy (control) and I_Kr‐blocker E‐4031‐induced aLQTS rabbit hearts. MEC was studied in vivo by acutely increasing cardiac preload, and ex vivo by using voltage optical mapping (OM) in beating hearts at different preloads. In aLQTS, electrical repolarization (heart rate corrected RT‐interval, RTn370) was prolonged compared to control (P < 0.0001) with increased spatial and temporal RT heterogeneity (P < 0.01). Changing electrical function (in aLQTS) resulted in significantly reduced diastolic mechanical function and prolonged contraction duration (EMC), causing increased apico‐basal mechanical heterogeneity. Increased preload acutely prolonged RTn370 in both control and aLQTS hearts (MEC). This effect was more pronounced in aLQTS (P < 0.0001). Additionally, regional RT‐dispersion increased in aLQTS. Motion‐correction allowed us to determine APD‐prolongation in beating aLQTS hearts, but limited motion correction accuracy upon preload‐changes prevented a clear analysis of MEC ex vivo. Mechano‐induced RT‐prolongation and increased heterogeneity were more pronounced in aLQTS than in healthy hearts. Acute MEC effects may play an additional role in LQT‐related arrhythmogenesis, warranting further mechanistic investigations. image Key points: Electromechanical reciprocity comprising excitation‐contraction coupling (EMC) and mechano‐electric feedback loops (MEC) is essential for physiological cardiac function. Alterations in electrical and/or mechanical heterogeneity are known to have potentially pro‐arrhythmic effects. In this study, we aimed to investigate how electrical changes impact on the mechanical function (EMC) and vice versa (MEC) both under physiological conditions (control) and in acquired long QT syndrome (aLQTS). We show that changing the electrical function (in aLQTS) results in significantly altered mechanical heterogeneity via EMC and, vice versa, that increasing the preload acutely prolongs repolarization duration and increases electrical heterogeneity, particularly in aLQTS as compared to control. Our results substantiate the hypothesis that LQTS is an ‛electro‐mechanical’, rather than a ‘purely electrical’, disease and suggest that acute MEC effects may play an additional role in LQT‐related arrhythmogenesis.

Neuroendocrine neoplasms (NENs) represent a rare, heterogeneous group of malignancies. Within this tumor entity, primary renal neuroendocrine tumors (PRNETs) are exceedingly rare, with only 160 cases reported worldwide. Due to the absence of native neuroendocrine cells in the renal parenchyma, their cellular origin remains unclear. Clinical and diagnostic challenges are reflected by the low incidence, non-specific clinical presentation, resemblance to common renal neoplasms, and the need for specialized histopathological diagnostic examination. Here, we present the case of a 61-year-old female with an incidentally diagnosed left-sided PRNET in September 2024. This case highlights the diagnostic complexity of PRNET and, importantly, underscores its genomic heterogeneity. It demonstrates a lack of typical renal cell carcinoma (RCC) or common NEN-associated gene alterations, emphasizing their unique molecular landscape.

Background/Objectives: Cardiac metastases (CM) represent a rare manifestation of neuroendocrine neoplasms (NEN). Detailed clinical characteristics and significance remain understudied. Methods: We retrospectively evaluated 1201 patients with NEN treated at an ENETS Center of Excellence to determine prevalence, clinical features, and outcomes of cardiac metastases. CM were identified in 15 patients (prevalence 1.25%) through multimodal imaging, incorporating somatostatin receptor positron emission tomography/computed tomography (SSTR PET/CT). Metachronous CM occurrence accounted for 93% of cases. Results: The majority of patients showed well-differentiated tumors (G1/G2), with ileum being the most frequent site of origin. Clinical symptoms attributable to CM were observed in 27% of affected patients. Following CM detection, therapeutic management was adjusted in 73% of cases, most frequently by initiating peptide receptor radionuclide therapy (PRRT) n = 8, 53%. Median overall survival (OS) from CM diagnosis was 95 months, with an estimated 5-year survival rate of 77%, with a 5-year OS from NEN diagnosis of 87%. Conclusions: CM in NEN are rare and often clinically silent, with SSTR PET/CT proving essential for detection. While treatment adjustments were frequently observed, particularly with PRRT, OS remained favorable, indicating that the presence of CM in NEN serves as an indicator of metastatic spread rather than a standalone diagnostic determinant of survival. Larger, prospective studies are needed to further validate these findings and to better define the clinical implications of CM in NEN.