Background: Cardiovascular magnetic resonance (CMR) is the clinical gold standard for assessing cardiac anatomy and function. However, the manual segmentation of cardiac structures and myocardial infarction (MI) is time-consuming, prone to inter-observer variability, and often depends on contrast-enhanced imaging. Although deep learning (DL) has enabled substantial automation, challenges remain in generalizability, particularly for MI detection from non-contrast cine CMR. Objective: This study proposes a comprehensive DL-based framework for automatic segmentation of cardiac structures and myocardial infarction using contrast-free cine CMR. Methods: The framework integrates multiple convolutional neural network (CNN) architectures for cardiac structure segmentation with an attention-based deep learning model for MI localization. Post-processing refinement using stacked autoencoders and active contour modeling is applied to improve anatomical consistency. Segmentation performance is evaluated using overlap-based and boundary-based metrics, including the Dice Similarity Coefficient (DSC), Mean Contour Distance (MCD), and Hausdorff Distance (HD). Results: The best-performing model achieved Dice scores of 0.93 ± 0.05 for the left ventricular (LV) cavity, 0.89 ± 0.04 for the LV myocardium, and 0.91 ± 0.06 for the right ventricular (RV) cavity, with consistently low boundary errors across all structures. Myocardial infarction segmentation achieved a Dice score of 0.80 ± 0.02 with high recall, demonstrating reliable infarct localization without the use of contrast agents. Conclusions: By enabling accurate cardiac structure and myocardial infarction segmentation from contrast-free cine CMR, the proposed framework supports broader clinical applicability, particularly for patients with contraindications to gadolinium-based contrast agents and in emergency or resource-limited settings. This approach facilitates scalable, contrast-independent cardiac assessment.

QRS fragmentation on the 12-lead electrocardiogram and its association to physiological cardiac adaptation in elite cyclists.

Pulmonary arterial hypertension (PAH) presents as increased pressure in the pulmonary arteries (PA) leading to cardiac right ventricular (RV) failure and death. Pulmonary arterial (PA) remodeling characterized by enhanced proliferation of pulmonary arterial smooth muscle cells (PASMC) and fibroblasts (PAFB) underlies PAH. There are currently no cures and PAH mortality remains high. PAH has a striking female-predominant incidence - 4:1 ratio - indicating that males may have a protective factor. However, to date only a few sex-biased factors in PAH have been investigated. Analyses were performed on a publicly available microarray dataset (GSE117261), comprising human lung tissues from PAH patients and healthy controls, as well as publicly available single-cell lung atlases of humans and mice. Lung tissue, plasma, PASMC and PAFB were collected from male and female PAH patients. Cell proliferation was assessed after recombinant HGF protein stimulation. PH was induced in male and female rats by monocrotaline (MCT). Lung-specific knockdown was performed by intratracheal siRNA instillation the first two weeks after MCT injection. PA and RV function were assessed by echocardiography, RV systolic pressure by catheterization, and PA remodeling by histology. HGF was only upregulated in lungs of male PAH patients compared to male control lungs, but not in female PAH patients vs. female controls. Elevated plasma HGF correlated with favorable clinical characteristics only in male PAH patients. HGF is highly expressed in vascular SMC and FB in the lung and recombinant HGF inhibited PASMC and PAFB proliferation to a greater extent in cells isolated from male PAH patients compared to female. Lung HGF expression is increased to a higher extent and longer duration at early stage of PH in male rats in MCT model vs. female rats. Finally, knockdown of HGF in the lungs in early disease stage exacerbated PH in male rats characterized by higher mortality, worsened RV and PA function as well as enhanced PA medial thickening and adventitial fibrosis. Lung HGF expression may be upregulated to counteract PAH disease progression by inhibiting proliferation of PASMC and PAFB. Elevated HGF in males might at least partially account for the lower incidence of male PAH patients.

The Sigma-1 receptor agonist PRE084 improves cardiopulmonary function and remodelling in an experimental model of pulmonary arterial hypertension.

Dynamic Changes in Right Ventricular-Pulmonary Arterial Coupling During Acute Heart Failure Hospitalization: Prognostic Implications.

Calcium, sodium and potassium are essential for the contractile function of cardiomyocytes. In pulmonary arterial hypertension (PAH), intracellular calcium dynamics are impaired, affecting contractility and leading to heart failure. Energy-dispersive X-ray spectroscopy associated with scanning electron microscopy (EDS-SEM) technique can be useful for mapping the distribution of these minerals in cardiac tissue. This study aimed to investigate chronic ionic imbalances in the cardiac tissue of a monocrotaline (MCT) induced PAH model, using EDS-SEM, and to evaluate the impact of these imbalances on the contractile function of isolated RV myocytes. Twenty-eight Wistar rats were assigned to Control and PAH groups, with PAH induced by MCT. Right ventricular (RV) function was assessed by echocardiography at day 24. On day 25, cardiac tissue was analyzed by EDS-SEM to quantify electrolytes and by Western blotting, and RV myocyte contractility was measured. Student's t-test was performed to compare the groups. Animals with PAH showed reduced final weight, increased cardiac and RV weight, and reduced RV systolic function compared to controls. EDS-SEM analysis revealed lower Ca and Na density in cardiac tissue of PAH animals. The expression of Ca2+ regulatory proteins was reduced in the PAH group, and the contractility of isolated myocytes was impaired, exhibiting decreased amplitude, contraction velocity, and relaxation velocity. In conclusion, the study demonstrates that MCT-induced ionic imbalances, specifically reduced Ca and Na, disrupt excitation-contraction coupling proteins, leading to impaired cardiomyocyte contractility and contributing to the RV dysfunction observed in PAH.

In secondary tricuspid regurgitation (STR) patients, the clinical value of right atrioventricular coupling (RAVC) and right atrial (RA) stiffness indices has never been evaluated. Accordingly, we explored the association with a composite outcome of all-cause mortality or heart failure hospitalization of: 1) RAVC index obtained either with speckle tracking echocardiography (RAVCSTE) or as the ratio between RA volume (RAV) and right ventricular (RV) stroke volume (RAVCVOL), and 2) RA stiffness index calculated as the ratio between RAV index and RA longitudinal reservoir strain (RALS). 513 patients with mild-to-severe STR (75±13 years, 58% severe) were included. After a mean follow-up of 18±15 months, 195 patients (38%) reached the composite endpoint. On spline curve modeling, the cut-off values associated with increased two-year event rates were: (1) <0.82 for RAVCSTE (reduced values of the ratio between RALS and RV free wall strain indicating impaired coupling, the RA not supporting effectively the RV filling, despite a good systolic function of the RV); (2) >1.23 for RAVCVOL (higher values suggesting greater RA remodeling relative to RV stroke volume and altered coupling); (3) >4.6 for RA stiffness index (higher values indicating a diminished RA compliance to filling). However, in multivariable Cox regression analyses and hierarchical χ2 analyses, only RAVCVOL maintained a significant association with the outcome (p<0.05). In STR patients, RAVC and RA stiffness indices are associated with the risk of events, with RAVCVOL yielding the strongest association.

Pulmonary arterial hypertension (PAH) is a chronic condition of elevated pulmonary arterial pressure caused by vascular remodeling due to increased proliferation of pulmonary arterial smooth muscle cells (PASMC). Initially described as a disease primarily affecting young women, it now increasingly affects the elderly. Age-related pathomechanisms of PAH remain, however, unclear. In a translational approach combining preclinical disease model and analyses of human cohorts, we probed for a role of the anti-aging protein Klotho which acts as co-receptor for fibroblast growth factor 23 (FGF23) in the pathogenesis of PAH. Mice aged 114-117 weeks showed moderate spontaneous PAH with right ventricular (RV) hypertrophy and dysfunction relative to young mice aged < 40 weeks. This effect was further pronounced upon hypoxic exposure (10% O2) for 14 days. Histological sections showed pulmonary vascular wall thickening of small pulmonary arterioles. Similar findings were obtained in mice with a partial Klotho deficiency (kl/+) that developed right ventricular (RV) systolic pressures (RVSP) of 72.58±3.3 mmHg within two weeks of hypoxia. Aged mice and kl/+ mice had elevated plasma levels of FGF23 further amplified by hypoxic exposure. ELISA based measurements in serum of patients from a cross-sectional study with PAH aged 60 years or older confirmed an increase in circulatory FGF23. Immunohistochemistry staining of lung tissue showed increased proliferative activity of PASMC in kl/+ mice and recombinant FGF23 elevated proliferative activity of PASMC in vitro. The hyperproliferative response to FGF23 was prevented by siRNA-mediated knockdown of fibroblast growth factor receptor 1 in PASMC. In kl/+ mice, FGF23 neutralization using an anti-FGF23 antibody reduced RVSP, improved RV dysfunction and RV hypertrophy and prevented pulmonary vascular remodeling. Our findings identify accumulation of FGF23 as novel mechanism of pulmonary vascular remodeling in PAH. Targeting dysregulated Klotho/FGF23 signaling may present a promising therapeutic strategy in elderly patients.

Pulmonary hypertension (PH) is a fatal complication of chronic obstructive pulmonary disease (COPD) that worsens its prognosis. However, the associated diagnostic markers are uncertain. We assess the diagnostic utility of microRNA-21 (miR-21) and NT-proBNP for PH diagnosis in COPD patients. We selected three groups of participants: Group 1 consisted of 25 patients with COPD who did not have PH (COPD); Group 2 included 35 patients with COPD and PH (COPD-PH); and Group 3 comprised 30 healthy controls. Demographic, spirometric, echocardiographic-Doppler study, and biochemical variables were recorded and compared among these three groups. Serum miR-21 was measured by quantitative real-time PCR. Serum miR-21 level in COPD-PH patients was significantly higher compared with that in COPD patients and controls (P < 0.001). Compared with the COPD group, the COPD-PH group had greater miR-21 and brain natriuretic peptide (BNP) levels but significantly reduced forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), tricuspid annular plane systolic excursion (TAPSE), 6-minute walk test, and right ventricular (RV) functional parameters. Receiver Operating Characteristic curve analysis revealed that miRNA-21 had good diagnostic value for PH diagnosis in COPD patients, with an area under the curve (AUC) of 1.000, 100% sensitivity, and 100% specificity at a cutoff >7.94. While NT-proBNP demonstrated good accuracy, with an AUC of 0.936, sensitivity of 88.6%, and specificity of 88% at a cutoff >390.1 pg/mL. miR-21 may serve as a useful and reliable biomarker for diagnosing PH in COPD patients, outperforming the traditional biomarker NT-proBNP.

Previously proposed staging classification based on cardiac damage highlighted that right ventricular (RV) damage reflects the most advanced stage in patients with severe aortic stenosis. This study aimed to investigate the association between RV damage detected by RV free wall longitudinal strain (RVFWLS) and outcomes in patients with severe aortic stenosis who underwent transcatheter aortic valve implantation (TAVI). A total of 768 patients with severe aortic stenosis who underwent TAVI and echocardiographic images for RV functional assessment were included from a retrospective multicenter TAVI registry. The primary outcome was a composite of all-cause death and hospitalization due to cardiovascular events. During a median follow-up of 21 (12-30) months, 213 patients (28%) experienced the primary end points. In the multivariable Cox proportional hazards model, a higher absolute RVFWLS value was independently associated with better outcomes (adjusted hazard ratio [HR], 0.88 [95% CI, 0.84-0.91]). RVFWLS demonstrated incremental values superior to those of conventional RV parameters. Adding RVFWLS <17% as an RV damage (Stage 4) criterion in staging classification identified 272 (35%) patients in Stage 4. Patients with RVFWLS-incorporated Stage 4 had lower event-free survival than did those in the other stages (adjusted HR, 1.55 [95% CI, 1.35-1.77]). In patients with severe aortic stenosis who underwent TAVI, RVFWLS was independently associated with outcomes and provided superior prognostic value than other conventional RV echocardiographic parameters. Incorporating RVFWLS in a staging classification for RV damage showed incremental value for predicting survival after TAVI over the original staging classification.

Pacing-induced cardiomyopathy (PIC) occurs in up to 30% of patients with conventional right ventricular (RV) pacing, often requiring upgrade to cardiac resynchronization therapy (CRT). Left bundle branch area pacing (LBBAP) offers a physiological alternative to biventricular pacing, but its role in PIC upgrades remains underexplored. We retrospectively analyzed 31 patients who underwent LBBAP upgrades for PIC between June 2020 and September 2024. Procedural success, electrical remodeling, echocardiographic changes, and clinical outcomes were assessed. LBBAP was successful in 30 (97%) cases. Average procedure time was 80 (60-120) min. QRS duration significantly decreased (175 ± 17 ms to 130 ± 18 ms, p < 0.001). After a median 19 months of follow up, left ventricular ejection fraction (LVEF) improved from 33 ± 8% to 42 ± 8% (p < 0.001). Three patients (9%) were hospitalized for heart failure, and five (16%) died during follow-up. LBBAP is a safe and effective upgrade strategy for PIC, offering significant electrical and functional improvements. Further studies are needed to confirm its long-term benefits compared to biventricular pacing.

Right ventricular (RV) failure is a principal determinant of morbidity and mortality in children with pulmonary hypertension, making accurate RV assessment a cornerstone of risk stratification and long-term management. Noninvasive imaging plays a central role in this evaluation; however, commonly used modalities, including 2- and 3-dimensional echocardiography and cardiac magnetic resonance imaging, each have distinct advantages and limitations in the pediatric population. Consequently, an integrated, multimodal imaging strategy is required. This review provides a contemporary, critical appraisal of the existing evidence and key knowledge gaps related to noninvasive multimodality imaging of the RV in pediatric pulmonary hypertension. The discussion is structured around fundamental aspects of RV physiology, including chamber size and mass, systolic function, diastolic function and stiffness, RV-left ventricle interactions, ventriculoarterial coupling, and exercise assessment. Echocardiography and cardiac magnetic resonance imaging are presented in parallel to highlight their complementary roles within a multimodality framework. Current prognostic thresholds in pediatric pulmonary hypertension imaging are largely supported by level of evidence C, underscoring persistent gaps that limit the development of definitive clinical recommendations and a unified approach. We propose a roadmap to guide future research efforts and collaborative initiatives among pediatric pulmonary hypertension and imaging specialists, emphasizing the role of professional networks in advancing the field.

Background/Objectives: It is widely acknowledged that healthy highlanders (HL) present with significantly higher pulmonary arterial pressure (PAP) compared to healthy lowlanders (LL). However, whether this elevated PAP solely signifies a response to hypoxia at altitude or is also linked to right ventricular (RV) dysfunction is still unknown. Therefore, we assessed RV function in HL and LL using speckle-tracking-derived strain analysis. Methods: This case-control study evaluates echocardiographic RV free wall strain (RVFWS) in LL and HL in Kyrgyzstan. A RVFWS over -20% for men and a RVFWS of -21% for women were considered indicators of RV dysfunction. Subgroup analysis included individuals with and without risk for pulmonary hypertension (PH), defined as a TRV > 2.8 m/s. Results: A total of 59 participants (21 LL, 38 HL), with a mean ± SD age of 43 ± 8 versus 48 ± 10 years, were included and assessed at their living altitude. RVFWS in HL and LL was -27.3% ± 4.7 versus -27.0% ± 6.0 (mean difference 0.13%, 95%CI -2.65 to 2.92, p = 0.852). The conventional RV indices RV FAC (42% ± 6 vs. 38% ± 8), TAPSE (2.2 cm ± 0.2 vs. 2.0 cm ± 0.3), and TDI S' (14.2 cm/s ± 1.9 vs. 12.1 cm/s ± 1.8), however, did differ significantly between LL and HL. HL with and without risk for PH did not differ in RVFWS and in the conventional RV indices. Conclusions: Despite significant differences in conventional RV markers, healthy highlanders generally did not differ in RVFWS compared with lowlanders, indicating maintained RV systolic function at high altitude. Our findings suggest that elevated PAP in HL reflects adaptation rather than RV dysfunction, underscoring the need for refined diagnostic criteria for clinically relevant high-altitude pulmonary hypertension.

Neonates with Ebstein anomaly or severe tricuspid valve dysplasia represent a high-risk patient cohort. The modified Starnes procedure was historically performed for cases incompatible with biventricular (BV) repair, leading them towards single-ventricle palliation. However, in recent years, a paradigm shift has emerged in which the Starnes procedure in the acute setting can provide a means for right ventricular (RV) rehabilitation, by providing relief of RV volume overload and time for recovery of RV function, thus serving as a bridge to subsequent one and a half ventricle or BV repair. Herein, we present two cases at our institution of successful transition to BV repair after the Starnes procedure, despite an initially failed index BV repair as a neonate. Both patients presented with severe tricuspid valve dysplasia. The first patient underwent Starnes procedure at 10 days of life and takedown at 4 years of age after bilateral cavopulmonary shunt (BCPS) failure from recurrent bilateral pulmonary artery stenoses. The 2nd patient received Starnes at 4 months of age and successfully underwent takedown at 18mo after being deemed an unsuitable candidate for BCPS. Improvement in RV function was noted throughout the Starnes course. By providing our center's experience in the context of other case reports and series of BV conversion post-Starnes procedure, summarizing clinical and surgical considerations advocated in recent guidelines, and highlighting the topical areas of management that remain to be elucidated, we hope this discussion can lead to appropriate adoption of this new treatment strategy.

Abstract Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome defined by diastolic dysfunction and limited therapeutic options, with increasing recognition of right ventricular (RV) involvement. Using invasive pressure-volume loop analysis, we assessed biventricular hemodynamics in lean and obese ZSF1 rats, a well-established rodent model of HFpEF. Obese rats exhibited significantly increased RV and left ventricular (LV) chamber stiffness, with a positive correlation between RV and LV stiffness constants, indicating biventricular diastolic dysfunction. RV end-systolic elastance was preserved, whereas LV contractility was increased. Despite elevated RV stiffness, myocardial fibrosis was unchanged, while RV and septal cardiomyocyte hypertrophy was significantly increased. These findings demonstrate that RV diastolic dysfunction in this HFpEF model is driven primarily by myocytic stiffening rather than fibrotic remodeling. Our data provide invasive hemodynamic evidence of RV involvement in HFpEF and further support the translational relevance of the ZSF1 rat model for studying biventricular HFpEF pathophysiology.

Although early right ventricular failure (eRVF) following durable left ventricular assist device (dLVAD) implantation is associated with a poor prognosis, reliable predictive parameters have not yet been established. In this study we evaluated the predictive value of right ventricular (RV) to pulmonary artery (PA) uncoupling, measured by the ratio of tricuspid annular plane systolic excursion (TAPSE) to PA systolic pressure (PASP), in patients undergoing dLVAD implantation. We conducted a single-center retrospective study of adult patients who underwent dLVAD implantation between January 2008 and December 2024. eRVF was defined as receiving short- or long-term right-sided circulatory support, or continuous inotropic support for more than 14 days within 30 days after dLVAD implantation. Preoperative echocardiographic variables, including the TAPSE/PASP ratio and right-sided heart catheter parameters, were analyzed using univariate and multivariate logistic regression models to identify eRVF predictors. We analyzed data for 111 patients who underwent dLVAD implantation and 46.8% developed eRVF postoperatively. The TAPSE/PASP ratio was an independent predictor of eRVF, even after adjustments for other echocardiographic variables (odds ratio [OR], 0.05; 95% confidence interval [CI], 0.004-0.67, P=0.024) and right-sided heart catheter variables (OR, 0.04; 95% CI, 0.002-0.69, P=0.027). Preoperative RV-PA uncoupling, assessed using the TAPSE/PASP ratio, may predict eRVF following dLVAD implantation. This parameter is clinically accessible and valuable for preoperative risk stratification and may facilitate improved perioperative management.

Pulmonary arterial hypertension (PAH) is characterized by progressive vascular remodeling and right ventricular (RV) dysfunction, processes that are increasingly associated with disturbances in cellular metabolism. We investigated whether transplantation of exogenous mitochondria derived from bone marrow mesenchymal stromal cells, alone or combined with sildenafil, could improve mitochondrial homeostasis and attenuate cardiopulmonary remodeling in monocrotaline-induced PAH. Male Wistar rats were assigned to control (CTRL, n = 8) or PAH (n = 32) groups. Fourteen days after induction of PAH, animals were randomized to receive saline, sildenafil (20 mg/kg/day for 14 days), intravenous mitochondrial transplantation (100 μg, days 14 and 21), or combined therapy. On day 28, echocardiography, invasive measurement of RV systolic pressure (RVSP), pulmonary vascular histology, gene expression analyses (vimentin, VE-cadherin, and mitochondrial metabolism-related genes), and high-resolution respirometry were performed. All treatments significantly reduced RVSP compared with untreated PAH. Mitochondrial therapy, alone or combined with sildenafil, decreased arteriolar α-smooth muscle actin content, whereas endothelial-mesenchymal transition was attenuated only with combined treatment. Mitochondrial transplantation and sildenafil increased Complex I-dependent respiration, whereas Complex IV activity improved exclusively with mitochondrial therapy. Combined treatment reduced plasma IL-6 and IL-1β levels compared with PAH. Thus, mitochondrial transplantation, particularly when combined with sildenafil, improved RV function, limited pulmonary vascular remodeling, reduced plasma inflammatory markers, and changed key mitochondrial pathways in experimental PAH.

Aortic root thrombosis (ART) in left ventricular assist device (LVAD) patients has gained attention due to potential clinical consequences. This study aims to assess the clinical outcomes associated with ART in LVAD patients. We retrospectively evaluated adult patients who received LVAD implants at our center between January 2020 and March 2022. Pre-operative data, including demographics, laboratory values, and echocardiographic assessments, were similar between the ART and non-ART groups. Composite outcomes such as cerebrovascular events, pump thrombosis, myocardial infarction, embolic events, bleeding, right ventricular (RV) failure, and mortality post-discharge were examined. The study included 44 outpatients (36 HeartMate 3, 8 HeartWare). ART was identified in 20 patients (45%) post-discharge. The "no ART" group had a mean age of 47±10 years (23 of 24 patients were male, 95.8%), while the "ART" group had a mean age of 48±12 years (15 of 20 patients were male, 75%), with no significant age difference (p>0.05). Thrombosis occurred at a median of 59 days post-implantation, primarily affecting the non-coronary cusp in 50% of the ART group. The median follow-up period was 416 days. No significant differences were found in composite outcomes (p=0.276), mortality (p=0.814), bleeding (p=0.808), or RV failure (p=0.197). ART may be under-recognized in LVAD patients, potentially leading to cardiac and end-organ damage. While ART does not significantly impact mortality, it emphasizes the need for careful management of LVAD patients.

ABSTRACTTraditional echocardiographic measures of right ventricular (RV) function, such as tricuspid annular plane systolic excursion (TAPSE) and peak systolic velocity at the tricuspid annulus (S’), may be unreliable after cardiac surgery due to changes in loading conditions and myocardial mechanics. This study aimed to evaluate RV function following pulmonary thromboendarterectomy (PTE) for chronic thromboembolic pulmonary hypertension (CTEPH) and to identify alternative echocardiographic indices that better reflect postoperative RV recovery. This retrospective, single‐center study included CTEPH patients who underwent PTE at Cleveland Clinic between January 2020 and March 2021. Echocardiographic evaluations were performed preoperatively and within 3 months postoperatively. Parameters assessed included RV size, function, volumes, pulmonary pressures, and tricuspid regurgitation (TR) severity. TAPSE and RV S’ significantly decreased postoperatively (mean changes −0.75 cm and −2.8 cm/s, respectively; p < 0.001). RV systolic pressure, end‐diastolic volume (RVEDV), and end‐systolic volume (RVESV) also declined (p < 0.05). RV diameter decreased (mean 4.57 cm; p = 0.012), and 2D RV ejection fraction (RVEF) increased significantly (mean change +7%; p = 0.003). TR severity improved, with 97.1% of patients showing only mild TR (p = 0.003). Fractional area change (FAC) did not change significantly. After PTE, RV size, volume, RVEF, and TR severity are more reliable indicators of RV recovery than TAPSE or S’. These findings reflect reverse RV remodeling due to reduced afterload and underscore the limitations of traditional longitudinal RV function metrics in the postoperative setting.

Background/Objective: Pacing-induced cardiomyopathy (PICM) is a common complication of right ventricular (RV) pacing, affecting 6-25% of patients with frequent RV pacing, due to electrical and mechanical dyssynchrony. Certain clinical and electrocardiographic risk factors have been identified, including high RV-pacing burden and longer paced QRS, but their ability to predict the development PICM remains limited. Additionally, other forms of PICM have been described, including heart failure with preserved ejection fraction and RV failure. The goal of this narrative review is to summarize the current evidence utilizing noninvasive imaging to identify patients predisposed to a high risk of PICM. Methods: Using a literature search in the PubMed, Scopus, Google Scholar, and the Cochrane databases from 2000 to 2025, which included but was not limited to the keywords right ventricular pacing, pacemaker-related cardiomyopathy, pacemaker-induced cardiomyopathy, biventricular pacing, conduction system pacing, His bundle pacing, left bundle pacing, echocardiography, computed tomography imaging, and cardiac magnetic resonance imaging, we reviewed randomized control trials, observational retrospective and prospective cohort studies, societal guidelines, and systematic review articles. Conclusions: Essential in the diagnosis of PICM, cardiac imaging can identify patients at risk, even before left ventricular (LV) dysfunction or symptoms develop. Pre- and early post-implantation 2- and 3-dimensional echocardiography with global longitudinal strain provides sensitive parameters for the potential development of PICM. Relative indices of contractile asymmetry have been described. Cardiac magnetic resonance imaging offers an accurate assessment of cardiac volumes and LV synchrony and can also quantify myocardial fibrosis, a significant predictor of PICM. Performing pre-device implantation imaging may help predict subsequent heart failure development and potentially can guide pacing modality selection that can mitigate this risk. Thus, an imaging-guided framework will advance the management of PICM.