Advanced Cardiovascular Imaging in Cardiomyopathy

Editor


E-Mail Website
Guest Editor
Department of Clinical Internal, Anesthesiologic and Cardiovascular Sciences, Sapienza Università di Roma, Rome, Italy
Interests: takotsubo cardiomyopathy; echocardiography; human study
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiomyopathies encompass a heterogeneous group of myocardial disorders with varied phenotypic expressions, ranging from asymptomatic subtle structural changes to life-threatening complications including sudden cardiac death, arrhythmias, and heart failure. Accurate characterization of these pathologies is critical for differential diagnosis, risk stratification, and therapy guidance. This Special Issue aims to highlight the pivotal role of advanced cardiovascular imaging in unraveling the complexity of cardiomyopathies. We welcome original research, state-of-the-art reviews, and perspectives that specifically address the following:

  • Phenotypic diversity of cardiomyopathies: Insights into the genetic, morphological, and functional spectrum of cardiomyopathies, including hypertrophic, dilated, non-dilated left ventricular, arrhythmogenic right ventricular, and restrictive phenotypes.
  • Multimodality approach: Contributions demonstrating the complementary roles of echocardiography, cardiac magnetic resonance, computed tomography, and nuclear imaging in diagnosis and disease staging.
  • Therapeutic implications: Studies showcasing how imaging informs personalized treatment strategies, from pharmacological tailored interventions to device therapy, and enables precise monitoring of treatment response.

This Special Issue seeks to bridge gaps between clinical imaging, pathophysiological understanding, and emerging therapeutics in cardiomyopathy care. Submissions from multidisciplinary teams and collaborative networks are especially encouraged. We look forward to your contributions to this timely and impactful Issue.

Dr. Luca Arcari
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiomyopathies
  • hypertrophic cardiomyopathy
  • dilated cardiomyopathy
  • cardiac amyloidosis
  • arrhythmogenic right ventricular cardiomyopathy
  • non-dilated left ventricular cardiomyopathy
  • cardiac magnetic resonance imaging
  • computed tomography
  • echocardiography
  • nuclear imaging

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 8817 KB  
Article
Relationships Between Regional Left Ventricular Myocardial Strain and Tissue Characteristics in Hypertrophic Cardiomyopathy
by Gabriela S. Galvao, Badr Bannan, Laura Jimenez-Juan, Huda S. Ismail, Faisal Alabdulkarim, Matias F. Callejas, Yin Ge, Djeven P. Deva and Andrew T. Yan
J. Cardiovasc. Dev. Dis. 2026, 13(9), 430; https://doi.org/10.3390/jcdd13090430 - 2 Sep 2026
Viewed by 162
Abstract
Both fibrosis and hypertrophy contribute to abnormal myocardial mechanics in hypertrophic cardiomyopathy (HCM). We sought to assess the relationships between regional structural and functional parameters in HCM by cardiac magnetic resonance (CMR). This was a retrospective single-center study of HCM patients and age-matched [...] Read more.
Both fibrosis and hypertrophy contribute to abnormal myocardial mechanics in hypertrophic cardiomyopathy (HCM). We sought to assess the relationships between regional structural and functional parameters in HCM by cardiac magnetic resonance (CMR). This was a retrospective single-center study of HCM patients and age-matched controls with either hypertensive heart disease (HHD) or normal CMRs. CMR feature tracking was performed to assess global and segmental 2D-radial, circumferential, and longitudinal LV strain, while native and post-contrast T1 parametric mapping analysis was performed to assess the global and regional T1 values and ECV fraction. Of 100 patients (age 56 ± 15 years; 66% male), 62 were in the HCM group and 38 in the control group (19 healthy individuals and 19 with HHD). Compared to the control group, global circumferential strain (−16.1 ± 5.9% vs. −20.8 ± 3.6%, p < 0.001) and radial strain (45.2 ± 14.1% vs. 32.1 ± 14.0%, p < 0.001) were worse in the HCM group. Among the HCM patients, there were significant correlations between segmental native T1 values at the most hypertrophied segment and global longitudinal strain (r = 0.27, p = 0.031), global circumferential strain (r = 0.34, p = 0.006), global radial strain (r = −0.29, p = 0.024), and left ventricular ejection fraction (LVEF) (r = −0.31, p = 0.014). In HCM, higher myocardial T1 at the most hypertrophied segment correlated with worse global LV myocardial strain and LVEF by CMR. Full article
(This article belongs to the Special Issue Advanced Cardiovascular Imaging in Cardiomyopathy)
Show Figures

Figure 1

19 pages, 6230 KB  
Article
Native T1 Mapping and Clinical Risk Characterization in Non-Ischemic Dilated Cardiomyopathy: A Cardiac Magnetic Resonance Study
by Manuela Montatore, Marco Rella, Eleonora Indolfi, Federica Masino, Ruggiero Tupputi, Eluisa Muscogiuri and Giuseppe Guglielmi
J. Cardiovasc. Dev. Dis. 2026, 13(6), 279; https://doi.org/10.3390/jcdd13060279 - 19 Jun 2026
Viewed by 502
Abstract
Background: Risk stratification in non-ischemic dilated cardiomyopathy (DCM) remains challenging because left ventricular ejection fraction (LVEF) and late gadolinium enhancement (LGE) do not fully capture the underlying myocardial substrate. Septal native T1 mapping provides a quantitative assessment of diffuse myocardial abnormalities and may [...] Read more.
Background: Risk stratification in non-ischemic dilated cardiomyopathy (DCM) remains challenging because left ventricular ejection fraction (LVEF) and late gadolinium enhancement (LGE) do not fully capture the underlying myocardial substrate. Septal native T1 mapping provides a quantitative assessment of diffuse myocardial abnormalities and may contribute to myocardial tissue characterization within a multiparametric CMR framework. Methods: This retrospective single-center study included 45 consecutive patients with non-ischemic DCM referred for clinically indicated CMR at Perrino Hospital, Brindisi, Italy, between November 2023 and November 2025. All examinations were performed using a standardized CMR protocol including cine imaging, LGE, and native T1 mapping on a 1.5-T Siemens Healthineers scanner. Septal native T1 was used as the primary mapping parameter because of its established reproducibility and robustness for myocardial tissue characterization. Patients were followed for a composite endpoint including all-cause mortality, major ventricular arrhythmic events, appropriate ICD therapy, and hospitalization for heart failure. Endpoint coding was verified, and all analyses were performed using the final validated dataset. Results: During a median follow-up of 15 months, 14 patients (31.1%) experienced the composite endpoint. Patients with events had lower LVEF (27.1 ± 7.8% vs. 48.3 ± 10.5%; p < 0.001), higher LVEDVi (142.6 ± 28.5 vs. 110.6 ± 23.4 mL/m2; p = 0.001), and higher septal native T1 values among patients with available T1 measurements (1047.5 ± 25.0 vs. 1031.5 ± 24.3 ms; p = 0.065). ROC analysis identified a septal native T1 threshold of 1042 ms for prediction of the composite endpoint, with an exploratory AUC of 0.70. Event-free survival was lower in patients with septal native T1 ≥ 1042 ms. Given the limited number of events, all regression and hierarchical analyses should be interpreted as exploratory and hypothesis-generating. Conclusions: Higher septal native T1 values were observed in patients experiencing adverse clinical outcomes; however, native T1 was not independently associated with the composite endpoint in exploratory Cox regression analyses. Full article
(This article belongs to the Special Issue Advanced Cardiovascular Imaging in Cardiomyopathy)
Show Figures

Figure 1

16 pages, 503 KB  
Article
Multi-Chamber Reverse Remodeling and Hemodynamic Force Realignment After SGLT2 Inhibitor Initiation in Real-World Heart Failure
by Silvia Prosperi, Sara Monosilio, Andrea D’Amato, Danilo Angotti, Domenico Filomena, Lucrezia Netti, Giovanni Tonti, Gianni Pedrizzetti, Sara Cimino, Roberto Badagliacca, Paolo Severino, Carmine Dario Vizza and Viviana Maestrini
J. Cardiovasc. Dev. Dis. 2026, 13(6), 260; https://doi.org/10.3390/jcdd13060260 - 11 Jun 2026
Viewed by 450
Abstract
Background: Sodium–glucose cotransporter 2 inhibitors (SGLT2i) promote beneficial effects on cardiac reverse remodeling (RR) in heart failure (HF). However, most imaging evidence focuses on single chambers, mainly the left ventricle (LV) or left atrium (LA), whereas integrated biventricular and atrial remodeling remains less [...] Read more.
Background: Sodium–glucose cotransporter 2 inhibitors (SGLT2i) promote beneficial effects on cardiac reverse remodeling (RR) in heart failure (HF). However, most imaging evidence focuses on single chambers, mainly the left ventricle (LV) or left atrium (LA), whereas integrated biventricular and atrial remodeling remains less explored. Moreover, real-world data are limited, and myocardial–flow coupling markers, such as hemodynamic forces (HDFs), are scarcely investigated, with uncertain sex-related differences. Purpose: To evaluate multi-chamber cardiac RR after SGLT2i initiation in a real-world HF population. Secondary aims are to assess whether changes in HDFs provide additional functional insight into myocardial–flow coupling beyond conventional echocardiographic indices, and to descriptively explore sex-related differences in echocardiographic remodeling. Methods: Patients with HF and ejection fraction (EF) ≤ 45%, naive to SGLT2i and on stable guideline-directed medical therapy for ≥3 months, were enrolled. Standard and advanced echocardiography were performed at baseline and follow-up, including speckle-tracking and HDFs assessment. NYHA class and NT-proBNP were collected. Analyses were performed overall and stratified by sex. Results: Sixty-eight patients were included. After 6 months, RR was observed across all chambers: LV-RR in 33 patients (49%), right ventricular (RV) RR in 35 (52%), biventricular RR in 18 (27%), and LA-RR in 14 (21%). HDFs showed significant realignment, suggesting association with improved myocardial–flow coupling. RR effects were comparable between sexes (p > 0.05). NT-proBNP significantly decreased. Conclusions: In this real-world cohort, SGLT2i therapy was associated with significant multi-chamber RR and HDFs realignment, supporting improved myocardial–flow coupling beyond conventional indices. Exploratory sex-related analyses showed no significant differences. Larger and longer-term randomized studies are warranted. Full article
(This article belongs to the Special Issue Advanced Cardiovascular Imaging in Cardiomyopathy)
Show Figures

Graphical abstract

Review

Jump to: Research

19 pages, 7134 KB  
Review
Imaging Cardiac Amyloidosis: From Early Diagnosis to Risk Stratification and Evaluation of Treatment Efficacy
by Matteo Sclafani, Domitilla Russo, Georgios Oikonomou, Giovanni Camastra, Emanuela Belmonte, Giacomo Tini, Rossella Rotunno, Cristina Chimenti, Chiara Lanzillo, Beatrice Musumeci, Teresa Castiello, Stefano Regondi, Roberto Ricci, Luca Cacciotti and Luca Arcari
J. Cardiovasc. Dev. Dis. 2026, 13(8), 401; https://doi.org/10.3390/jcdd13080401 - 21 Aug 2026
Viewed by 898
Abstract
Cardiac amyloidosis (CA) is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins, most commonly immunoglobulin light chains (AL) or transthyretin (ATTR). Once considered a rare disease, CA is increasingly recognised due to improved diagnostic strategies and the availability of disease-modifying therapies. [...] Read more.
Cardiac amyloidosis (CA) is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins, most commonly immunoglobulin light chains (AL) or transthyretin (ATTR). Once considered a rare disease, CA is increasingly recognised due to improved diagnostic strategies and the availability of disease-modifying therapies. Early diagnosis is crucial, as treatment efficacy and clinical outcomes are strongly influenced by the stage of cardiac involvement. Multimodality cardiac imaging plays a central role in the diagnostic pathway, risk stratification, and evaluation of therapeutic response in CA. Echocardiography represents the first-line imaging modality and is essential for raising clinical suspicion through the identification of characteristic structural and functional abnormalities, including ventricular wall thickening, diastolic dysfunction, and distinctive strain patterns. Bone scintigraphy has revolutionised the non-invasive diagnosis of ATTR-CA, allowing accurate identification of transthyretin-related disease in the absence of monoclonal gammopathy, which needs to be excluded via serum and urinary immunofixation. Cardiovascular magnetic resonance provides advanced tissue characterisation through late gadolinium enhancement and quantitative mapping techniques, enabling detection of early myocardial involvement and robust prognostic stratification. Emerging imaging modalities, including dual-energy (spectral) computed tomography and positron emission tomography tracers, show promise in myocardial amyloid quantification and subtype differentiation, although their role is still evolving. Integration of imaging findings with clinical and laboratory parameters allows comprehensive disease assessment, facilitating early diagnosis, guiding therapeutic decisions, and improving risk stratification. This review summarises the current role of multimodality imaging in CA, highlighting its contribution from early detection to prognostic evaluation and monitoring of treatment efficacy, with particular emphasis on the emerging role of quantitative imaging in monitoring treatment response. Full article
(This article belongs to the Special Issue Advanced Cardiovascular Imaging in Cardiomyopathy)
Show Figures

Figure 1

Back to TopTop