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Life
Special Issues
Pathology, Diagnosis, and Treatment of Cardiomyopathies
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Pathology, Diagnosis, and Treatment of Cardiomyopathies

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 1302

Editor

Dr. Sanjay Sivalokanathan

E-Mail Website
Guest Editor
Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: cardiomyopathy; cardiac sarcoidosis; sports cardiology; HCM
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiomyopathy comprises a heterogeneous group of myocardial disorders characterized by structural and functional impairments of the heart. Major phenotypic classifications include hypertrophic cardiomyopathy, dilated cardiomyopathy, restrictive cardiomyopathy, and inflammatory cardiomyopathy.

The pathogenetic mechanisms underlying cardiomyopathy are multifactorial and complex, frequently involving interactions between genetic predisposition, environmental influences and lifestyle factors. These contribute to a cascade of pathophysiological alterations—including myocardial hypertrophy, ventricular dilation, compromised pumping capacity and cardiomyocyte damage—that culminate in distinct cardiomyopathy phenotypes.

Diagnostic evaluation encompasses detailed clinical history-taking, physical examination, advanced cardiac imaging and endomyocardial biopsy when indicated. Ongoing refinements in imaging modalities and histological techniques have significantly improved diagnostic precision.

Management strategies include pharmacotherapy, device-based interventions and other options. Adjunctive lifestyle modification and structured exercise training also contribute to functional recovery. Treatment must be individualized and multimodal, based on disease etiology, stage and clinical profile.

This Special Issue seeks to synthesize current understanding of pathogenic pathways, highlight emerging diagnostic technologies and evaluate novel therapeutic approaches, with the ultimate goal of facilitating personalized management in cardiomyopathy.

Dr. Sanjay Sivalokanathan
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. Life 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 2600 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
  • pathogenetic mechanisms
  • diagnoses

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Published Papers (2 papers)

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Review

17 pages, 1069 KB  
Review
Coronary Microvascular Dysfunction in Stress Cardiomyopathy: At the Heart of the Problem
by Giorgio Piccolboni, Giovanni Civieri and Francesco Tona
Life 2026, 16(7), 1091; https://doi.org/10.3390/life16071091 - 29 Jun 2026
Viewed by 370
Abstract
Takotsubo syndrome (TTS) is an acute disorder characterized by transient left ventricular dysfunction with typical regional wall motion abnormalities, most commonly apical ballooning. It accounts for 1–3% of all suspected acute coronary syndromes and up to 5–6% in women presenting with ST-segment elevation [...] Read more.
Takotsubo syndrome (TTS) is an acute disorder characterized by transient left ventricular dysfunction with typical regional wall motion abnormalities, most commonly apical ballooning. It accounts for 1–3% of all suspected acute coronary syndromes and up to 5–6% in women presenting with ST-segment elevation myocardial infarction requiring coronary angiography to exclude obstructive coronary artery disease. The pathophysiology of TTS is complex and not fully elucidated, with sympathetic hyperactivation playing a central role through calcium dysregulation, oxidative stress, and metabolic alterations. Both clinical and experimental data demonstrate the importance of inflammation, with cell infiltration and persistent immune activation exceeding the acute phase. Increasing evidence highlights the impact of coronary microvascular disfunction (CMVD) as a secondary phenomenon, with some findings that support its role as a causative substrate. Beyond well-known predisposing conditions such as female sex, postmenopausal age, and neurological and psychiatric disorders with the trigger of a physical or psychological event, numerous case reports associate the syndrome with chronic autoimmune diseases, even if clear experimental evidence remains poor and worthy of further study. Echocardiography and advanced imaging techniques, including cardiac magnetic resonance and positron emission tomography, have provided insights into transient CMVD, reversible myocardial edema, and metabolic impairment, strengthening our knowledge of the syndrome as a dynamic process. It is also of growing interest to perform invasive hemodynamic assessment to explain the increase in microvascular resistance. This review offers a comprehensive and up-to-date overview of these techniques in the context of TTS. Since clinically, TTS may be associated with significant morbidity and mortality, with some unexplained cases of long-term myocardial disfunction or even recurrence, a deeper understanding of the interplay between catecholamines, inflammation, immune substrate, and CMVD may improve risk stratification and lead to the development of targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Pathology, Diagnosis, and Treatment of Cardiomyopathies)
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29 pages, 1054 KB  
Review
Micro- and Nanoplastics as Potential Drivers of Dilated Cardiomyopathy
by Joshua Xu and Sanjay Sivalokanthan
Life 2026, 16(6), 916; https://doi.org/10.3390/life16060916 - 29 May 2026
Viewed by 580
Abstract
Dilated cardiomyopathy (DCM) is a leading cause of heart failure, but up to 50% of cases have no definitive etiology. Genetic susceptibility alone does not account for phenotypic inconsistency, so a ‘two-hit’ model has been proposed to explore the spectrum of gene-environment interactions. [...] Read more.
Dilated cardiomyopathy (DCM) is a leading cause of heart failure, but up to 50% of cases have no definitive etiology. Genetic susceptibility alone does not account for phenotypic inconsistency, so a ‘two-hit’ model has been proposed to explore the spectrum of gene-environment interactions. Certain triggers, such as alcohol, chemotherapy agents, and viral myocarditis, are well-established second hits in the pathogenesis of DCM. The exposome, which encompasses environmental and social exposures across the lifespan, provides a more comprehensive framework to understand these interactions. In patients with DCM, air pollution and heavy metals have already been associated with higher rates of mortality and heart failure hospitalization. Microplastics and nanoplastics (MNPs) are novel components of the exposome. They form from the degradation of plastics and enter the circulatory system primarily through ingestion and inhalation. They have recently been found in human cardiovascular tissue, including atherosclerotic plaques and the myocardium. In vivo and in vitro models consistently demonstrate that MNPs induce oxidative stress, mitochondrial dysfunction, and calcium dysregulation. These pathways are shared with established cardiotoxins and converge on cardiomyocyte death, fibrosis, and eccentric ventricular remodeling, which is consistent with the pathogenesis and phenotype of DCM. In genetically susceptible individuals, MNP exposure may therefore contribute to the progression from subclinical myocardial injury to overt systolic dysfunction. This narrative review synthesizes preclinical mechanistic evidence linking MNP exposure to myocardial injury, compares the underlying mechanisms with those of other environmental pollutants and cardiovascular toxins, and integrates these findings within the proposed ‘two-hit’ model of DCM. Whether MNP exposure contributes to DCM in humans remains to be established, but understanding the potential consequences of MNPs has important implications for prevention, therapeutic development and health policy. Standardization of detection methods, chronic low-dose exposure models, and prospective human studies using functional cardiac assessment are needed before translating these experimental findings into clinical practice. Full article
(This article belongs to the Special Issue Pathology, Diagnosis, and Treatment of Cardiomyopathies)
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