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Dear Colleagues,

It is my pleasure to invite you to contribute to the Special Issue entitled "Cardiomyopathy: Clinical Diagnosis and Treatment: Part II”. This is a follow-up volume to the previous one, where we published six papers. For more details, please visit:

https://0-www-mdpi-com.brum.beds.ac.uk/journal/jcm/special_issues/Clinical_Takotsubo_Syndrome

Cardiomyopathy entails a broad group of diseases, acquired or genetic, which result in a similar phenotype. Furthermore, cardiomyopathy is a clinically heterogeneous disease with large differences depending on gender, age of onset and rate of progression, which are thought to be explained by a complex interplay of genetic susceptibility and environmental factors. Because of the wide variety of conditions that can lead to cardiomyopathy, a systematic approach is needed to facilitate the identification and management of specific cardiomyopathies. The diagnosis, management and follow-up of patients with cardiomyopathy is a multifactorial process. In this Special Issue, we would like to present the latest findings on cardiomyopathy from various viewpoints, and share this information with readers.

Dr. Keiichi Hirono
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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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 Clinical Medicine is an international peer-reviewed open access semimonthly 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.

Related Special Issue

Published Papers (2 papers)

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Research

11 pages, 1416 KiB

Open AccessArticle

Retinal Vascular Changes in Heart Failure with Preserved Ejection Fraction Using Optical Coherence Tomography Angiography

by Jerremy Weerts, Anne G. Raafs, Birgit Sandhoefner, Frank C. T. van der Heide, Sanne G. J. Mourmans, Nicolas Wolff, Robert P. Finger, Peyman Falahat, Maximilian W. M. Wintergerst, Vanessa P. M. van Empel and Stephane R. B. Heymans

J. Clin. Med. 2024, 13(7), 1892; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm13071892 - 25 Mar 2024

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Abstract

Background: Systemic microvascular regression and dysfunction are considered important underlying mechanisms in heart failure with preserved ejection fraction (HFpEF), but retinal changes are unknown. Methods: This prospective study aimed to investigate whether retinal microvascular and structural parameters assessed using optical coherence tomography angiography (OCT-A) differ between patients with HFpEF and control individuals (i.e., capillary vessel density, thickness of retina layers). We also aimed to assess the associations of retinal parameters with clinical and echocardiographic parameters in HFpEF. HFpEF patients, but not controls, underwent echocardiography. Macula-centered 6 × 6 mm volume scans were computed of both eyes. Results: Twenty-two HFpEF patients and 24 controls without known HFpEF were evaluated, with an age of 74 [68–80] vs. 68 [58–77] years (p = 0.027), and 73% vs. 42% females (p = 0.034), respectively. HFpEF patients showed vascular degeneration compared to controls, depicted by lower macular vessel density (p < 0.001) and macular ganglion cell-inner plexiform layer thickness (p = 0.025), and a trend towards lower total retinal volume (p = 0.050) on OCT-A. In HFpEF, a lower total retinal volume was associated with markers of diastolic dysfunction (septal e’, septal and average E/e’: R² = 0.38, 0.36, 0.25, respectively; all p < 0.05), even after adjustment for age, sex, diabetes mellitus, or atrial fibrillation. Conclusions: Patients with HFpEF showed clear levels of retinal vascular changes compared to control individuals, and retinal alterations appeared to be associated with markers of more severe diastolic dysfunction in HFpEF. OCT-A may therefore be a promising technique for monitoring systemic microvascular regression and cardiac diastolic dysfunction. Full article

(This article belongs to the Special Issue Cardiomyopathy: Clinical Diagnosis and Treatment: Part II)

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Graphical abstract

10 pages, 2326 KiB

Open AccessCommunication

Novel Genetic Microvascular Dysplasia Causing Hypoperfusion of Cardiac, Renal, and Cerebral Circulation

by Andrea Frustaci, Rosario Cianci, Romina Verardo, Bruna Cerbelli, Maria Cecilia D’Asdia and Alessandro De Luca

J. Clin. Med. 2023, 12(22), 7150; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm12227150 - 17 Nov 2023

Viewed by 647

Abstract

Background: Microvascular disorders represent an uncommon site of tissue hypo-perfusion and damage. Various genetic and acquired causes can be involved. A 65-year-old man was admitted because of refractory angina, which he had had since the age of 30 years, micro-hematuria, and recurrent transitory ischemic attacks from the age of 64. Methods: Hematochemical studies, ECG, Holter monitoring, 2D-echo, cardiac magnetic resonance (CMR), CTA of cerebral vessels, endomyocardial coronary angiography, and kidney biopsy processes were undertaken. Gene mutation analysis was conducted using next-generation sequencing, which included more than 5000 genes associated with inherited diseases. Results: Hematochemical findings were unremarkable. The ECG, Holter, 2D-echo, and CTA of brain vessels were normal. Cerebral magnetic resonance showed the presence of multiple small foci of ischemia. Coronary and ventricular angiography showed normal arteries with remarkably slow flow and multiple biventricular micro-aneurysms. At the endomyocardial biopsy, five of seven arterioles presented severe lumen obstruction due to hypertrophy and disarray of the muscular coat. Similarly, obstructed pre-glomerular arteries with glomerular sclerosis were seen at the renal biopsy. Genetics identified mutations in the ABCC6, MMP2, and XYLT1 genes, which play pivotal roles in the extracellular matrix. Conclusion: This study described a new genetic microvascular obstructive disease causing progressive hypo-perfusion of the human brain, heart, and kidney. Full article

(This article belongs to the Special Issue Cardiomyopathy: Clinical Diagnosis and Treatment: Part II)

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