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Cardiomyopathy: Clinical Diagnosis and Treatment: Part II
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Cardiomyopathy: Clinical Diagnosis and Treatment: Part II

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cardiology".

Deadline for manuscript submissions: closed (25 October 2024) | Viewed by 5377

Special Issue Editor

Dr. Keiichi Hirono

E-Mail Website
Guest Editor
Department of Pediatrics, University of Toyama, Toyama, Japan
Interests: cardiomyopathy; left ventricualr noncomapction; genetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

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://www.mdpi.com/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.

Keywords

  • cardiomyopathy
  • heart failure
  • arrhythmia
  • genetics
  • clinical diagnosis and treatment
  • management

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Related Special Issue

Published Papers (5 papers)

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Research

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11 pages, 967 KiB  
Article
Time Course of Left Ventricular Strain Assessment via Cardiovascular Magnetic Resonance Myocardial Feature Tracking in Takotsubo Syndrome
by Hiroki Goto, Ken Kato, Yoichi Imori, Masaki Wakita, Noriko Eguchi, Hiroyuki Takaoka, Tsutomu Murakami, Yuji Nagatomo, Toshiaki Isogai, Yuya Mitsuhashi, Mike Saji, Satoshi Yamashita, Yuichiro Maekawa, Hiroki Mochizuki, Yoshimitsu Takaoka, Masafumi Ono, Tetsuo Yamaguchi, Yoshio Kobayashi, Kuniya Asai, Wataru Shimizu and Tsutomu Yoshikawaadd Show full author list remove Hide full author list
J. Clin. Med. 2024, 13(11), 3238; https://doi.org/10.3390/jcm13113238 - 30 May 2024
Viewed by 721
Abstract
Background: Although takotsubo syndrome (TTS) is characterized by transient systolic dysfunction of the left ventricle (LV), the time course and mechanism of LV function recovery remain elusive. The aim of this study is to evaluate cardiac functional recovery in TTS via serial cardiac [...] Read more.
Background: Although takotsubo syndrome (TTS) is characterized by transient systolic dysfunction of the left ventricle (LV), the time course and mechanism of LV function recovery remain elusive. The aim of this study is to evaluate cardiac functional recovery in TTS via serial cardiac magnetic resonance feature tracking (CMR-FT). Methods: In this Japanese multicenter registry, patients with newly diagnosed TTS were prospectively enrolled. In patients who underwent serial cardiovascular magnetic resonance (CMR) imaging at 1 month and 1 year after the onset, CMR-FT was performed to determine the global circumferential strain (GCS), global radial strain (GRS) and global longitudinal strain (GLS). We compared LV ejection fraction, GCS, GRS and GLS at 1 month and 1 year after the onset of TTS. Results: Eighteen patients underwent CMR imaging in one month and one year after the onset in the present study. LV ejection fraction had already normalized at 1 month after the onset, with no significant difference between 1 month and 1 year (55.8 ± 9.2% vs. 58.9 ± 7.3%, p = 0.09). CMR-FT demonstrated significant improvement in GCS from 1 month to 1 year (−16.7 ± 3.4% vs. −18.5 ± 3.2%, p < 0.01), while there was no significant difference in GRS and GLS between 1 month and year (GRS: 59.6 ± 24.2% vs. 59.4 ± 17.3%, p = 0.95, GLS: −12.8 ± 5.9% vs. −13.8 ± 4.9%, p = 0.42). Conclusions: Serial CMR-FT analysis revealed delayed improvement of GCS compared to GRS and GLS despite of rapid recovery of LV ejection fraction. CMR-FT can detect subtle impairment of LV systolic function during the recovery process in patients with TTS. Full article
(This article belongs to the Special Issue Cardiomyopathy: Clinical Diagnosis and Treatment: Part II)
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8 pages, 578 KiB  
Article
Troponin T Assessment Allows for Identification of Mutation Carriers among Young Relatives of Patients with LMNA-Related Dilated Cardiomyopathy
by Przemysław Chmielewski, Ilona Kowalik, Grażyna Truszkowska, Ewa Michalak, Joanna Ponińska, Agnieszka Sadowska, Katarzyna Kalin, Krzysztof Jaworski, Ilona Minota, Jolanta Krzysztoń-Russjan, Tomasz Zieliński, Rafał Płoski and Zofia Teresa Bilińska
J. Clin. Med. 2024, 13(11), 3164; https://doi.org/10.3390/jcm13113164 - 28 May 2024
Viewed by 803
Abstract
Background: LMNA-related dilated cardiomyopathy (LMNA-DCM) caused by mutations in the lamin A/C gene (LMNA) is one of the most common forms of hereditary DCM. Due to the high risk of mutation transmission to offspring and the high [...] Read more.
Background: LMNA-related dilated cardiomyopathy (LMNA-DCM) caused by mutations in the lamin A/C gene (LMNA) is one of the most common forms of hereditary DCM. Due to the high risk of mutation transmission to offspring and the high incidence of ventricular arrhythmia and sudden death even before the onset of heart failure symptoms, it is very important to identify LMNA-mutation carriers. However, many relatives of LMNA-DCM patients do not report to specialized centers for clinical or genetic screening. Therefore, an easily available tool to identify at-risk subjects is needed. Methods: We compared two cohorts of young, asymptomatic relatives of DCM patients who reported for screening: 29 LMNA mutation carriers and 43 individuals from the control group. Receiver operating characteristic (ROC) curves for potential indicators of mutation carriership status were analyzed. Results: PR interval, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and high-sensitivity cardiac troponin T (hscTnT) serum levels were higher in the LMNA mutation carrier cohort. Neither group differed significantly with regard to creatinine concentration or left ventricular ejection fraction. The best mutation carriership discriminator was hscTnT level with an optimal cut-off value at 5.5 ng/L, for which sensitivity and specificity were 86% and 93%, respectively. The median hscTnT level was 11.0 ng/L in LMNA mutation carriers vs. <3.0 ng/L in the control group, p < 0.001. Conclusions: Wherever access to genetic testing is limited, LMNA mutation carriership status can be assessed reliably using the hscTnT assay. Among young symptomless relatives of LMNA-DCM patients, a hscTnT level >5.5 ng/L strongly suggests mutation carriers. Full article
(This article belongs to the Special Issue Cardiomyopathy: Clinical Diagnosis and Treatment: Part II)
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11 pages, 1416 KiB  
Article
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://doi.org/10.3390/jcm13071892 - 25 Mar 2024
Viewed by 1317
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 [...] Read more.
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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10 pages, 2326 KiB  
Communication
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://doi.org/10.3390/jcm12227150 - 17 Nov 2023
Viewed by 1014
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 [...] Read more.
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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Review

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11 pages, 1369 KiB  
Review
Tachycardia-Induced Cardiomyopathy in an Infant with Atrial Flutter and Prolonged Recovery of Cardiac Function
by Tomohide Sakai, Kaori Tsuboi, Shinya Takarada, Mako Okabe, Hideyuki Nakaoka, Keijiro Ibuki, Sayaka W. Ozawa, Yukiko Hata, Shojiro Ichimata, Naoki Nishida and Keiichi Hirono
J. Clin. Med. 2024, 13(11), 3313; https://doi.org/10.3390/jcm13113313 - 4 Jun 2024
Cited by 1 | Viewed by 986
Abstract
Background: Tachycardia-induced cardiomyopathy (TIC) is caused by prolonged tachycardia, leading to left ventricular dilatation and systolic dysfunction with heart failure. Although TIC is more common in adults, it is rare in early infancy. Methods: Clinical testing was performed as part of medical evaluation [...] Read more.
Background: Tachycardia-induced cardiomyopathy (TIC) is caused by prolonged tachycardia, leading to left ventricular dilatation and systolic dysfunction with heart failure. Although TIC is more common in adults, it is rare in early infancy. Methods: Clinical testing was performed as part of medical evaluation and management. Next-generation sequencing (NGS) was conducted for a patient with TIC. A literature review on TIC was also conducted. Results: The case involved a 5-month-old infant referred to the hospital due to symptoms of heart failure lasting at least two months. The infant’s heart rate was 200 beats per minute, the left ventricular ejection fraction fell below 14%, and electrocardiograms showed atrial flutter, suggesting TIC. After cardioversion, there was no recurrence of atrial flutter, and cardiac function improved 98 days after tachycardia arrest. The NGS did not identify any pathogenic variants. The literature review identified eight early infantile cases of TIC. However, no previous reports described a case with such a prolonged duration of TIC as ours. Conclusions: This is the first report of a case of prolonged TIC in a child with the documented time to recover normal cardiac function. The improvement of cardiac function depends on the duration of TIC. Early recognition and intervention in TIC are essential to improve outcomes for infantile patients, as timely treatment offers the potential for recovery. Full article
(This article belongs to the Special Issue Cardiomyopathy: Clinical Diagnosis and Treatment: Part II)
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