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Biomedicines
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Advanced Research in Hypertrophic Cardiomyopathy
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Advanced Research in Hypertrophic Cardiomyopathy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 1311

Special Issue Editors

Dr. Said Alsidawi

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Guest Editor
Department of Cardiovascular Medicine, Mayo Clinic, Phoenix, AZ 85054, USA
Interests: hypertrophic cardiomyopathy; the role of myosin inhibitors in positive cardiac remodeling; valvular heart disease research
Dr. Juan Farina

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Guest Editor
Department of Cardiovascular Medicine, Mayo Clinic, Phoenix, AZ 85054, USA
Interests: cardiology research; research methodologies and biostatistics
Dr. Celestino Sardu

E-Mail Website
Guest Editor
Department of Medical, Surgical, Neurological, Metabolic and Aging Sciences, University of Campania "Luigi Vanvitelli", Piazza Miraglia, 80138 Naples, Italy
Interests: clinical cardiology; myocardial infarction; cardiovascular genetics; clinical electrophysiology; molecular cardiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will focus on everything new in the risk stratification and management of hypertrophic cardiomyopathy, addressing the following:

  • New trends in the treatment of hypertrophic cardiomyopathy (HCM) and the role of myosin inhibitors;
  • Advantages and disadvantages of traditional and new therapies for HCM: septal reduction therapy vs. myosin inhibitors;
  • Risk of arrhythmias while on myosin inhibitors;
  • Treatment on the horizon for hypertrophic cardiomyopathy beyond myosin inhibitors;
  • Gene therapy for hypertrophic cardiomyopathy;
  • Contemporary trends in the risk stratification of sudden cardiac death in HCM;
  • New research on understanding the genetic nature of HCM, focusing on the management and follow up of patients with genetically positive/phenotypically negative HCM profiles.

Dr. Said Alsidawi
Dr. Juan Maria Farina
Dr. Celestino Sardu
Guest Editors

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. Biomedicines 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

  • hypertrophic cardiomyopathy
  • myosin inhibitors
  • genetic therapy
  • risk stratification

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Published Papers (3 papers)

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11 pages, 427 KiB  
Article
Temporal Patterns of Holter-Detected Arrhythmias in Hypertrophic Cardiomyopathy Patients Treated with Mavacamten
by Amro Badr, Kaitlin Roehl, Mustafa Suppah, Humam Abo Abdullah, Reza Arsanjani, Konstantinos C. Siontis, Jeffrey B. Geske, Steve R. Ommen, John R. Giudicessi and Said Alsidawi
Biomedicines 2025, 13(4), 1005; https://doi.org/10.3390/biomedicines13041005 - 21 Apr 2025
Viewed by 309
Abstract
Background: Hypertrophic cardiomyopathy (HCM) is a genetic cardiomyopathy marked by increased left ventricular wall thickness, leading in some cases to left ventricular outflow tract (LVOT) obstruction, heart failure, and arrhythmias. Mavacamten, a selective allosteric inhibitor of cardiac myosin, has demonstrated benefits in improving [...] Read more.
Background: Hypertrophic cardiomyopathy (HCM) is a genetic cardiomyopathy marked by increased left ventricular wall thickness, leading in some cases to left ventricular outflow tract (LVOT) obstruction, heart failure, and arrhythmias. Mavacamten, a selective allosteric inhibitor of cardiac myosin, has demonstrated benefits in improving hemodynamics and reducing LVOT obstruction. However, its impact on arrhythmic burden remains unclear, with reports of early atrial fibrillation (AF) risk contrasting with long-term reductions in arrhythmias. This study assesses the temporal patterns of Holter-detected arrhythmias in HCM patients treated with mavacamten. Methods: This retrospective study included HCM patients from three Mayo Clinic sites. Baseline demographic, clinical, and echocardiographic data were collected. Holter monitoring was performed at baseline, short-term (<6 months), and long-term (>6 months) follow-up. Arrhythmic events, including premature atrial contractions (PACs), premature ventricular contractions (PVCs), and supraventricular tachycardia (SVT), were analyzed using standardized rates per 24 h. Statistical comparisons utilized the Wilcoxon signed-rank test. Results: Twenty-seven patients (56% female, median age 66 years) were included. PACs, PVCs, and SVT duration transiently but not significantly increased at short-term follow-up but returned to baseline at long-term follow-up. No sustained or high-risk ventricular arrhythmias were observed. Conclusions: Mavacamten is associated with transient arrhythmic fluctuations early in treatment, followed by stabilization. These findings support its long-term electrophysiological safety and underscore the need for early rhythm monitoring. Further research should explore its role in arrhythmic risk stratification in HCM patients. Full article
(This article belongs to the Special Issue Advanced Research in Hypertrophic Cardiomyopathy)
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12 pages, 1983 KiB  
Article
Effect of CBC-Derived Inflammatory Indicators in Predicting Chronic Kidney Disease Risk in Hypertrophic Cardiomyopathy Patients
by Changying Zhao, Luqin Yan, Yong Liu, Siyuan Chen, Beidi Lan, Ruohan Liu, Jinqi Xin, Tao Shi and Xiaohong Yang
Biomedicines 2025, 13(4), 997; https://doi.org/10.3390/biomedicines13040997 - 20 Apr 2025
Viewed by 169
Abstract
Background: Hypertrophic cardiomyopathy (HCM) is a prevalent condition that often coexists with chronic kidney disease (CKD), significantly impacting patient prognosis. This study aimed to investigate the predictive value of complete blood cell counts derived inflammatory indicators in assessing CKD risk in HCM patients. [...] Read more.
Background: Hypertrophic cardiomyopathy (HCM) is a prevalent condition that often coexists with chronic kidney disease (CKD), significantly impacting patient prognosis. This study aimed to investigate the predictive value of complete blood cell counts derived inflammatory indicators in assessing CKD risk in HCM patients. Methods: This study enrolled HCM patients and categorized them into CKD and non-CKD group based on discharge diagnoses. Analyzed indicators included systemic inflammation response index (SIRI), systemic immune inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR). Least absolute shrinkage and selection operator (LASSO) logistic and multivariable logistic regression were employed to identified independent risk factors for CKD, which were subsequently utilized to develop a nomogram. Results: A total of 1795 HCM patients were included, including 112 (6.24%) individuals assigned to the CKD group. In univariate analyses, NLR (AUC: 0.755; 95%CI: 0.711–0.800) demonstrated superior accuracy compared to others. Eighteen baseline characteristics exhibiting statistical difference were incorporated into LASSO-logistic regression. Six factors were further selected by multivariable logistic regression. The results identified male gender (OR: 2.622; 95% CI: 1.565–4.393, p < 0.001), Hb (OR: 0.972; 95% CI: 0.962–0.981, p < 0.001), Pro-BNP (OR: 1.000; 95% CI: 1.000–1.000, p < 0.001), SIRI (OR: 1.037; 95% CI: 1.026–1.049, p < 0.001), and SII (OR: 1.000; 95% CI: 1.000–1.001, p = 0.003) as risk factors. These five factors were used to construct a nomogram, which exhibited good accuracy and consistency. Conclusions: Male gender, Hb, Pro-BNP, SIRI, and SII were identified as risk factors for CKD risk in HCM patients. A nomogram was developed using these factors, which may facilitate early identification and management of high-risk individuals. Full article
(This article belongs to the Special Issue Advanced Research in Hypertrophic Cardiomyopathy)
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13 pages, 31619 KiB  
Article
PRKAG2 Syndrome: Clinical Features, Imaging Findings and Cardiac Events
by Maria Sudomir, Przemysław Chmielewski, Grażyna Truszkowska, Mariusz Kłopotowski, Mateusz Śpiewak, Marta Legatowicz-Koprowska, Monika Gawor-Prokopczyk, Justyna Szczygieł, Joanna Zakrzewska-Koperska, Mariusz Kruk, Jolanta Krzysztoń-Russjan, Jacek Grzybowski, Rafał Płoski and Zofia T. Bilińska
Biomedicines 2025, 13(3), 751; https://doi.org/10.3390/biomedicines13030751 - 19 Mar 2025
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Abstract
Background/Objectives: PRKAG2 syndrome (PS) is a rare genocopy of hypertrophic cardiomyopathy (HCM). Our goal was to expand knowledge about PS by analyzing patient clinical, imaging, and follow-up data. Methods: The study included carriers of likely pathogenic or pathogenic PRKAG2 variants identified [...] Read more.
Background/Objectives: PRKAG2 syndrome (PS) is a rare genocopy of hypertrophic cardiomyopathy (HCM). Our goal was to expand knowledge about PS by analyzing patient clinical, imaging, and follow-up data. Methods: The study included carriers of likely pathogenic or pathogenic PRKAG2 variants identified in the years 2011–2022. Cardiac involvement was assessed by electrocardiography, echocardiography, cardiac magnetic resonance imaging, and endomyocardial biopsy (EMB). We recorded concomitant diseases and cardiac events, including the implantation of electronic cardiac devices, arrhythmia, heart failure (HF), and death. Results: Seven patients from four families (median age 43 years) with PRKAG2 variants: Phe293Leu, Val336Leu, Arg302Gln, and His530Arg were included. At the first evaluation, 3 carriers were in New York Heart Association (NYHA) functional class II–III, while the remaining were in NYHA class I. Left ventricular hypertrophy (LVH) was present in 5 patients; 2 had ventricular pre-excitation, one was in atrial flutter and pacemaker-dependent; 2 had bradycardia. Two female carriers had concomitant chronic renal disease. In the EMB of one of the patients, staining for glycogen deposits was positive. Furthermore, we provide a link between the Val336Leu PRKAG2 variant and autophagy identified on EMB. After a median follow-up of 13.1 years, 6 carriers had LVH, 3 required admission for HF, and 1 had sustained ventricular tachycardia with subsequent cardioverter defibrillator implantation, and despite this, died suddenly; there were two de novo pacemaker implantations due to symptomatic bradycardia. Conclusions: PR is a distinctive disorder with an early onset of arrhythmic events, often leading to HF. Full article
(This article belongs to the Special Issue Advanced Research in Hypertrophic Cardiomyopathy)
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