All Articles

Volker Walhorn¹, Mareike Dieding¹, Jana Davina Debus², Raimund Kerkhoff¹, Anna Gärtner-Rommel², Hendrik Milting², and Dario Anselmetti¹

¹Experimental Biophysics, Physics Faculty, Bielefeld University, D-33615 Bielefeld, Germany

²Erich & Hanna Klessmann Institute for Cardiovascular Research and Development, Heart and Diabetes Center NRW,University Hospital of the Ruhr-University Bochum, D- 32545 Bad Oeynhausen, Germany

Cadherins are calcium dependent adhesion proteins that bridge the intercellular gap and establish a tight connection to adjacent cells. Desmoglein-2 (DSG2) is a specific cadherin of the cell-cell contact in cardiac desmosomes. Mutations in the DSG2 gene are associated with rare but severe heart muscle diseases such as arrhythmogenic right ventricular cardiomyopathy (ARVC). However, the molecular pathomechanism of many DSG2 mutations is unknown. In our recently published research, we report on the homophilic binding properties of wildtype DSG2 and two mutations thereof. We found that wildtype DSG2 binding kinetics differs significantly from the two analyzed mutations whereas thermodynamic properties such as the difference in Gibbs free energy are virtually unaffected. Here, we comment on (bio-) physical concepts how non-covalent bonds are characterized and we highlight the limitations of these concepts. Furthermore, we consistently link molecular binding properties of DSG2 with the macroscopic stability of cellular networks overexpressing a distinct DSG2 species. Finally, on the basis of DSG2 binding kinetics, we draft a biophysically inspired hypothesis of a molecular pathomechanism leading to ARVC.

Lu Feng¹, Gexin Zhao^2*, Beidong Chen^1*

^*1The MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Beijing, 100730, China

^*2Technology Center for Genomics & Bioinformatics. Department of Pathology & Laboratory Medicine, David Geffen School of Medicine, University of California, California 90095, USA

Atherosclerosis is a chronic inflammation disease that is initiated by endothelial cell injury. Hyperlipidemia is an independent risk factor for atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) is a major component of hyperlipidemia and contributes to atherosclerosis. Ox-LDL and ox-LDL-related reactive oxygen species (ROS) and inflammation have deleterious effects on vascular endothelial cells. Previous studies have demonstrated that thioredoxin-1 (Trx) is one of the key regulators of intracellular redox, which may play a role in the pathogenesis of atherosclerosis. This review will summarize the protective mechanisms of Trx on endothelial injury induced by ox-LDL.

Alvaro D. B. Bordalo*

*Consultant in Cardiology (ret.), Preoperative Outpatient Clinic (former Head), Cardio-Thoracic Surgery Department, Hospital de Santa Maria, University of Lisbon School of Medicine, Lisbon, Portugal

HDL complex has multiple functions. There is some parallelism between the plasma HDL-cholesterol (HDL-C) concentrations and the HDL complex atheroprotective function, but those values only measure the reverse C-transport. Multiple epidemiological studies have shown that a high HDL-C level is a strong marker of protection against atherosclerotic vascular disease (AVD) development, but in about 10% of patients, there is no correlation between AVD presence or absence and low or high HDL-C values, respectively. Plasma HDL-C concentrations have multiple genetic determinants, but most of the genetic profiles responsible for the association of high HDL-C levels with atheroprotection are not yet identified. A meta-analysis demonstrated that the HDL capacity of C-acceptance from macrophages is inversely associated with AVD prevalence but is independent of HDL-C values. CETP-inhibition therapies, in spite of up to 133% HDL-C increases, failed to improve AVD secondary prevention. As a consequence, the main focus of research has changed and resides now on attempts to improve HDL complex functionality. Elderly AVD-free aortic stenosis patients represent a natural laboratory terrain for use in studies to identify the HDL complex components responsible for successful atheroprotection. However, the reasons why HDL complex, competent for AVD protection for several decades, fails to prevent aortic sclerosis/calcification in the same patients, remain unknown.

Tobias-Raphael Wenzel¹, Matthias Morfeld^1,2*

¹Institute for Healthcare research, Intervention, Therapy and Evaluation e.V., Stendal, Germany

^*2University of Applied Sciences Magdeburg-Stendal, Rehabilitation Psychology, Stendal, Germany

In Germany, the International Classification of Functioning, Disability and Health (ICF) is anchored in social law and it provides an important theoretical basis for rehabilitative action. Basically, there is an information deficit regarding the use of the ICF in rehabilitative practice in Germany. From the few publications available it can be concluded that the ICF in the practice of medical rehabilitation in Germany is used differently in nature and extent by social insurance agencies and service providers. There is a need for research to better map, support and develop the utilization of the ICF in the practice of medical rehabilitation in Germany.

Ulrich Julius^1*

^*1Lipidology and Center for Extracorporeal Treatment, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Germany

Ping-Shuan Dong^1*, Jing-Jing Jia¹, Lai-Jing Du¹

^*1Department of Cardiology, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China

Various forms of interventional programs have been suggested to help reduce the risk factors for cardiovascular diseases. However, little is known about the effects of physician-based interventional program on the long-term disease prognoses of patients after percutaneous coronary intervention (PCI). A number of studies have demonstrated the intensive secondary prevention provide effective risk factor reduction in coronary artery disease patients, while few studies focused on important cardiovascular outcomes and long-term clinical prognoses. This study is the first prospective randomized controlled study to demonstrate the impact of professional physician-coordinated intensive follow-up on the long-time prognosis of PCI in acute coronary syndrome (ACS) patients in China. We have shown that this intensive follow-up program robustly prolongs the survival time and reduces the controllable risk factors for cardiovascular disease control of cardiovascular risk factors, thereby markedly improve the prognosis of PCI in ACS patients. The study was the first to demonstrate the cost-effect benefit of intensive secondary prevention in ACS patients in Chinese populations, and this benefit was long-term.

Mohsin Khan D.O.^1*, Mitchell S. Karl¹, Ashwin Durairaj¹, and Antonello Santini²

^*1Florida Atlantic University, Schmidt School of Medicine, 777 Glades Road, Boca Raton, FL 33431, United States

²Department of Pharmacy, School of Medicine, University of Napoli Federico II, Via D. Montesano 49, 80131 Napoli, Italy

Martina Mason*, Ian Smith

Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, CB23 3RE, UK

Obstructive sleep apnoea (OSA) is common and high prevalence has been described amongst patients undergoing cardiac revascularisation surgery. An excess of postoperative complications has been reported in patients with untreated Obstructive Sleep Apnoea (OSA) following surgical procedures, including those undergoing cardiac surgery. This has led some clinicians towards pre-operative screening for OSA though the best screening methodology has not yet been established. Moreover, the effect of screening and of treatment for OSA on surgical outcomes remains unknown. Does current evidence justify screening and treating patients before they present for surgery? Is this leading to potential delay in surgery whilst awaiting sleep diagnostics and commencing the treatment? This review article will examine the available evidence base and endeavour to answer these questions and identify implications for future research.

Alexandar A. Iliev^1*, Georgi N. Kotov¹, Iva N. Dimitrova² and Boycho V. Landzhov¹

¹Department of Anatomy, Histology and Embryology, Medical University of Sofia, Bulgaria

²Department of Cardiology, University Hospital ‘St. Ekaterina’, Medical University of Sofia, Bulgaria

Introduction: Spontaneously hypertensive rats are often used as a model of arterial hypertension in humans. Cardiomyocytic hypertrophy, focal myocytolysis and ventricular fibrosis are only a part of the alterations in the morphology of the myocardium observed in spontaneously hypertensive rats with the progression of hypertension. The present manuscript reviews our studies on spontaneously hypertensive rats, with focus on the microscopic changes in the myocardial architectonics and analysis of several morphometric parameters.

Materials and methods: A total of 12 male spontaneously hypertensive rats, distributed in two age groups, each containing six animals: 1-month-old (young) and 6-months-old (adult) were used. We also used 12 male normotensive Wistar rats, distributed in two age groups, each containing six animals: 1-month-old (young) and 6-months-old (adult). Routine haematoxylin and eosin staining and Mallory’s trichrome stain were conducted. Quantitative data were obtained with a computerized system for image analysis NIS-Elements Advanced Research (Ver. 2.30).

Results: Changes in the normal morphology of the myocardium included cardiomyocytic hypertrophy, focal myocytolysis and ventricular fibrosis. As aging progressed, we noted a significant increase in the thickness of the free wall and cross-sectional area of the cardiomyocytes and the cardiomyocytic nuclei and a decrease in cardiomyocytic density.

Conclusion: The manuscript presents a detailed qualitative and quantitative study of changes in the normal structure of the myocardium initiated by arterial hypertension.

Federico Paredes Vignoli*

Awad Magbri, Eusera El-Magbri, Mariam El-Magbri, Brar Balhinder and Shauket Rashid

Nausica Català Tella^1*, Catalina Serna Arnaiz¹, Jordi Real Gatius^2,3, Oriol Yuguero Torres⁴ and Leonardo Galván Santiago⁵

Martin Rosas-Peralta¹, Gabriela Borrayo-Sánchez², Erick Ramirez Arias³, Janaí Santiago-López⁴, Eduardo Almeida-Gutiérrez⁵,  Jose de Jesús Arriaga-Dávila⁶

Gabriela Borrayo-Sánchez¹, Martin Rosas-Peralta^2*, Erick Ramirez Arias³, Janaí Santiago-López⁴, Eduardo Almeida-Gutiérrez⁵, Hector David Martínez-Chapa⁶, Jose de Jesús Arriaga-Dávila⁷

¹Head of Evaluation and Accountability Division for Medical Care, CUMAE-IMSS, Mexico

²Head of Special Projects Area, Coordination of High Specialty Units, CUMAE-IMSS, Mexico

³Head of Emergency Room, Hospital of Cardiology of the National Medical Center, XXI Century, IMSS, Mexico

⁴Special Projects Area, CUMAE-IMSS, Mexico

⁵Titular of the Directorate of Education and Research in Health of the Hospital of Cardiology of the National Medical Center XXI century, IMSS, Mexico

⁶Titular of Medical Attention Unit, IMSS, Mexico

⁷Head of Medical Benefits of IMSS, Mexico