TY - JOUR AU - Nádasy, György László AU - Patai, B.B. AU - Molnár, Andrea Ágnes AU - Hetthéssy, Judit AU - Tőkés, Anna-Mária AU - Varady, Z. AU - Bednárikné Dörnyei, Gabriella TI - Vicious Circle With Venous Hypertension, Irregular Flow, Pathological Venous Wall Remodeling, and Valve Destruction in Chronic Venous Disease: A Review JF - ANGIOLOGY J2 - ANGIOLOGY PY - 2024 SN - 0003-3197 DO - 10.1177/00033197241256680 UR - https://m2.mtmt.hu/api/publication/35059257 ID - 35059257 N1 - Export Date: 3 July 2024 CODEN: ANGIA Correspondence Address: Nadasy, G.L.; Department of Physiology, Hungary; email: nadasy.gyorgy@med.semmelweis-univ.hu AB - Substantial advances occurred in phlebological practice in the last two decades. With the use of modern diagnostic equipment, the patients’ venous hemodynamics can be examined in detail in everyday practice. Application of venous segments for arterial bypasses motivated studies on the effect of hemodynamic load on the venous wall. New animal models have been developed to study hemodynamic effects on the venous system. In vivo and in vitro studies revealed cellular phase transitions of venous endothelial, smooth muscle, and fibroblastic cells and changes in connective tissue composition, under hemodynamic load and at different locations of the chronically diseased venous system. This review is an attempt to integrate our knowledge from epidemiology, paleoanthropology and anthropology, clinical and experimental hemodynamic studies, histology, cell physiology, cell pathology, and molecular biology on the complex pathomechanism of this frequent disease. Our conclusion is that the disease is initiated by limited genetic adaptation of mankind not to bipedalism but to bipedalism in the unmoving standing or sitting position. In the course of the disease several pathologic vicious circles emerge, sustained venous hypertension inducing cellular phase transitions, chronic wall inflammation, apoptosis of cells, pathologic dilation, and valvular damage which, in turn, further aggravate the venous hypertension. © The Author(s) 2024. LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Pásztor, Dorottya Tímea AU - Tarcza, Zsófia AU - Merkely, Béla Péter TI - Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 24 PY - 2023 IS - 24 PG - 23 SN - 1661-6596 DO - 10.3390/ijms242417129 UR - https://m2.mtmt.hu/api/publication/34450917 ID - 34450917 N1 - Export Date: 20 March 2024 Correspondence Address: Molnár, A.Á.; Heart and Vascular Center, Hungary; email: molnarandreaagnes@gmail.com AB - Aging is a major risk factor of atherosclerosis through different complex pathways including replicative cellular senescence and age-related clonal hematopoiesis. In addition to aging, extracellular stress factors, such as mechanical and oxidative stress, can induce cellular senescence, defined as premature cellular senescence. Senescent cells can accumulate within atherosclerotic plaques over time and contribute to plaque instability. This review summarizes the role of cellular senescence in the complex pathophysiology of atherosclerosis and highlights the most important senotherapeutics tested in cardiovascular studies targeting senescence. Continued bench-to-bedside research in cellular senescence might allow the future implementation of new effective anti-atherosclerotic preventive and treatment strategies in clinical practice. LA - English DB - MTMT ER - TY - JOUR AU - Merkely, Béla Péter AU - Hatala, Robert AU - Wranicz, Jerzy K AU - Duray, Gábor Zoltán AU - Földesi, Csaba László AU - Som, Zoltán AU - Németh, Marianna AU - Goscinska-Bis, Kinga AU - Gellér, László Alajos AU - Zima, Endre István AU - Osztheimer, István AU - Molnár, Levente Domonkos AU - Karády, Júlia AU - Hindricks, Gerhard AU - Goldenberg, Ilan AU - Klein, Helmut AU - Szigeti, Mátyás AU - Solomon, Scott D AU - Kutyifa, Valentina AU - Kovács, Attila AU - Kosztin, Annamária ED - Behon, Anett / Collaborator ED - Czimbalmos, Csilla / Collaborator ED - Deményi, Boglárka / Collaborator ED - Fábián, Alexandra / Collaborator ED - Ferencz, Andrea / Collaborator ED - Mervai-Kuthi, Luca / Collaborator ED - Ladányi, Zsuzsanna / Collaborator ED - Lakatos, Bálint / Collaborator ED - Masszi, Richárd / Collaborator ED - Pólos-Merkel, Eperke Dóra / Collaborator ED - Molnár, Andrea Ágnes / Collaborator ED - Papp, Roland / Collaborator ED - Ruppert, Mihály / Collaborator ED - Schwertner, Walter Richard / Collaborator ED - Tarcza, Zsófia / Collaborator ED - Tokodi, Márton / Collaborator ED - Ujvári, Adrienn / Collaborator ED - Veres, Boglárka / Collaborator ED - Polgár, Balázs / Collaborator ED - Kohári, Mária / Collaborator ED - Csanádi, Zoltán / Collaborator ED - Clemens, Marcell / Collaborator ED - Sándorfi, Gábor / Collaborator ED - Gaszner, Balázs / Collaborator ED - Tardi-Szabó, Judit / Collaborator TI - Upgrade of right ventricular pacing to cardiac resynchronization therapy in heart failure : a randomised trial JF - EUROPEAN HEART JOURNAL J2 - EUR HEART J VL - 44 PY - 2023 IS - 40 SP - 4259 EP - 4269 PG - 11 SN - 0195-668X DO - 10.1093/eurheartj/ehad591 UR - https://m2.mtmt.hu/api/publication/34113078 ID - 34113078 AB - De novo implanted cardiac resynchronisation therapy with defibrillator (CRT-D) reduces the risk of morbidity and mortality in patients with left bundle branch block, heart failure and reduced ejection fraction (HFrEF). However, among HFrEF patients with right ventricular pacing (RVP), the efficacy of CRT-D upgrade is uncertain.In this multicentre, randomised, controlled trial, 360 symptomatic (New York Heart Association class II-IVa) HFrEF patients with a pacemaker or implantable cardioverter defibrillator (ICD), high RVP burden ≥20%, and a wide, paced QRS complex duration ≥150 ms were randomly assigned to receive CRT-D upgrade (n = 215) or ICD (n = 145) in a 3:2 ratio. The primary outcome was the composite of all-cause mortality, heart failure hospitalisation or <15% reduction of left ventricular end-systolic volume assessed at 12 months. Secondary outcomes included all-cause mortality or heart failure hospitalisation.Over a median follow-up of 12.4 months, the primary outcome occurred in 58/179 (32.4%) in the CRT-D arm vs. 101/128 (78.9%) in the ICD arm [odds ratio 0.11; 95% confidence interval (CI) 0.06-0.19; p < 0.001]. All-cause mortality or heart failure hospitalization occurred in 22/215 (10%) in the CRT-D arm vs. 46/145 (32%) in the ICD arm (hazard ratio 0.27; 95% CI 0.16-0.47; p < 0.001). The incidence of procedure- or device-related complications was similar between the two arms [CRT-D group 25/211 (12.3%) vs. ICD group 11/142 (7.8%)].In pacemaker or ICD patients with significant RVP burden and reduced ejection fraction, upgrade to CRT-D compared to ICD therapy reduced the combined risk of all-cause mortality, heart failure hospitalisation or absence of reverse remodelling. LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Sánta, A. AU - Merkely, Béla Péter TI - Echocardiography Imaging of the Right Ventricle: Focus on Three-Dimensional Echocardiography JF - DIAGNOSTICS J2 - DIAGNOSTICS VL - 13 PY - 2023 IS - 15 PG - 22 SN - 2075-4418 DO - 10.3390/diagnostics13152470 UR - https://m2.mtmt.hu/api/publication/34105005 ID - 34105005 N1 - Cited By :1 Export Date: 30 April 2024 Correspondence Address: Molnár, A.Á.; Heart and Vascular Center, Hungary; email: molnarandreaagnes@gmail.com LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Sánta, A. AU - Pásztor, Dorottya Tímea AU - Merkely, Béla Péter TI - Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives JF - CELLS J2 - CELLS-BASEL VL - 12 PY - 2023 IS - 13 PG - 26 SN - 2073-4409 DO - 10.3390/cells12131796 UR - https://m2.mtmt.hu/api/publication/34074932 ID - 34074932 N1 - Funding Agency and Grant Number: Thematic Excellence Programme of the Ministry for Innovation and Technology in Hungary, within Semmelweis University; National Research, Development, and Innovation Office (NKFIH) of Hungary [2020-4.1.1.-TKP2020]; [K135076] Funding text: The manuscript was financed by the Thematic Excellence Programme (2020-4.1.1.-TKP2020) of the Ministry for Innovation and Technology in Hungary, within the framework of the Therapeutic Development and Bioimaging thematic programs of Semmelweis University. This project was supported by grants from the National Research, Development, and Innovation Office (NKFIH) of Hungary (K135076 to B.M.). AB - This review discusses the evolving topic of atrial cardiomyopathy concerning valvular heart disease. The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can trigger atrial tachyarrhythmia. The complex interaction between valvular disease and atrial cardiomyopathy creates a vicious cycle of aggravating atrial enlargement, dysfunction, and valvular disease severity. Furthermore, atrial remodeling and arrhythmia can predispose to atrial thrombus formation and stroke. The underlying pathomechanism of atrial myopathy involves molecular, cellular, and subcellular alterations resulting in chronic inflammation, atrial fibrosis, and electrophysiological changes. Atrial dysfunction has emerged as an essential determinant of outcomes in valvular disease and heart failure. Despite its predictive value, the detection of atrial fibrosis and dysfunction is challenging and is not included in the clinical routine. Transthoracic echocardiography and cardiac magnetic resonance imaging are the main diagnostic tools for atrial cardiomyopathy. Recently published data have revealed that both left atrial volumes and functional parameters are independent predictors of cardiovascular events in valvular disease. The integration of atrial function assessment in clinical practice might help in early cardiovascular risk estimation, promoting early therapeutic intervention in valvular disease. © 2023 by the authors. LA - English DB - MTMT ER - TY - JOUR AU - Lakatos, Bálint AU - Ladányi, Zsuzsanna AU - Ruppert, Mihály AU - Fábián, Alexandra AU - Ujvári, Adrienn AU - Molnar, L AU - Straub, E AU - Molnár, Andrea Ágnes AU - Nagy, Anikó Ilona AU - Kovacs, A AU - Merkely, Béla Péter TI - Left ventricular deformation and non-invasive myocardial work after transcatheter aortic valve replacement: a prospective echocardiographic study JF - EUROPEAN JOURNAL OF HEART FAILURE J2 - EUR J HEART FAIL VL - 24 PY - 2022 IS - Suppl. S2 SP - 216 EP - 216 PG - 1 SN - 1388-9842 UR - https://m2.mtmt.hu/api/publication/34000272 ID - 34000272 LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Pásztor, Dorottya Tímea AU - Merkely, Béla Péter TI - Cellular Senescence, Aging and Non-Aging Processes in Calcified Aortic Valve Stenosis: From Bench-Side to Bedside JF - CELLS J2 - CELLS-BASEL VL - 11 PY - 2022 IS - 21 PG - 17 SN - 2073-4409 DO - 10.3390/cells11213389 UR - https://m2.mtmt.hu/api/publication/33259810 ID - 33259810 N1 - Funding Agency and Grant Number: National Research, Development, and Innovation Fund of Hungary [NVKP 16-1-2016-0017]; Thematic Excellence Programme of the Ministry for Innovation and Technology in Hungary of the Semmelweis University [2020-4.1.1.-TKP2020] Funding text: Project no. NVKP 16-1-2016-0017 (`National Heart Program') has been implemented with the support provided by the National Research, Development, and Innovation Fund of Hungary, financed under the NVKP 16 funding scheme. The research was financed by the Thematic Excellence Programme (2020-4.1.1.-TKP2020) of the Ministry for Innovation and Technology in Hungary, within the framework of the Therapeutic Development and Bioimaging thematic programs of the Semmelweis University. AB - Aortic valve stenosis (AS) is the most common valvular heart disease. The incidence of AS increases with age, however, a significant proportion of elderly people have no significant AS, indicating that both aging and nonaging pathways are involved in the pathomechanism of AS. Age-related and stress-induced cellular senescence accompanied by further active processes represent the key elements of AS pathomechanism. The early stage of aortic valve degeneration involves dysfunction and disruption of the valvular endothelium due to cellular senescence and mechanical stress on blood flow. These cells are replaced by circulating progenitor cells, but in an age-dependent decelerating manner. When endothelial denudation is no longer replaced by progenitor cells, the path opens for focal lipid deposition, initiating subsequent oxidation, inflammation and micromineralisation. Later stages of AS feature a complex active process with extracellular matrix remodeling, fibrosis and calcification. Echocardiography is the gold standard method for diagnosing aortic valve disease, although computed tomography and cardiac magnetic resonance are useful additional imaging methods. To date, no medical treatment has been proven to halt the progression of AS. Elucidation of differences and similarities between vascular and valvular calcification pathomechanisms may help to find effective medical therapy and reduce the increasing health burden of the disease. LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Merkely, Béla Péter TI - The Added Value of Atrial Strain Assessment in Clinical Practice JF - DIAGNOSTICS J2 - DIAGNOSTICS VL - 12 PY - 2022 IS - 4 PG - 16 SN - 2075-4418 DO - 10.3390/diagnostics12040982 UR - https://m2.mtmt.hu/api/publication/32792956 ID - 32792956 N1 - Export Date: 12 June 2024 Correspondence Address: Molnár, A.Á.; Heart and Vascular Center, Hungary; email: molnarandreaagnes@gmail.com LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Ábrahám, Pál AU - Merkely, Béla Péter AU - Nardai, Sándor TI - Echocardiographic Evaluation of Atrial Communications before Transcatheter Closure JF - JOVE-JOURNAL OF VISUALIZED EXPERIMENTS J2 - JOVE-J VIS EXP VL - 2022 PY - 2022 IS - 180 PG - 8 SN - 1940-087X DO - 10.3791/61240 UR - https://m2.mtmt.hu/api/publication/31851073 ID - 31851073 N1 - Molnar AA and Abraham P contributed equally. LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Nádasy, György László AU - Bednárikné Dörnyei, Gabriella AU - Patai, Bernadett Bettina AU - Delfavero, J. AU - Fülöp, Gábor Áron AU - Kirkpatrick, A.C. AU - Ungvári, Zoltán István AU - Merkely, Béla Péter TI - The aging venous system: from varicosities to vascular cognitive impairment JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 43 PY - 2021 IS - 6 SP - 2761 EP - 2784 PG - 24 SN - 2509-2715 DO - 10.1007/s11357-021-00475-2 UR - https://m2.mtmt.hu/api/publication/32505562 ID - 32505562 AB - Aging-induced pathological alterations of the circulatory system play a critical role in morbidity and mortality of older adults. While the importance of cellular and molecular mechanisms of arterial aging for increased cardiovascular risk in older adults is increasingly appreciated, aging processes of veins are much less studied and understood than those of arteries. In this review, age-related cellular and morphological alterations in the venous system are presented. Similarities and dissimilarities between arterial and venous aging are highlighted, and shared molecular mechanisms of arterial and venous aging are considered. The pathogenesis of venous diseases affecting older adults, including varicose veins, chronic venous insufficiency, and deep vein thrombosis, is discussed, and the potential contribution of venous pathologies to the onset of vascular cognitive impairment and neurodegenerative diseases is emphasized. It is our hope that a greater appreciation of the cellular and molecular processes of vascular aging will stimulate further investigation into strategies aimed at preventing or retarding age-related venous pathologies. © 2021, The Author(s). LA - English DB - MTMT ER -