@article{MTMT:35059257,
	title = {Vicious Circle With Venous Hypertension, Irregular Flow, Pathological Venous Wall Remodeling, and Valve Destruction in Chronic Venous Disease: A Review},
	url = {https://m2.mtmt.hu/api/publication/35059257},
	author = {Nádasy, György László and Patai, B.B. and Molnár, Andrea Ágnes and Hetthéssy, Judit and Tőkés, Anna-Mária and Varady, Z. and Bednárikné Dörnyei, Gabriella},
	doi = {10.1177/00033197241256680},
	journal-iso = {ANGIOLOGY},
	journal = {ANGIOLOGY},
	unique-id = {35059257},
	issn = {0003-3197},
	abstract = {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.},
	keywords = {Hemodynamics; Pathomechanism; chronic venous disease; varicosity; cell pathology},
	year = {2024},
	eissn = {1940-1574},
	orcid-numbers = {Nádasy, György László/0000-0003-2057-2391; Hetthéssy, Judit/0000-0001-8274-5257; Tőkés, Anna-Mária/0000-0002-9581-7536; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252}
}

@article{MTMT:34450917,
	title = {Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice},
	url = {https://m2.mtmt.hu/api/publication/34450917},
	author = {Molnár, Andrea Ágnes and Pásztor, Dorottya Tímea and Tarcza, Zsófia and Merkely, Béla Péter},
	doi = {10.3390/ijms242417129},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {34450917},
	issn = {1661-6596},
	abstract = {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.},
	year = {2023},
	eissn = {1422-0067},
	orcid-numbers = {Pásztor, Dorottya Tímea/0009-0001-8399-1019; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:34113078,
	title = {Upgrade of right ventricular pacing to cardiac resynchronization therapy in heart failure : a randomised trial},
	url = {https://m2.mtmt.hu/api/publication/34113078},
	author = {Merkely, Béla Péter and Hatala, Robert and Wranicz, Jerzy K and Duray, Gábor Zoltán and Földesi, Csaba László and Som, Zoltán and Németh, Marianna and Goscinska-Bis, Kinga and Gellér, László Alajos and Zima, Endre István and Osztheimer, István and Molnár, Levente Domonkos and Karády, Júlia and Hindricks, Gerhard and Goldenberg, Ilan and Klein, Helmut and Szigeti, Mátyás and Solomon, Scott D and Kutyifa, Valentina and Kovács, Attila and Kosztin, Annamária},
	doi = {10.1093/eurheartj/ehad591},
	journal-iso = {EUR HEART J},
	journal = {EUROPEAN HEART JOURNAL},
	volume = {44},
	unique-id = {34113078},
	issn = {0195-668X},
	abstract = {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.},
	keywords = {heart failure; right ventricular pacing; UPGRADE; cardiac resynchronisation therapy; pacing-induced cardiomyopathy},
	year = {2023},
	eissn = {1522-9645},
	pages = {4259-4269},
	orcid-numbers = {Merkely, Béla Péter/0000-0001-6514-0723; Duray, Gábor Zoltán/0000-0003-1286-6576; Németh, Marianna/0009-0004-3920-1392; Gellér, László Alajos/0000-0001-6802-6360; Zima, Endre István/0000-0001-5132-6009; Osztheimer, István/0000-0002-8209-990X; Karády, Júlia/0000-0002-6640-6260; Kutyifa, Valentina/0000-0002-0016-289X; Kovács, Attila/0000-0003-2320-6434; Kosztin, Annamária/0000-0001-6647-2623; Behon, Anett/0000-0002-9852-2768; Czimbalmos, Csilla/0000-0001-6311-9920; Fábián, Alexandra/0000-0002-8449-0638; Ferencz, Andrea/0009-0007-6747-4373; Mervai-Kuthi, Luca/0000-0002-6563-5862; Ladányi, Zsuzsanna/0000-0002-6258-1985; Lakatos, Bálint/0000-0002-7627-5620; Masszi, Richárd/0000-0002-0162-6043; Schwertner, Walter Richard/0000-0002-6206-243X; Tokodi, Márton/0000-0003-3036-4131; Ujvári, Adrienn/0000-0002-7625-6761; Veres, Boglárka/0000-0002-3889-3794}
}

@article{MTMT:34105005,
	title = {Echocardiography Imaging of the Right Ventricle: Focus on Three-Dimensional Echocardiography},
	url = {https://m2.mtmt.hu/api/publication/34105005},
	author = {Molnár, Andrea Ágnes and Sánta, A. and Merkely, Béla Péter},
	doi = {10.3390/diagnostics13152470},
	journal-iso = {DIAGNOSTICS},
	journal = {DIAGNOSTICS},
	volume = {13},
	unique-id = {34105005},
	issn = {2075-4418},
	year = {2023},
	eissn = {2075-4418},
	orcid-numbers = {Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:34074932,
	title = {Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives},
	url = {https://m2.mtmt.hu/api/publication/34074932},
	author = {Molnár, Andrea Ágnes and Sánta, A. and Pásztor, Dorottya Tímea and Merkely, Béla Péter},
	doi = {10.3390/cells12131796},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {12},
	unique-id = {34074932},
	abstract = {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.},
	keywords = {Fibrosis; Aortic valve stenosis; mitral valve regurgitation; atrial cardiomyopathy},
	year = {2023},
	eissn = {2073-4409},
	orcid-numbers = {Pásztor, Dorottya Tímea/0009-0001-8399-1019; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:34000272,
	title = {Left ventricular deformation and non-invasive myocardial work after transcatheter aortic valve replacement: a prospective echocardiographic study},
	url = {https://m2.mtmt.hu/api/publication/34000272},
	author = {Lakatos, Bálint and Ladányi, Zsuzsanna and Ruppert, Mihály and Fábián, Alexandra and Ujvári, Adrienn and Molnar, L and Straub, E and Molnár, Andrea Ágnes and Nagy, Anikó Ilona and Kovacs, A and Merkely, Béla Péter},
	journal-iso = {EUR J HEART FAIL},
	journal = {EUROPEAN JOURNAL OF HEART FAILURE},
	volume = {24},
	unique-id = {34000272},
	issn = {1388-9842},
	year = {2022},
	eissn = {1879-0844},
	pages = {216-216},
	orcid-numbers = {Lakatos, Bálint/0000-0002-7627-5620; Ladányi, Zsuzsanna/0000-0002-6258-1985; Fábián, Alexandra/0000-0002-8449-0638; Ujvári, Adrienn/0000-0002-7625-6761; Nagy, Anikó Ilona/0000-0002-0519-5172; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:33259810,
	title = {Cellular Senescence, Aging and Non-Aging Processes in Calcified Aortic Valve Stenosis: From Bench-Side to Bedside},
	url = {https://m2.mtmt.hu/api/publication/33259810},
	author = {Molnár, Andrea Ágnes and Pásztor, Dorottya Tímea and Merkely, Béla Péter},
	doi = {10.3390/cells11213389},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {11},
	unique-id = {33259810},
	abstract = {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.},
	year = {2022},
	eissn = {2073-4409},
	orcid-numbers = {Pásztor, Dorottya Tímea/0009-0001-8399-1019; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:32792956,
	title = {The Added Value of Atrial Strain Assessment in Clinical Practice},
	url = {https://m2.mtmt.hu/api/publication/32792956},
	author = {Molnár, Andrea Ágnes and Merkely, Béla Péter},
	doi = {10.3390/diagnostics12040982},
	journal-iso = {DIAGNOSTICS},
	journal = {DIAGNOSTICS},
	volume = {12},
	unique-id = {32792956},
	issn = {2075-4418},
	year = {2022},
	eissn = {2075-4418},
	orcid-numbers = {Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:31851073,
	title = {Echocardiographic Evaluation of Atrial Communications before Transcatheter Closure},
	url = {https://m2.mtmt.hu/api/publication/31851073},
	author = {Molnár, Andrea Ágnes and Ábrahám, Pál and Merkely, Béla Péter and Nardai, Sándor},
	doi = {10.3791/61240},
	journal-iso = {JOVE-J VIS EXP},
	journal = {JOVE-JOURNAL OF VISUALIZED EXPERIMENTS},
	volume = {2022},
	unique-id = {31851073},
	issn = {1940-087X},
	year = {2022},
	eissn = {1940-087X},
	orcid-numbers = {Ábrahám, Pál/0000-0001-5645-9855; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:32505562,
	title = {The aging venous system: from varicosities to vascular cognitive impairment},
	url = {https://m2.mtmt.hu/api/publication/32505562},
	author = {Molnár, Andrea Ágnes and Nádasy, György László and Bednárikné Dörnyei, Gabriella and Patai, Bernadett Bettina and Delfavero, J. and Fülöp, Gábor Áron and Kirkpatrick, A.C. and Ungvári, Zoltán István and Merkely, Béla Péter},
	doi = {10.1007/s11357-021-00475-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {43},
	unique-id = {32505562},
	issn = {2509-2715},
	abstract = {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).},
	keywords = {Aging; Veins; Ageing; deep vein thrombosis; Venous Insufficiency; Varicose Veins; Vascular cognitive impairment; geroscience},
	year = {2021},
	eissn = {2509-2723},
	pages = {2761-2784},
	orcid-numbers = {Nádasy, György László/0000-0003-2057-2391; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252; Patai, Bernadett Bettina/0000-0003-1631-1607; Ungvári, Zoltán István/0000-0002-6035-6039; Merkely, Béla Péter/0000-0001-6514-0723}
}