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34 results on '"Jazwiec, Tomasz"'

16. Effect of variable annular reduction on functional tricuspid regurgitation and right ventricular dynamics in an ovine model of tachycardia-induced cardiomyopathy

Author

Jazwiec, Tomasz, primary, Malinowski, Marcin, additional, Ferguson, Haley, additional, Wodarek, Jeremy, additional, Quay, Nathan, additional, Bush, Jared, additional, Goehler, Matthew, additional, Parker, Jessica, additional, Rausch, Manuel, additional, and Timek, Tomasz A., additional

Published
2021
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26. The Tricuspid Valve Leaflets Also Adapt to Functional Regurgitation

Author

Tomasz A. Timek, Manuel K. Rausch, William D. Meador, Jazwiec Tomasz, Malinowski Marcin, and Mrudang Mathur

Subjects
medicine.medical_specialty, Tricuspid valve, medicine.anatomical_structure, business.industry, Internal medicine, medicine, Cardiology, Regurgitation (circulation), Cardiology and Cardiovascular Medicine, business
Published
2020

31. Symetis Acurate Neo transfemoral aortic bioprosthesis — initial Polish experience

Author

Zembala, Michał, primary, Hawranek, Michał, additional, Wacławski, Jacek, additional, Niklewski, Tomasz, additional, Nadziakiewicz, Paweł, additional, Koba, Rafał, additional, Przybylski, Roman, additional, Walas, Ryszard, additional, Głowacki, Jan, additional, Jazwiec, Tomasz, additional, Garbacz, Marcin, additional, Gąsior, Mariusz, additional, and Zembala, Marian, additional

Published
2016
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33. Untangling the mechanisms of pulmonary hypertension-induced right ventricular stiffening in a large animal model.

Author

Kakaletsis S, Malinowski M, Mathur M, Sugerman GP, Lucy JJ, Snider C, Jazwiec T, Bersi M, Timek TA, and Rausch MK

Abstract

Background: Pulmonary arterial hypertension (PHT) is a devastating disease with low survival rates. In PHT, chronic pressure overload leads to right ventricle (RV) remodeling and stiffening; thus, impeding diastolic filling and ventricular function. Multiple mechanisms contribute to RV stiffening, including wall thickening, microstructural disorganization, and myocardial stiffening. The relative importance of each mechanism is unclear. Our objective is to use a large animal model as well as imaging, experimental, and computational approaches to untangle these mechanisms., Methods: We induced PHT in eight sheep via pulmonary artery banding. After eight weeks, the hearts underwent anatomic and diffusion tensor MRI to characterize wall thickening and microstructural disorganization. Additionally, myocardial samples underwent histological and gene expression analyses to quantify compositional changes and mechanical testing to quantify myocardial stiffening. All findings were compared to 12 control animals. Finally, we used computational modeling to disentangle the relative importance of each stiffening mechanism., Results: First, we found that the RVs of PHT animals thickened most at the base and the free wall. Additionally, we found that PHT induced excessive collagen synthesis and microstructural disorganization, consistent with increased expression of fibrotic genes. We also found that the myocardium itself stiffened significantly. Importantly, myocardial stiffening correlated significantly with excess collagen synthesis. Finally, our model of normalized RV pressure-volume relationships predicted that myocardial stiffness contributes to RV stiffening significantly more than other mechanisms., Conclusions: In summary, we found that PHT induces wall thickening, microstructural disorganization, and myocardial stiffening. These remodeling mechanisms were both spatially and directionally dependent. Using modeling, we show that myocardial stiffness is the primary contributor to RV stiffening. Thus, myocardial stiffening may be an important predictor for PHT progression. Given the significant correlation between myocardial stiffness and collagen synthesis, collagen-sensitive imaging modalities may be useful for non-invasively estimating myocardial stiffness and predicting PHT outcomes.

Published
2023
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34. Impact of tricuspid annular size reduction on right ventricular function, geometry and strain.

Author

Malinowski M, Jazwiec T, Goehler M, Bush J, Quay N, Ferguson H, Rausch MK, and Timek TA

Abstract

Objectives: Restrictive tricuspid annuloplasty is a clinically accepted approach to treat functional tricuspid regurgitation. We set out to investigate the effect of varying degrees of tricuspid annular reduction on the right ventricular (RV) function, geometry and strain., Methods: Eight, healthy sheep (45 ± 4 kg) had 6 sonomicrometry crystals implanted around the tricuspid annulus and 20 onto the epicardium of the right ventricle defining 3 free wall regions: basal, mid and lower. A polypropylene annuloplasty suture was placed around the tricuspid annulus and externalized to an epicardial tourniquet. Simultaneous echocardiographic, haemodynamic and sonomicrometry data were acquired at baseline and during 5 consecutive annular reduction steps (TAR 1-5) with successive (5-7 mm) suture cinching. RV free wall circumferential, longitudinal and areal cardiac and interventional strains, RV radius of curvature (ROC), cross-sectional area and tricuspid annular dimensions were calculated from 3-dimensional crystal coordinates., Results: TAR 1-5 resulted in 19 ± 15%, 35 ± 15%, 51 ± 15%, 60 ± 15% and 68 ± 13% tricuspid annular area reduction, respectively. TAR 1 and 2 had minimal influence on the RV function, RV-ROC and strains. TAR 4 and 5 decreased RV-ROC in basal and mid-regions, but reduced the RV cross-sectional area change (from 19 ± 4% at baseline to 14 ± 3% and 13 ± 2%, respectively, P < 0.001) and circumferential and areal strains. TAR 3 significantly decreased free wall RV-ROC from 44.0 ± 1.5 to 42.6 ± 2.4 mm P < 0.001 at the RV base but maintained the regional ventricular function and strains., Conclusions: In healthy ovine hearts, a tricuspid annular area reduction of ∼50% provides optimal conditions for reducing RV-ROC while maintaining regional RV function and strain patterns.

Published
2019
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