Spontaneous splenic rupture following mitral valve replacement for infective endocarditis successfully managed with splenic artery embolisation

2020 ◽  
Vol 35 (12) ◽  
pp. 3638-3641
Author(s):  
Ahmed Mohamed Abdel Shafi ◽  
Michelle Lee ◽  
Damian Balmforth ◽  
Kulvinder Lall
Keyword(s):  
Infective Endocarditis ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Splenic Artery ◽  
Splenic Rupture ◽  
Spontaneous Splenic Rupture

Spontaneous splenic rupture after mitral valve replacement for infective endocarditis

1998 ◽  
Vol 46 (5) ◽  
pp. 482-485 ◽  
Author(s):  
Tsutomu Sugimoto ◽  
Takashi Minowa ◽  
Hideaki Uchino ◽  
Takao Shimanuki ◽  
Chiharu Nakamura
Keyword(s):  
Infective Endocarditis ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Splenic Rupture ◽  
Spontaneous Splenic Rupture

scholarly journals Fatal rupture of splenic artery mycotic aneurysm after mitral valve replacement for infective endocarditis

2009 ◽  
Vol 36 (4) ◽  
pp. 783-784 ◽  
Author(s):  
Nicholas A. Charokopos ◽  
Christophoros N. Foroulis ◽  
Efthymia G. Rouska ◽  
Christos Papakonstantinou
Keyword(s):  
Infective Endocarditis ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Splenic Artery ◽  
Mycotic Aneurysm

Infective endocarditis and outcomes of mitral valve replacement

2021 ◽  
Author(s):  
Vesa Anttila ◽  
Markus Malmberg ◽  
Jarmo Gunn ◽  
Päivi Rautava ◽  
Ville Kytö
Keyword(s):  
Infective Endocarditis ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement

Infective endocarditis in hypertrophic cardiomyopathy: Analysis of 5 patients requiring mitral valve replacement

1982 ◽  
Vol 49 (4) ◽  
pp. 949 ◽  
Author(s):  
Joan C. Kishel ◽  
Altagracia M. Chavez ◽  
Barry J. Maron ◽  
Stephen E. Epstein ◽  
Andrew G. Morrow ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Hypertrophic Cardiomyopathy ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement

scholarly journals Septic cardiomyopathy: evidence for a reduced force-generating capacity of human atrial myocardium in acute infective endocarditis

2017 ◽  
Vol 2 (2) ◽  
pp. 81-87 ◽  
Author(s):  
Katja Buschmann ◽  
Ryan Chaban ◽  
Anna Lena Emrich ◽  
Marwan Youssef ◽  
Angela Kornberger ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Isometric Force ◽  
Active Force ◽  
Atrial Myocardium ◽  
Force Amplitude ◽  
Generating Capacity

AbstractBackground:This study analyzes the myocardial force-generating capacity in infective endocarditis (IE) using an experimental model of isolated human atrial myocardium. In vivo, it is difficult to decide whether or not alterations in myocardial contractile behavior are due to secondary effects associated with infection such as an altered heart rate, alterations of preload and afterload resulting from valvular defects, and altered humoral processes. Our in vitro model using isolated human myocardium, in contrast, guarantees exactly defined experimental conditions with respect to preload, afterload, and contraction frequency, thus not only preventing confounding by in vivo determinants of contractility but also excluding effects of other factors associated with sepsis, hemodynamics, humoral influences, temperature, and medical treatment.Methods:We analyzed right atrial trabeculae (diameter 0.3–0.5 mm, initial length 5 mm) from 32 patients undergoing aortic and/or mitral valve replacement for acute valve incompetence caused by IE and 65 controls receiving aortic and/or mitral valve replacement for nonendocarditic valve incompetence. Isometric force amplitudes and passive resting force values measured at optimal length in the two groups were compared using Student’s t-test.Results:There were no significant differences between the groups in terms of the passive resting force. The isometric force amplitude in the endocarditis group, however, was significantly lower than in the nonendocarditis group (p=0.001). In the endocarditis group, the calculated active force, defined as the isometric force amplitude minus the resting force, was significantly lower (p<0.0001) and the resting force/active force ratio was significantly higher (p<0.0001). Using linear regression to describe the function between resting force and active force, we identified a significant difference in slope (p<0.0001), with lower values found in the endocarditis group.Conclusion:Our data suggest that the force-generating capacity of atrial myocardium is significantly reduced in patients with IE. In these patients, an elevated resting force is required to achieve a given force amplitude. It remains unclear, however, whether this is due to calcium desensitization of the contractile apparatus, presence of myocardial edema, fibrotic remodeling, disruption of contractile units, or other mechanisms.

scholarly journals Spleen Rupture After Mitral Valve Replacement for Infective Endocarditis

2008 ◽  
Vol 46 (4) ◽  
pp. 191-193 ◽  
Author(s):  
Mei-Hui Yang ◽  
Chia-Chan Wu ◽  
Wei-Horng Jean ◽  
Cheng-Wei Lu ◽  
Yueh-Hsun Chuang ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Spleen Rupture

scholarly journals Surgical removal of atrial septal defect occlusion device and mitral valve replacement in a 39-year-old female patient with infective endocarditis

2018 ◽  
Vol 99 (1) ◽  
pp. 140-143
Author(s):  
A S Zotov ◽  
D V Borisov ◽  
T V Klypa ◽  
S A Vachev
Keyword(s):  
Infective Endocarditis ◽  
Mitral Valve ◽  
Atrial Septal Defect ◽  
Female Patient ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Septal Defect ◽  
Surgical Removal ◽  
Occlusion Device

Дефекты межпредсердной перегородки - вторые по частоте после дефектов межжелудочковой перегородки среди врождённых пороков сердца. Эндоваскулярное закрытие дефекта межпредсердной перегородки выполняют по строгим показаниям у пациентов со значимым сбросом крови слева направо. Развитие инфекционного эндокардита после транскатетерной имплантации окклюдера бывает чрезвычайно редким осложнением. В данном клиническом наблюдении рассмотрен случай развития инфекционного эндокардита митрального клапана (с развитием выраженной недостаточности) через 13 лет после эндоваскулярного закрытия дефекта межпредсердной перегородки у пациентки 39 лет. Перед выполнением хирургического вмешательства проведена комплексная антибиотикотерапия. В ходе операции выполнены удаление окклюдера дефекта межпредсердной перегородки, протезирование митрального клапана, пластика дефекта межпредсердной перегородки и резекция ушка левого предсердия. Послеоперационный период протекал без особенностей.

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