Purposes: Predicting hemodynamic changes of stenotic mitral valve (MV) lesions with mitral annular calcification (MAC) following transcatheter aortic valve implantation (TAVI) may inform clinical decision-making. This study aimed to investigate the association between the MAC severity quantified by computed tomography (CT) and changes in mean transmitral gradient (mTMG), mitral valve area (MVA) and stroke volume index (SVi) following TAVI.
Methods And Results: A total of 708 patients (median age 81, 52% male) with severe aortic stenosis (AS) underwent pre-procedural CT and pre- and post-TAVI transthoracic echocardiography. According to the classification of MAC severity determined by CT, 299 (42.2%) patients had no MAC, 229 (32.3%) mild MAC, 102 (14.4%) moderate MAC, and 78 (11.0%) severe MAC. After adjusting for age and sex, there was no significant change in mTMG following TAVI (Δ mTMG = 0.07 mmHg, 95% CI -0.10 to 0.23, P = 0.92) for patients with no MAC. In contrast, patients with mild MAC (Δ mTMG = 0.21 mmHg, 95% CI 0.01 to 0.40, P = 0.018), moderate MAC (Δ mTMG = 0.31 mmHg, 95% CI 0.02 to 0.60, P = 0.019) and severe MAC (Δ mTMG = 0.43 mmHg, 95% CI 0.10 to 0.76, P = 0.0012) had significant increases in mTMG following TAVI, with greater changes associated with increasing MAC severity. In contrast, there was no significant change in MVA or SVi following TAVI.
Conclusion: In patients with severe AS undergoing TAVI, MAC severity was associated with greater increases in post-procedural mTMG whereas MVA or SVi remained unchanged. MAC severity should be considered for potential subsequent MV interventions if TAVI does not improve symptoms.
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http://dx.doi.org/10.1007/s10554-023-02931-w | DOI Listing |
Eur J Med Res
December 2024
Department of Bone and Joint Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, China.
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BMJ Open Gastroenterol
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Department of Gastroenterology, National Center for Global Health and Medicine, Shinjuku-ku, Japan
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View Article and Find Full Text PDFCan J Cardiol
December 2024
GMV Care & Research, Maria Cecilia Hospital, Cotignola, Italy.
Mitral annular calcification (MAC) is a chronic degenerative process linked to increased cardiovascular disease and mortality. In patients with degenerative mitral stenosis (DMS), management is typically pharmacological until severe symptoms arise, with surgery often deemed too high-risk. Balloon valvuloplasty has never been a viable option due to the extensive mitral calcifications of DMS anatomies; however, lithotripsy-assisted percutaneous mitral commissurotomy recently emerged as a new alternative for surgery-ineligible patients.
View Article and Find Full Text PDFIntern Med
December 2024
Division of Pulmonary Medicine, Department of Medicine, Jichi Medial University, Japan.
A 21-year-old male with hereditary hemorrhagic telangiectasia underwent coil embolization for three pulmonary arteriovenous malformations (right Sc, right Sa, and left Sb). Three years after coil embolization, coil migration was observed in the right Sc and Sa, and a cavitary lesion developed between the two coils. Four years after embolization, the two coil lesions were found to have merged within the cavity.
View Article and Find Full Text PDFFree Radic Biol Med
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Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China; Key Laboratory of Viral Heart Diseases, National Health Commission, Shanghai, China; Key Laboratory of Viral Heart Diseases, Chinese Academy of Medical Sciences, Shanghai, China; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Backgrounds: Bruton tyrosine kinase (BTK), which is highly expressed in immune cells, plays a critical role in regulating the function of macrophages. A growing body of evidence has demonstrated that the accumulation of macrophages in cardiac tissue after myocardial infarction (MI) significantly affects wound healing and ventricular remodeling during the early phase of repair after MI. However, the role of BTK in cardiac repair post-MI, especially in macrophage-mediated repair, remains unclear.
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