Acute torrential mitral regurgitation during transcatheter aortic valve replacement: a case report

Abstract Background Transcatheter aortic valve replacement (TAVR) is a minimally invasive approach to aortic valve replacement. However, critical cardiovascular collapse can occur during the procedure for various reasons. Case presentation A 90-year-old man with severe aortic stenosis and left circumflex artery stenosis developed acute torrential mitral regurgitation (MR) during TAVR. The valve deployment process induced left ventricular dyssynchrony due to left bundle-branch block and myocardial ischemia in the left circumflex artery region with torrential MR. Transesophageal echocardiography clearly demonstrated the mechanisms of MR, which was successfully bailed out by left ventricular pacing and intra-aortic balloon pumping. Conclusions MR can be seriously exaggerated by various and complicated mechanisms during TAVR and should be rapidly assessed and appropriately managed depending on its mechanisms

Transgenic Expression of the Formin Protein Fhod3 Selectively in the Embryonic Heart: Role of Actin-Binding Activity of Fhod3 and Its Sarcomeric Localization during Myofibrillogenesis.

Fhod3 is a cardiac member of the formin family proteins that play pivotal roles in actin filament assembly in various cellular contexts. The targeted deletion of mouse Fhod3 gene leads to defects in cardiogenesis, particularly during myofibrillogenesis, followed by lethality at embryonic day (E) 11.5. However, it remains largely unknown how Fhod3 functions during myofibrillogenesis. In this study, to assess the mechanism whereby Fhod3 regulates myofibrillogenesis during embryonic cardiogenesis, we generated transgenic mice expressing Fhod3 selectively in embryonic cardiomyocytes under the control of the β-myosin heavy chain (MHC) promoter. Mice expressing wild-type Fhod3 in embryonic cardiomyocytes survive to adulthood and are fertile, whereas those expressing Fhod3 (I1127A) defective in binding to actin die by E11.5 with cardiac defects. This cardiac phenotype of the Fhod3 mutant embryos is almost identical to that observed in Fhod3 null embryos, suggesting that the actin-binding activity of Fhod3 is crucial for embryonic cardiogenesis. On the other hand, the β-MHC promoter-driven expression of wild-type Fhod3 sufficiently rescues cardiac defects of Fhod3-null embryos, indicating that the Fhod3 protein expressed in a transgenic manner can function properly to achieve myofibril maturation in embryonic cardiomyocytes. Using the transgenic mice, we further examined detailed localization of Fhod3 during myofibrillogenesis in situ and found that Fhod3 localizes to the specific central region of nascent sarcomeres prior to massive rearrangement of actin filaments and remains there throughout myofibrillogenesis. Taken together, the present findings suggest that, during embryonic cardiogenesis, Fhod3 functions as the essential reorganizer of actin filaments at the central region of maturating sarcomeres via the actin-binding activity of the FH2 domain

Genotypes of offspring from mating of β-MHC-Fhod3-IA × B6.

<p>Genotypes of offspring from mating of β-MHC-Fhod3-IA × B6.</p

Genotypes of embryos from mating of β-MHC-Fhod3-IA#4 × B6.

<p>Genotypes of embryos from mating of β-MHC-Fhod3-IA#4 × B6.</p