PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 16500504

Rapid ventricular remodeling with left ventricular unloading postventricular assist device placement: new insights with strain imaging.

Luke Havemann·Colin J McMahon·Javier Ganame·Jack Price·Charles D Fraser·Benjamin W Eidem·Ricardo H Pignatelli
View original source ↗Export metadata ↓

Abstract

We report the case of a 6-year old girl who presented with severe dilated cardiomyopathy. Cross-sectional echocardiography demonstrated a severely dilated hypokinetic left ventricle with an ejection fraction less than 10%. She developed intractable ventricular tachyarrhythmias and subsequently had a left ventricular assist device implanted. Within 1 week of mechanical support, echocardiography demonstrated dramatic reverse remodeling of the left ventricle with marked improvement in myocardial deformation using strain rate imaging. This report further highlights the potential for rapid remodeling after mechanical support of the failing myocardium.

Explore related subjects

Cardiomyopathy, DilatedChildEchocardiography, DopplerFemaleHeart-Assist DevicesHumansRecovery of FunctionTreatment OutcomeVentricular Dysfunction, LeftVentricular RemodelingCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Luke Havemann, Colin J McMahon, Javier Ganame, Jack Price, Charles D Fraser, Benjamin W Eidem, Ricardo H Pignatelli. 2006. Rapid ventricular remodeling with left ventricular unloading postventricular assist device placement: new insights with strain imaging.. https://doi.org/10.1016/j.echo.2005.11.010

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

The bidirectional genetic causality between immunocyte phenotypes and dilated cardiomyopathy: A bidirectional Mendelian randomization study.

The association between immunocyte phenotypes and dilated cardiomyopathy (DCM) has been explored, however the exact pathogenesis of the relationship between immune cells and DCM is unclear. This bidirectional two-sample Mendelian randomization (MR) research aims to further validate the causal link between 731 immunocyte phenotypes and DCM. Summary statistics from a genome-wide association study data of individuals with European ancestry were utilized, including 1444 DCM cases and 353,937 controls, as well as 3757 European adults for the 731 immunocyte phenotypes. Causal effects were estimated using inverse variance weighted, MR-Egger regression, weight median estimator, weighted mode, and simple mode. Sensitivity analysis was conducted to confirm data robustness and feasibility. Based on the inverse variance weighted findings, 14 immunocyte phenotypes were risk factors for DCM (P&#x2005;<&#x2005;.05, odds ratio [OR]&#x2005;>&#x2005;1), while 15 immunocyte phenotypes exhibited a protective effect on DCM (P&#x2005;<&#x2005;.05, OR&#x2005;<&#x2005;1). The results of reverse MR analysis suggested evidence that DCM occurrence might elevate the levels of 17 immunocyte phenotypes (P&#x2005;<&#x2005;.05, OR&#x2005;>&#x2005;1) and decrease the levels of 9 immunocyte phenotypes (P&#x2005;<&#x2005;.05, OR&#x2005;<&#x2005;1). Our research indicated that CD28 on secreting regulatory T cell could mitigate the occurrence of DCM, and reciprocally, the progression of DCM could reduce the level of CD28 on secreting regulatory T cell. This study confirmed the bidirectional genetic predictive relationship between immunocyte phenotypes and DCM, underscoring the complex interplay between DCM and the immune system.

Cardiomyopathy, Dilated↗
PubMed2008

Neuroblastoma presenting with dilated cardiomyopathy.

We report an infant with neuroblastoma who presented with dilated cardiomyopathy. A 3-month-old girl presented with dilated cardiomyopathy diagnosed as stage III neuroblastoma. Since total resection was impossible, chemotherapy was started. Cardiomyopathy was normalized by improvement of neuroblastoma. The prompt improvement of cardiac function following treatment of neuroblastoma suggested that cardiomyopathy in this patient was caused by the increase in catecholamines secreted by neuroblastoma and that reduction in catecholamines by treatment of neuroblastoma led to improvement in the cardiomyopathy.

Cardiomyopathy, Dilated↗