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Case Reports
. 2022 Dec 23:7:101716.
doi: 10.1016/j.jaccas.2022.101716. eCollection 2023 Feb 1.

1,1-Difluoroethane Hydrocarbon Cardiomyopathy

Affiliations
Case Reports

1,1-Difluoroethane Hydrocarbon Cardiomyopathy

Kristen N Brown et al. JACC Case Rep. .

Abstract

1,1-Difluoroethane (DFE) cardiomyopathy results from the direct inhalation of toxic halogenated hydrocarbons. We present a case series of acute DFE cardiomyopathy illustrating the typical presentation of severe DFE cardiomyopathy along with a detailed description of its mechanism of injury. (Level of Difficulty: Advanced.).

Keywords: 1,1-difluoroethane hydrocarbon; DFE, 1,1-difluoroethane; ECMO, extracorporeal membrane oxygenation; EF, ejection fraction; huffing; nonischemic cardiomyopathy; toxic cardiomyopathy.

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Conflict of interest statement

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Figures

None
Graphical abstract
Figure 1
Figure 1
Molecular and Cellular Effects DFE (A) Saturation of myocytes. (B) Calcium chelation. (C) Directly binding of calcium channels. (D) Saturating gap junction channels. (E) Blockade of potassium channels. (F) DFE molecule. (G) Myofibril. (H) Interstitial edema. (I) Intramyocardial hemorrhage. (J) Myocardial necrosis. (K) Extracellular space. (L) Blocks actin and myosin binding. (M) Long-term exposure results in disruption in myocyte DNA resulting in disorganized and malfunctioning muscle tissue.
Figure 2
Figure 2
Multiorgan Effects of DFE Toxicity Microsoft Word stock images were used to create the illustration.

References

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