Gerbode Defect following Tetralogy of Fallot Repair: The Role of Transesophageal Echocardiography

ABSTRACT Gerbode defect is a rare type of left ventricle (LV) to right atrium (RA) shunt. It is congenital in origin, but acquired cases are also described, usually following infective endocarditis, valve replacement, trauma, or myocardial infarction. We, hereby, report two cases of acquired Gerbode defect after tetralogy of Fallot (TOF) repair, and describe the role of echocardiography in the complete visualization of the anatomical defect, and in differentiation of this shunt from other conditions. The role of transesophageal echocardiography (TEE) is highlighted during reintervention for successful shunt closure. How to cite this article Ladha S, Balasubramaniam U, Kiran U, Makhija N, Devagourou V. Gerbode Defect following Tetralogy of Fallot Repair: The Role of Transesophageal Echocardiography. J Perioper Echocardiogr 2017;5(2):70-73.

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Reliability of Intraoperative Transesophageal Echocardiography During Tetralogy of Fallot Repair

Echocardiography ◽

10.1111/j.1540-8175.2000.tb01143.x ◽

2000 ◽

Vol 17 (4) ◽

pp. 319-327 ◽

Cited By ~ 18

Author(s):

JAMES J. JOYCE ◽

EUGENE Y. HWANG ◽

HENRY B. WILES ◽

CHARLES H. KLINE ◽

SCOTT M. BRADLEY ◽

...

Keyword(s):

Transesophageal Echocardiography ◽

Tetralogy Of Fallot ◽

Intraoperative Transesophageal Echocardiography ◽

Tetralogy Of Fallot Repair

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Role of transesophageal echocardiography in the diagnosis of papillary muscle rupture secondary to myocardial infarction

American Heart Journal ◽

10.1016/0002-8703(89)90026-4 ◽

1989 ◽

Vol 118 (6) ◽

pp. 1330-1333 ◽

Cited By ~ 28

Author(s):

Ashokakumar M. Patel ◽

Fletcher A. Miller ◽

Bijoy K. Khandheria ◽

Charles J. Mullany ◽

James B. Seward ◽

...

Keyword(s):

Myocardial Infarction ◽

Transesophageal Echocardiography ◽

Papillary Muscle ◽

Papillary Muscle Rupture ◽

Muscle Rupture

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Abstract 12648: Deletion of 12/15 Lipoxygenase Improves Left Ventricle Function and Survival by Resolving Inflammation Post Myocardial Infarction

Circulation ◽

10.1161/circ.130.suppl_2.12648 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Vasundhara Kain ◽

Kevin A Ingle ◽

Janusz Kabarowski ◽

Sumanth D Prabhu ◽

Ganesh V Halade

Keyword(s):

Myocardial Infarction ◽

Left Ventricle ◽

Survival Rates ◽

Coronary Artery Ligation ◽

Artery Ligation ◽

Lv Remodeling ◽

Early Expression ◽

Cox 2

12/15 lipoxygenase (LOX) is crucial in the inflammatory process leading to diabetes and atherosclerosis. However, the role of 12/15 LOX in myocardial infarction (MI) and left ventricle (LV) remodeling is unclear. We assessed the role of 12/15 LOX in resolving inflammation in post-MI LV remodeling. 8-12 weeks old C57BL/6J wild-type (WT; n=67) and 12/15 LOX (LOX –/– ; n=78) male mice were subjected to permanent coronary artery ligation surgery and monitored through day (d)1 and d5. No MI surgery mice were maintained as d0 naïve controls. LOX -/- mice showed higher survival rate, improved fractional shortening with reduced remodeling and edema index than WT at d1 and d5 post-MI (all p<0.05). LOX -/- mice showed increased Cxcl5 expression at d1 post-MI, consistent with stimulated neutrophil recruitment in the infarct region that was decreased at d5 compared to WT. LOX -/- mice infarct had increased expression of Ccl2 and Cxcl1, that stimulated an earlier recruitment of monocytes with increased macrophages population at d5 (all p<0.05) compared to WT. The altered kinetics of immune cells post-MI indicates a rapid resolving phase, through increase in alternative macrophage phenotypes with reduced collagen density in LOX -/- mice compared to WT mice at d5 post-MI. LOX -/- mice showed a coordinated COX-1 and COX-2 response at d1 post MI, leading to an evident increase in 5-LOX and hemoxygenase-1 (HO-1) at d5 post-MI. 12/15 LOX deletion enhanced the recruitment of alternative macrophages with secretion of HO-1 to resolve inflammation. In-vitro addition of LOX metabolite 12 hydroxyeicosatetraenoic acid to LOX -/- fibroblast induced early expression of COX-2 and 5-LOX compared to WT, indicating 5LOX role in resolution of inflammation. Post-MI increased expression of TIMP-1 and decrease in MMP-9 at d1 and α-SMA at d5 in LOX -/- mice suggested controlled differentiation of fibroblast-to-myofibroblast which is key event during ventricular tissue repair and resolving phase. This change is supported by increased expression of tgf-βi, ctgf and admats-2 (all P<0.05) at d5 post MI. In conclusion, absence of 12/15 LOX improves post-MI survival rates and attenuates LV dysfunction by resolving inflammation through coordination of 5-LOX and HO-1 as key inflammation resolving enzymes.

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