Complete Left Pericardial Defect with Dual Passage of the Phrenic Nerve: A Challenge to the Widely Accepted Embryogenic Theory

Kaneko, Yukihiro; Okabe, Hideo; Nagata, Nanae

doi:10.1007/s002469900338

Cited by 15 publications

(8 citation statements)

References 10 publications

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“…Perna (1909) proposed that the premature atrophy of the left duct of Cuvier results from insufficient blood supply to the PPMs 19. Alternatively, altered growth of the heart may inappropriately stretch and tear the PPMs 20. To our knowledge, normal and abnormal pericardial development has not been described in any detail in the mouse.…”

Section: Discussionmentioning

confidence: 95%

Wt1 and Retinoic Acid Signaling in the Subcoelomic Mesenchyme Control the Development of the Pleuropericardial Membranes and the Sinus Horns

Norden

Grieskamp²,

Lausch³

et al. 2010

Circulation Research

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Rationale: The cardiac venous pole is a common focus of congenital malformations and atrial arrhythmias, yet little is known about the cellular and molecular mechanisms that regulate its development. T he systemic venous return of the mature mammalian heart, which terminates in the right atrium, consists of multiple anatomic components including the myocardial sleeves of the right superior and inferior caval veins, the sinoatrial node (SAN), the coronary sinus (persisting left caval vein in the mouse), and the sinus venarum. 1 The systemic venous return is a focus of congenital malformations and atrial arrhythmias, 2,3 necessitating insight into the cellular and molecular programs by which it arises during cardiac development. Most myocardial components of the heart are not represented in its initial anlage, but are continuously added by recruitment and differentiation of precursor cells. 4 The sinus horns, the myocardial parts of the common cardinal veins upstream of the venous valves that bulge into the pericardial cavity, form from pericardial precursors that differentiate into sinus venosus myocardium around the systemic venous connection to the atrium. 5 They form only after embryonic day (E)9.5, when outflow tract, left and right ventricle, and the common atrium have already been established. In adults, most of the right sinus horn myocardium is incorporated into the right atrium to form the sinus venarum. In humans, the left sinus horn will lose its connection to the body and form the coronary sinus, whereas in mouse it will persist as the left superior caval vein.Few genes regulating venous pole development have been characterized, including the Tbx18 (T-box transcription factor 18) that marks the sinus horn lineage. 14 which harbors a tetrameric repeat of the RAR␤2 RARE linked to the Hsp68 minimal promoter used to determine RA signaling, were all described before. For the Wt1 BAC-IRES-EGFPCre transgenic line, the BAC clone RP23-266M16 was modified by inserting an IRES/EGFP-Cre cassette 17bp downstream of the translation stop site of the Wt1 gene. (The generation and evaluation of this line will be described elsewhere.) In Wt1 tTA mice, the coding sequence of an improved tetracyclinedependent transactivator tTA2S 15 was introduced into the Wt1 locus by gene targeting (E Lausch, S Fees, C Steinwender, C Spangenberg, L Eshkind, E Bockamp, B Zabel, manuscript in preparation). All mouse lines were maintained on an outbred (NMRI or FvB) background.An expanded Materials and Methods section is available in the Online Data Supplement at http://circres.ahajournals.org. Results Defects in the Systemic Venous Return of Wt1-Deficient Hearts Wt1Ϫ/Ϫ mice maintained on an NMRI outbred background died during midgestation presenting defects reported on earlier, including lack of kidneys, diaphragmatic hernia, and defects in coronary vessel formation the latter of which may underlie embryonic lethality. Yet, histological inspection of surviving embryos at E14.5 revealed an undescribed variation in the systemic venous ...

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Section: Discussionmentioning

confidence: 95%

Wt1 and Retinoic Acid Signaling in the Subcoelomic Mesenchyme Control the Development of the Pleuropericardial Membranes and the Sinus Horns

Norden

Grieskamp²,

Lausch³

et al. 2010

Circulation Research

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“…An alternative theory proposes that a traction induced tear may develop in the pleuropericardial membrane, with a resultant pericardial defect. Kaneko et al's case of pericardial absence associated with a divided phrenic nerve,[ 4 ] passing both ventrally and dorsally to the defect, illustrates this conjecture. A third theory attributes the developmental failure of the pericardial membrane to premature atrophy of the cardinal veins (duct of Cuvier) supplying the pleuropericardial folds.…”

Section: Introductionmentioning

confidence: 99%

Congenital Absence of the Right Pericardium: Embryology and Imaging

Koo

Newburg

2015

Journal of Clinical Imaging Science

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Though congenital pericardial absence is often asymptomatic, complications can be life threatening. To date, few short case reports, primarily from the pre-CT and MR era, describe congenital absence of the right pericardium. We present a more comprehensive discussion of the embryologic derangements causing such defects and offer an up-to-date review of characteristic radiologic findings. Recognition of characteristic imaging findings of congenital pericardial absence is crucial in guiding diagnosis and management.

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“…Its persistence may be due to inadequate blood supply following premature atrophy of the left common cardinal vein (the duct of Cuvier), which is an event that could account for both the defect and its tendency to occur on the left side (2). A recent article suggests that some defects may be due to a tear in the pleuro-pericardial membrane rather than failure of the pleuro-pericardial foramen to close (3). …”

Section: Discussionmentioning

confidence: 99%

“…It has rarely been reported that the left phrenic nerve runs behind it (9, 10). Kaneko and associates (3) report a patient with a complete left pericardial defect whose phrenic nerve, split into two portions, passes both ventral and dorsal to the defect. Our case is an example where the phrenic nerve runs behind the defect.…”

Section: Discussionmentioning

confidence: 99%

Partial Pericardial Defect Incidentally Discovered During Coronary Bypass Surgery

Son

Choi

et al. 2010

J Korean Med Sci

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A 71-yr-old male patient with three vessel coronary artery disease underwent a coronary artery bypass graft. The patient was found to have a large pericardial defect at the apex of the heart that measured approximately 18 cm in circumference. The edge of the pericardial defect impinged on the epicardial coronary arteries. The left phrenic nerve descended via the dorsal boundary of the pericardial defect. Following coronary artery bypass grafting, the pericardial defect was repaired with a polytetrafluorethylene patch. The patient had an uncomplicated postoperative course.

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Complete Left Pericardial Defect with Dual Passage of the Phrenic Nerve: A Challenge to the Widely Accepted Embryogenic Theory

Cited by 15 publications

References 10 publications

Wt1 and Retinoic Acid Signaling in the Subcoelomic Mesenchyme Control the Development of the Pleuropericardial Membranes and the Sinus Horns

Wt1 and Retinoic Acid Signaling in the Subcoelomic Mesenchyme Control the Development of the Pleuropericardial Membranes and the Sinus Horns

Congenital Absence of the Right Pericardium: Embryology and Imaging

Partial Pericardial Defect Incidentally Discovered During Coronary Bypass Surgery

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