Talk:Cardiovascular System - Ventricular Septal Defects

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Cite this page: Hill, M.A. (2024, March 29) Embryology Cardiovascular System - Ventricular Septal Defects. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Cardiovascular_System_-_Ventricular_Septal_Defects

2011

Complete Repair of Coarctation of the Aorta and a Ventricular Septal Defect in a 1,480 g Low Birth Weight Neonate

Korean J Thorac Cardiovasc Surg. 2011 Apr;44(2):183-5. Epub 2011 Apr 14.

Lee H, Cho JY, Kim GJ. Source Department of Thoracic and Cardiovascular Surgery, Kyungpook University Hospital, Korea. Abstract Although outcomes of neonatal cardiac surgery have dramatically improved in the last two decades, low body weight still constitutes an important risk factor for morbidity and mortality. In particular, cardiac surgery in neonates with very low birth weight (≤1.5 kg) is carried out with greater risk because most organ systems are immature. We report here on a successful case of early one-stage total repair of coarctation of the aorta and a ventricular septal defect in a 1,480 gram neonate.

PMID 22263148

When was ventricular septal defect first defined?

Anadolu Kardiyol Derg. 2011 Mar;11(2):179. doi: 10.5152/akd.2011.041. Epub 2011 Feb 23.

Ulus AT, Songur M, Kahya E. Source Department of Cardiovascular Surgery, Türkiye Yüksek İhtisas Education and Research Hospital, Ankara, Turkey. uluss@yahoo.com


"Almost all of the cardiac, cardiovascular guidelines and the textbooks mention that one of the first clinical descriptions of ventricular septal defect was made by Henri Roger in 1879 (1). Henri Roger’s experience and skill as a pediatrician, combined with his interest in auscultation, led to his discovery of a simple but important interventricular communication which later became known as ‘’maladie de Roger’’(2). He described the clinical and auscultatory findings of 6 acyanotic patients and autopsy finding of a child with ventricular septal defect (1). We could not find any earlier descriptions about the definition of the ventricular septal defects in these texts. All of the authors agree in that ventricular septal defect was first described clinically by Henri Roger (2).

We found out that before Henri Roger, Mansur b. Muhammed b. Ahmed who lived in the 14th century described ventricular septal defects. He wrote the book named “Kitab-ı Teşhirü’l- Ebdan Min e’t -Tıb” (A Work on Human Anatomy) in 1386 and mentioned about all of the anatomical systems of the human body. Moreover, this book is known to be one of the three illustrated medical books in the Turkish medical globe history (3). He described the ventricular septal defects clearly noticing the existence of a passage between the two ventricles; the part of the passage on the right side was larger becoming narrower through the left side (3).

The scientists who are interested in medical history should accept that Mansur b. Muhammad b. Ahmed was of Turkish origin as they can easily define it from his poor Persian and the figures in his works (3). However, there are three illustrated anatomical works in the historical period of that time in Old Turkish Medical History and two of them were written in Persian. The other illustrated anatomical work was written by Nasir al-Din Tusi in the 13th century; it was named Tansuhname-i Ilhani (A Work on General Anatomy of Ilhani). The third one was written in Turkish. It was named Tashrih al-Abdan (Illustrated Work on Human Anatomy); his author was Shams al-Itaki. When we compared their illustrations, we can define interesting resemblances among them. Principally Mansur b.Muhammad b. Ahmed explained at first simple organs and then the complex organs, which were called as main systems in modern anatomical works. Finally, he explained the creation and the improvement of embryo. Rhazes claimed that firstly liver occurred in fetus, Ibn Sina claimed umbilical cord, Hippocrates said brain is the first organ in fetus but, contrarily Mansur b. Muhammad b. Ahmed mentioned that firstly heart occurred in fetus (3). He also gave several illustrations that show the anatomical systems but several physicians used these in their works in the following periods without giving as a reference (3)."

PMID 21342858


1986

Pulmonary arterial changes in patients with ventricular septal defects and severe pulmonary hypertension

Pediatr Cardiol. 1986;7(3):147-54.

Fried R, Falkovsky G, Newburger J, Gorchakova AI, Rabinovitch M, Gordonova MI, Fyler D, Reid L, Burakovsky V.

Abstract

In 25 patients, aged eight months to 31 years, with ventricular septal defect (VSD; isolated in 15, the others with atrial septal defect, PDA, coarctation or patent ductus arteriosus + coarctation), each with severe pulmonary artery hypertension (pulmonary artery systolic pressure [Ppa] at least 75% of systemic and an elevated pulmonary vascular resistance), we related morphologic and morphometric data from open-lung biopsy to hemodynamic measurements obtained at cardiac catheterization during the same hospital admission. Of the hemodynamic features measured, only the ratios of pulmonary-to-systemic flow and pulmonary-to-systemic resistance correlated significantly with structure. Neither pulmonary artery pressure (Ppa) nor pulmonary vascular resistance correlated significantly with any structural feature studied. The increased external diameter of respiratory bronchiolar arteries in those with the more advanced Heath-Edwards grades reflects dilatation and suggests that it is in the small arteries of the distal arterial bed that the changes of pulmonary hypertension are most significant. Neither age nor body weight correlated significantly with the degree of structural or hemodynamic abnormality. In the ten patients who underwent VSD closure, Ppa was measured postoperatively. The Heath-Edwards grade (no more than one grade-III lesion) and arterial density (at least one-half that normal for age) were the best correlates of the difference between preoperative Ppa and Ppa immediately after corrective surgery. The presurgical catheterization data, including pulmonary resistance and the resistance ratio, did not correlate significantly with change in Ppa following VSD closure.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID 3808993

1981

Pulmonary arterial changes and hemodynamic parameters in isolated ventricular septal defect

Thorac Cardiovasc Surg. 1981 Dec;29(6):355-8. Hoffmeister HM, Fischbach H, Hoffmeister HE. Abstract Lung biopsy specimens of 20 patients (aged 6 months to 29 years) with isolated ventricular septal defect (VSD) and various degrees of pulmonary hypertension were obtained at operation. The cross-section area of the pulmonary arteries was measured by a morphometrical method in each biopsy specimen and the grade of the hypertensive pulmonary vascular disease was determined according to the Health and Edwards classification. These findings were correlated to the pulmonary-to-systemic pressure ratio, to the pulmonary-to-systemic resistance ratio, and to the pulmonary-to-systemic flow ratio. The thickness of the media of pulmonary arteries (measured as area ratio) was well correlated to both the systolic blood pressure ratio and the resistance ratio resulting in a product moment correlation of r = 0.73. No direct relationship was found between the hypertrophy and the pulmonary-to-systemic flow ratio. Our quantitative morphometric data were well correlated with the qualitative Health and Edwards classification. Medial wall thickness was not significantly higher in grade III when compared to grade II. The mean values of the hemodynamic parameters were not significantly different in the Health and Edwards grade II and grade III groups. Our results indicate that the calculation of the mean pulmonary pressure and of the pulmonary-to-systemic resistance ratio are of no higher predictive value than the systolic pressure ratio. The classification of Health and Edwards appears to the sufficient for clinical evaluation.

PMID 6179217

1847

Case of cyanosis, with a description of the appearances presented on dissection, illustrated by the preparation, and a drawing, of the heart

Med Chir Trans. 1847;30:112.2-120.

Clark Fle G.

PMID 20895864

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2104017 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2104017/pdf/medcht00051-0145.pdf