Ventricular Septal Defect

Transcatheter closure of ventricular septal defect in aortic valve prolapse and aortic regurgitation

“…AVP and AR are well known to be associated with VSDs. Incidence of AVP is 5–8% in case of perimembranous VSD and as high as 30% in doubly committed subarterial VSD 9 . In case of perimembranous VSD, AVP occurs initially during diastole due to Venturi effect produced by the left to right shunting of the blood.…”

“…Incidence of AVP is 5–8% in case of perimembranous VSD and as high as 30% in doubly committed subarterial VSD. 9 In case of perimembranous VSD, AVP occurs initially during diastole due to Venturi effect produced by the left to right shunting of the blood. During later phase, prolapse occurs during systole also; because, damaged aortic valve becomes unable withstand the high aortic pressure.…”

Canadian Cardiovascular Society 2022 Guidelines for Cardiovascular Interventions in Adults With Congenital Heart Disease

“…Of patients with restrictive VSD deemed not to require surgical closure during childhood, long-term survival is expected and favourable. [60][61][62] Occasionally, isolated VSDs are not identified in childhood and might subsequently present in adulthood with left ventricular (LV) volume overload, infective endocarditis, progressive aortic regurgitation (AR), or PAH.…”

“…There are 4 types of VSD: muscular, perimembranous, supracristal (outlet or conal [if located above the crista supraventricularis]) and AVSD (or inlet-type VSD) spectrum. 60 The type of VSD is important because there are differences in the natural history and indications for closure. Patients with an isolated VSD that is surgically repaired in childhood and those with small restrictive (without significant shunt) VSDs not requiring repair, have an excellent long-term prognosis, although they are not completely free from morbidity or mortality (Fig.…”

Simulation of Eisenmenger syndrome with ventricular septal defect using equivalent electronic system

“…Irreversible pulmonary vascular obstructive disease, Eisenmenger syndrome, develops in 10-15% of patients with ventricular septal defects, most commonly in the second and third decades of life. [3][4][5][6] The Eisenmenger syndrome consists of a congenital communication between the systemic and pulmonary circulation, with resultant pulmonary arterial hypertension and right-to-left reversal of flow through the defect. When pulmonary vascular resistance exceeds systemic vascular resistance, it results in hypoxaemia and cyanosis.…”