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143 Natural History of Repaired and Unrepaired VSD – an Experience of a District General Hospital with Dedicated Adult Congenital Heart Disease Clinics
  1. Isma Rafiq1,
  2. Leisa Freeman1,
  3. Mateusz Orzalkiewicz1,
  4. Nadine Hiari2,
  5. Clive Lewis2
  1. 1Norfolk and Norwich University Hospital
  2. 2Papworth NHS Trust

Abstract

Background Ventricular septal defect are the most common congenital defect but only accounts for 10% of congenital defects in the adults due to spontaneous closure. The objective of this study is to review the natural course and outcomes of the repaired and unrepaired VSD in this large follow up cohort in non surgical (CHD) centre.

Methods We reviewed the NORPAP database (n = 2322) and found 300 patients with ventricular septal defect (12.9% incidence)

Results 137/300 were male, 163/300 (54%) were female. Age range 17–83, median age at FU was 39 years. Spectrum of type of ventricular septal defect is described Table 1 and associated concomitant cardiac lesions.

Abstract 143 Table 1

Anatomical location of ventricular septal defects in NORPAP ACHD Clinics

Surgical closure of VSD occurred in 122 and percutaneous closure in 3 (total 125). 24/125 had redo surgery and 10/24 had 3rd operation. 1/10 had 4th, 5th and 6th procedure for repeated tricuspid valve obstruction (thrombus and pannus).

175 patients were unoperated at transition to adult clinic, 26 have since had spontaneous closure, 6 partial closure; 1 is waiting VSD closure. Arrhythmia incidence was low (33) and equal in both operated and unoperated. Atrial arrhythmias in 21, ventricular in 9, bradycardia requiring pacemaker in 3; overall incidence of device therapy was low (7).

22 patients had endocarditis – 9 had had previous surgery, 13 unoperated (1 twice). 12/163 (7.3%) females and 10 males/137 (7.3%) was against male preponderance. IHD disease was not a common associated feature of VSD n = 4.

10 patients had RVOT – obstruction associated VSD out of which 6 required resection and repair of VSD- 1 patient required further intervention due to LVOT-obstruction caused by aneurysmal septal patch

38 patients developed pulmonary hypertension out of which 21 patients had Eisenmenger syndrome. 32 patients were unoperated in this group while 6 patients developed pulmonary hypertension post repair

Conclusion Ventricular septal defects associated with concomitant lesions require long term follow up in dedicated adult CHD clinics. Small unoperated VSD’s and repaired VSD’s can be followed in physiologist led echo clinics with ACH-CSN review as required to watch for late outflow tract obstruction or other sequelae. No death was reported in our cohort up to date. Over 50% of endocarditis in this cohort occurred in unoperated VSD’s

Abstract 143 Table 2

VSD: Concomitant cardiac lesions from NORPAP database


  • Ventricular Septal defect
  • Repaired and Unrepaired
  • Natural Outcome

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