Silent VSD—Revisited

Silent VSD—Revisited

583 Screening for Congenital Heart Disease by Prenatal Ultrasound. A Comparison of Two Decades in Western Australia J. McLean ∗ , C. Bower, J. Sharpe,...

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583 Screening for Congenital Heart Disease by Prenatal Ultrasound. A Comparison of Two Decades in Western Australia J. McLean ∗ , C. Bower, J. Sharpe, L. D’Orsogna, D. Kothari Maternal Fetal Medicine Unit, King Edward Memorial Hospital, Australia Background: Worldwide trends have demonstrated that there is a significant increase in detection rates of congenital heart disease (CHD) by prenatal screening. Aim: This study was aimed at assessing detection rates of CHD by prenatal ultrasound screening, comparing two decades (1990–1999 and 2000–2009). Method: A retrospective review of trends in the detection of CHD anomalies in Western Australia was undertaken between the periods of 1990 and 2009. Data were extracted from the Western Australian Register of Developmental Anomalies. This included four major anomalies – Atrioventricular Septal Defects (AVSD), Tetralogy of Fallot (TOF), Complete Transposition of Great arteries (TGA) and Single Ventricles and compared the pre and post natal detection rates including post mortem findings over two decades. Results: The number of patients diagnosed with CHD in Western Australia has remained unchanged over the previous two decades, accounting for approximately 1% of live births. Overall prenatal detection rates have increased from 14% (1990–1999) to 44% (2000–2009) era. Individually the rates of detection have also significantly increased; TOF 4.3–25.2%, AVSD 28–46.7%, single ventricle 43.5–85.7% and TGA 4–40%. Despite the increase there is still a significant proportion of CHD that remains undetected by prenatal ultrasound screening. Conclusion: This study has demonstrated an increase in the detection rates of CHD over two decades. Improvements are required at the screening level to further reduce the proportion of undetected cases of major cardiac anomalies. doi:10.1016/j.hlc.2011.05.587 584 Silent VSD—Revisited T. Goh ∗ Monash Medical Centre, Australia Objective: Clinical course of small VSD is a loud pansystolic murmur that progressively softens and eventually disappears as the VSD closes. The condition where the murmur is silent clinically yet a VSD persists on echo has been recently described (2009). Dynamics of closing VSD: Progressive diminution of turbulent energy conversion to acoustic energy occurs as VSD becomes smaller until a critical low level of acoustic energy is reached which makes the murmur inaudible to



the human ear – hence “Silent VSD”[SVSD] (VSD persists on ECHO). Methods and results: Of more than 160 patients followed up[fu] by serial clinical and echo for more than 20 years, 17 patients [age 24–164 months] fu12–163 months (12 pvsd, five musvsd) have SVSD (examined at rest). Four patients SVSD have since had complete echo closure fu 5–36 months median 17 months. Four patients have since been exercised and this has brought on the VSD murmur momentarily. One patient has a soft VSD murmur on review having not had a murmur on previous annual review. All patients remain well. Dynamics of SVSD with exercise: Increasing cardiac output (CO) levels causes increasing turbulent energy conversion to acoustic energy to the level for the human ear to hear momentarily. Conclusion: 1. SVSD is a benign echo/clinical entity with good outcome thus far. 2. Exercise may resurrect the VSD murmur momentarily. 3. Patients with clinical spontaneous closure of VSD should be exercised and reexamined for VSD murmur. 4. SVSD sound dynamics is related to CO levels. doi:10.1016/j.hlc.2011.05.588 585 Surgery for Ebstein’s Anomaly: A Single Centre Experience V. Wijesekera ∗ , D. Radford, P. Pohlner Adult Congenital Heart Disease Service, The Prince Charles Hospital, Australia Background: First described by Wilhelm Ebstein in 1866, the condition was managed conservatively for many years. With improvements in surgery, tricuspid valve repair began to be undertaken and techniques evolved. We evaluated the results of surgical intervention at our institution. Method: Available records of patients who had surgery for Ebstein’s Anomaly between January 1990 and January 2010 were analysed. Results: Records for 22 patients were reviewed. Ages ranged from 2 to 74 years and 59% were female. Associated conditions included ASD (9), PDA (1) and pulmonary stenosis with hypoplastic RV (1). Only seven had a diagnosis of SVT of whom three had AF. Resting cyanosis was associated with ASD. Fifty-two percent had less than NYHA class III dyspnoea. Two had clinical signs of right heart failure and 95% had at least Grade 3/4 tricuspid regurgitation prior to surgery. Forty-two percent (eight patients) had RV dysfunction preoperatively. RV dilatation was present in most and nine were classified as severe. Valve repair without ring insertion was successful in 13 of 22, four had successful TV ring insertion and the remaining five required valve replacement. Three had concomitant reduction of RA size. At early follow-up 89% had improvement in dyspnoea by at least one NYHA class. Degree of TR improved in 16 post-operatively; however three had worsening TR. Nine patients required redo-TV surgery for TR or TS. There were no deaths.


Heart, Lung and Circulation 2011;20S:S156–S251