Late results (30 to 35 years) after operative closure of isolated ventricular septal defect from 1954 to 1960

doi:10.1016/0002-9149(91)90284-R

The American Journal of Cardiology

Volume 68, Issue 15, 1 December 1991, Pages 1491-1497

https://doi.org/10.1016/0002-9149(91)90284-R Get rights and content

Abstract

This study was designed to determine the clinical status, cause of death, and effects of pulmonary vascular disease and conduction abnormalities 30 to 35 years after surgery in 296 consecutive surviving patients of closure of ventricular septal defect. Of the 296 patients, current status was determined by contact with patient and physician in 290 cases, with 6 (2%) lost to follow-up (7,912 patient years are included). Cardiac catheterization after surgery in 168 patients showed complete closure of the defect in 80%. Death occurred in 59 patients (20%), with higher mortality rates in those operated on after the age of 5 years, those with pulmonary vascular resistance >7 units (51%), and those with complete heart block (78%). Of 37 patients with transient heart block after surgery, 8 (22%) have died (3 pulmonary vascular disease, 2 sudden death, 2 unknown causes and 1 complete heart block). Twenty other patients had a dysrrhythmia after surgery, and none of these died. Nine episodes of endocarditis occurred ( $11.4 10,000$ patient years). Nine of 296 (3%) offspring had cardiac malformation. Most patients are in New York Heart Association class I, 57% attended college and 15% received an advanced degree.

The data show good results for this group of patients operated on during an early era (1954 to 1960) of open cardiac surgery. They support the current trend toward operation in patients with ventricular septal defects at an early age and with low pulmonary vascular resistance.

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Citation Excerpt :
All patients were evaluated locally including assessment of functional class, echocardiography and invasive hemodynamic right heart catheterization. Patients with significant PAH that were deemed “non-correctable” according to the most reasonable published data at the time of presentation [11–13], and initiated on PAH-targeted therapy were included. In general, the data available that spanned the study timeframe suggests that a PVR >4.6–7 Wood units would be considered high-risk and therefore, a “non-correctable” defect.
Adults presenting with an unrepaired atrial septal defect and pulmonary arterial hypertension (ASD-PAH) are typically classified as “correctable” or “non-correctable”. The use of directed PAH medical therapy in non-correctable ASD-PAH leading to favorable closure candidacy, repair status and long-term follow-up is not well studied. We therefore sought to characterize response to PAH targeted therapy in ‘non-correctable’ ASD-PAH.
Nine North American tertiary care centers submitted retrospective data from adults with unrepaired ASD-PAH that did not meet recommendations for repair at initial presentation (1996–2017). Sixty-nine patients (women 51(74%), 40 ± 15 years, mean pulmonary artery pressure (mPA) 51 ± 13 mm Hg, pulmonary vascular resistance (PVR) 8.7 ± 4.9 Wood units, Qp:Qs 1.6 ± 0.4) were enrolled. All patients were prescribed PAH targeted therapy and late shunt repair occurred in 19(28%) (Women 15(29%) vs. Men 4(22%), p = 0.6). At late follow-up (4.4 ± 2.9 years) 6-minute walk test distance (6MWTD) was significantly better in the group that underwent repair (486 ± 89 m vs. 375 ± 139 m, p < 0.05). Transthoracic echo showed significant improvement in right ventricular (RV) function (severe dysfunction in repaired 8(40%) vs. unrepaired groups 35(69%), p < 0.05). Divergent survival curves suggest that with larger studies and more follow-up, differences in survival between repaired and unrepaired groups may be important. (repaired: 17(94%) vs. unrepaired: 32(81%), p = 0.18).
This is the first and largest multicenter study evaluating the “treat-to-close” approach in non-correctable ASD-PAH. Our new data supports further study of this strategy in patients who have reversibility of PAH in response to targeted therapy. We demonstrate that in the carefully selected patient with non-correctable ASD-PAH, successful shunt repair is possible if post-therapy PVR is ≤6.5 Wood units. Patients who underwent repair had improved RV function following PAH targeted therapy. Divergent survival curves suggest that with further study, defect repair may affect medium-term to late survival.
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Patients undergoing transatrial VSD repair were identified from our institutional database. Follow-up echocardiography and patient data were obtained from medical records. Between January 2005 and August 2016, 130 isolated conoventricular VSDs were repaired. Among these, 26 patients underwent leaflet detachment, 15 underwent chordal detachment, and 89 underwent regular VSD repair (reference group).
The groups did not differ significantly in age, weight, postoperative length of stay, genetic/syndromic abnormalities, time to extubation, and left and right ventricular systolic function. The cardiopulmonary bypass and cross-clamp time were significantly longer in the leaflet detachment group than in the reference group (118 ± 28 vs 102 ± 32 minutes [p = 0.02] and 73 ± 20 vs 61 ± 23 minutes [p = 0.01], respectively). Echocardiographic follow-up was available for 87 patients at a mean of 2.6 years (range, 1 month to 11 years). Tricuspid regurgitation was rated as none or trivial in 66 (76%), mild in 20 (23%), and moderate in 1 reference group patient. There was no difference in presence of residual VSD or degree of tricuspid regurgitation among the three groups. There was no reoperation for tricuspid regurgitation.
Tricuspid valve leaflet and chordal detachment techniques provide an equally viable and safe alternative to closure of hard-to-expose VSDs while maintaining appropriate tricuspid valve function. Their use in our series did not lead to increased tricuspid valve dysfunction at early-to-midterm echocardiographic assessment.
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^☆: This study was supported by the Paul F. Dwan Chair in Education in Pediatric Cardiology.

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Late results (30 to 35 years) after operative closure of isolated ventricular septal defect from 1954 to 1960☆

Abstract

J Am Coll Cardiol

Am Heart J

Am Heart J

J Thorac Cardiovasc Surg

J Thorac Cardiovasc Surg

The direct-vision intracardiac correction of congenital anomalies by controlled cross circulation. Results in 32 patients with ventricular septal defects, tetralogy of Fallot, and atrioventricularis communis defects

Surgery

Physiologic changes after closure of ventricular septal defects

Lancet

Clinical and hemodynamic changes after closure of ventricular septal defects

JAMA

Pre and postoperative cardiac catheterization in 200 patients undergoing closure of ventricular septal defects

Surgery

High-pressure ventricular septal defects

JAMA

Post-operative follow-up of patients with ventricular septal defect

Circulation

Prognosis for patients with ventricular septal defect and severe pulmonary vascular obstructive disease

Circulation

Haemodynamic studies after repair of ventricular septal defect

Br Heart J

Effects of surgical closure of ventricular septal defects upon pulmonary vascular disease

Br Heart J

Ventricular septal defect. Incidence, morbidity, and mortality in various age groups

Br Heart J

Closure of pulmonary hypertension following surgical closure of ventricular septal defect

Adv Cardiol