, et al
Mortality and complications in 3495 children with isolated ventricular septal defects
Arch Dis Child
; doi:

Investigators from Norway conducted a nationwide cohort study to determine the mortality rate and occurrence of cardiac complications in children with isolated ventricular septal defects (VSDs). Four Norwegian nationwide health registers were used to identify all live-born children in Norway from 1994–2009 and determine their medical history as well as causes of death for those who died. Children with congenital heart disease (CHD), and specifically those with isolated VSD, were identified using specific CHD diagnosis codes documented in the health registers. The primary outcome was mortality, defined as the proportion of deaths in the cohort regardless of cause through 2012. A secondary outcome was occurrence of cardiac complications (eg, endocarditis, aortic regurgitation, pulmonary hypertensions, and arrhythmias) among children with isolated VSD as determined by routine diagnostic and procedure codes in the health registers. Survival among children with isolated VSDs was compared to survival among children without CHD using a hazard ratio (HR).

Of 943,871 live-born children identified, 11,272 had CHD and 3,495 (0.4%) had an isolated VSD. Surgical or catheter-based treatment of VSD was performed in 5.2% of the cases. Twelve children (0.3%) with isolated VSDs died during the study period compared to 4,015 (0.4%) of children without CHD (adjusted HR, 0.8; 95% CI, 0.5–1.4; P = .48). Among children with isolated VSDs, endocarditis occurred in 0.9%, aortic regurgitation in 3.4%, pulmonary hypertension in 0.3%, and arrhythmias in 4.6%.

The investigators conclude that children with isolated VSDs have a favorable prognosis without excess mortality.

Dr. Spar has disclosed no financial relationship relevant to this commentary. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.

VSDs are the most common CHD defect in children (excluding bicuspid aortic valve), occurring in nearly half of patients with CHD. VSDs occur in various anatomic locations including membranous, muscular, outlet, and inlet locations. After birth, these defects often lead to left to right shunts as the pulmonary vascular resistance decreases. There are variations in the size of the defect and intracardiac shunt, from small to large. Large shunts can lead to increased pulmonary circulation (symptoms including tachypnea, poor feeding and weight gain, tachycardia, hepatomegaly). VSD closure is indicated in patients with heart failure symptoms despite maximal therapy, large shunts, and defects associated with aortic valve prolapse and aortic regurgitation.

The natural history of VSDs had been well described. Most small defects close within the first 2 years of life. If small defects persist into adulthood, the VSDs are usually benign (rare reports of endocarditis and arrhythmia). Large VSDs rarely close and often lead to pulmonary overcirculation and failure to thrive, which ultimately require surgical intervention. If unrepaired, large defects can lead to irreversible pulmonary hypertension. Complications of VSDs include endocarditis, aortic regurgitation, subaortic...

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