Ventricular septal defect epidemiology and demographics

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] and Leida Perez, M.D.

Associate Editor-in-Chief: Keri Shafer, M.D. [2]

Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

Epidemiology and Demographics

The ventricular septal defect is the most common congenital cardiac malformation with an incidence of 1.5 to 2.5 per 1,000 live births, corresponding to 30% of all newborns with a congenital heart defect. There is no predilection based on sex.

The several known risk factors for VSD, including a family history of congenital heart disease and exposure to certain drugs, infectious agents, and maternal metabolic disturbances, explain few cases. Incidence rates are similar in different races and seasons and are unrelated to maternal age, birth order, sex, and socioeconomic status. Congential VSDs are frequently associated with other congential conditions, such as Down syndrome. [1]

Only in the United States, there are approximately 1 million adults with congenital heart disease, with 20,000 new patients reaching adolescence each year. Due to the improvement in early diagnosis in childhood and improved medical, surgical and ICU care, the number of adults will continue to rise. However, despite improved survival to adulthood, many patients will continue to have problems with residual shunts, valvular heart disease, ventricular dysfunction, heart failure and arrhythmias. The risk of sudden death in adults with congenital heart disease is nearly 25-50 times greater than would be expected for their age.

In adults, a VSD can form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead (heart) tissue.

References

  1. Giuliani et al, Cardiology: Fundamentals and Practice, Second Edition, Mosby Year Book, Boston, 1991.

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