Ventricular septal defect epidemiology and demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Priyamvada Singh, MBBS [2]; Cafer Zorkun, M.D., Ph.D. [3]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [4]

Overview

The ventricular septal defect is the most common congenital cardiac malformation with an incidence of 300 to 350 per 100,000 live births,^[1] corresponding to 30% of all newborns with a congenital heart defect. There is no predilection based on sex. 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 congenital conditions, such as Down syndrome. ^[2]

Epidemiology and Demographics

Incidence in United States of America

Only in the United States, there are approximately 1 million adults with congenital heart disease, with 20,000 new patients reaching adolescence each year.

Age

Pediatrics

The incidence has been found to be approximately 300 to 350 infants per 100,000 live births. ^[1]

Adults

The prevalence of ventricular septal defects is less in adults compared to the infants. This might be due to the fact that many small ventricular septal defects have spontaneous closure in childhood. ^[3]^[4] 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 (without congenital heart defects), a VSD can form a few days after a myocardial infarction (heart attack). It might be due to mechanical tearing of the septal wall, before scar tissue forms and macrophages start remodeling the dead (heart) tissue.

Gender

There is no predilection based on gender.

Race

There is no significant difference in incidences of ventricular septal defects based on race.

References

↑ ^1.0 ^1.1 Hoffman JI, Kaplan S (2002). “The incidence of congenital heart disease”. J Am Coll Cardiol. 39 (12): 1890–900. PMID 12084585.
↑ Giuliani et al, Cardiology: Fundamentals and Practice, Second Edition, Mosby Year Book, Boston, 1991.
↑ Du ZD, Roguin N, Wu XJ (1998). “Spontaneous closure of muscular ventricular septal defect identified by echocardiography in neonates”. Cardiol Young. 8 (4): 500–5. PMID 9855105.
↑ Kidd L, Driscoll DJ, Gersony WM, Hayes CJ, Keane JF, O’Fallon WM; et al. (1993). “Second natural history study of congenital heart defects. Results of treatment of patients with ventricular septal defects”. Circulation. 87 (2 Suppl): I38–51. PMID 8425321.

Template:WikiDoc Sources

[pmid12084585-1] 1.0 ^1.1 Hoffman JI, Kaplan S (2002). “The incidence of congenital heart disease”. J Am Coll Cardiol. 39 (12): 1890–900. PMID 12084585.

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

[pmid9855105-3] Du ZD, Roguin N, Wu XJ (1998). “Spontaneous closure of muscular ventricular septal defect identified by echocardiography in neonates”. Cardiol Young. 8 (4): 500–5. PMID 9855105.

[pmid8425321-4] Kidd L, Driscoll DJ, Gersony WM, Hayes CJ, Keane JF, O’Fallon WM; et al. (1993). “Second natural history study of congenital heart defects. Results of treatment of patients with ventricular septal defects”. Circulation. 87 (2 Suppl): I38–51. PMID 8425321.

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