The pulmonic valve is normally a thin tricuspid structure that prevents blood from regurgitating into the right ventricle once ejected into the low-pressure pulmonary circulation. Pulmonic regurgitation refers to retrograde flow from the pulmonary artery into the right ventricle during diastole. Physiologic (trace-to-mild) pulmonic regurgitation is present in nearly all individuals, particularly in those with advanced age. However, pathologic conditions that produce excessive and clinically significant regurgitation can result in impairment of right ventricular function and eventual clinical manifestations of right-sided volume overload and heart failure. Often, pulmonic regurgitation is not the primary process but a finding secondary to an underlying process such as pulmonary hypertension or dilated cardiomyopathy.
Incompetence of the pulmonic valve occurs by 1 of 3 basic pathologic processes: dilatation of the pulmonic valve ring, acquired alteration of pulmonic valve leaflet morphology, or congenital absence or malformation of the valve.
Physiologic pulmonic regurgitation is present in nearly all individuals and is a normal echocardiographic finding. Pulmonic regurgitation detected by physical examination is not a normal finding in healthy adults. Congenital pulmonic regurgitation and congenital absence of the pulmonic valve are rare conditions.
No difference in international incidence is known.
The morbidity and mortality rates associated with pulmonic regurgitation vary considerably, depending on the underlying etiology.
No racial or ethnic predilection exists.
Differing frequency of pulmonic regurgitation between men and women corresponds to the specific etiology resulting in pulmonic regurgitation.
Except for congenital absence of the pulmonic valve, which is more likely to cause right-sided ventricular decompensation early in life, the age at which clinical symptoms of pulmonic regurgitation occur is variable and is primarily related to the underlying process causing the pulmonic regurgitation.
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