[Pulmonary regurgitation with special reference to the shape of the pulmonary valve ring: a pulsed Doppler and angiographic study].

Using pulsed Doppler echocardiography and cineangiography, the significance of pulmonic valve ring dimensions in the genesis of pulmonic regurgitation (PR) was studied in 40 patients, including 12 with valvular disease, 19 with coronary artery disease and nine with the normal heart. In nine of the 40 subjects, pulmonary hypertension (mean pulmonary artery pressure greater than or equal to 20 mmHg) was observed. The criterion for diagnosing PR was disturbed flow patterns recorded just below the pulmonic valve which spanned more than 40% of diastole, exceeding 1.5 KHz in peak frequency (corresponding to a flow velocity of about 50 cm/sec). Sagittal and transverse diameters of the pulmonic valve ring (PRDs, PRDt) at the upper edge of the pulmonary sinus, and the sagittal diameter of the pulmonary sinus (PSD) at the level of its maximal bulging were measured using pulmonary angiography. PR was detected in 15 subjects (37.5%). The prevalence of PR among three groups regardless of the absence or presence of pulmonary hypertension was not significantly different. The peak frequency of the regurgitant flow signals as well as the farthest point of the signals detected did not differ among the three groups irrespective of pulmonary hypertension. The ratio of the PRDs to the PRDt (PRDs/PRDt) was greater in patients with PR than in those without PR (p less than 0.001), but no correlation was established between PRDs/PRDt and mean pulmonary artery pressure. The PRDt index and PRDs index (normalized by body surface area) correlated well with the mean pulmonary artery pressure (r = 0.70, p less than 0.001 and r = 0.62, p less than 0.001, respectively). PSD also correlated with the mean pulmonary artery pressure (r = 0.49, p less than 0.01), whereas, PSD/PRDs correlated inversely with the mean pulmonary artery pressure (r = 0.40, p less than 0.01), indicating a relatively more prominent dilatation of the PRDs than of the PSD in cases with pulmonary hypertension. These results suggest that the etiology of PR in our series of patients was primarily attributable to the distortion of the pulmonic valve ring. The wide-spread concept that pulmonary hypertension dilates the pulmonic valve ring, leading to the development of PR, should be criticized.