Second, the area of color-flow jet used to assess the severity of valvular regurgitation may be dependent on factors other than regurgitant volume, such as jet velocity, chamber compliance, ventricular function, and the eccentricity of the jet. Third, although the same criteria for determining valvular sclerosis and annular calcification were utilized both in older and in younger patients, it is possible that valves in the “normal” older patients may actually be thicker than those of younger patients. Fourth, the low prevalence of aortic regurgitation and of moderate regurgitation of any valve (particularly aortic) did not allow for reliable determination of intraobserver and interobserver variabilities. In addition, since only four patients had moderate aortic regurgitation, data from the three different methods (color flow, pressure halftime, and pulsed Doppler evaluation of descending aortic flow) cannot be compared in a meaningful way. Finally, pulmonic regurgitation was not emphasized in this report, since detailed evaluations for pulmonic regurgitation were not as routinely and vigorously performed in our laboratory and, on many occasions during the period of our study, trivial pulmonic regurgitation was not reported or entered into our database. Therefore, the pulmonic regurgitation signal was not utilized for the estimation of pulmonary artery diastolic pressure and mean pulmonary artery pressure.
Despite these limitations, these data indicate a very high prevalence of valvular regurgitation, particularly trivial and mild mitral and tricuspid regurgitation, in patients with completely normal M-mode and 2D echocardiograms, suggesting that these findings are physiologically normal. These factors must be considered when addressing management (eg, patient wellbeing, employability, insurability, and particularly provision of endocarditis prophylaxis recommendations) in patients with Doppler-detected valvular regurgitation in order to prevent “iatrogenic heart disease.”