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Rao. Vessel Plus 2022;6:22  https://dx.doi.org/10.20517/2574-1209.2021.105      Page 15 of 24


















                Figure 4. Artist’s rendition of ejection systolic murmur (secondary to stenotic aortic or pulmonary valve or due to increased flow across
                the semilunar valve because of valvar regurgitation) and early diastolic decrescendo murmur (due to aortic or pulmonary regurgitation).

               and Quinke’s pulse (flushing and blanching alternatively of the capillary beds of the tips of finger) are seen
               in subjects with moderate to severe AR; however, these signs do not automatically identify that the AR is
               severe.

               The ECG is normal in mild AR cases. In moderate to severe AR patients, signs of LV enlargement are seen.
               Chest roentgenogram reveals cardiac enlargement (mostly due to LV dilatation). Classically, there is no
               evidence for LA enlargement unless mitral valve disease is also present. Echo-Doppler studies demonstrate
               LV volume overloading. The anterior mitral leaflet may be seen to flutter on echocardiography and is
               indicative of AR, and corresponds to the Austin-Flint murmur described above. The LV fractional
               shortening is normal initially, but increases with time in response to increased volume to be pumped by the
               LV. With the onset of myocardial failure either due to very severe and/or prolonged AR, the LV fractional
               shortening decreases. Doppler study shows flow reversal in the LV outflow region. Color flow imaging
               unmistakably demonstrates the jet of AR, which is of use in assessing the magnitude of AR. In moderate to
               severe AR cases, flow reversal in the descending aorta may be observed; such findings may indicate that the
               AR is significant. Pressure ½ time of AR jet is useful in semi-quantification of AR.


               The early diastolic murmur of AR must be distinguished from the early diastolic murmur associated with
               pulmonary regurgitation (PR) and pulmonary hypertension. These will be reviewed in the next section. The
               causes of AR are multiple, and these are: rheumatic heart disease; bicuspid aortic valve; prolapse of the
               aortic valve leaflet in an attempt to spontaneously close a VSD; perforation of aortic valve leaflet, which may
               be congenital in origin or is due to prior bacterial endocarditis; aortic root dilatation secondary to Marfan’s
               syndrome; aorta-to-LV tunnel, and perhaps others. It may also be due to surgical valvotomy or balloon
               aortic valvuloplasty for AS. Information from history, other physical findings, and echo-Doppler
               examination are valuable in determining the correct cause of AR.


               Pulmonary regurgitation
               The murmur of PR is also an early diastolic decrescendo murmur and is best auscultated at the LUSB and
               LMSBs. Sometimes, it radiates inferiorly to the LLSB. It is different from the murmur of AR because it is of
               low pitch quality in contradistinction to the high pitch of AR murmur. In addition, there are no peripheral
               manifestations of AR. Furthermore, the murmur of PR is best auscultated with the stethoscope’s bell, with
               the patient lying flat. The RV impulse is usually prominent. Heart sounds usually exhibit wide splitting of
               the 2nd heart sound. Single 2nd heart sound may be heard in some disease entities as reviewed in the next
               section. A systolic ejection murmur [Figure 4] may be appreciated at LUSB and is likely to be related to
               augmented volume of blood flow via the pulmonary valve, and does not automatically suggest associated PS.
               Nevertheless, pulmonary valve stenosis or pulmonary valve annular hypoplasia can also produce systolic
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