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Page 18 of 24 Rao. Vessel Plus 2022;6:22 https://dx.doi.org/10.20517/2574-1209.2021.105

Tricuspid stenosis
Congenital or rheumatic tricuspid valve narrowing, although uncommon, may result in mid-diastolic
murmur heard best at lower left sternal border. There is usually a pre-systolic accentuation of the murmur.

Presystolic murmurs
Presystolic murmur (Figure 3; bottom) is infrequent in children in developed countries and is produced by
stenotic AV valves. The etiology of presystolic murmurs is tabulated [Table 8]. The murmur location on
auscultation and the findings in history and physical examination are useful in differentiating the causes of
these murmurs.

Mitral stenosis
Most commonly, mitral stenosis is rheumatic in origin. Mitral stenosis results in a presystolic murmur as
well as a preceding low-pitched mid-diastolic murmur. The mid-diastolic murmur becomes more intense in
late diastole and is generally described as presystolic accentuation. The murmur ends in S . The murmur is
1
produced by rapid blood flow via the stenotic mitral valve all through the atrial systole. Consequently, the
murmur cannot be auscultated in subjects who are in atrial fibrillation. The murmur is better auscultated at
the apical region and is best heard with the stethoscope’s bell. The murmur is better heard when the patient
is in lateral decubitus. The RV impulse is usually increased, but with a normal LV impulse. Frequently, a
thrill in diastole is felt at the apex. Unless carefully timed, the diastolic thrill of rheumatic mitral stenosis
may be erroneously interpreted as a systolic thrill. On auscultation, the 1st heart sound is loud. The
pulmonary component of the 2nd heart sound is accentuated in patients who have high PA pressures. An
opening snap of high-frequency quality may be auscultated at the apex; the snap is thought to be caused by
the sudden opening of the stiffened mitral valve leaflets. It is important to differentiate the opening snap
from a loud 3rd sound and the pulmonary component of the 2nd sound. A systolic murmur can be heard at
the apex in patients who have additional MR. The BP and arterial pulses are usually normal; however, in
patients with very severe mitral stenosis, the pulse volume (pulse pressure) is decreased.

The ECG demonstrates LA enlargement and RVH. Chest roentgenogram illustrates LA dilatation, dilated
main PA, and congestion of the pulmonary venous structures. Cephalization of pulmonary vascular
markings and Kerley B lines, indicative of dilated lymphatics may be visualized. M-mode echo reveals
decreased anterior mitral leaflet’s E to F slope and reduced movement of the posterior leaflet of the mitral
valve. 2D echo helps estimation of the mitral valve area. Doppler interrogation of the LV inflow region,
measuring mitral inflow gradient is useful in determining gradient through the stenotic mitral valve.

Patients who have mitral stenosis of congenital origin are likely to exhibit similar murmurs; however, the
patients are clearly younger. In addition, a loud first sound is not present, and an opening snap is not heard
because the mitral valve leaflets are not mobile with short and thick chordae in babies with congenital mitral
stenosis. Other CHDs with comparable pathophysiology are cor triatriatum and parachute mitral valve.
Such conditions do not exhibit distinctive presystolic murmur.

Tricuspid stenosis
Tricuspid valve stenoses, both congenital and rheumatic, are uncommon. Frequently, tricuspid stenosis is
seen in association with other CHDs. In such situations, the clinical features are largely determined by the
associated defects. Occasionally tricuspid valve may be involved in a severe rheumatic process causing
tricuspid stenosis. The presystolic murmur of tricuspid stenosis is auscultated best at LLSB; the intensity of
murmur increases with inspiration. In tricuspid stenosis opening snap is not commonly heard. Increased
“a” waves in the jugular venous pulse and presystolic hepatic pulsations may be seen/felt. However, if there