If aortic
regurgitation is the sole lesion, its severity may be gauged from
the degree of left ventricular volume overload, but the duration
and severity of the mitral or septal flutter are of no help in this
regard.
It has long been appreciated that most patients tolerate even quite
severe aortic regurgitation for many years, but that deterioration
is rapid once left ventricular failure occurs. Thus, a major contribution
of echocardiography to the management of aortic regurgitation is
in determining the pathogenesis, and in providing a noninvasive
method for monitoring left ventricular function.
As with other flow lesions, Doppler echocardiography is now the
noninvasive standard for detecting the presence and severity of
aortic regurgitation.
 |
| Fig. 49 |
In rheumatic heart disease, the most common presentation after pure
mitral stenosis is a combination of this with aortic regurgitation.
The changes in the aortic valve can be minimal, causing only slight
thickening of the cusp echoes. The aortic root diameter, measured
at the level of the cusps, is normal. Evidence of the etiology comes
from the mitral valve, which almost always shows some echocardiographic
signs of rheumatic disease. The mitral valve abnormality may be
confined to slight reduction in amplitude of the posterior leaflet
motion without any clinical manifestations (Fig. 49). If, on the
other hand, the mitral valve is heavily calcified, any flutter caused
by aortic regurgitation may be difficult to detect. Magnified views
of the valve and interventricular septum, recorded by M-mode using
higher paper speed and low gain settings, may help to demonstrate
diastolic fluttering.
 |
| Fig. 50 |
Where vegetations on the aortic valve result from the infection,
they are best detected by using two-dimensional long-axis and short-axis
views, shown in (Fig. 50). Vegetations larger than 2-3 mm can usually
be visualized clearly and their approximate size can be determined,
along with the cusps to which they are attached.
 |
| Fig. 51 |
Aortic valve endocarditis is sometimes complicated by the development
of a mycotic aneurysm, which can rupture into one of the other cardiac
chambers, or by the spread of the infection to the tricuspid valve.
Although M-mode recordings may demonstrate the resulting hemodynamic
changes, direct visualization of such defects is normally possible
only by two-dimensional echocardiography (Fig. 51).
In many cases, however, endocarditis infection of an aortic valve
does not produce vegetations, but rather causes erosion of the cusp
tissue that leads to rupture or perforation. The echocardiographic
sign of such lesions is rapid fluttering of the aortic cusps during
diastole, caused by a turbulent jet of blood passing through a defect
in the otherwise closed valve.
Many infected aortic valves also appear to be bicuspid, and it is
well known that any abnormality of the valve greatly increases its
susceptibility to infection. But only about one percent of the population
has a bicuspid valve, and roughly half of the patients requiring
valve replacement for severe aortic regurgitation caused by endocarditis
have a normal three-cusp configuration.
Not infrequently, the regurgitant jet of blood spreads the infection
to the mitral valve, producing the signs described previously.
2004
