MYOCARDIAL ISCHEMIA: DETECTION AND LIMITATIONS
Within seconds of the onset of myocardial ischemia, affected segments
of the heart cease contracting normally.[65]
This
fact is the basis for the use of TEE for the detection of myocardial ischemia. For
example, in 50 patients undergoing cardiovascular surgery, new severe segmental wall
motion abnormalities (SWMAs) occurred in 24 patients and ischemic ST-segment changes
in only 6.[66]
In three patients who sustained
intraoperative myocardial infarctions, severe SWMAs developed in the corresponding
area of myocardium and persisted until the end of surgery, but only one of these
three patients had ischemic ST-segment changes intraoperatively. Subsequent studies
in comparable patients confirmed these advantages of TEE over electrocardiographic
monitoring.[67]
[68]
[69]
Moreover, when multiple TEE cross sections
are monitored (not just the one cross section as was done in the aforementioned studies),
the detection rate of SWMAs more than doubles.[70]
[71]
Limitations of TEE in the detection of ischemia should be recognized.
When an area of myocardium is clearly in view, segmental contraction can be difficult
to evaluate if the heart rotates or translates markedly during systole or if discoordinated
contraction occurs because of bundle branch block or ventricular pacing. Consequently,
a valid system for assessment of SWMAs must first compensate for global motion of
the heart and then evaluate both regional endocardial motion and myocardial thickening.
Marked worsening of segmental wall motion and wall thickening (in the absence of
similar global changes) is required to make the diagnosis of ischemia ( Table
33-5
); less pronounced changes are not consistently interpreted even by
experts. Interpretation of septal motion is the most problematic because it is often
confounded by discoordinated contraction patterns. However, a simple rule applies:
when the septum is viable and nonischemic, it thickens appreciably during systole,
although its inward motion may begin slightly before or after the inward motion of
the other ventricular segments. Thus, new SWMAs can be detected during bundle branch
block, ventricular pacing, and marked global movements of the heart, but not by assessment
of endocardial motion alone—wall thickening must also be assessed. Because
not all hearts contract normally and not all parts of a normal heart contract to
the same degree, not all SWMAs are indicative of myocardial ischemia. For
TABLE 33-5 -- Classes of segmental wall motion and thickening
*
|
Class of Wall Motion |
Wall Thickening |
Change in Radius |
|
1. Normal or hyperkinesis |
Marked |
>30% ↓ |
|
2. Mild hypokinesis |
Moderate |
10%–30% ↓ |
|
3. Severe hypokinesis |
Minimal |
<10%, >0% ↓ |
|
4. Akinesis |
None |
No change |
|
5. Dyskinesis |
Thinning |
↑ |
|
From Cahalan MK: Intraoperative Transesophageal Echocardiography:
An Interactive Text and Atlas. New York, Churchill Livingstone, 1996. |
*Assessment
of segmental wall motion is subjective, but this grading system helps limit the variability
among readers by defining categories of inward endocardial motion and myocardial
thickening. "Change in radius" refers to the percentage of change during systole
in the radius from the endocardium to the imaginary center of the left ventricle.
Because normal myocardial thickening is 2 to 5 mm and inward endocardial motion
is 5 to 10 mm, thickening is more difficult to assess than endocardial motion. Nevertheless,
thickening is the more reliable guide to myocardial function because it is unaffected
by variables that confound assessment of endocardial motion: translational motion
of the heart, conduction abnormalities, and ventricular pacing. In the absence of
these variables, endocardial motion is usually an adequate indicator of function
of the underlying myocardium.
instance, myocardial infarction, myocardial stunning, and myocarditis can cause SWMAs.
However, a sudden, severe decrease or cessation of segmental contraction is almost
certainly due to myocardial ischemia. One exception to this rule occurs when LV
preload is severely reduced.[72]
Echocardiographic contrast agents can delineate myocardial blood
flow, but to date, they have not proved to be a practical method to differentiate
infarcted from acutely stunned myocardium.[73]
Fortunately, dobutamine may facilitate this differential diagnosis because it can
improve segmental function in stunned, but not infarcted myocardium.[74]
[75]
[76]
For clinical
purposes, when stunned myocardium is suspected after cardiopulmonary bypass, graft
status should be re-evaluated and segmental myocardial function closely monitored
for signs of improvement. A trial of low- to moderate-dose dobutamine may improve
the function of stunned myocardium. If worsening occurs, if graft status is questionable,
or if the patient's hemodynamics is tenuous, additional revascularization should
be considered. Intraoperative stress testing has been evaluated and appears to be
safe in the setting of cardiac surgery.[77]
[78]
