(Circulation. 1998;98:625-627.)
© 1998 American Heart Association, Inc.
Assessing the Myocardium After Attempted Reperfusion
Should We Bother?
Sanjiv Kaul, MD
From the Cardiovascular Division, University of Virginia School of
Medicine, Charlottesville, Virginia.
Correspondence to Sanjiv Kaul, MD, Cardiovascular Division, Box 158, Medical Center, University of Virginia, Charlottesville, VA 22908. E-mail sk@virginia.edu
Key Words: Editorials • myocardium • echocardiography • microcirculation • myocardial infarction
In
patients with AMI who have undergone attempted reperfusion, two
questions need to be answered. The first, and the most obvious, is
whether the myocardium has been successfully reperfused.
The second, and perhaps equally important, is how much of the
myocardium has been salvaged, and how much can still
potentially be salvaged? To answer these questions, one must have the
tools to accurately assess myocardial perfusion and infarct size. The
ultimate indicator of tissue perfusion is capillary flow, whereas that
of myocardial infarction is myocyte necrosis. The farther we deviate
from a direct assessment of these indicators, the more imprecise we
become. The Figure
depicts the findings generally used
in the clinical setting to determine whether reperfusion has actually
occurred and the extent of myocardial salvage achieved.
View larger version (21K):
[in this window]
[in a new window]
|
Figure 1. Figure depicts the findings generally used in the clinical
setting to determine whether reperfusion has actually occurred and the
extent of myocardial salvage achieved.
|
|
Although the presence of a wall motion abnormality is valuable for
the diagnosis of prior infarction and resting or inducible
ischemia,1 it is of limited value in
patients with AMI who have recently undergone reperfusion therapy. In
these patients, a wall motion abnormality is likely to be present
whether or not reperfusion has been successful. Regional function will
be normal only if the period of ischemia was very short
(minutes), which is uncommon in the clinical setting. The degree of
wall thickening also does not reflect the transmural extent of
myocardial necrosis because dysfunction may be present . . . [Full Text of this Article]
This article has been cited by other articles:
|
|
|
|
 
T. Ibrahim, S. G. Nekolla, M. Hornke, H. P. Bulow, J. Dirschinger, A. Schomig, and M. Schwaiger
Quantitative measurement of infarct size by contrast-enhanced magnetic resonance imaging early after acute myocardial infarction: Comparison with single-photon emission tomography using Tc99m-sestamibi
J. Am. Coll. Cardiol.,
February 15, 2005;
45(4):
544 - 552.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y Nohtomi, M Takeuchi, K Nagasawa, K Arimura, K Miyata, K Kuwata, T Yamawaki, S Kondo, A Yamada, and S Okamatsu
Persistence of systolic coronary flow reversal predicts irreversible dysfunction after reperfused anterior myocardial infarction
Heart,
April 1, 2003;
89(4):
382 - 388.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Panteghini, C. Cuccia, G. Bonetti, R. Giubbini, F. Pagani, and E. Bonini
Single-Point Cardiac Troponin T at Coronary Care Unit Discharge after Myocardial Infarction Correlates with Infarct Size and Ejection Fraction
Clin. Chem.,
September 1, 2002;
48(9):
1432 - 1436.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Mahrholdt, A. Wagner, R.M. Judd, and U. Sechtem
Assessment of myocardial viability by cardiovascular magnetic resonance imaging
Eur. Heart J.,
April 2, 2002;
23(8):
602 - 619.
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. M. Kramer, W. J. Rogers Jr., S. Mankad, T. M. Theobald, D. L. Pakstis, and Y.-L. Hu
Contractile reserve and contrast uptake pattern by magnetic resonance imaging and functional recovery after reperfused myocardial infarction
J. Am. Coll. Cardiol.,
November 15, 2000;
36(6):
1835 - 1840.
[Abstract]
[Full Text]
[PDF]
|
|
|
