Myocardial infarct expansion: recognition, significance and pathology.
Infarct expansion can be defined pathologically as a distortion of ventricular topography produced by thinning and disproportionate dilation of the infarct segment. Large transmural infarcts tend to be associated with greater propensity for infarct expansion. Two-dimensional echocardiography has made it feasible to detect these acute alterations in cardiac topography by serial examination of patients with acute myocardial infarction. A practical approach to the echocardiographic quantification of expansion involves analysis of end-diastolic cross-sectional echo views at the papillary muscle level, which can be used as fixed internal landmarks to divide the left ventricle into 2 segments, anterior and posterior. An off-line computer system can be used to track relative lengths of these segments as well as their thicknesses over time. In the initial clinical study, one third of patients with acute anterior transmural infarcts showed an average 50% increase in the infarct segment length beginning within the first 3 days of infarction, characterized by disproportionate progressive dilation and transmural thinning of this zone. These patients demonstrated a significantly higher mortality than those without expansion. Later studies demonstrated not only continuing dilation of the infarcted anterior wall, but also progressive dilation of the noninfarcted posterior wall, underscoring the importance of continuing long-term noninvasive follow-up. Not only is expansion associated with a poor clinical outcome; it has also been shown experimentally and clinically to be modifiable or even preventable by various therapeutic maneuvers, which may well improve survival. Because of the limitations of the echocardiographic window, it is often possible to obtain only a single cross-sectional view of high quality, and even then technical quality may not be sufficiently high to enable detailed quantitative analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
Weiss
J L
JL
Johns Hopkins University School of Medicine, Division of Cardiology, Baltimore, Maryland.
Marino
P N
PN
Shapiro
E P
EP
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology*; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology*; D009206:Myocardium / Q000473:pathology