Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion.

Abstract

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p < .0 1), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p < .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p < .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p < .05) and significant increases in angiographic cardiac index (p < .01) and LVESV index (p < .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akineticdyskinetic segments and volume-overload hypertrophy of noninfarcted segments. The magnitude of the remodeling process is directly proportional to infarct size as assessed by the extent of wall motion abnormality present during the acute phase of infarction. Moreover, the remodeling changes that occur are associated with hemodynamic improvement, including lower left ventricular filling pressures and increased cardiac output, but these hemodynamic changes appear to occur at the expense of a significant increase in left ventricular chamber volumes.

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

“…This global enlargement has been observed in both clinical and experimental studies of infarction27-31 and has been hypothesized to represent a compensatory remodeling of the left ventricle in response to alterations in systolic function. 28 Clinically silent infarct extension was observed in 14% of this population with acute Q wave myocardial infarction. This is similar to previous reports in which the prevalence of silent extension of infarction ranged from 13% to 25%.32,33 The significant increase in ESA in association with infarct extension has not been previously described.…”

Predictive value of the serum level of N‐terminal pro‐brain natriuretic peptide and high‐sensitivity C‐reactive protein in left ventricular remodeling after acute myocardial infarction

“…Long-and short-axis views were acquired from the left edge of the sternum between the third and fourth ribs, and four-and twochamber views were acquired from the apical region. A 20% increase in LVEDV from the basal level was defined as LV remodeling (8,9). Serum NT-proBNP was measured by electrochemiluminescence immunoassay with 2100 (Roche, Basel, Switzerland).…”

Cellular basis of chronic ventricular remodeling after myocardial infarction in rats.

“…12 The Laplace load on the remaining myocytes will be highly dependent on the anatomic rearrangements that govern the relation between wall thickness, number of cells in the wall, chamber radius, and resultant myocardial function. [13][14][15][16] The inability of the heart to reestablish normal wall stress may be the critical factor in the evolution of ischemic cardiomyopathy after infarction. Therefore, the present study was undertaken to characterize the structural and functional properties of the infarcted heart at the completion of the healing process to identify how the remodeling of the ventricle interacts with cardiac hemodynamic parameters in the definition of the loading state of the myocardium after ischemic necrosis.…”