Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.

Abstract

An acute myocardial infarction, particularly one that is large and transmural, can produce alterations in the topography of both the infarcted and noninfarcted regions of the ventricle. This remodeling can importantly affect the function of the ventricle and the prognosis for survival. In the early period, infarct expansion has been recognized by echocardiography as a lengthening of the noncontractile region. The noninfarcted region also undergoes an important lengthening that is consistent with a secondary volume-overload hypertrophy and that can be progressive. The extent of ventricular enlargement after infarction is related to the magnitude of the initial damage to the myocardium and, although an increase in cavity size tends to restore stroke volume despite a persistently depressed ejection fraction, ventricular dilation has been associated with a reduction in survival. The process of ventricular enlargement can be influenced by three interdependent factors, that is, infarct size, infarct healing, and ventricular wall stresses. A most effective way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in attenuating ventricular enlargement. The process of scarification can be interfered with during the acute infarct period by the administration of glucocorticosteroids and nonsteroidal antiinflammatory agents, which result in thinner infarcts and greater degrees of infarct expansion. Modification of distending or deforming forces can importantly influence ventricular enlargement. Even short-term augmentations in afterload have deleterious long-term effects on ventricular topography. Conversely, judicious use of nitroglycerin seems to be associated with an attenuation of infarct expansion and long-term improvement in clinical outcome. Long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions on the left ventricle and reduce progressive ventricular enlargement as demonstrated in both experimental and clinical studies. With the former therapy, this attenuation of ventricular enlargement was associated with a prolongation in survival. The long-term clinical consequences of long-term angiotensin converting enzyme inhibitor therapy after myocardial infarction is currently being evaluated. Although studies directed at attenuating left ventricular remodeling after infarction are in the early stages, it does seem that this will be an important area in which future research might improve long-term outcome after infarction. (Circulation 1990;81:1161-1172 Tennant and Wiggers' classic description of regional wall motion changes after acute coronary artery ligation describes "local enfeeblement of contraction" as well as "systolic expansion."1 Thes...

The Structure-function remodeling in rabbit hearts of myocardial infarction

“…1995; Rungwerth et al. 2004), which presented high similarity to the large animal models of MI (Pfeffer and Braunwald 1990; Moainie et al. 2002).…”

In vivo chronic myocardial infarction characterization by spin locked cardiovascular magnetic resonance

“…The water 1  H longitudinal relaxation rate, 1/T1,at 3 T is affected by both the chemical and pharmacologic properties of low molecular weight paramagnetic contrast agents. Paramagnetic relaxation enhancement is believed to have two contributions: [1] relaxation enhancement of a water molecule directly coordinated to the gadolinium ion, which is dominated by the rotational correlation time of the Gd (III) complex and [2] relaxation enhancement of water 1  H through dipolar coupling and translational diffusion nearthe gadolinium complex [14,15]. Gd-chelates also function as drugsand distribute nonspecifically throughout the plasma and interstitium.…”

“…The size, location and extent of a myocardial infarction (MI) are important criteria for the evaluation of post-infarction left ventricular (LV) remodeling [1-3]. To detect MI, it is desirable to inject Gd-DTPA as an exogenous, T1 relaxation time shortening contrast agent.…”

Relation of circulating interleukin‐6 to left ventricular remodeling in patients with reperfused anterior myocardial infarction

“…It was interesting to note that multivariate analyses demonstrated that circulating IL-6 at the acute phase was a powerful inde- Healing after MI involves inflammatory cell infiltrations followed by fibroblast proliferation, collagen deposition, and remodeling in the infarct myocardium. 2 In addition, reperfusion of the ischemic myocardium has been shown to trigger the release of cytokines and other mediators of inflammation. 6,7 Previous clinical studies have indicated the presence of activated circulating leukocytes and inflammatory cytokines, as well as acute-phase reactants such as CRP in patients with AMI.…”