New insights into the open artery hypothesis.

Factors Affecting Left Ventricular Remodeling Early coronary artery reperfusion is clearly the most important therapy for acute ST segment elevation myocardial infarcts. Early reperfusion reduces myocardial infarct size and in so doing helps to prevent or minimize deleterious consequences of a large myocardial infarction, including infarct expansion (thinning and dilation of the infarct), subsequent eccentric hypertrophy and dilation of the noninfarcted ventricular muscle, and global dilation of the left ventricle.1–4 These processes encompass the phenomenon of ventricular remodeling. One of the major determinants of death at 1 year after a myocardial infarction is the degree of dilation of the left ventricle (LV).5 However, suppose early reperfusion is not available. A number of manipulations and pharmacological therapies can be administered beyond the time frame of reducing myocardial infarct size and still reduce the extent of infarct expansion and LV remodeling (Table 1). Angiotensin converting enzyme inhibitors6 and angiotensin receptor blockers7 have been shown to reduce LV dilation and remodeling and in some studies reduce major cardiovascular events. Cell therapy and even some noncellular therapies (collagen, alginate) may thicken the infarct scar and prevent ventricular wall dyskinesis.8–10 Aneurysmectomy and certain suturing techniques have been attempted to prevent infarct expansion and remodeling.11 Late reperfusion—too late to reduce myocardial infarct size, but early enough to favorably affect infarct healing1—also appears to limit infarct expansion and limit LV remodeling, and is the subject of the accompanying article.12 Certain features are associated with worse LV remodeling (Table 2), including a large myocardial infarct, lack of any reperfusion,1 a large zone of no reflow,13 and certain antiinflammatory agents14 (such as steroids and a host of nonsteroidal antiinflammatory agents) introduced early enough to inhibit the healing phase of myocardial infarction.