科研之友
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摘要
Myocardial infarcts are wounds inflicted by ischemic injury of the heart muscle. As in any other wound, a sufficient healing process after acute injury is prerequisite to the recovery and integrity of the organ's function. If infarct healing derails, fibrosis may be insufficient or too widespread, either endangering the left ventricle's geometry or increasing its stiffness, especially if fibrosis occurs in the remote myocardium. The imminent threat of insufficient healing is a weak scar that may rupture, often a deadly complication. More frequently, the weak infarct scar acutely maintains the ventricle's integrity but expands over time, thus causing chronic post-myocardial infarction (MI) remodeling and heart failure. Macrophages are centrally involved in wound healing, including healing of the heart (1). These cells are also part of the causal pathology leading to ischemia of the heart because macrophages destabilize atherosclerotic plaques, rendering them prone to rupture (1).
- 出版日期2013-11-12
