Post-Infarction Inflammation and Left Ventricular Remodeling

Abstract

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp non-specific response to tissue damage. 1 However, an investigation into the relation between the peak body temperature during the first week and in-hospital complications since the event of MI showed that the incidence of complications of pump failure (grade of class 2 or greater according to Killip's classification or subset II or greater according to Forrester's classification) and ventricular aneurysm, as well as the incidence of cardiovascular events such as cardiac death, pump failure, fatal ventricular arrhythmias and cardiac rupture, increased in proportion to the body temperature increase. 2 Although the peak creatine kinase (CK) level, an indicator of infarct size, was similar, LV end-diastolic and LV end-systolic volumes measured by left ventriculography before discharge had increased and the LV ejection fraction decreased in proportion to the peak body temperature, demonstrating an association between body temperature increase after MI and LV remodeling. 2 Post-MI Inflammation and Infarct ExpansionDuring the acute phase of MI, resident macrophages in the myocardial tissue are activated following neutrophil infiltration into the infarcted region. CD11b/18 on the surface of neutroeft ventricular (LV) remodeling after myocardial infarction (MI) is the process of infarct expansion followed by non-infarct hypertrophy and progressive LV dilation, and is associated with adverse clinical outcomes. Defective infarct healing, as well as infarct size and wall stress, is a major determinant of infarct expansion. A well-orchestrated inflammatory response after MI leads to an appropriate infarct healing process and formation of a scar with tensile strength, preventing infarct expansion. Despite the importance of the inflammatory response and healing process in post-MI LV remodeling, the mechanisms that initiate and control these processes have not been fully elucidated. Numerous clinical and experimental studies have focused on the role of inflammation and its regulatory mechanism as a novel therapeutic target for post-infarction LV remodeling. Increase in Body Temperature and Post-MI ComplicationsThe 4 classical signs of inflammation are dolor, tumor, rubor and calor. It has also been recognized for a long time that body temperature increases after MI, reflecting the development of inflammation after tissue necrosis, but it was believed to be a After myocardial infarction (MI), inflammatory cells such as neutrophils, followed by monocytes and macrophages, infiltrate and phagocytose the necrotic tissues, as well as secreting a variety of inflammatory cytokines. The vulnerable myocardium, which consists of necrotic tissue and inflammatory cells, is susceptible to wall stress, resulting in infarct expansion. Subacute cardiac rupture is an extreme form of infarct expansion, whereas ventricular aneurysm is its chronic form and a trigger for subsequent left ventricular (LV) remodeling. Although post-infarction inflammation...

Retracted: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction

“…Moreover, left ventricular remodelling (LVR) in ischaemic cardiomyopathy has been determine as the main cause of heart failure and is an established prognostic factor for cardiovascular complications 5. LVR after MI is the process by which the initial infarction leads to cardiac expansion followed by non‐infarct hypertrophy and progressive left ventricular dilation, and is associated with adverse clinical outcome 6. A previous study demonstrates that the acute inflammatory response in the early phase of MI could be a potential target for treating patients with MI 7…”

Increase in cholinergic modulation with pyridostigmine induces anti-inflammatory cell recruitment soon after acute myocardial infarction in rats

“…(10,41) A deregulated immune reaction can lead to changes in ventricular shape, size, and function and can, thus, induce the development of heart failure syndrome. (4,15) Therefore, it would be desirable to develop new therapeutic strategies to modulate immune response and improve healing after MI (1).…”

Extracorporeal Low-Energy Shock-Wave Therapy Exerts Anti-Inflammatory Effects in a Rat Model of Acute Myocardial Infarction

“…14 Infiltration of inflammatory cells (eg, macrophages) is critically important in wound healing after AMI, while excessive inflammatory responses deteriorates LV remodeling in the chronic phase. [15][16][17] In the present study, we thus examined whether SW therapy exerts beneficial anti-inflammatory effects in a rat model of AMI.…”