Role of Inflammation in Cardiac Remodeling After Acute Myocardial Infarction

Abstract

Atherosclerosis is defined as an inflammatory disease. Low-grade inflammation is present in all phases of the cardiovascular continuum, since the establishment of cardiovascular risk factors and ischemic heart disease until cardiovascular events, such as myocardial infarction, heart failure and death. Not all inflammatory pathways are linked to cardiovascular outcomes, and thus, not all anti-inflammatory approaches decrease cardiovascular events. The most common cause of ventricular remodeling and heart failure is ischemic heart disease. Biomarkers such as high-sensitivity C-reactive protein can identify individuals at risk of major cardiovascular complications, but this biomarker has no causal effect on cardiovascular disease. On the other hand, interleukin 6 appears to be causally associated with cardiovascular disease. CANTOS was the first proof of concept study showing that anti-inflammatory therapy reduces major cardiovascular outcomes. Based on many anti-inflammatory trials, only therapies acting on the NLRP3 inflammasome, or interleukin 1beta, showed benefits on cardiovascular disease. Ventricular remodeling, particularly after myocardial infarction seems also influenced by the intensity of inflammatory responses, suggesting that anti-inflammatory therapies may reduce the residual cardiovascular risk. Inflammasome (NLRP3) activation, subtypes of lymphocytes, interleukin 6, and some inflammatory biomarkers, are associated with larger infarct size and impaired ventricular function after myocardial infarction. Cardiovascular risk factors commonly present in patients with myocardial infarction, and advanced age are associated with higher inflammatory activity.

Ribosome biogenesis in disease: new players and therapeutic targets

“…Atherosclerosis is also a chronic inflammatory disease, as an inflammatory response accompanies its onset. 180 Macrophages are one of the cells responsible for atherosclerosis; they form foam cells by phagocytosing lipid droplets and accelerating the progression of atherosclerosis. 181 , 182 Basu et al 183 reported that macrophage-specific deletion of RPL13 increases the susceptibility of ApoE knockout mice to high-fat diet-induced atherosclerosis.…”

Effect of levosimendan on ventricular remodelling in patients with left ventricular systolic dysfunction: a meta‐analysis

“…Previous studies have shown a causal relationship between IL‐6 and cardiovascular disease 119 . Additionally, IL‐6 has been associated with ventricular dysfunction 120 . The meta‐analysis revealed that levosimendan has the potential to reduce IL‐6 levels.…”

The Protective Role of TREM2 in the Heterogenous Population of Macrophages during Post-Myocardial Infarction Inflammation

“…LV remodeling is a process in which the heart adapts to mechanical, neurohormonal, and inherited changes by regulating the size, shape, and function of the ventricle. It is commonly observed in infarcted hearts [ 4 ]. Adverse LV remodeling following MI involves various processes, including the transformation of LV geometry, myocardial fibrosis, a shift in energy metabolism, neurohormonal activation, and inflammation.…”

“…After myocardial infarction, ventricular remodeling or recurrent ischemic events are both reported to be associated with inflammation [ 4 ]. In particular, during the early phase of cardiac injury, inflammation plays a crucial role in determining the extent of myocardial injury, including cardiomyocyte necrosis and the degradation of extracellular matrix components.…”