Myocardial Infarction and Inflammation

Abstract

A therosclerosis as a persistent arterial disease is characterized by an imbalanced lipid metabolism and maladaptive immune response, resulting in subendothelial lipoprotein retention and endothelial activation with continuous migration of leukocytes and smooth muscle cells to the inflamed intima. 1,2 Over decades, this leads to the formation of stable atheromas that induce chronic tissue ischemia or of vulnerable plaques that cause acute occlusive atherothrombotic complications, such as myocardial infarction and stroke. As such, atherosclerosis and its consequences remain the leading causes of mortality and morbidity in Western countries. Acute myocardial infarction (AMI) often occurs as the first and fatal manifestation of atherosclerotic coronary artery disease. In general, AMI represents a typical sterile inflammation with release of inflammatory cytokines, platelet activation, leukocytosis, and hyperglycemia. The pathophysiological and laboratory parameters of AMI are monitored at admission after confirming the diagnosis only; however, this hampers any consideration and distinction of the very critical interval between initiation of myocardial ischemia, with the first symptoms of AMI often being imprecise or rather nontypical, and hospitalization. Numerous animal studies have provided detailed experimental data on AMI pathophysiology starting with the time of induction of ischemia by coronary artery ligation, whereas comparable data in men remain largely elusive and obscure. Article, see p 867In this issue of the journal, Liebetrau et al provide intriguing evidence in humans by taking advantage of ethanol-based transcoronary ablation of septal hypertrophy (TASH) in 21 patients with hypertrophic obstructive cardiomyopathy as a clinical model to induce AMI. 3 This model allows for precise definition of the exact time point of myocardial ischemia. By using TASH, the authors intended to screen early release kinetics of some soluble inflammatory biomarkers and leukocyte subsets within 24 hours of myocardial injury. They found a sustained elevation in interleukin (IL)-6, C-reactive protein, neutrophils and classical CD14 ++ CD16− monocytes, whereas sCD40L levels were decreased (Figure).In fact, the same group has recently published studies with identical design and on the same patient collective.4-7 Their results revealed the release kinetics of additional early ischemic biomarkers in the setting of TASH-induced AMI, such as cardiac troponin-T, NT-proBNP, s-Flt1, microRNAs, ischemia-modified albumin, and heart-type fatty acid-binding protein.4-7 A common conclusion implied that all these biomarkers may harbor a certain diagnostic value in the setting of AMI. Yet, the questions remained unanswered which of the biomarkers has a major effect and whether a single biomarker or rather the combination of >1 biomarker (eg, in a panel) are useful for routine measurement during the onset of AMI? This clearly mandates the need for more conclusive research with solid prospective data on outcome and correlation to cardiac fun...

The utility of inflammation and platelet biomarkers in patients with acute coronary syndromes

“…Atherosclerosis is a chronic inflammatory arterial disease developing over decades, characterized by an impaired lipid metabolism and imbalanced immune response, which lead to the subendothelial lipoprotein retention and activation of endothelial cells with continuous migration of leukocytes and smooth muscle cells to the inflamed intima. Acute occlusive atherothrombotic complications, such as myocardial infarctions (MI) and strokes, result from the formation of vulnerable atherosclerotic plaque (Hristov and Weber, 2015).…”

Causal effects for neurodegenerative diseases on the risk of myocardial infarction: a two-sample Mendelian randomization study

“…Besides, immunomodulatory treatments such as interferon β have been found to be associated with the risk of CVD in MS patients [69]. In genetic terms, the causality found may be due to alterations in Human Leukocyte Antigen (HLA), CD40, and PINK1/Parkin genes in patients with MS and PD, which modulate the body's immune-inflammatory response and mitochondrial autophagy, thereby influencing the occurrence of myocardial infarction [70][71][72][73]. It's essential to acknowledge potential biases in these observational studies, such as confounding variables and subjective viewpoints.…”

Hydrogen Sulfide Alleviates Acute Myocardial Ischemia Injury by Modulating Autophagy and Inflammation Response under Oxidative Stress

“…Enhanced inflammation response may lead to increased secretion of inflammatory cytokines such as TNF- α and IL-6. It was suggested that high levels of TNF- α or IL-6 may promote cardiomyocyte apoptosis [ 50 , 51 ]. Finally, excessive oxidative stress resulted in aggravated cardiac injury.…”