Inflammation and C-reactive protein in atrial fibrillation: cause or effect?

Atrial fibrillation is associated with substantial morbidity and mortality rates. The incompletely understood pathogenesis of this cardiac dysrhythmia makes it difficult to improve approaches to primary and secondary prevention. Evidence has accumulated in regard to a relationship between inflammation and atrial fibrillation. Investigators have correlated the dysrhythmia with myocarditis, pericardiotomy, and C-reactive protein levels, suggesting that inflammation causes atrial fibrillation or participates in its onset and continuation. Conversely, other investigators suggest that atrial fibrillation induces an inflammatory response. In this review, we summarize and critically discuss the nature and clinical role of inflammation and C-reactive protein in atrial fibrillation.

Adaptive immunity, inflammation, and cardiovascular complications in type 1 and type 2 diabetes mellitus.

Diabetes mellitus (DM) is a pandemics that affects more than 170 million people worldwide, associated with increased mortality and morbidity due to coronary artery disease (CAD). In type 1 (T1) DM, the main pathogenic mechanism seems to be the destruction of pancreatic ß -cells mediated by autoreactive T-cells resulting in chronic insulitis, while in type 2 (T2) DM primary insulin resistance, rather than defective insulin production due to ß -cell destruction, seems to be the triggering alteration. In our study, we investigated the role of systemic inflammation and T-cell subsets in T1- and T2DM and the possible mechanisms underlying the increased cardiovascular risk associated with these diseases.

Increasing specificity of high-sensitivity troponin: new approaches and perspectives in the diagnosis of acute coronary syndromes.

In the past years, new generations of assays to detect cardiac troponin (cTn), called sensitive or high sensitivity troponin (hs-Tn), have been introduced. Progressive improvement in the analytical sensitivity of cTn assays has led to a more rapid diagnosis of acute myocardial infarction (AMI) and improved risk stratification in patients with non ST-elevation acute coronary syndromes (NSTE-ACS) but, at the same time, has introduced the problem of a lower diagnostic specificity. As a matter of fact, hs-Tn assays are able to detect very small increases in the biomarker concentration and therefore result "positive" in a wide range of non-ischemic clinical conditions, acute and chronic, cardiac and extra-cardiac. The reduced specificity of hs-Tn versus the previous generation cTn assays may, therefore, lead to an increased number of inappropriate hospitalizations, i.e. patients with high cTn due to no-ACS conditions, and requires a more careful evaluation, not only on the clinical side, but also on the information that hs-Tn assessment may provide. Several approaches to increase this specificity have been used, but the most promising appear to be the "delta approach", which tries to quantify the relative or absolute change in cTn concentration, and the "age approach", which highlights the need for a different cutoff with a better diagnostic efficiency in the elderly population, often affected by other conditions, different from ACS, that can cause an increased level of cTn.

Polymorphonuclear neutrophils and instability of the atherosclerotic plaque: a causative role?

OBJECTIVE: The aim of this review is to examine the role of polymorphonuclear neutrophils (PMNs) in the evolution of atherosclerosis. INTRODUCTION: While the role of PMNs in the evolution of atherosclerosic process has failed until recently to attract much attention, a body of research carried out over the last decade has disclosed the unexpectedly complex behavior of these cells, unraveling an unexpected key role for PMNs in the onset and progression of atheroma. METHODS: A PubMed database search was performed for studies providing evidences on the role of PMNs in the development and progression of atherosclerotic lesion. RESULTS AND CONCLUSIONS: Activated PMNs were shown to produce and release reactive oxygen species, inflammatory leukotrienes and proteolytic lysosomal enzymes, directly inducing vascular damage. Activated PMNs also secrete myeloperoxidase, involved in lipoprotein oxidation. PMNs have a finite lifespan and typically die through apoptosis, which thus represents a counter-regulatory mechanism limiting the toxic potential of these short-lived, terminally differentiated cells. Dysregulation of this process probably contributes to the pathogenesis and progression of several inflammatory diseases. Moreover, high circulating levels of PMN-platelet aggregates have been reported in patients with clinical atherosclerosis, and recent studies suggest that these aggregates may play a role in vascular response to injury. It has been suggested that this heterotypic interaction between platelets and leukocytes might represent a link between hemostasis/thrombosis and the inflammatory response.

Potential therapeutic role of microRNAs in ischemic heart disease.

Cardiovascular disease (CVD) is the most important cause of death and illness in the western world. Atherosclerosis constitutes the single most important contributor to CVD. miRNAs are small ribonucleic acids (RNAs) that negatively regulate gene expression on the post-transcriptional level by inhibiting mRNA translation or promoting mRNA degradation. Several studies demonstrated that miRNAs dysregulation have a key role in the disease process and, focusing on atherosclerotic disease, in every step of plaque formation and destabilization. These data suggest a possible therapeutic application of miRNA modulation, in particular dysregulated miRNAs can be modulated in disease process antagonizing miRNAs up-regulated and increasing miRNAs down-regulated. In this review we summarize the miRNA therapeutic techniques (antimiR, mimics, sponges, masking, and erasers) underlining their therapeutic advantages and evaluating their risks and challenges. In particular, the use of miRNA modulators as a therapeutic approach opens a novel and fascinating area of intervention in the therapy of ischemic heart disease.

A case of unusual acute coronary syndrome.

Pheochromocytoma is a rare tumor that usually develops ahead of the neuroectodermal chromaffin cells of the adrenal medulla, but it may arise anywhere within plexus of sympathetic adrenergic nerves. Headache, palpitations, tremor, excessive sweating, abdominal pain, and hypertensive paroxysm are the common clinical presentations of the tumor, but it has also been reported several cardiac symptoms.

[Myeloperoxidase as possible diagnostic and prognostic marker of acute coronary syndrome]. / Il ruolo della mieloperossidasi come marker diagnostico e prognostico nella cardiopatia ischemica.

Myeloperoxidase (MPO) is an enzyme stored in azurophilic granules of polymorphonuclear neutrophils and macrophages and released into extracellular fluid during inflammatory processes. Several studies have shown its involvement into oxidative stress and inflammation. Recently, MPO has been considered its role as a possible marker of plaque instability and a useful tool for the prognostic evaluation of patients with coronary artery disease. Aim of this review is to provide an overview of patophysiological, analytical and clinical characteristics of MPO and to summarize the evidence about its usefulness as diagnostic and prognostic marker in the setting of acute coronary syndrome.