Listing 1 - 2 of 2 |
Sort by
|
Choose an application
In spite of the large volume of associated research, the pathophysiological mechanisms involved in atrial fibrillation (AF) onset and recurrence remain uncertain. This may explain why the performances of thromboembolic and bleeding prediction scores in AF patients are limited. In the past few years, the concept of atrial cardiopathy has emerged as a promising lead to connect AF to stroke, heart failure, and inflammatory processes: indeed, all of the mechanisms associated with atrial remodeling and the development of atrial cardiopathy are also likely to promote the development of AF. This recent concept of atrial cardiopathy suggests that the real trigger of stroke may be an abnormal atrial substrate rather than atrial rhythm itself. In this setting, AF could be seen as a symptom of atrial cardiopathy rather than a risk factor of stroke. In the absence of validated clinical markers of atrial cardiopathy, the search for the mechanism of AF remains the cornerstone of cardioembolic stroke prevention for now.The aim of this Special Issue is to gather basic research as well as pathophysiological and epidemiological papers focused on the relationship between atrial substrates and atrial fibrillation onset, recurrence, and outcomes.
postoperative atrial fibrillation --- biomarkers --- coronary artery bypass grafting --- miRNA --- circRNA --- mtDNA --- SNPs --- atrial fibrillation --- acute myocardial infarction --- heart rate variability --- autonomic nervous system --- bleeding risk --- age --- left atrial appendage closure --- coronary artery disease --- prognosis --- anticoagulation --- antiplatelet therapy --- hypertension --- elderly --- prevention --- ganglionated plexi --- ablation --- dementia --- early-onset --- n/a --- ischemic stroke --- risk factor --- new oral anticoagulants --- mitochondria --- cardiac remodeling --- pharmacotherapy --- electroporation --- pulsed field ablation --- cardiac --- heart --- arrhythmia --- NOAC --- VKA --- statin --- outcome --- mortality --- paroxysmal atrial fibrillation --- catheter ablation --- epicardial adipose tissue --- persistent atrial fibrillation --- posterior wall --- hybrid ablation --- convergent ablation --- atrial tachycardia --- mechanism --- spatiotemporal dispersion --- left atrial appendage occlusion --- BNP --- atrial remodeling --- atrial cardiopathy --- cardiac ablation --- irreversible electroporation
Choose an application
The natriuretic peptides (NPs) family includes a class of hormones and their receptors needed for the physiological control of cardiovascular functions. The discovery of NPs provided a fundamental contribution into our understanding of the physiological regulation of blood pressure, and of heart and kidney functions. NPs have also been implicated in the pathogenesis of several cardiovascular diseases (CVDs), including hypertension, atherosclerosis, heart failure, and stroke. A fine comprehension of the molecular mechanisms dependent from NPs and underlying the promotion of cardiovascular damage has contributed to improve our understanding of the molecular basis of all major CVDs. Finally, the opportunity to target NPs in order to develop new therapeutic tools for a better treatment of CVDs has been developed over the years. The current Special Issue of the Journal covers all major aspects of the molecular implications of NPs in physiology and pathology of the cardiovascular system, including NP-based therapeutic approaches.
postmortem biochemistry --- medulla --- animal models --- remodeling --- BNP --- PCSK9 --- guanylyl cyclase/natriuretic peptide receptor-A --- cardiorenal syndrome --- forensic medicine --- preserved ejection fraction --- kidney --- renin-angiotensin-aldosterone system --- atrial fibrillation --- vasopressor --- congestive heart failure --- atrial natriuretic peptide --- gene-knockout --- obesity --- heart failure --- angiogenesis --- adipose tissue --- vascular --- LDL receptor --- metabolic syndrome --- linkage analysis --- cardiometabolic disease --- cardiomyocyte --- cardiac dysfunction --- cardiac hypertrophy --- insulin --- lipid metabolism --- cGMP --- Idiopathic Pulmonary Arterial Hypertension (IPAH) --- Natriuretic Peptide Clearance Receptor (NPR-C) signaling --- gene-duplication --- renin–angiotensin system --- natriuretic peptides --- angiotensin receptor–neprilysin inhibitor --- cardiac remodelling --- ARNi --- NT-proBNP --- inflammation --- pulmonary arterial hypertension --- vascular homeostasis --- endothelial cell --- Atrial Natriuretic peptide --- natriuretic peptide --- vasodilator --- stroke --- genetic variants --- arterial hypertension --- fibroblast --- MANP --- hypertension --- guanylyl cyclase receptor A
Listing 1 - 2 of 2 |
Sort by
|