ABSTRACT
Myocardial stunning is a temporary post-ischemic cardiac mechanical dysfunction. As such, it is a heterogeneous entity and different conditions can promote its occurrence. Transient coronary occlusion, increased production of catecholamines and endothelin, and myocardial inflammation are all possible causes of myocardial stunning. Possible underlying mechanisms include an oxyradical hypothesis, calcium overload, decreased responsiveness of myofilaments to calcium, and excitation-contraction uncoupling due to sarcoplasmic reticulum dysfunction. The aim of this review is to summarize the clinical conditions that may be responsible for stunned myocardium.
Subject(s)
Myocardial Contraction , Myocardial Stunning/etiology , Myocardium/metabolism , Myofibrils/metabolism , Sarcoplasmic Reticulum/metabolism , Animals , Calcium/metabolism , Catecholamines/metabolism , Endothelins/metabolism , Excitation Contraction Coupling , Humans , Inflammation Mediators/metabolism , Myocardial Stunning/diagnosis , Myocardial Stunning/metabolism , Myocardial Stunning/physiopathology , Myocardium/pathology , Myofibrils/pathology , Reactive Oxygen Species/metabolism , Risk Factors , Sarcoplasmic Reticulum/pathologyABSTRACT
In recent years, bioresorbable vascular scaffolds (BVS) have been introduced into clinical practice. The main advantage of BVS is that they overcome the problem of the foreign body in the treated artery. BVS, once placed into narrowed coronary vessels, behave like a conventional drug-eluting stent, but a device that disappears over time can preserve the anatomy and physiology of the treated vessel. The progression of stenosis after stenting has been attributed, at least in part, to inflammation around metallic struts, that, however, disappears gradually when using BVS. BVS have proven to be effective and safe as drug-eluting stents; in fact, the rate of adverse cardiovascular events and scaffold thrombosis in patients is low. The aim of this review article is to provide a comprehensive and updated description of the status of the art on BVS, highlighting the current evidence and future perspectives of this technology.
Subject(s)
Absorbable Implants , Blood Vessel Prosthesis , Coronary Artery Disease/surgery , Tissue Scaffolds , Coronary Restenosis , Humans , Percutaneous Coronary Intervention/instrumentation , Percutaneous Coronary Intervention/methodsSubject(s)
Brachial Artery/physiopathology , Colitis, Ulcerative/physiopathology , Crohn Disease/physiopathology , Endothelium, Vascular/physiopathology , Vasodilation , Adult , Body Mass Index , C-Reactive Protein/metabolism , Carotid Intima-Media Thickness , Case-Control Studies , Colitis, Ulcerative/drug therapy , Crohn Disease/drug therapy , Dilatation, Pathologic , Female , Humans , Male , Middle Aged , Severity of Illness Index , Triglycerides/bloodABSTRACT
Hyperpolarization and Cyclic Nucleotide (HCN) -gated channels represent the molecular correlates of the "funny" pacemaker current (I(f)), a current activated by hyperpolarization and considered able to influence the sinus node function in generating cardiac impulses. HCN channels are a family of six transmembrane domain, single pore-loop, hyperpolarization activated, non-selective cation channels. This channel family comprises four members: HCN1-4, but there is a general agreement to consider HCN4 as the main isoform able to control heart rate. This review aims to summarize advanced insights into the structure, function and cellular regulation of HCN channels in order to better understand the role of such channels in regulating heart rate and heart function in normal and pathological conditions. Therefore, we evaluated the possible therapeutic application of the selective HCN channels blockers in heart rate control.
Subject(s)
Cyclic Nucleotide-Gated Cation Channels/metabolism , Heart Rate/physiology , Animals , Arrhythmias, Cardiac/drug therapy , Arrhythmias, Cardiac/genetics , Biological Clocks/drug effects , Biological Clocks/physiology , Cardiovascular Agents/pharmacology , Cardiovascular Agents/therapeutic use , Circadian Rhythm/drug effects , Circadian Rhythm/physiology , Cyclic Nucleotide-Gated Cation Channels/drug effects , Cyclic Nucleotide-Gated Cation Channels/genetics , Disease Models, Animal , Heart Rate/drug effects , Humans , Membrane Transport Modulators/pharmacology , Membrane Transport Modulators/therapeutic use , Mice , Mice, Knockout , Mutation , Sinoatrial Node/drug effects , Sinoatrial Node/physiologyABSTRACT
Polycystic ovary syndrome (PCOS), or Stein-Leventhal syndrome, is a common endocrine disorder defined by two of the three following features: i) oligoovulation or anovulation, ii) clinical and/or biochemical signs of hyperandrogenism, or iii) polycystic ovaries, once the related endocrinological and gynaecological disorders have been excluded. PCOS does not exclusively involve the reproductive apparatus , it has a complex number of systemic relevancy symptoms. It leads to Metabolic Syndrome, with severe consequences on the cardiovascular apparatus. Many clinical studies have underlined the connection between PCOS and the cardiovascular risk profile of such female patients, due to a lipid/glucose altered metabolism, hypertension, systemic inflammatory condition (assessable by markers such as VES, TNF-alfa, citokines and C-reactive protein (hsPCR) levels), and vascular injuries. Considering the early onset of the disease, PCOS could be considered as a real cardiovascular risk factor which affects the quality of life seriously. The current review aimed to point out the main connections between PCOS and cardiovascular risk factors according to the latest findings coming from literature data analysis, and try to depict the great influences that such a common disease can have on the patients' health integrity.
