scholarly journals Pathophysiological role of major adipokines in Atrial Fibrillation

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Saira Rafaqat ◽  
Sana Rafaqat ◽  
Simon Rafaqat
Keyword(s):  
Atrial Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Review Article ◽  
Atrial Remodeling ◽  
Main Body ◽  
Tnf Α ◽  
Pathophysiological Role

Abstract Background The adipokines, secreted from adipose tissue or body fats, are also called adipocytokines which are cytokines, cell signaling proteins or cell–cell communication. However, AF is a common cardiac arrhythmia in which the heart beats so fast by abnormal beating and is a serious public health disease associated with increased heart failure, systemic thromboembolism, and death. Adipokines are cardiovascular disease (CVD) mediators or biomarkers that affect the heart as well as blood vessels, by increasing the cardiac contractility and action potential duration, which result in the extent of left ventricular and atrial remodeling. Main body Google Scholar, PubMed, and science direct were used to review the literature. Many keywords were used for searching the literature such as Adipokines, Leptin, Apelin, Adiponectin, Omentin-1, Chemerin, CTRP3, TNF-α, IL-6, IL-10, and AF. According to the literature, much more data are available for numerous adipokines, but this review article only has taken few major adipokines which played their major role in Atrial Fibrillation. The review article did not limit the time frame. Conclusion In conclusion, adipokines play a significant role in the development and progress of atrial fibrillation. Also, there are major adipokines such as adiponectin, apelin, C1q/TNF-Related Protein 3 (CTRP3), Chemerin, Omentin-1, interleukin-6, Leptin, TNF-α, resistin, and interleukin-10, which played their pathophysiological role in atrial fibrillation by causing cardiac hypertrophy, increasing the cardiac contractility and action potential duration, atrial fibrosis, electrical and structural remodeling of atrial tissue.

Biomarkers of Atrial Fibrillation in Hypertension

2019 ◽  
Vol 26 (5) ◽  
pp. 888-897 ◽  
Author(s):  
Costas Tsioufis ◽  
Dimitris Konstantinidis ◽  
Ilias Nikolakopoulos ◽  
Evi Vemmou ◽  
Theodoros Kalos ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Left Ventricular ◽  
P Wave ◽  
Diagnostic Tools ◽  
Atrial Remodeling ◽  
Hypertensive Patients ◽  
Risk Patients ◽  
Underlying Mechanisms ◽  
Prompt Diagnosis ◽  
The Ideal

Background: Atrial fibrillation (AF) is the most frequently encountered cardiac arrhythmia globally and substantially increases the risk for thromboembolic disease. Albeit, 20% of all cases of AF remain undiagnosed. On the other hand, hypertension amplifies the risk for both AF occurrences through hemodynamic and non-hemodynamic mechanisms and cerebrovascular ischemia. Under this prism, prompt diagnosis of undetected AF in hypertensive patients is of pivotal importance. Method: We conducted a review of the literature for studies with biomarkers that could be used in AF diagnosis as well as in predicting the transition of paroxysmal AF to sustained AF, especially in hypertensive patients. Results: Potential biomarkers for AF can be broadly categorized into electrophysiological, morphological and molecular markers that reflect the underlying mechanisms of adverse atrial remodeling. We focused on P-wave duration and dispersion as electrophysiological markers, and left atrial (LA) and LA appendage size, atrial fibrosis, left ventricular hypertrophy and aortic stiffness as structural biomarkers, respectively. The heterogeneous group of molecular biomarkers of AF encompasses products of the neurohormonal cascade, including NT-pro BNP, BNP, MR-pro ANP, polymorphisms of the ACE and convertases such as corin and furin. In addition, soluble biomarkers of inflammation (i.e. CRP, IL-6) and fibrosis (i.e. TGF-1 and matrix metalloproteinases) were assessed for predicting AF. Conclusion: The reviewed individual biomarkers might be a valuable addition to current diagnostic tools but the ideal candidate is expected to combine multiple indices of atrial remodeling in order to effectively detect both AF and adverse characteristics of high risk patients with hypertension.

scholarly journals P496Remodeling of atrial action potential duration and atrial chamber deformation: a potential link in the development of atrial fibrillation?

2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S120-S120
Author(s):  
L Sartiani ◽  
L Sartiani ◽  
M Cameli ◽  
L Dini ◽  
S Modillo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Potential Link

scholarly journals Echocardiography in Patients with Atrial Fibrillation - What Should the Internist Doctor Know?

2020 ◽  
Vol 17 (4) ◽  
pp. 49-60
Author(s):  
Maria-Luiza Toplicianu-Dimitriu ◽  
Ioan Tiberiu Nanea
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Structural Changes ◽  
Excess Mortality ◽  
Ventricular Dysfunction ◽  
Imaging Technique ◽  
Left Ventricular ◽  
Clinical Impact ◽  
Atrial Remodeling ◽  
Routine Imaging

AbstractAtrial fibrillation (AF) is the most common cardiac arrhythmia, with an increasing prevalence and an enormous clinical impact due to the high stroke rate, left ventricular dysfunction and excess mortality. The occurrence and maintenance of AF is favored by both the degree of left atrial (LA) dilation and the association of fibrotic lesions of the myocardium. The LA is a marker of adverse cardiovascular events in patients with AF. Atrial remodeling can be electrical (shortening atrial refractory), structural (altering geometry and altering collagen content) and contractile (loss of contractility). Cardiac imaging plays a central role in the clinical management of this arrhythmia. Echocardiography represents the routine imaging technique used in patients with AF, with a role in detecting LA dysfunction and cardiac structural changes that predispose to this arrhythmia, also having the ability to predict the maintenance of sinus rhythm after cardioversion and after ablation.

Hypertensive-diabetic cardiomyopathy in rats

1990 ◽  
Vol 258 (3) ◽  
pp. H793-H805 ◽  
Author(s):  
F. S. Fein ◽  
B. E. Zola ◽  
A. Malhotra ◽  
S. Cho ◽  
S. M. Factor ◽  
...  
Keyword(s):  
Action Potential ◽  
Right Ventricular ◽  
Action Potential Duration ◽  
Stimulus Frequency ◽  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Resting Membrane Potential ◽  
Contraction And Relaxation ◽  
And Control ◽  
Myocardial Pathology

Left ventricular papillary muscle function, transmembrane action potentials, myosin adenosinetriphosphatase (ATPase) and isoenzyme distribution, and myocardial pathology were studied in hypertensive (H), diabetic (D), hypertensive-diabetic (HD), and control (C) rats. There was approximately 50% relative left ventricular hypertrophy in H and HD rats. Relative lung and liver weights were greater in HD rats. Peak velocity of shortening tended to decrease progressively in H, D, and HD rats. The duration of contraction and relaxation was markedly prolonged in Ds and HDs. The length-developed tension relation was blunted in HDs. The negative inotropic effect of verapamil was similar in all groups. Resting membrane potential and amplitude were decreased in D and HD rats. Action potential duration was increased in H, D, and especially HD rats. The shortening of action potential duration with increased stimulus frequency was greater in H, D, and especially HD rats than in Cs. Left ventricular myosin ATPase and V1 isoenzyme content decreased progressively in H, D, and HD rats. Right ventricular V1 isoenzyme content was not affected in H rats but was markedly decreased in D and HD rats. Left (and right) ventricular pathology was unchanged in rats with diabetes but was increased in rats with hypertension. These data suggest that the combination of myocardial pathology (due to hypertension) and cellular dysfunction (caused mainly by diabetes) may result in cardiomyopathy and congestive heart failure in the HD rat.

Atrial fibrillation surgery with a focus on patients with reduced left ventricular function and heart failure

EP Europace ◽  
2020 ◽  
Vol 22 (4) ◽  
pp. 517-521
Author(s):  
Johannes Petersen ◽  
Hermann Reichenspurner ◽  
Simon Pecha
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Surgical Treatment ◽  
Left Ventricular Function ◽  
Treatment Options ◽  
Left Ventricular ◽  
Review Article ◽  
Surgical Ablation ◽  
Ablation Therapy ◽  
Patients With Heart Failure

Abstract This review article aims to give an overview on the different surgical treatment options for atrial fibrillation It includes concomitant- as well as stand-alone surgical ablation therapy and outlines the main issues in patients with heart failure and reduced LVEF.

Regression of LV hypertrophy with captopril normalizes membrane currents in rabbits

1998 ◽  
Vol 275 (4) ◽  
pp. H1216-H1224 ◽  
Author(s):  
Seth J. Rials ◽  
Xiaoping Xu ◽  
Ying Wu ◽  
Roger A. Marinchak ◽  
Peter R. Kowey
Keyword(s):  
Cell Membrane ◽  
Action Potential ◽  
Renal Artery ◽  
Current Density ◽  
Action Potential Duration ◽  
Left Ventricular ◽  
Membrane Current ◽  
Membrane Capacitance ◽  
Membrane Currents ◽  
Cell Membrane Capacitance

Recent studies indicate that regression of left ventricular hypertrophy (LVH) normalizes the in situ electrophysiological abnormalities of the left ventricle. This study was designed to determine whether regression of LVH also normalizes the abnormalities of individual membrane currents. LVH was induced in rabbits by renal artery banding. Single ventricular myocytes from rabbits with LVH at 3 mo after renal artery banding demonstrated increased cell membrane capacitance, prolonged action potential duration, decreased inward rectifier K+ current density, and increased transient outward K+ current density compared with myocytes from age-matched controls. Additional rabbits were randomized at 3 mo after banding to treatment with either vehicle or captopril for an additional 3 mo. Myocytes from LVH rabbits treated with vehicle showed persistent membrane current abnormalities. However, myocytes isolated from LVH rabbits treated with captopril had normal cell membrane capacitance, action potential duration, and membrane current densities. Captopril had no direct effect on membrane currents of either control or LVH myocytes. These data support the hypothesis that the action potential prolongation and membrane current abnormalities of LVH are reversed by regression. Normalization of membrane currents probably explains the reduced vulnerability to ventricular arrhythmia observed in this LVH model after treatment with captopril.

scholarly journals Ion Channel and Structural Remodeling in Obesity-Mediated Atrial Fibrillation

2020 ◽  
Vol 13 (8) ◽  
Author(s):  
Mark D. McCauley ◽  
Liang Hong ◽  
Arvind Sridhar ◽  
Ambili Menon ◽  
Srikanth Perike ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Action Potential ◽  
Ion Channel ◽  
Sodium Channel ◽  
Action Potential Duration ◽  
Obese Mice ◽  
Atrial Fibrosis ◽  
Structural Remodeling ◽  
Cardiac Sodium Channel ◽  
Channel Expression

Background: Epidemiological studies have established obesity as an independent risk factor for atrial fibrillation (AF), but the underlying pathophysiological mechanisms remain unclear. Reduced cardiac sodium channel expression is a known causal mechanism in AF. We hypothesized that obesity decreases Nav1.5 expression via enhanced oxidative stress, thus reducing I Na , and enhancing susceptibility to AF. Methods: To elucidate the underlying electrophysiological mechanisms a diet-induced obese mouse model was used. Weight, blood pressure, glucose, F 2 -isoprostanes, NOX2 (NADPH oxidase 2), and PKC (protein kinase C) were measured in obese mice and compared with lean controls. Invasive electrophysiological, immunohistochemistry, Western blotting, and patch clamping of membrane potentials was performed to evaluate the molecular and electrophysiological phenotype of atrial myocytes. Results: Pacing-induced AF in 100% of diet-induced obese mice versus 25% in controls ( P <0.01) with increased AF burden. Cardiac sodium channel expression, I Na and atrial action potential duration were reduced and potassium channel expression (Kv1.5) and current ( I Kur ) and F 2 -isoprostanes, NOX2, and PKC-α/δ expression and atrial fibrosis were significantly increased in diet-induced obese mice as compared with controls. A mitochondrial antioxidant reduced AF burden, restored I Na , I Ca,L , I Kur , action potential duration, and reversed atrial fibrosis in diet-induced obese mice as compared with controls. Conclusions: Inducible AF in obese mice is mediated, in part, by a combined effect of sodium, potassium, and calcium channel remodeling and atrial fibrosis. Mitochondrial antioxidant therapy abrogated the ion channel and structural remodeling and reversed the obesity-induced AF burden. Our findings have important implications for the management of obesity-mediated AF in patients. Graphic Abstract: A graphic abstract is available for this article.

Sign in / Sign up

Export Citation Format

Share Document