Common Cause Of Atrial Fibrillation Research Articles

СТРАТИФИКАЦИЯ РИСКА ПРОГРЕССИРОВАНИЯ ФИБРИЛЛЯЦИИ ПРЕДСЕРДИЙ У ПАЦИЕНТОВ С АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИЕЙ И ВОЗМОЖНОСТИ ВТОРИЧНОЙ ПРОФИЛАКТИКИ

Progression of atrial fibrillation (AF) is a process of steady development of arrhythmia from short paroxysms to the permanent form. Arterial hypertension (AH) is the most common cause of AF. The aim of this review is to highlight the role of possible predictors of AF progression in hypertensive patients. The role of general risk factors in the maintenance of arrhythmia, the significance of high blood pressure and its individual characteristics in the progression of AF are analyzed. Echocardiographic predictors of arrhythmia recurrence and the transition of AF to a permanent form in hypertension are described. Various existing scales for assessing the risk of AF progression are presented. The ways of secondary prevention of arrhythmia in AH are considered.

Management of atrial fibrillation in rheumatic heart disease.

Rheumatic heart disease (RHD) is the underlying cause of a significant proportion of atrial fibrillation (AF) in the low- and middle-income countries, while nonvalvular AF is the most common cause of AF in high-income countries. RHD is also common among African Americans, migrants, and the indigenous population of high-income countries. The onset of AF in RHD patients is a clinical marker of worse outcomes and is associated with significant morbidity and mortality. Despite RHD being a major cause of morbidity and mortality in the young in many parts of the world, it is often neglected by policymakers, the media, and even the medical fraternity. Stroke risk assessment using various risk scores has not been systematically evaluated in rheumatic AF patients. Rate control may not be ideal for symptom control in rheumatic AF patients considering the young age and an active lifestyle. There is limited information regarding the nonpharmacological management of rheumatic AF. The current management guidelines based on nonvalvular AF do not apply to rheumatic AF patients who are often younger, are women, and have fewer comorbidities. This review critically looks at specific areas such as stroke prevention with reference to direct oral anticoagulants, cardioversion, rate and rhythm control strategies, and the role of nonpharmacological methods in rheumatic AF management. Future recommendations must be cognizant of local health care systems and resourcing considering the geographic distribution of the disease.

Prevalence and risk factors for persistent atrial fibrillation in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a common cause of atrial fibrillation (AF). The prevalence rate of OSA in AF is highest at 80%. There is limited data if who will develop AF in OSA patients. This study aimed to evaluate the prevalence of AF in patients with OSA and find clinical factors predictive of AF in patients with OSA. This was a cross-sectional study. We enrolled consecutive patients diagnosed with obstructive sleep apnea diagnosed by polysomnography. The primary outcome was persistent AF identified by electrocardiogram. Prevalence and predictors of AF in patients with OSA were analyzed. During the study period, there were 199 patients with OSA enrolled in the study. Of those, 31 patients (15.57%) had AF. There were five factors in the final model predictive for AF in OSA patients. Among those factors, three factors were independently associated with AF in OSA including age, tiredness, and glomerular filtration rate. The latter two factors were protective factors, while age was a predictor for AF with an adjusted odds ratio (95% confidence interval) of 1.052 (1.004, 1.103). The prevalence of AF in patients with OSA was 15.57%. Elderly patients with renal deterioration are at risk of AF but AF risk was decreasing in patients with tiredness.

Risk Factors for New Onset Atrial Fibrillation during Thyroid Gland Surgery

Objective: Thyroid dysfunction is a common cause of atrial fibrillation (AF). Incidence of AF is high in patients with both expressed and subclinical hyperthyroidism. The aim of our study was to determine the incidence and predictors of new onset atrial fibrillation (NOAF) in euthyroid patients undergoing thyroid surgery. Subject and Methods: The study included 1,252 euthyroid patients with American Society of Anesthesiologists (ASA) physical status ASA 2 and ASA 3, who were 18 years and older and were in sinus rhythm. Patients without comorbidity and patients with persistent AF were excluded. We investigated the influence of the following preoperative characteristics on the occurrence of NOAF: age, sex, body mass index, ASA score, admission diagnoses, and comorbidity. We noted the influence of difficult intubation of trachea, type and duration of surgery, and time under general anaesthesia. Univariate and multivariate logistic regression were used to determine predictors of occurrence of NOAF. Results: NOAF was noted in 0.72% of patients. Patients with NOAF were older (63.11 vs. 56.81 years) than patients without NOAF, but this was not statistically significant. Significantly more patients from the NOAF group had preoperative heart rhythm disturbance and a history of angina pectoris, in contrast to patients without registered NOAF (p = 0.001; p = 0.017). Multivariate analysis showed that a history of heart rhythm disturbance was an independent predictor of NOAF. Conclusions: Incidence of NOAF during thyroid surgery is similar to the other type of surgery, if the values of thyroid hormones are normal.

Atrial Fibrillation in Patients With Cardiomyopathy: Prevalence and Clinical Outcomes From Real‐World Data

BackgroundCardiomyopathy is a common cause of atrial fibrillation (AF) and may also present as a complication of AF. However, there is a scarcity of evidence of clinical outcomes for people with cardiomyopathy and concomittant AF. The aim of the present study was therefore to characterize the prevalence of AF in major subtypes of cardiomyopathy and investigate the impact on important clinical outcomes.Methods and ResultsA retrospective cohort study was conducted using electronic medical records from a global federated health research network, with data primarily from the United States. The TriNetX network was searched on January 17, 2021, including records from 2002 to 2020, which included at least 1 year of follow‐up data. Patients were included based on a diagnosis of hypertrophic, dilated, or restrictive cardiomyopathy and concomitant AF. Patients with cardiomyopathy and AF were propensity‐score matched for age, sex, race, and comorbidities with patients who had a cardiomyopathy only. The outcomes were 1‐year mortality, hospitalization, incident heart failure, and incident stroke. Of 634 885 patients with cardiomyopathy, there were 14 675 (2.3%) patients with hypertrophic, 90 117 (7.0%) with restrictive, and 37 685 (5.9%) with dilated cardiomyopathy with concomitant AF. AF was associated with significantly higher odds of all‐cause mortality (odds ratio [95% CI]) for patients with hypertrophic (1.26 [1.13–1.40]) and dilated (1.36 [1.27–1.46]), but not restrictive (0.98 [0.94–1.02]), cardiomyopathy. Odds of hospitalization, incident heart failure, and incident stroke were significantly higher in all cardiomyopathy subtypes with concomitant AF. Among patients with AF, catheter ablation was associated with significantly lower odds of all‐cause mortality at 12 months across all cardiomyopathy subtypes.ConclusionsFindings of the present study suggest AF may be highly prevalent in patients with cardiomyopathy and associated with worsened prognosis. Subsequent research is needed to determine the usefulness of screening and multisdisciplinary treatment of AF in this population.

Trans-esophageal Echocardiographic Assessment of Left Atrial and Left Atrial Appendage Function in Atrial Fibrillation and Rheumatic Heart Disease.

Introduction: Rheumatic heart disease (RHD) is one of the most typical causes of atrial fibrillation in developing countries like India. The left atrial and left atrial appendage structure and function are deranged in atrial fibrillation and are a major source of thromboembolism. The goal of this study was to assess the left atrial and left atrial appendage function by transesophageal echocardiography in patients with atrial fibrillation and their comparison in patients with or without RHD.Methods: A total of 172 consecutive patients with atrial fibrillation with or without RHD were subjected to trans-esophageal echocardiography to assess and compare left atrial (LA) and left atrial appendage (LAA) function.Results: Out of 172 patients with atrial fibrillation, 100 were female (58.1%) and 72 were male (48.9%). The mean age was 54.11±12.3 years, and rheumatic heart disease (RHD) was the commonest cause of atrial fibrillation found in 121 (70.3%) patients. The mean left atrium diameter was significantly higher in RHD patients than in Non-RHD patients (52.08±10.13 vs. 46.67±6.78 mm, p=0.001). Mean left atrial ejection fraction was significantly lower in RHD patients as compared to Non-RHD patients (33.53±5.06 vs. 35.49±5.40%, p=0.024). The mean LAA orifice area of RHD patients was significantly higher than the Non-RHD patients (7.52±1.22 vs 6.94±1.17 mm2, p=0.005). Mean LAA emptying velocity was significantly lower in RHD patients than Non-RHD (20.49±3.95 vs. 22.8±5.96 ml/s, p=0.002).Conclusion: Rheumatic heart disease is still a common cause of atrial fibrillation in developing countries. LA and LAA function is impaired in atrial fibrillation, more in patients with rheumatic heart disease.

Prevention and Treatment of Atrial Fibrillation via Risk Factor Modification

Atrial fibrillation (AF) is the most common clinically significant arrhythmia, and it increases stroke risk. A preventive approach to AF is needed because virtually all treatments such as cardioversion, antiarrhythmic drugs, ablation, and anticoagulation are associated with high cost and carry significant risk. A systematic review was performed to identify effective lifestyle-based strategies for reducing primary and secondary AF. A PubMed search was performed using articles up to March 1, 2021. Search terms included atrial fibrillation, atrial flutter, exercise, diet, metabolic syndrome, type 2 diabetes mellitus, obesity, hypertension, stress, tobacco smoking, alcohol, Mediterranean diet, sodium, and omega-3 fatty acids. Additional articles were identified from the bibliographies of retrieved articles. The control of hypertension, ideally with a renin-angiotensin-aldosterone system inhibitor, is effective for preventing primary AF and recurrence. Obstructive sleep apnea is a common cause of AF, and treating it effectively reduces AF episodes. Alcohol increases the risk of AF in a dose-dependent manner, and abstinence reduces risk of recurrence. Sedentary behavior and chronic high-intensity endurance exercise are both risk factors for AF; however, moderate physical activity is associated with lower risk of AF. Recently, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 agonists have been associated with reduced risk of AF. Among overweight/obese patients, weight loss of ≥10% is associated with reduced AF risk. Lifestyle changes and risk factor modification are highly effective for preventing AF.

Regulatory adaptive status in determining the effectiveness of treatment with bisoprololum and nebivololum in patients with paroxysmal atrial fibrillation and hypertension

Increase in mortality from cardiovascular causes, systemic thromboembolism, congestive heart failure, increased frequency of hospitalization and deterioration in quality of life is associated with atrial fibrillation (AF). Essential hypertension (EH) is the most common cause of AF. To prevent recurrence of AF in patients with hypertension b-blockers (b-AB) can be used. Taking into account the possible effect of multidirectional b-AB on the functional condition of the body, in order to determine the effectiveness of therapy, it is advisable to apply a quantitative assessment of the regulatory-adaptive status (RAS). Goal - compare the effectiveness of bisoprololum and nebivololum in patients with paroxysmal AF and EH, given their impact on the RAS. Materials and methods. 50 patients with AF against the background of EH of stages II-III were randomized into two groups for treatment with bisoprololum (5.4±1.8 mg/day, n=25) or nebivololum (5.6±1.6 mg/day, n=25). As part of combination therapy, patients were administered lisinoprilum (14.2±3.8 and 14.3±3.7 mg/day), when required also atorvastatinum (19.1±3.7 and 18.8±4.4 mg/day), acetylsalicylic acid (90.0±4.6 and 91.2±4.1 mg/day), respectively. Initially and in 6 months, the following was done: quantitative assessment of the RAS (cardio-respiratory synchronism test), echocardiography, triplex scanning of brachiocephalic arteries, treadmill test, six-minute walk test, daily monitoring of blood pressure and electrocardiogram, subjective assessment of the quality of life. Results. Both drug regimens comparably suppressed arrhythmia, controlled hypertension, improved the structural and functional condition of the heart. The use of nebivololum positively affected the RAS, to a greater extent increased exercise capacity and improved the quality of life. Conclusion. In patients with paroxysmal AF against the background of EH of stages II-III, the use of nebivololum as part of combination therapy may be preferable to bisoprololum due to its positive impact on the RAS.

Co-existence of ischemic stroke in Rheumatic and non-rheumatic atrial Fibrillation in a tertiary care teaching hospital of Western Nepal

Background & Objectives: Stroke is a major public health burden worldwide leading to long-term morbidity and even mortality. Atrial fibrillation (AF) is the most common sustained arrhythmia and is an independent factor to increase risk of ischemic stroke. The risk of stroke further enhanced in rheumatic atrial fibrillation and affects younger population of developing countries. The study has aimed to find out frequency of co-existence of stroke in AF and secondarily to look for age distribution of stroke and risk factors of AF.Materials & Methods: A retrospective analysis of trans-thoracic echocardiographic records of patients from 1st June 2009 to 31st June 2016 was done. Data were collected in a pre-structured proforma and analyzed.Results: Among 15767 echocardiographies, 577 (3.65%) cases were recorded to have atrial fibrillation. Mean age 65(±15) years ranging from 14 to 100 years. Rheumatic heart disease was the second most common cause of atrial fibrillation after hypertension. The co-existence of ischemic stroke was seen in 87(15.07%) cases with male to female ratio of 1:1.3. The proportion of stroke in rheumatic Atrial fibrillation was 21(18.75%) which was higher than in non-Rheumatic atrial fibrillation 66(14.2%).Conclusion: Rheumatic heart disease is contributing as second most common cause of atrial fibrillation after hypertension, nearly one fourth of total stroke and most common (93%) cause of stroke below the age of 45 years. Preventive strategies aimed at health awareness about rheumatic fever, screening programs at community level, early detection and treatment for hypertension and Rheumatic heart disease can contribute in reduction of stroke burden.

Clinical and Etiological Profile of Patients with Atrial Fibrillation (AF): Analysis and implications

Background and Objectives: Atrial fibrillation (AF) is a frequently encountered cardiac arrhythmia which may be either symptomatic or asymptomatic. So, this study was conducted to know clinical presentation and to find out possible clinical and etiological profile of patients with AF.Material and Methods: This cross sectional study was conducted at Osh Regional Integrated Clinical Hospital, Osh Territorial City Clinical Hospital, The Kyrgyz Republic in collaboration with Janaki Medical College Teaching Hospital, Janakpurdham, Nepal. Sixty consecutive patients with AF were taken. Presenting complaints, past history, personal history was recorded. A thorough clinical examination was done, electrocardiogram, chest X-Ray posterio-anterior view, echocardiogram, thyroid function test and relevant test were done and analyzed.Results: Forty percent of the patients complained palpitation. Systemic thrombo-embolism was found in 15% of the patients. Other presenting complaints were cough, chest pain, shortness of breath, dizziness, swelling of the legs, tremors. Eighteen percent of patients presented with features of congestive cardiac failure and 30% of the patients gave history of rheumatic heart disease, 16.6% and 11.6% hypertension and ischemic heart disease respectively. Etiology-wise, rheumatic heart disease was the most common (46.6%) followed by hypertension (21.6%), ischemic heart disease (11.6%), dilated cardiomyopathy (6.6%), hyperthyroidism (5%), pneumonia (5%).Conclusion: Rheumatic heart disease, especially mitral stenosis is the most common cause of AF in this study. Systemic hypertension was next common etiology of AF, followed by ischaemic heart disease, dilated cardiomyopathy, thyroid disease. Heart failure, Systemic thromboembolism, decreased exercise tolerance are a major determinants for development of significant morbidity and mortality.Janaki Medical College Journal of Medical Sciences (2016) Vol. 4 (1): 5-12

Regulatory and adaptive status: bisoprolol vs sotalol in co-existent hypertension and paroxysmal atrial fibrillation

Background. Atrial fibrillation (AF) is associated with the increase in mortality from cardiovascular causes, systemic thromboembolism, congestive heart failure, high rate of hospitalization and deterioration of quality of life. Hypertension (HTN) is the most common cause of AF. Beta-blockers are the therapy of choice for AF prevention. To predict the therapy efficiency, one should assess the regulatory and adaptive status (RAS). The aim of our study was to compare bisoprolol vs sotalol in patients with HTn and paroxysmal AF taking into account quantitative indices of the regulatory adaptive status (RAS). Design and methods. We included 50 patients with HTN stages II–III and paroxysmal AF and randomized them into two groups for treatment with bisoprolol (6,4 ± 1,8 mg/day, n = 25) or sotalol (157,0 ± 38,3 mg/day, n = 25). As part of combination therapy, lisinopril (14,2 ± 3,8 and 14,0 ± 4,8 mg/day), atorvastatin (17,1 ± 3,7 mg/day, n = 11 and 16,0 ± 5,1 mg/day, n = 11), acetylsalicylic acid were prescribed (90,0 ± 14,6 mg/day, n = 12 and 92,1 ± 16,8 mg/day, n = 12), respectively. At baseline and 6 months after therapy, quantitative assessment of RAS (by cardio-respiratory synchronism test), echocardiography, triplex scanning of brachiocephalic arteries, treadmill test, six-minute walk test, 24‑hour blood pressure and electrocardiogram monitoring, subjective assessment of quality of life. Results. Both schemes comparably improved structural and functional parameters of the heart, increased exercise tolerance, controlled arterial hypertension, effectively suppressed AF paroxysms, improved quality of life. At the same time, sotalol led to the decrease of RAS to a lesser degree than bisoprolol. Conclusions . In patients with HTN stages II–III and paroxysmal AF sotalol as a component of the combination therapy may be preferable to bisoprolol due to its lower impact on the RAS.

5. Newly developed atrial fibrillation in liver transplant patient with intravenous dexmedetomedine sedation

Introduction Atrial fibrillation (AF) is the commonest type of arrhythmias in common population and critically ill as well. Intensive care patients are vulnerable to develop AF due to numerous causing and risk factors during their illness. Drug-induced AF is a group of underestimated causes known to induce arrhythmias in severely ill patients one of these medications is. Dexmetedomedine (precedx™) one of relatively new sedative-analgesic is effectively used in mechanically ventilated patients and as a consequence recent critical care society recommendations claimed dexmedetomidine may be preferred over sedation with benzodiazepines. Case report We present a case report of newly developed resistant AF in post living-related liver transplant lady who received intravenous dexmedetomidine as recommended sedative to liberate her from the ventilator. Discussion Despite the presence of other clinical risk factors pertinent to the patient to develop AF which took place after starting dexmedetomidine, yet the resolution of AF had occurred subsequent to cessation of dexmedetomidine. Retrospective analysis of critical care department database of king Fahad specialist hospital Dammam from January 2011 till July 2014 up to revealed about 20% of patients received intravenous dexmedetomidine had experienced AF. In fact these results are higher than the reported information by the literature. Conclusion Intravenous dexmedetomidine (precedex™) is a common cause of AF in critically ill patients. This kind of side effect needs scrutinized assessment and follow up to find out the risk factors involved in its development especially in the era of increasing dexmedetomidine as a state-of-art recommended sedative agent in intensive care units and perioperative as well.

Comprehensive mutation scanning of KCNQ1 in 111 Han Chinese patients with lone atrial fibrillation

ObjectiveTo determine the extent to which genetic variation in the potassium channel gene KCNQ1 causes atrial fibrillation (AF).DesignCase–control study.SettingNational University Hospital, Singapore.PatientsHan Chinese patients (n=111) with lone AF (onset <60...

Noninvasive real-time mapping of an incomplete pulmonary vein isolation using electrocardiographic imaging

Establishing entrance and exit block from pulmonary veins is an endpoint for pulmonary vein isolation (PVI) procedures (1). Reestablished pulmonary vein connection is a common cause of atrial fibrillation (AF) recurrence in patients who have previously undergone PVI. Here we provide images from a noninvasive cardiac electrophysiology imaging system (ECGI) performed during PVI. The ECGI procedure has been described previously (2) (3). 250 carbon electrodes were applied to the patient’s torso before a pre-procedural contrast-enhanced CT scan, which provided torso-electrode positions and atrial geometry in the same reference frame. The electrodes were removed, then replaced on the day of the PVI procedure in the same configuration, and remained on the patient throughout the procedure. ECGI performed during the procedure noninvasively generated epicardial isochrone activation maps. After circumferential ablation around the antrum of the right pulmonary veins, a lasso catheter in the right inferior pulmonary vein (RIPV) demonstrated entrance block. However, high-output pacing from within the RIPV captured the atrium, revealing incomplete exit block. Panel A displays the real-time ECGI isochrone map during RIPV pacing, showing earliest activation in the superior-posterior antrum of the RIPV (red is earliest), with radial spread across the posterior LA. A 60-ms delay is seen from the pacing breakthrough (red) to posterior LA (green) activation, consistent with incomplete line of block created by the ablation. The invasive electroanatomic map (Panel B) shows the final ablation lesion set and the additional ablation necessary for exit block from the RIPV (pink marker). This location on the invasive electroanatomic map corresponds closely to the exit site determined by ECGI in Panel A. Panel C shows an ECGI isochrone map during high-output pacing from within the RIPV after the complete ablation. Pacing failed to capture the atrium, and the earliest LA activation in sinus rhythm was near Bachmann’s bundle (red). Posterior LA activation is limited superiorly and inferiorly with lines of block (white dotted lines) corresponding to the ablation lines on the LA roof and posterior wall seen in panel B. Three PV’s also demonstrate electrical isolation (blue). Although the RSPV in Panel C appears to have electrical connection in sinus rhythm, the appearance of activation is due to far-field signal from the posterior right atrium in close proximity. Invasive testing of the RSPV demonstrated entrance and exit block. Rigorous prospective study is needed, but if real-time ECGI can accurately identify areas of incomplete PVI isolation, it may shorten procedure time and improve long-term success rates by pinpointing sites of incomplete linear ablation.

Calcium-Handling Abnormalities Underlying Atrial Arrhythmogenesis and Contractile Dysfunction in Dogs With Congestive Heart Failure

Congestive heart failure (CHF) is a common cause of atrial fibrillation. Focal sources of unknown mechanism have been described in CHF-related atrial fibrillation. The authors hypothesized that abnormal calcium (Ca(2+)) handling contributes to the CHF-related atrial arrhythmogenic substrate. CHF was induced in dogs by ventricular tachypacing (240 bpm x2 weeks). Cellular Ca(2+)-handling properties and expression/phosphorylation status of key Ca(2+) handling and myofilament proteins were assessed in control and CHF atria. CHF decreased cell shortening but increased left atrial diastolic intracellular Ca(2+) concentration ([Ca(2+)](i)), [Ca(2+)](i) transient amplitude, and sarcoplasmic reticulum (SR) Ca(2+) load (caffeine-induced [Ca(2+)](i) release). SR Ca(2+) overload was associated with spontaneous Ca(2+) transient events and triggered ectopic activity, which was suppressed by the inhibition of SR Ca(2+) release (ryanodine) or Na(+)/Ca(2+) exchange. Mechanisms underlying abnormal SR Ca(2+) handling were then studied. CHF increased atrial action potential duration and action potential voltage clamp showed that CHF-like action potentials enhance Ca(2+)(i) loading. CHF increased calmodulin-dependent protein kinase II phosphorylation of phospholamban by 120%, potentially enhancing SR Ca(2+) uptake by reducing phospholamban inhibition of SR Ca(2+) ATPase, but it did not affect phosphorylation of SR Ca(2+)-release channels (RyR2). Total RyR2 and calsequestrin (main SR Ca(2+)-binding protein) expression were significantly reduced, by 65% and 15%, potentially contributing to SR dysfunction. CHF decreased expression of total and protein kinase A-phosphorylated myosin-binding protein C (a key contractile filament regulator) by 27% and 74%, potentially accounting for decreased contractility despite increased Ca(2+) transients. Complex phosphorylation changes were explained by enhanced calmodulin-dependent protein kinase IIdelta expression and function and type-1 protein-phosphatase activity but downregulated regulatory protein kinase A subunits. CHF causes profound changes in Ca(2+)-handling and -regulatory proteins that produce atrial fibrillation-promoting atrial cardiomyocyte Ca(2+)-handling abnormalities, arrhythmogenic triggered activity, and contractile dysfunction.

Association of Prolidase Activity, Oxidative Parameters, and Presence of Atrial Fibrillation in Patients with Mitral Stenosis

Mitral stenosis (MS) is a common cause of atrial fibrillation (AF). Oxidative stress and inflammation factors were shown to be involved in atrial remodeling. The study aim was to compare the oxidative parameters and prolidase activity in severe MS patients with and without AF. The study population was comprised of 33 patients with MS and sinus rhythm (group I), 27 patients with MS and AF (group II), and 25 healthy controls (group III). Plasma prolidase activity, total antioxidant capacity (TAC), total oxidative status (TOS), and oxidative stress index (OSI) were determined. Additionally, we measured tissue TOS and TAC in patients with mitral valve replacement. TAC and OSI were higher, but TOS and prolidase were lower in patients with MS than control (all p <0.001). These parameters were similar in group I and group II (ANOVA p >0.05). Tissue TAC was significantly lower in group II than group I (0.015 +/- 0.01 vs. 0.026 +/- 0.01 mmol Trolox equiv/L, p = 0.014), tissue TOS was similar between groups I and II (0.24 +/- 0.06 vs. 0.22 +/- 0.05 mmol Trolox equiv/L, p = 0.161). Presence of AF was correlated with systolic blood pressure, left atrial diameter, plasma TAC, tissue TAC, plasma TOS, plasma OSI, and plasma prolidase activity. Tissue TAC level (beta = -0.435, p = 0.006) and left atrial diameter (beta = 0.460, p = 0.003) were independently related with presence of AF in patients with MS. This study suggested that the presence of AF in patients with severe MS may be associated with the plasma prolidase activity, tissue and plasma oxidative parameters.

Effects of simvastatin on the development of the atrial fibrillation substrate in dogs with congestive heart failure☆

Congestive heart failure (CHF) is a common cause of atrial fibrillation (AF). Oxidative stress and inflammation (profibrotic) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha, antifibrotic) factors may be involved in CHF-related remodeling. We evaluated the effects of simvastatin (antioxidant, anti-inflammatory) and fenofibrate (PPAR-alpha activator) on CHF-related atrial remodeling. Dogs were subjected to 2-week ventricular tachypacing (VTP) in the absence and presence of simvastatin (20 or 80 mg/day) or fenofibrate. Induced AF duration (DAF) was increased by VTP from 36+/-14 (non-paced controls) to 1005+/-257 s (p<0.01). Simvastatin prevented VTP-induced DAF increases (147+/-37 and 84+/-37 s at 20 and 80 mg/day, respectively), but fenofibrate did not (1018+/-352 s). Simvastatin also attenuated CHF-induced conduction abnormalities (heterogeneity-index reduced from 1.5+/-0.1 to 1.1+/-0.1 and 1.0+/-0.1 at 20 and 80 mg/day, p<0.01) and atrial fibrosis (from 19.4+/-1.3% to 10.8+/-0.8% and 9.9+/-0.8% at 20 and 80 mg/day, p<0.01), while fenofibrate did not. Simvastatin (but not fenofibrate) also attenuated VTP-induced left-ventricular nitric-oxide synthase and nitrotyrosine increases, along with hemodynamic dysfunction. Atrial fibroblast proliferation increased with 24-h fetal bovine serum (FBS) stimulation from 654+/-153 to 7264+/-1636 DPM (p<0.001). Simvastatin, but not fenofibrate, suppressed fibroblast proliferation (664+/-192 DPM, p<0.001). Simvastatin also significantly attenuated transforming growth factor-beta1-stimulated alpha-smooth muscle actin (alpha-SMA) expression (indicating myofibroblast differentiation) from 1.3+/-0.1 to 1.0+/-0.1 times baseline (p<0.05). CHF-induced atrial structural remodeling and AF promotion are attenuated by simvastatin, but not fenofibrate. Statin-induced inhibition of profibrotic atrial fibroblast responses and attenuation of left-ventricular dysfunction may contribute to preventing the CHF-induced fibrotic AF substrate.

Atrial fibrillation in intensive care units

Summary Atrial fibrillation (AF) is an abnormal irregular heart rhythm whereby electrical signals are generated apparently randomly throughout the atria. It is the most common of all cardiac arrhythmias. The occurrence of AF has been poorly studied in general intensive care units (ICUs), but extensively studied in the postoperative period, when it is a cause of admission to surgical ICUs (S-ICUs) or can delay patient transfer from S-ICUs. The most frequently identified risk factors are increased age, valvular heart disease, atrial enlargement, preoperative atrial arrhythmias, and chronic lung diseases. Ischaemic heart disease is probably the most common cause of AF, followed by hypertension, rheumatic heart disease, thyrotoxicosis, cardiomyopathy, mitral valve disease, haemochromatosis and infection (e.g. pneumonia or systemic sepsis). The onset of AF or faster rates of chronic AF may be precipitated by acid–base disturbances, electrolyte abnormalities (in particular, hypokalaemia or hypomagnesaemia), hypovolaemia, myocardial ischaemia, and surgical manipulation in the thorax. Postoperative AF resolves spontaneously in most patients, but can recur. Two main therapeutic strategies can be adopted in perioperative AF: rhythm control and rate control. The former is based on electrical or pharmacological treatment, while the latter is only pharmacological. No clear superiority has been pointed out by comparative studies, but the choice is influenced by clinical conditions. Rhythm control strategy should be chosen in the presence of contraindications to anticoagulation, which is indicated if spontaneous conversion to sinus rhythm does not occur within 48h.

Hyperthyroidism as a Cause of Atrial Fibrillation in Long-term Care

We measured sensitive thyrotropin-stimulating hormone (sTSH) in 50 consecutive nursing home patients (39 men) with atrial fibrillation to determine the frequency of hyperthyroidism. Patients were identified in a long-term care facility by an electrocardiogram demonstrating atrial fibrillation. The sensitive thyrotropin-stimulating hormone assay had a detection limit of less than or equal to 0.02 mU/L (normal range, 0.46 to 3.60 mU/L). No subject had a suppressed sensitive thyrotropin-stimulating hormone. Hyperthyroidism is not a common cause of atrial fibrillation in male nursing home residents.