Post-surgery Atrial Fibrillation Research Articles

Assessment of the frequency and possible risk factors for paroxysmal atrial fibrillation in the early postoperative period after transapical implantation of the MedLab-CT valve

Aim. To study the incidence and possible risk factors for atrial fibrillation (AF) in the early postoperative period after transapical implantation of the first Russian aortic valve (TAP-AVI).Methods. The study included 118 patients after successful TAP-AVI. Patients with open aortic valve replacement due to dislocation of the prosthesis were excluded, as well as subjects with permanent AF and who died in the early postoperative period. The mean age of the patients was 71.1±4.9 years, body mass index 31.1±5.9 kg/m2 , males - 39.8%, hypertension was present in 93.2%, diabetes mellitus (DM) - in 27.9%, paroxysmal AF - in 12.7%, coronary artery disease (CAD) was in 56.7%, 8.4% were smokers. The median follow-up time corresponded to the hospital stay - 9.5 days. To identify cardiac arrhythmias, regular daily ECG recording in 12 leads was initiated from the first day after TAP-AVI. In the presence of palpitations, 24-hour ECG monitoring was performed. Indicators such as age, male gender, DM, history of AF, interatrial block before surgery, CAD, and echocardiographic parameters were studied as possible predictors of AF development in the early postoperative period after TAP-AVI. There were no significant differences in the baseline parameters in patients with AF paroxysms and sinus rhythm.Results. In the early postoperative period, AF was encountered in 46 (39%) of patients. New-onset AF occurred in 38 (32.2%) patients. No cerebrovascular event occurred in patients with post-surgery AF. The only statistically significant risk factor for AF in the postoperative period was CAD (OR 5.756; 95% CI 1.009-8.132; p = 0.048).Conclusion. In the early postoperative period, the only significant predictor of AF was the presence of documented CAD.

Cholinergic activity regulates the secretome of epicardial adipose tissue: Association with atrial fibrillation.

Botulinum toxin injection on epicardial fat, which inhibits acetylcholine (ACh) release, reduced the presence of atrial fibrillation (AF) in patients after heart surgery. Thus, we wanted to study the profile of the released proteins of epicardial adipose tissue (EAT) under cholinergic activity (ACh treatment) and their value as AF predictors. Biopsies, explants, or primary cultures were obtained from the EAT of 85 patients that underwent open heart surgery. The quantification of muscarinic receptors (mAChR) by real-time polymerase chain reaction or western blot showed their expression in EAT. Moreover, mAChR Type 3 was upregulated after adipogenesis induction (p < 0.05). Cholinergic fibers in EAT were detected by vesicular ACh transporter levels and/or acetylcholinesterase activity. ACh treatment modified the released proteins by EAT, which were identified by nano-high-performance liquid chromatography and TripleTOF analysis. These differentially released proteins were involved in cell structure, inflammation, or detoxification. After testing the plasma levels of alpha-defensin 3 (inflammation-involved protein) of patients who underwent open heart surgery ( n = 24), we observed differential levels between the patients who developed or did not develop postsurgery AF (1.58 ± 1.61 ng/ml vs. 6.2 ± 5.6 ng/ml; p < 0.005). The cholinergic activity on EAT might suggest a new mechanism for studying the interplay among EAT, autonomic nervous system dysfunction, and AF.

Myocardial fibrosis and atrial fibrillation

Atrial fibrillation is the most prevalent arrhythmia, and tends to progress. Any structural changes in the heart may lead to its progressive remodelling with increased deposition of connective tissue and fibrosis. Predominance of collagen types I and III synthesis over its degradation leads to accumulation of fibers and to fibrosis. Increase of atrial fibrosis is usually found on autopsy and biopsy. There is relation revealed, of atrial fibrosis grade and postsurgery atrial fibrillation. The mechanisms participating in the structural remodelling and progression of atrial fibrosis are not studied well enough, but there is known role of renin-angiotensinaldosterone system, transforming growth factor, inflammation and matrix metalloproteases. As an alternative, one should consider non-invasive diagnostic methods: magnetic resonance imaging of the heart and biomarkers level measurement. Hyperactivation of the renin-angiotensin-aldosterone system facilitates structural remodelling of the heart and progression of atrial fibrosis. Hyperexpression of the transforming growth factor leads to selective atrial fibrosis, heterogeneity of excitation conduction and fibrillation onset. Matrix metalloproteases are the marker of extracellular degradation. Study of fibrosis biomarkers makes it to increase significantly the efficacy of atrial fibrillation course prediction.

A ROLE OF SUPEROXIDE DISMUTASE IN DEVELOPMENT OF POST-OPERATION ATRIAL FIBRILLATION IN CORONARY HEART DISEASE PATIENTS

Aim. To evaluate the level of superoxide dismutase (SOD) in coronary heart disease (CHD) patients underwent coronary bypass (CBG), and to estimate its importance in development of post-surgery atrial fibrillation (PSAF). Material and methods . Totally, 96 patients studied, with CHD, admitted for CBG. Patients were selected to 2 groups: 1 group — non-PSAF (67 patients, 80,6% males, mean age 57,9±7,3 y.o.), 2 group — with first time AF in early period of CBG (29 patients, 86% males, mean age 64,0±8,4 y.o.). Results. During study period PSAF developed in 30,2% cases, mean on 4,9±3,8 day after surgery. Comparing with group 1, level of SOD was higher in group 2 patients (2589,8±1999,3 U/g vs 1572,8±1275,2 U/g, р=0,034). Patients of group 2 were older 4 years in average (64,0±8,4 vs 57,9±7,3 y., р=0,048), had longer duration of cardiovascular pathology (86,9±76,1 months vs 44,3±38,4 m., р=0,002). Patients with PSAF had III functional class of angina (72,4% vs 47,8%, р=0,028) and III functional class of congestive heart failure (38,0% vs 7,5%, р=0,006), they had larger left atrium (43,5±4,1 mm vs 37,9±3,4 mm, р<0,001). After multifactorial analysis, predictive value remained for the following: left atrium larger than 41 mm — 5,1 (95% CI, 2,1-9,8, р=0,0005), SOD more than 2948 U/g — 4,4 (95% CI, 1,1-8,9, р=0,04). Conclusion. The study showed that CBG operation is followed by activation of oxidation stress which is followed by the decrease of SOD concentration, probably due to its consumption. However, among patients with PSAF there is higher activity of this enzyme.

Coronary artery anatomy and the occurrence of atrial fibrillation after coronary artery bypass surgery

Background: Atrial fibrillation (AF) is one of the most common complications occurring after cardiac surgeries. The incidence of post-operative AF is increasing continuously over the past decades and it is associated with lengthened hospital stay and risk of stroke. Objectives: This study was designed to examine the relationship between coronary artery involvement and the occurrence of AF after coronary artery bypass graft (CABG). Methods: This prospective observational study was to assess the relationship between the coronary artery involvement and the occurrence of post CABG surgery AF. Patients with chronic and paroxysmal AF before surgery were excluded. All patients had a complete evaluation by echocardiography, electrocardiography, and laboratory testing. The patients were monitored for 3 days after surgery and any tachycardia monitored as AF was noted. Patients were also divided into two groups of having post-operative AF and not having AF. Coronary artery involvement was defined using the Rentrop system. The coronary arteries were divided into 14 segments for better understanding of the lesions. Results: In this study 232 patients were selected, from which 106 patients had AF and 126 patients had sinus rhythm. The results of the present study confirmed that the older patients had a more frequent occurrence of AF after CABG (P < 0.001). There was no significant relationship between the right coronary artery (RCA) lesion and the development of AF after CABG. Proximal left anterior descending (LAD) artery lesion was associated with a higher occurrence of AF after CABG (P = 0.022). Patients with single vessel or two-vessel coronary artery disease had a more frequent occurrence of AF after CABG versus those with three vessel disease (P = 0.021). Conclusions: Although age has been the most important predictor for occurrence of AF after CABG in the past and present studies, there are many other variables affecting its occurrence. Out of the variables evaluated in this study, higher PAP, proximal LAD lesion, higher levels of BNP, and D dimer as well as single vessel and two vessel coronary artery diseases were noted to significantly predict a higher occurrence of AF after CABG.

Cardiovascular interactions assessed via conditional joint transfer entropy in patients developing atrial fibrillation after coronary artery bypass graft surgery.

Assigned the universe of knowledge Ω as composed by one target and two exogenous signals, the conditional joint transfer entropy (CJTE), assessing the amount of information jointly transferred from the two sources to the target that can be uniquely linked to one of the two sources, was found useful to study cardiovascular control. We propose the assessment of CJTE from systolic arterial pressure (SAP) and respiration (R) to heart period (HP) conditioned on R (CJTESAP, R→HP|R) along the baroreflex, and from HP and R to SAP conditioned on R (CJTEHP, R→SAP|R) along the feedforward mechanical pathway, in 134 patients undergoing coronary artery bypass graft surgery before (PRE) and after (POST) the induction of general anesthesia. In this group 38 patients developed atrial fibrillation (AF) after surgery, while the remaining individuals did not (noAF, n=96). Both CJTESAP, R→HP|R and CJTEHP, R→SAP|R distinguished AF from noAF individuals in the PRE condition, suggesting an impairment of HP-SAP closed-loop regulation in AF group and the possibility to identify subjects at higher risk to develop post-surgery AF.

Acute effects of unilateral temporary stellate ganglion block on human atrial electrophysiological properties and atrial fibrillation inducibility

In experimental models, stellate ganglion block (SGB) reduces the induction of atrial fibrillation (AF), while data in humans are limited. The aim of this study was to assess the effect of unilateral SGB on atrial electrophysiological properties and AF induction in patients with paroxysmal AF. Thirty-six patients with paroxysmal AF were randomized in a 2:1 order to temporary, transcutaneous, pharmaceutical SGB with lidocaine or placebo before pulmonary vein isolation. Lidocaine was 1:1 randomly infused to the right or left ganglion. Before and after randomization, atrial effective refractory period (ERP) of each atrium, difference between right and left atrial ERP, intra- and interatrial conduction time, AF inducibility, and AF duration were assessed. After SGB, right atrial ERP was prolonged from a median (1st-3rd quartile) of 240 (220-268) ms to 260 (240-300) ms (P < .01) and left atrial ERP from 235 (220-260) ms to 245 (240-280) ms (P < .01). AF was induced by atrial pacing in all 24 patients before SGB, but only in 13 patients (54%) after the intervention (P < .01). AF duration was shorter after SGB: 1.5 (0.0-5.8) minutes from 5.5 (3.0-12.0) minutes (P < .01). Intra- and interatrial conduction time was not significantly prolonged. No significant differences were observed between right and left SGB. No changes were observed in the placebo group. Unilateral temporary SGB prolonged atrial ERP, reduced AF inducibility, and decreased AF duration. An equivalent effect of right and left SGB on both atria was observed. These findings may have a clinical implication in the prevention of drug refractory and postsurgery AF and deserve further clinical investigation.

POLYMORPHISM OF THE INTERLEUKIN-6, INTERLEUKIN-10, SUPEROXIDE DISMUTASE AND ANGIOTENSIN CONVERTING ENZYME GENES, AND THE RISK OF ATRIAL FIBRILLATION AFTER CARDIOSURGERY

Aim. To reveal the relation of gene polymorphisms of interleukin-6 (IL6, C174G), interleukin-10 (IL10, C592A), superoxide dismutase (SOD1, G8958A) and angiotensin converting enzyme (ACE, Alu Ins/Del) with postsurgery atrial fibrillation (PSAF) after coronary bypass grafting (CBG) in coronary heart disease patients (CHD). Material and methods. Totally, 80 CHD patients studied, had been admitted for CBG. Genotype assessed for IL6 C174G, IL10 C592A, SOD1 G8958A and ACE Alu Ins/Del. According to PSAF, patients were selected to 2 groups: 1 group — non- PSAF (56 patients, 78,6% males, mean age 61,0±7,5 years), 2 group — with PSAF (24 patients, 83,3% males, mean age 64,7±7,9 years). Results. Analysis of genetic polymorphisms showed the prevalence of СG IL6 C174G (57,2%) genotype, СС IL10 C592A (62,5%), GG SOD1 G8958A (87,5%), I/D ACE Alu Ins/Del (60,8%) among non-arrhythmic patients. In PSAF most prevalent were genotypes СG IL6 C174G (54,2%), СА IL10 C592A (54,2%), GG SOD1 G8958A (79,2%), I/D ACE Alu (58,4%). In multifactor regression analysis, odds ratio for PSAF in allele G IL6 C174G was 1,5 (95% CI, 0,69-3,44, р=0,29), for allele A IL10 C592A — 2,7 (95% CI, 1,2-6,9, р=0,04), for allele A SOD1 G8958A — 2,1 (95% CI, 0,7-6,2, р=0,19), for allele D gene ACE Alu Ins/Del — 0,9 (95% CI, 0,27-3,1, р=0,89). Conclusion. Therefore, presence of allele A of candidate gene IL10 C592A might force the onset of atrial fibrillation during early postsurgery period in coronary bypass.

The future of atrial fibrillation therapy: intervention on heat shock proteins influencing electropathology is the next in line

Atrial fibrillation (AF) is the most common age-related cardiac arrhythmia accounting for one-third of hospitalisations. Treatment of AF is difficult, which is rooted in the progressive nature of electrical and structural remodelling, called electropathology, which makes the atria more vulnerable for AF. Importantly, structural damage of the myocardium is already present when AF is diagnosed for the first time. Currently, no effective therapy is known that can resolve this damage.Previously, we observed that exhaustion of cardioprotective heat shock proteins (HSPs) contributes to structural damage in AF patients. Also, boosting of HSPs, by the heat shock factor-1 activator geranylgeranylacetone, halted AF initiation and progression in experimental cardiomyocyte and dog models for AF. However, it is still unclear whether induction of HSPs also prolongs the arrhythmia-free interval after, for example, cardioversion of AF.In this review, we discuss the role of HSPs in the pathophysiology of AF and give an outline of the HALT&REVERSE project, initiated by the HALT&REVERSE Consortium and the AF Innovation Platform. This project will elucidate whether HSPs (1) reverse cardiomyocyte electropathology and thereby halt AF initiation and progression and (2) represent novel biomarkers that predict the outcome of AF conversion and/or occurrence of post-surgery AF.