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Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulate fluid homoeostasis. [...]atrial cells (both cardiomyocytes and non-cardiomyocyte elements like fibroblasts, endothelial cells, and neurons) react briskly and extensively to pathological stimuli [3] and are susceptible to a range of genetic influences [7]. [...]atrial pathologies have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk [1,8]. [...]while some pathological processes may affect the atria very selectively (e.g. atrial fibrillation-induced remodelling), most cardiomyopathies that affect the atria also involve the ventricles to a greater or lesser extent. [...]we have proposed here a working histological/ pathopysiological classification scheme for atrial cardiomyopathies ( Table 1; Fig. 1). [...]this classification is purely descriptive and in contrast to other classifications (NYHA class, CCS class etc.), there is no progression in severity from EHRAS class I to EHRAS IV ( Table 2). Unlike ventricular cardiomyocytes, atrial cardiomyocytes do not possess an extensive T-tubule network but they do have prominent sarcoplasmic reticulum (SR) elements known as Z-tubules [33]. [...]the atrial sarcolemma does not protrude into the cell, and voltage-operated Ca2+ channels mainly function at the cell periphery [34].

A thorough understanding of advanced device algorithms designed to promote intrinsic atrioventricular conduction is mandatory to allow appropriate management of arrhythmias induced by pacing, particularly when other types of tachycardia are involved. A thorough understanding of advanced device algorithms designed to promote intrinsic atrioventricular conduction is mandatory to allow appropriate management of arrhythmias induced by pacing, particularly when other types of tachycardia are involved.

Table of Contents 1 Introduction 3 1.1 Evidence review 3 1.2 Relationships with industry and other conflicts 4 2 Decline of cognitive function: terminology and epidemiology 4 2.1 Terminology: cognitive decline, mild cognitive impairment, and dementia 4 2.2 Epidemiology of dementia 4 3 Methods for assessment of cognitive function 4 4 Role of imaging 5 5 Atrial fibrillation and cognitive function 8 5.1 Atrial fibrillation, overt stroke, and cognitive function 8 5.2 Atrial fibrillation, silent stroke, and cognitive function 9 5.3 Atrial fibrillation and cognitive function in the absence of stroke 10 5.4 Assessment of cognitive function in atrial fibrillation patients in clinical practice 11 5.5 Prevention of cognitive dysfunction in atrial fibrillation patients 12 6 Other arrhythmias and cognitive dysfunction 13 6.1 Cognitive dysfunction in patients with regular supraventricular tachycardias 13 6.2 Cognitive impairment after cardiac arrest 13 6.2.1 Brain injury after non-fatal cardiac arrest 13 6.2.2 Memory impairment after cardiac arrest 14 6.2.3 Therapeutic hypothermia to prevent cognitive impairment after cardiac arrest 14 6.3 Cardiac implantable electronic devices and cognitive dysfunction 14 6.4 Catheter ablation 15 6.5 Implications for electrophysiological procedures and cognitive function 16 7 Current knowledge gaps, future directions, and areas for research 19 8 Recommendations 20 References 20 INTRODUCTION This expert consensus statement of the European Heart Rhythm Association (EHRA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), and the Latin American Heart Rhythm Society (LAHRS) summarizes the consensus of the international writing group and is based on a thorough review of the medical literature regarding cognitive function in arrhythmias. SEE PDF.] 2This categorization for our consensus document should not be considered as being directly similar to that used for official society guideline recommendations which apply a classification (I-III) and level of evidence (A, B, and C) to recommendations. [...]a green heart indicates a “should do this” consensus statement or indicated treatment or procedure that is based on at least one randomized trial, or is supported by strong observational evidence that it is beneficial and effective. [...]this is a consensus document that includes evidence and expert opinions from several countries. In 2010, 58% of all people with dementia lived in countries with low or middle incomes, with this proportion anticipated to rise to 63% in 2030 and 71% in 2050. [...]dementia is a burgeoning global public health problem that prompts an urgent and more comprehensive understanding of its risk factors with the aim to discover novel prevention strategies.

We evaluated the factors affecting epicardial radiofrequency (RF) lesion formation in normal ventricular myocardium. In 16 dogs, a minithoracotomy was made and a sheath was placed in the pericardial space. Standard ablation lesions (4-mm tip catheter; 70 ( composite function) C/60 seconds) were created in each ventricle under fluoroscopy guidance (n = 7) or hand-held with direct visualization of the catheter to assure optimal electrode-tissue contact (n = 6). In the latter, thermally-shielded (TS) electrodes (50% tip surface along its 4 mm length) were used in 3/6 dogs. Catheter tip (4 mm) irrigation (13 mL/minutes; 40 ( composite function) C/60 seconds) was employed with conventional techniques in 3 additional dogs. With optimal electrode-tissue contact (11 lesions), power (3.4 +/- 2.3 W vs. 16 +/- 13 W; p < 0.001) and pacing thresholds (0.2 +/- 0.0 mA vs. 3.6 +/- 5.7 mA; p = 0.004) were lower than standard RF (25 lesions). However, lesion dimensions were similar and transmural lesions did not occur (depth 2.8 +/- 1.1 mm vs. 3.0 +/- 1.5 mm). Catheter irrigation allowed high power outputs (43 +/- 6.1 W; p < 0.001) generating transmural lesions, 5/9 (55%), depth 6.4 +/- 2.1 mm. At constant power (2 W), catheter-tip temperature (52 +/- 5.2( composite function) C vs. 57 +/- 6.6( composite function) C; p = NS) and lesion (10 in each group) dimensions were similar for conventional and TS electrodes, but damage to parietal pericardium and lungs occurred with conventional electrodes only (70% vs. 0% p = 0.02). Standard epicardial RF ablation does not produce deep lesions and exhibits a significant energy loss probably due to poor electrode-tissue contact. Catheter irrigation allows delivery of high power outputs to the epicardium consistently creating deeper lesions than standard ablation. TS electrodes may reduce damage to neighboring structures during epicardial RF ablation.

Purpose Late lesion extension may be involved in the genesis of delayed radiofrequency (RF) effects. Because RF lesion is thermally mediated, we hypothesized that induction of heat shock response (thermotolerance) would modulate lesion healing. We evaluated the effects of thermotolerance on the dimensions and remodeling of RF lesions in a rat model of heart failure. Methods Wistar rats (weight 300 g) subjected to heat stress ( n  = 22, internal temperature of 42 °C for 10 min) were compared to controls ( n  = 22, internal temperature of 37 °C for 10 min). After 48 h (peak of HSP70 myocardial concentration), a modified unipolar RF lesion (customized catheter, tip 4.5 mm in diameter; 12 W; 10 s) was created on the left ventricular free wall. Animals were sacrificed 2 h ( n  = 10 per group) and 4 weeks ( n  = 12 per group) after ablation for lesion analysis. An echocardiogram was obtained at 4 weeks. Results There was no difference between groups regarding the size of acute (controls 27 ± 2 vs. treated 27 ± 3 mm 2 ) and chronic lesions (controls 17 ± 1 vs. treated 19 ± 1 mm 2 ). Histology of lesions did not differ between groups. The echocardiogram revealed dilation of the cavities and moderate systolic dysfunction without difference between groups. Acute lesion dimensions were similar between control and treated animals over time (ablation undertaken 3, 12, 24, 48, and 72 h after hyperthermia) and also using a conventional ablation catheter (50 °C; 15 W; 10 s). Conclusion Thermotolerance does not reduce the size or remodeling of RF lesions in the rat myocardium.