Risk Of Atrial Arrhythmias Research Articles

Assessment of the atrial electromechanical properties of patients with human immunodeficiency virus.

The relationship between atrial fibrillation and human immunodeficiency virus (HIV) infection was evaluated. Electro-echocardiographic methods can be used to predict the development of atrial fibrillation (AF). In this study, we aimed to investigate the atrial electromechanical delay (AEMD) parameters of HIV (+) patients. Forty-two HIV (+) patients and 40 HIV (-) healthy volunteers were prospectively enrolled in this study. The electromechanical properties of the subjects' atria were evaluated with tissue Doppler imaging. The left-AEMD, right-AEMD and inter-AEMD were increased in the HIV (+) patients relative to the controls (p=0.003, p<0.001, and p<0.001, respectively). The CD4 count was inversely correlated with the inter-AEMD (r=-0.428, p<0.001). The CD4 count was an independent predictor of the inter-AEMD (β=0.523, p=0.007). Our study demonstrated that both the inter- and intra-atrial electromechanical delays were prolonged in the patients with HIV. This non-invasive and simple technique may provide significant contributions to the assessment of the risk of atrial arrhythmia in patients with HIV.

Effectiveness of Early Invasive Therapy for Atrial Tachycardia in Adult Atrial-Baffle Survivors.

Adults who underwent complex atrial baffling as children via Mustard or Senning procedures are at heightened risk for atrial arrhythmias. Antiarrhythmic therapies are typically ineffective in this population. Accordingly, our team of pediatric and adult electrophysiologists investigated the effectiveness of early invasive transbaffle-access techniques to perform early radiofrequency ablation at the source of these clinically significant arrhythmias. For this retrospective study, we selected 11 adult survivors of atrial baffling (mean age, 34 ± 9 yr) who underwent clinically indicated electrophysiologic study after no more than one trial of antiarrhythmic therapy. Using transbaffle-access techniques and 3-dimensional mapping of the venous atria, we found 12 inducible arrhythmias in 10 patients: intra-atrial reentrant tachycardia (n=6), atrioventricular nodal reentrant tachycardia (n=3), focal atrial tachycardia (n=2), and repetitive double firing of the atrioventricular node (n=1). Defining success as short- and midterm freedom from arrhythmia, we analyzed outcomes of radiofrequency ablation at 1 and 6 months. At 1 month, ablation was 100% successful. At 6 months, after 11 ablations in 9 patients, 5 patients had no clinical recurrence, 2 had improved arrhythmia control from minimal medical therapy, and 2 were to undergo repeat study for recurrent tachycardia. In the recurrence-free patients, arrhythmias during electrophysiology study matched the types found clinically before the study. To our knowledge, this is the largest one-year cohort of adult survivors of atrial baffling to have undergone study by a combined pediatric-adult electrophysiology team. We conclude that early invasive transbaffle access for ablating diverse atrial tachyarrhythmias was effective in these patients.

Atrial tachyarrhythmia in adult congenital heart disease.

The adult congenital heart disease (ACHD) population continues to grow and most cardiologists, emergency room physicians and family doctors will intermittently come into contact with these patients. Oftentimes this may be in the setting of a presentation with atrial tachyarrhythmia; one of the commonest late complications of ACHD and problem with potentially serious implications. Providing appropriate initial care and ongoing management of atrial tachyarrhythmia in ACHD patients requires a degree of specialist knowledge and an awareness of certain key issues. In ACHD, atrial tachyarrhythmia is usually related to the abnormal anatomy of the underlying heart defect and often occurs as a result of surgical scar or a consequence of residual hemodynamic or electrical disturbances. Arrhythmias significantly increase mortality and morbidity in ACHD and are the most frequent reason for ACHD hospitalization. Intra-atrial reentrant tachycardia and atrial fibrillation are the most prevalent type of arrhythmia in this patient group. In hemodynamically unstable patients, urgent cardioversion is required. Acute management of the stable patient includes anticoagulation, rate control, and electrical or pharmacological cardioversion. In ACHD, rhythm control is the preferred management strategy and can often be achieved. However, in the long-term, medication side-effects can prove problematic. Electrophysiology studies and catheter ablation are important treatments modalities and in certain cases, surgical or percutaneous treatment of the underlying cardiac defect has a role. ACHD patients, especially those with complex CHD, are at increased risk of thromboembolic events and anticoagulation is usually required. Female ACHD patients of child bearing age may wish to pursue pregnancies. The risk of atrial arrhythmias is increased during pregnancy and management of atrial tachyarrhythmia during pregnancy needs specific consideration.

Fine particulate air pollution and premature atrial contractions: The REasons for Geographic And Racial Differences in Stroke study.

Several reports have suggested that particulate matter (PM) exposure increases the risk for atrial arrhythmias. However, data from large-scale epidemiologic studies supporting this hypothesis are lacking. We examined the association of PM <2.5 μm in diameter (PM2.5) concentration with premature atrial contractions (PACs) in 26,609 (mean age=65±9.4 years; 55% female; 41% black) participants from the REGARDS (REasons for Geographic And Racial Differences in Stroke) study. Estimates of short- (2 weeks) and long-term (1 year) PM2.5 exposure were computed before each participant's baseline visit using geographic information system data on the individual level at the coordinates of study participants' residences. PACs were identified from baseline electrocardiograms. A total of 2140 (8.2%) participants had evidence of PACs on the baseline electrocardiogram. Short-term PM2.5 (per 10 μg/m3) exposure was not associated with PACs (OR=1.09, 95% CI=0.98, 1.23). Increases in long-term PM2.5 (per 10 μg/m3) were associated with PACs (OR=1.40, 95% CI=1.10, 1.78). Interactions were not detected for short- and long-term PM2.5 exposure by age, sex, or race. Long- but not short-term PM2.5 exposure is associated with PACs. This suggests a role for long-term PM2.5 exposure in initiating supraventricular arrhythmias that are triggered by PACs.

SOLUBLE ST2 AND HIGH SENSITIVITY CARDIAC TROPONIN-T LEVELS PREDICT ATRIAL FIBRILLATION ABLATION OUTCOME

ST2 is associated with cardiac hypertrophy and fibrosis. High sensitivity cardiac troponin-T (hs-cTnT) is a marker of cardiac injury. Our hypothesis is that hs-cTnT stratifies ST2 defined risk of atrial arrhythmia (AA) recurrence. 23 patients undergoing AF ablation were enrolled. All underwent wide

High fat diet induced alterations of atrial electrical activities in mice.

Obesity is a well-known risk factor for various cardiovascular diseases. Recent clinical data showed that overweight and obese patients have higher incidence of atrial fibrillation (AF) compared with individuals with normal body weights, but the underlying mechanisms remain to be elucidated. In this study, we investigated the effects of a high fat diet on atrial activities in mice. ICR male mice were fed a regular diet (RD) or a high fat diet (HFD) for 8 weeks. Mice fed HFD showed significantly greater body weight gains and visceral fat accumulation compared with RD mice. Under anesthetic condition, baseline arterial blood pressure and heart rate were not significantly different between RD and HFD groups. Although no spontaneous or atrial stimulation-induced atrial fibrillation was observed, this study revealed several alterations in the activities and protein levels in the atria in HFD mice. Surface electrocardiogram (ECG) revealed significantly shortened PR interval in HFD mice. In the atrial stimulation experiments, the sinoatrial (SA) node recovery time was significantly prolonged whereas the atrial effective refractory period was significantly reduced in HFD mice as compared with RD mice. Western blot showed protein levels of two major potassium channels, Kv1.5 and Kv4.2/3, were significantly increased in atria of HFD mice. These data indicate that HFD induces atrial electrophysiological remodeling in mice, which may be a potential mechanism underlying the increased risk for atrial arrhythmias in obesity and metabolic disorders.

Differential atrial performance at rest and exercise in athletes: Potential trigger for developing atrial dysfunction?

Highly trained athletes show an increased risk of atrial arrhythmias. Little is known about atrial volumes and function during exercise in this population. Our aim was to analyze atrial size and contractile function during exercise. Fifty endurance athletes with 11±8h of training per week and 30 sedentary control subjects were included. Echocardiography was performed at baseline and during exercise. Left (LA) and right atrial (RA) size and function were assessed by two-dimensional echocardiography. Peak negative strain (Sa) during atrial contraction and active atrial emptying volume (AEV) were measured. Athletes and control subjects showed a significant increment of deformation and AEV of both atria with exercise (P<0.01 vs baseline for LA and RA). Among athletes, a subgroup with significant LA (n=8)/RA (n=15) dilatation (≥40mL/m2 ) showed a significantly lower increment in AEV with exercise (LA∆AEV: 1.4±1.1mL/m2 vs 2.1±0.9mL/m2 , P=0.04; RA∆AEV: 0.9±0.8mL/m2 vs 2.3±1.1mL/m2 , P<0.01) and lower increment in deformation vs other athletes (LA∆Sa: -3.2±2.9% vs -9.5±4.4%, P<0.01; RA∆Sa: -2.5±3.3% vs. -9.8±3.3%, P<0.01). During exercise, active atrial strain increases, but less in athletes compared to controls, but due to larger atrial volumes, they reached similar increases in atrial emptying volume. However, this overall lesser deformation increases from a subgroup with significant atrial dilatation showing impairment in atrial contractile reserve.

Rosuvastatin Alleviates Type 2 Diabetic Atrial Structural and Calcium Channel Remodeling.

Recent evidence has indicated that type 2 diabetes mellitus is related to an increased risk of atrial arrhythmias, which might result from atrial structural and electrical remodeling. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins), known as lipid-lowering agents, have been shown to exert antiarrhythmic effects both in experimental models and in humans. In this study, we postulate that atrial structural and calcium channel remodeling may occur in streptozotocin-induced type 2 diabetic rats and can be alleviated by rosuvastatin (RSV) therapy. We randomly divided Wistar rats into control, untreated diabetic, RSV-treated control, and RSV-treated diabetic animals. After treatment with RSV for 4 weeks, rats were assessed by metabolic tests, histopathology, and transmission electron microscopy. The expression of Cav1.2, Cav3.1, and Cav3.2 in atrial tissues was detected by real-time reverse transcriptase polymerase chain reaction and Western blot, and inward calcium currents (l(Ca-L) and l(Ca-T)) were recorded in isolated atrial myocytes using patch-clamp techniques. Compared with controls, diabetic rats displayed severe metabolic disorders and a disorganized cellular ultrastructure. In diabetic rats, the expression of Cav1.2 mRNA and protein was significantly decreased, whereas that of Cav3.1 was significantly increased. Long-term RSV treatment partially relieved some pathological changes in diabetic rats. However, Cav3.2 mRNA and protein remained unchanged in control and diabetic groups and was unaffected by RSV. Diabetic atrial myocytes showed significantly reduced L-type but increased T-type, Ca (2+) currents, and this effect was significantly reversed by RSV. In conclusion, long-term RSV therapy can alleviate structural and calcium channel remodeling in the type 2 diabetic rat atrium.

Circulation : Clinical Summaries

<i>Circulation</i> : Clinical Summaries

Electrocardiographic P-Wave Duration, QT Interval, T Peak to End Interval and Tp-e/QT Ratio in Pregnancy with Respect to Trimesters.

P-wave duration helps to determine the risk of atrial arrhythmia, especially atrial fibrillation. QT interval, T peak to end interval (Tp-e), and Tp-e/QT ratio are electrocardiographic indices related to ventricular repolarization which are used to determine the risk of ventricular arrhythmias. We search for any alterations in electrocardiographic indices of arrhythmia in the pregnancy period with respect to trimesters. We enrolled 154 pregnant and 62 nonpregnant, healthy women into this cross-sectional study. Maximum and minimum P-wave durations (Pmax, Pmin), and QT intervals (QTmax, QTmin) were measured from 12 leads. QT measurements were corrected using Fridericia (QTc-Fr) and Bazett's (QTc-Bz) correction. Tp-e interval was obtained from the difference between QT interval, and QT peak interval (QTp) measured from the beginning of the QRS until the peak of the T wave. Tp-e/QT ratio was calculated using these measurements. Pmax were 93.0 ± 9.1, 93.9 ± 8.9, 97.9 ± 5.6, 99.0 ± 6.1 in nonpregnant women, first, second, third trimesters of pregnancy, respectively (P = 0.001); whereas Pmin values were not significantly different. QTc-Fr max were 407.4 ± 14.2, 408.5 ± 16.1, 410.1 ± 13.1, 415.1 ± 10.1 (P = 0.007); Tp-e were 72.7 ± 6.2, 73.2 ± 6.5, 77.2 ± 8.9, 87.2 ± 9.6 (P < 0.001); and Tp-e/QT were 0.17 (0.14-0.20), 0.17 (0.14-0.20), 0.18 (0.15-0.23), 0.20 (0.16-0.25) in nonpregnant women, first, second, and third trimesters of pregnancy respectively (P < 0.001). None of the participants experienced any arrhythmic event. P-wave duration is prolonged in the second trimester, and resumes a plateau thereafter. Maximum QTc interval, Tp-e interval and Tp-e/QT ratio are increased in the late pregnancy. Although these indices are altered during the course of pregnancy, they all remain in the normal ranges.

Congenital heart disease in the older adult: a scientific statement from the American Heart Association.

The population of adults with congenital heart disease (ACHD) has increased dramatically over the past few decades, with many people who are now middle-aged and some in the geriatric age range. This improved longevity is leading to increased use of the medical system for both routine and episodic care, and caregivers need to be prepared to diagnose, follow up, and treat the older adult with congenital heart disease (CHD). The predictable natural progression of CHD entities and sequelae of previous interventions must now be treated in the setting of late complications, acquired cardiac disease, multiorgan effects of lifelong processes, and the unrelenting process of aging. Despite the advances in this field, death rates in the population from 20 to >70 years of age may be twice to 7 times higher for the ACHD population than for their peers.1 This American Heart Association (AHA) scientific statement will focus on the older adult (>40 years old) with CHD. It is meant to be complementary to the 2008 American College of Cardiology (ACC)/AHA guidelines for ACHD and orient the reader to the natural history, ramifications of childhood repair, and late initial diagnosis of CHD in the older adult. This population with CHD is unique and distinct from both the pediatric and young adult populations with CHD. Much of the information we provide is from scientific research combined with clinical experience from longitudinal care. We emphasize that this is the beginning of a discussion regarding this rapidly growing population, and continued research aimed at the progression of disease and complications reviewed here is necessary to advance the field of ACHD with the scientific rigor it deserves. ACHD encompass a broad range of presentations. There are people who are diagnosed for the first time in adulthood, as well as those with prior palliative repair …

Effect of Vitamin D Replacement on Atrial Electromechanical Delay in Subjects with Vitamin D Deficiency.

Limited data are available regarding cardiac arrhythmias in vitamin D (VitD) deficiency. Therefore, we aimed to assess whether atrial electromechanical delay (AEMD) measured by tissue Doppler imaging (TDI), which is an indicator for atrial fibrillation (AF) development, is prolonged in patients with VitD deficiency as compared to the control group. The effect of vitD replacement on AEMD was also evaluated. In this prospective study a total of 28 VitD-deficient and 56 age-, gender-, and BMI-matched VitD-sufficient healthy participants were enrolled. P-wave dispersion (PWd) was calculated on the 12-lead electrocardiogram. Both intra- and inter-AEMD were calculated by TDI. Measurements were performed at baseline in both groups and were repeated after 6-month replacement therapy in subjects with vitD deficiency. PWd and inter- and left intra-AEMD were significantly prolonged in patients with VitD deficiency compared to the control group (P < 0.001). While serum 25(OH)D levels were significantly and negatively correlated with left intra-AEMD (r = -0.657, P < 0.001), there was a positive correlation between serum 25(OH)D level and PWd (r = 0.523, P < 0.001). The serum 25(OH)D level was found as the independent predictor of the both left intra- and inter-AEMD in the multivariate linear regression analysis (β:-0.552, P < 0.001 and β:-0.555, P < 0.001, respectively). The serum 25(OH)D level was significantly increased after replacement therapy. While inter-AEMD was significantly decreased (P = 0.013), there was no change in PWD and left and right intra-AEMD (P > 0.05) following replacement therapy. PWd and left intra- and inter-AEMD are increased in patients with VitD deficiency. The serum 25(OH)D level was found as an independent predictor for AEMD in patients with VitD deficiency. Also a significant decrement was observed in inter-AEMD following vitD replacement therapy. Studies with longer follow-up are needed to investigate whether vitD-deficient patients with prolonged AEMD develop clinical arrhythmia and vitD replacement reduces the risk of atrial arrhythmias.

Progressive age-associated activation of JNK associates with conduction disruption in the aged atrium

Connexin43 (Cx43) is critical for maintaining electrical conduction across atrial muscle. During progressive ageing atrial conduction slows associating with increasing susceptibility to arrhythmias. Changes in Cx43 protein expression, or its phosphorylation status, can instigate changes in the conduction of the cardiac action potential. This study investigated whether increased levels of activated c-jun N-terminal kinase (JNK) is responsible for the decline of Cx43 during ageing. Right atria from guinea pigs aged between 1 day and 38 months of age were examined. The area of the intercalated disc increased with age concurrent with a 75% decline in C43 protein expression. An age-dependent increase in activated-JNK correlated with a rise in phosphorylated Cx43, but also slowing of action potential conduction velocity across the atria from 0.38±0.01m/s at 1 month of age to 0.30±0.01m/s at 38 months. The JNK activator anisomycin increased activated JNK in myocytes and reduced Cx43 protein expression simulating ageing. The JNK inhibitor SP600125, was found to eradicate almost all trace of Cx43 protein. We conclude that in vivo activation of JNK increases with age leading to the loss of Cx43 protein resulting in impaired conduction and contributing to the increasing risk of atrial arrhythmias with advancing age.

Preoperative brain natriuretic peptide and atrial arrhythmias after coronary artery bypass graft surgery.

To assess the association of preoperative brain natriuretic peptide with atrial arrhythmias and length of stay after cardiac surgery. A retrospective data analysis. All data were collected from patients who underwent cardiac surgery at a single institution, an academic hospital, between 2005 and 2010. Patient data were collected from the authors' institution's Perioperative Health Documentation System of cardiac surgeries. None. The major findings were that individuals with a 10-pg/mL increase in brain natriuretic peptide were 1.005 (95% CI: 1.002, 1.009) times more likely to have an atrial arrhythmia than those with no increase in brain natriuretic peptide. A brain natriuretic peptide value ≥306 pg/mL was calculated to best predict an atrial arrhythmia. Those above the threshold were 1.455 (95% CI: 1.087, 1.947) times more likely to have an atrial arrhythmia than those below the threshold. Individuals above the threshold had a median of 3 days in the intensive care unit compared to 1 day for those below the threshold, as well as median hospital stays of 11 days for those below the threshold. The results indicated that elevated brain natriuretic peptide was associated with increased risk of atrial arrhythmias and prolonged length of hospital stay after cardiac surgery. Identifying at-risk patients is important to guide preventative strategies for postoperative atrial arrhythmias.

Perturbed atrial calcium handling in an ovine model of heart failure: Potential roles for reductions in the L-type calcium current

Heart failure (HF) is commonly associated with reduced cardiac output and an increased risk of atrial arrhythmias particularly during β-adrenergic stimulation. The aim of the present study was to determine how HF alters systolic Ca2+ and the response to β-adrenergic (β-AR) stimulation in atrial myocytes. HF was induced in sheep by ventricular tachypacing and changes in intracellular Ca2+ concentration studied in single left atrial myocytes under voltage and current clamp conditions. The following were all reduced in HF atrial myocytes; Ca2+ transient amplitude (by 46% in current clamped and 28% in voltage clamped cells), SR dependent rate of Ca2+ removal (kSR, by 32%), L-type Ca2+ current density (by 36%) and action potential duration (APD90 by 22%). However, in HF SR Ca2+ content was increased (by 19%) when measured under voltage-clamp stimulation. Inhibiting the L-type Ca2+ current (ICa-L) in control cells reproduced both the decrease in Ca2+ transient amplitude and increase of SR Ca2+ content observed in voltage-clamped HF cells. During β-AR stimulation Ca2+ transient amplitude was the same in control and HF cells. However, ICa-L remained less in HF than control cells whilst SR Ca2+ content was highest in HF cells during β-AR stimulation. The decrease in ICa-L that occurs in HF atrial myocytes appears to underpin the decreased Ca2+ transient amplitude and increased SR Ca2+ content observed in voltage-clamped cells.

Effect of Years of Endurance Exercise on Risk of Atrial Fibrillation and Atrial Flutter

Emerging evidence suggests that endurance exercise increases the risk for atrial fibrillation (AF) in men, but few studies have investigated the dose-response relation between exercise and risk for atrial arrhythmias. Both exposure to exercise and reference points vary among studies, and previous studies have not differentiated between AF and atrial flutter. The aim of this study was to assess the risk for atrial arrhythmias by cumulative years of regular endurance exercise in men. To cover the range from physical inactivity to long-term endurance exercise, the study sample in this retrospective cohort study was based on 2 distinct cohorts: male participants in a long-distance cross-country ski race and men from the general population, in total 3,545 men aged ≥ 53 years. Arrhythmia diagnoses were validated by electrocardiograms during review of medical records. Regular endurance exercise was self-reported by questionnaire. A broad range of confounding factors was available for adjustment. The adjusted odds ratios per 10 years of regular endurance exercise were 1.16 (95% confidence interval 1.06 to 1.29) for AF and 1.42 (95% confidence interval 1.20 to 1.69) for atrial flutter. In stratified analyses, the associations were significant in cross-country skiers and in men from the general population. In conclusion, cumulative years of regular endurance exercise were associated with a gradually increased risk for AF and atrial flutter.

Association of thoracic epidural analgesia with risk of atrial arrhythmias after pulmonary resection: a retrospective cohort study.

Atrial arrhythmias are common after non-cardiac thoracic surgery. We tested the hypothesis that TEA reduces the risk of new-onset atrial arrhythmias after pulmonary resection. We evaluated patients who had pulmonary resection. New-onset atrial arrhythmias detected before hospital discharge was our primary outcome. Secondary outcomes included other cardiovascular complications, pulmonary complications, time-weighted average pain score over 72 h, and duration of hospitalization. Patients with combination of general anesthesia and TEA were matched on propensity scores with patients given general anesthesia only. The matched groups were compared by use of logistic regression, linear regression, or Cox proportional hazards regression, as appropriate. Among 1,236 patients who had pulmonary resections, 937 received a combination of general anesthesia and TEA (TEA) and 299 received general anesthesia only (non-TEA). We successfully matched 311 TEA patients with 132 non-TEA patients. We did not find a significant association between TEA and postoperative atrial arrhythmia (odds ratio (95 % CI) of 1.05 (0.50, 2.19), P = 0.9). TEA was not significantly associated with length of hospital stay or postoperative pulmonary complications (odds ratio (95 % CI) of 0.71 (0.22, 2.29), P = 0.47). TEA patients experienced fewer postoperative cardiovascular complications; although the association was not statistically significant (odds ratio (95 % CI) of 0.30 (0.06, 1.45), P = 0.06). Time-weighted average pain scores were similar in the two groups. TEA was not associated with reduced occurrence of postoperative atrial arrhythmia. Although postoperative pulmonary complications were similar with and without TEA, TEA patients tended to experience fewer cardiovascular complications.

The Contribution of the Common Single-nucleotide Polymorphisms of β1-Adrenoreceptor Gene to Cardiovascular Alteration in Patients with Thyrotoxicosis

The detection of a genetic organization of common diseases is one of the first key direction in modern medicine. In thyrotoxicosis, identification of genetic predictors, defining remission and the risk of cardiovascular complications is of a great importance. We gave attention to the second of above mentioned aspects. Candidates for genetic prediction are the genes regulated by triiodothyronine and playing a key role in changing of the myocardial contractility and arrhythmogenesis. There are SNPs of the β1-adrenergic receptor (ADRB1) gene among them: polymorphism in the 389 codon (Gly389Arg) and polymorphism in codon 49 (Ser49Gly). The investigation goal was to determine whether the deleterious effects on cardiovascular system of the thyroid hormones excess in people with thyrothoxicosis were modified by polymorphic variants of ADRB1 gene. So we investigated the possible link of these two SNPs with clinicopathologic findings, echocardiographic parameters and the changes during therapy in 165 patients with a thyrotoxicosis caused by Gravesdisease without any nonthyrotoxic cardiovascular disorders. The data analysis demonstrates that both Gly389Arg and Ser49Gly polymorphisms have very moderate influence on the risk of atrial arrhythmias, left ventricular hypertrophy and its type (concentric or eccentric). Genotype Gly389Gly (Gly389Arg polymorphism) or genotype Gly49Gly (Ser49Gly polymorphism) carriers have tendency to the lowest risk of cardiovascular complications during thyrohoxicosis, but no statistically significant effects were revealed.

P-wave duration dispersion in patients with lichen planus

Dear Editors, We have read the article “Increased P-wave dispersion (PWD) in patients with newly diagnosed lichen planus (LP)” by Sahin et al. (1). These researchers aimed to investigate PWD in patients with LP, and they concluded that PWD increased in the surface electrocardiographic measurements of LP patients. This result may be important for the early detection of subclinical cardiac involvement. This study provides important information on this clinically relevant condition. The ready availability of this parameter at no additional cost may encourage its wider use in clinical practice in the future. The authors should be commended for their contribution. LP is a chronic inflammatory autoimmune mucocutaneous disease. Although its pathogenesis is not fully understood, it is recognized as a chronic disease that is almost certainly immunologically mediated. Several studies have shown that prolonged PWD has predictive value for the development of atrial fibrillation (AF) in patients with or without apparent heart disease. In addition to predicting AF, prolonged PWD has also been observed in various clinical settings. Cross-sectional studies have demonstrated that subjects with hypertension, obesity, diabetes, and coronary artery disease have prolonged PWD compared with controls. Apart from the above-mentioned diseases, some conditions, such as seasonal variation, alcohol intake, and caffeine ingestion, have been demonstrated to affect PWD. Hepatic steatosis is associated with metabolic and hemodynamic abnormalities induced by insulin resistance and severe inflammation. Increased PWD may indicate a risk of atrial arrhythmia in patients with inflammation-based hepatic steatosis (2). Prolonged PWD has also been observed in patients with stable asthma (3). Furthermore, PWD is independently associated with renal function. In a previous study, researchers showed that PWD is a novel parameter that may accurately predict AF and was increased in renal failure patients (4). Prolonged atrial electromechanical coupling time and impaired mechanical atrial functions may be related to the increased incidence of arrhythmias. Thyroid hormone levels may affect atrial electromechanical function. In a previous study, researchers demonstrated prolonged PWD in patients with thyroid disorders (5). Additionally, some medications, such as propylthiouracil and methimazole, were found to reduce the P wave duration and dispersion (6). Furthermore, antihypertensive therapy, such as short-term treatment with quinapril, irbesartan, atenolol, and nebivolol, reduces the duration of PWD. This effect is independent of blood pressure and heart rate changes. Additionally, lipid-lowering therapy significantly reduced PWD, a finding that may be important in the prevention of AF in hyperlipidemic patients. In conclusion, although prolonged PWD was observed in the surface electrocardiographic measurements of LP patients as presented in the current study, PWD may be affected by various conditions and medications. Therefore, further studies should evaluate prolonged PWD-related conditions.

Atrial functional and geometrical remodeling in highly trained male athletes: for better or worse?

Highly trained athletes have an increased risk of atrial arrhythmias. Atrial geometrical and functional remodeling may be the underlying substrate. We analyze and relate atrial size, deformation and performance in professional handball players compared with non-sportive subjects. 24 Professional handball players and 20 non-sportive males were compared. All subjects underwent an echocardiographic study with evaluation of left (LA), right atrial (RA) dimensions and deformation by strain (Sa) and strain rate (SRa). Atrial performance was assessed from the atrial stroke volume (SV). With computational geometrical models, we studied the relation between atrial volumes, strains and SV and compared atrial working conditions. We estimated the functional reserve and a resulting average wall stress. LA and RA volumes were larger in athletes than in controls (35.2 ± 8.8 vs. 24.8 ± 4.3 ml/m(2), p < 0.01 and 29.0 ± 8.4 vs. 19.0 ± 5.1 ml/m(2), p < 0.01 respectively). LASa and RASa during active atrial contraction were decreased in athletes (-12.2 ± 2.0 vs. -14.5 ± 2.1%, p < 0.01 and -12.1 ± 1.8 vs. -14.2 ± 1.5%, p < 0.01 respectively). LASV was similar between groups (6.6 ± 1.4 vs. 7.3 ± 1.1 ml, p = 0.19) and RASV was lower in athletes (6.2 ± 1.3 vs. 7.2 ± 1.1 ml, p < 0.01). Computational models showed that this different operational mode potentially increases performance reserve, but at the cost of higher atrial wall stress. A proportion of athletes with enlarged LA and RA showed different atrial contractile performance, likely resulting in atria working at higher wall stress.