Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. The understanding of the pathophysiology of AF has changed during the last several decades, and a significant role of inflammation and of the renin–angiotensin–aldosterone system has been postulated both experimentally and clinically. There is emerging evidence of an association between inflammation and AF, and mounting evidence links increased C-reactive protein levels not only to already existing AF but also to the risk of developing future AF. The beneficial effects of statins on AF have been reported in several studies. Several randomized clinical and large observational studies have shown similar result that show the beneficial effect of statins in AF. In clinical studies, statins were considered effective in preventing AF after electrical cardioversion, post-ablation, and after permanent pacemaker and implantable cardioverter defibrillator insertion. The antiarrhythmic mechanisms of statins regarding AF prevention in patients with heart failure are still not clear. Perioperative statin use has been associated with favorable postoperative outcome in both cardiovascular and noncardiovascular conditions. Despite a growing body of evidence that drugs with anti-inflammatory properties such as statins may prevent AF, the observed positive effects of statins on the burden of AF appeared to be independent of their cholesterol-reducing properties. However, further data from large-scale randomized trials are clearly needed.
statins; pleiotropic effects; atrial fibrillation
Observational clinical and ex vivo studies have established a strong association between atrial fibrillation and inflammation1. However, whether inflammation is the cause or the consequence of atrial fibrillation and which specific inflammatory mediators may increase the atria's susceptibility to fibrillation remain elusive. Here we provide experimental and clinical evidence for the mechanistic involvement of myeloperoxidase (MPO), a heme enzyme abundantly expressed by neutrophils, in the pathophysiology of atrial fibrillation. MPO-deficient mice pretreated with angiotensin II (AngII) to provoke leukocyte activation showed lower atrial tissue abundance of the MPO product 3-chlorotyrosine, reduced activity of matrix metalloproteinases and blunted atrial fibrosis as compared to wild-type mice. Upon right atrial electrophysiological stimulation, MPO-deficient mice were protected from atrial fibrillation, which was reversed when MPO was restored. Humans with atrial fibrillation had higher plasma concentrations of MPO and a larger MPO burden in right atrial tissue as compared to individuals devoid of atrial fibrillation. In the atria, MPO colocalized with markedly increased formation of 3-chlorotyrosine. Our data demonstrate that MPO is a crucial prerequisite for structural remodeling of the myocardium, leading to an increased vulnerability to atrial fibrillation.
Clinicians involved in the care of patients with cardiovascular conditions have recently been confronted with an important body of literature linking inflammation and cardiovascular disease. Indeed, the level of systemic inflammation as measured by circulating levels of C-reactive protein (CRP) has been linked to prognosis in patients with atherosclerotic disease, congestive heart failure, atrial fibrillation, myocarditis, aortic valve disease and heart transplantation. In addition, a number of basic science reports suggest an active role for CRP in the pathophysiology of cardiovascular diseases. This article explores the potential role of CRP in disease initiation, progression, and clinical manifestations and reviews its role in the prediction of future events in clinical practice. Therapeutic interventions to decrease circulating levels of CRP are also reviewed.
C-reactive protein; inflammation; atherosclerosis; risk prediction; cardiovascular disease; acute coronary syndrome
Increasing evidence supports a role for inflammation in promoting atrial fibrillation (AF) and statins have anti-inflammatory effects that may be relevant for the prevention of AF. However, studies of statin therapy and incident AF have yielded mixed results and not focused on individuals with an underlying pro-inflammatory response. We studied whether high-sensitivity C-reactive protein is associated with incident AF and whether treatment with rosuvastatin is associated with a lower incidence of AF compared with placebo.
Methods and results
We randomized men and women with LDL cholesterol <130 mg/dL and high-sensitivity C-reactive protein ≥2 mg/L to receive either rosuvastatin 20 mg daily or placebo. Atrial fibrillation was determined from treatment-blind adverse event reports. Among 17 120 participants without prior history of arrhythmia, each increasing tertile of baseline high-sensitivity C-reactive protein was associated with a 36% increase in the risk of developing AF (95% CI: 1.16–1.60; P-trend < 0.01). Allocation to rosuvastatin when compared with placebo was associated with a 27% reduction in the relative risk of developing AF during the trial period; specifically, AF was reported among 138 participants in the placebo group and 100 in the rosuvastatin group (incidence rate 0.78 vs. 0.56/100 person-years, HR: 0.73, 95% CI: 0.56–0.94, P = 0.01). The exclusion of participants who developed a major cardiovascular event prior to the report of AF yielded similar results.
Within the JUPITER trial cohort of individuals selected for underlying inflammation, increasing levels of high-sensitivity C-reactive protein were associated with an increased risk of incident AF and random allocation to rosuvastatin significantly reduced that risk.
C-reactive protein; Atrial fibrillation; Statins
Atrial fibrillation (AF) is the most common sustained arrhythmia that is associated with significant morbidity and mortality. Current available therapies remain inadequate in symptom control and secondary prevention and are often associated with significant side effects. The mechanisms underlying the pathogenesis of AF are poorly understood, although electrophysiological remodeling has been described as an important initiating step. Recently, increasing evidence implicates oxidative stress and inflammation in the pathogenesis of AF. We searched the literature for evidence to support the use of antioxidant vitamins C and E in the prevention of AF. These vitamins, through their reactive-oxygen-species- (ROS-) scavenging effect, have shown a role in AF prevention in both animal and small clinical studies. The available evidence, however, is currently insufficient to support recommendations for their use in the wider patient population. Larger-scale clinical studies are required to confirm these preliminary results. Research is also required to further the understanding of the processes involved in the pathogenesis of AF and the role of antioxidant therapies to prevent the arrhythmia.
The aim of this study was to evaluate whether risk for postoperative atrial fibrillation in women is related to pre-existing inflammation as detected by plasma C-reactive protein (CRP) concentrations. We further sought to assess for the importance of atrial fibrillation for outcome after cardiac surgery in women.
CRP was measured before coronary artery bypass grafting and/or valvular surgery using cardiopulmonary bypass in 141 women. Univariate and multivariate analysis were used to evaluate for differences in CRP levels between women with and without atrial fibrillation, and to assess for the importance of the arrhythmia and postoperative outcomes.
Atrial fibrillation developed in 46 (33%) women. Neither CRP concentrations (median±SE, 13.3±2.5 mg/L vs 11.7±1.4 mg/L, p=0.847), nor the frequency of elevated levels (defined as > upper 95% CI or > 19.2 mg/L) (19% vs 21%, p=0.807) differed between women with or without atrial fibrillation. Patient age and previous stroke, but not CRP levels, were independently associated with atrial fibrillation. Women with atrial fibrillation were more likely to have low cardiac output syndrome (p= 0.018), stroke (p=0.031), longer duration of hospitalization in the intensive care unit (p=0.012) and on the postoperative (p=0.0008) ward, and they were more likely to require an extended care facility after surgery (p=0.046).
In contrast to findings from studies that have included mostly men, preoperative CRP concentrations are not associated with risk for atrial fibrillation after cardiac surgery for women. Postoperative atrial fibrillation in women is associated with increased risk for stroke, longer hospitalization, and extended care facility admission.
Arrhythmia; Atrial Fibrillation; Gender; Inflammation; On-pump
Inflammation and oxidative stress are associated with atrial fibrillation (AF). Statins have antioxidant and anti-inflammatory properties. We tested if atorvastatin reduced AF recurrence after DC cardioversion (CV) by modifying systemic oxidative stress and inflammation. (NCT00252967)
Methods and Results
In a randomized, double-blinded, placebo-controlled trial, patients with atrial fibrillation/flutter (AF) were randomized to receive either atorvastatin 80 mg (n=33) or placebo (n=31) before CV. Treatment was continued for 12 months or until AF recurred. Serum oxidative stress markers (ratios of oxidized to reduced glutathione and cysteine, derivatives of reactive oxygen species, isoprostanes) and inflammatory markers [ high sensitivity C- reactive protein (hs-CRP), interleukin-6 (IL-6), interleukin-1β(IL-1β), tumor necrosis factor-α (TNFα)] were measured at baseline and on follow-up. AF recurred in 22 (66.7%) of atorvastatin and 26 (83.9%) of placebo group (p=0.2). The adjusted hazard ratio of having recurrence on atorvastatin versus on placebo was 0.99 (95% CI: 0.98-1.01, p=0.3). There was no significant difference in the time to recurrence using Kaplan-Meier survival estimates (median (IR): 29 (2-145) days vs. 22 (7-70) days, p=0.9). While no significant effect was seen on oxidative stress, 2 of 4 inflammatory markers, IL-6 (adjusted OR: 0.59, 95% CI: 0.35-0.97, p= 0.04) and hs-CRP (adjusted OR: 0.59, 95% CI: 0.37-0.95, p=0.03) were significantly lowered with atorvastatin. Cholesterol levels significantly decreased with atorvastatin (p=0.03).
High dose atorvastatin did not reduce the recurrence of AF after CV. It reduced selective markers of inflammation without affecting systemic oxidative stress. Failure of atorvastatin to prevent AF recurrence may be due to its failure to affect oxidative stress.
atrial fibrillation; statin; cardioversion; inflammation; oxidative stress
A decrease in inflammation after cure of atrial arrhythmias suggests that such arrhythmias are pro-inflammatory, and lower inflammatory marker levels in the coronary sinus suggest that atrial arrhythmias result in the intracardiac appropriation of inflammatory cytokines.
To investigate the effect of atrial fibrillation on inflammatory markers drawn from intra and extracardiac chambers.
We performed a case control study of 167 AF patients and 207 controls. Blood from intra and extracardiac sites was obtained from a subset of patients undergoing curative AF ablation (n=46).
There were no significant differences in C-Reactive Protein (CRP) or interleukin-6 (IL-6) between those with and without a history of AF. Both were significantly higher when blood was drawn during AF compared to in sinus rhythm: median CRP 3.1 mg/dL (interquartile range [IQR] 1.0–6.0) versus 1.7 mg/dL (IQR 0.7 – 3.9, p=0.0005); median IL-6 2.3 ng/ml (IQR 1.5–3.9) versus 1.5 ng/ml (IQR 0.7–2.5; p=0.007). This finding persisted after adjusting for potential confounders. AF ablation patients in AF exhibited a positive median left atrial minus coronary sinus (LA-CS gradient) CRP (0.3 mg/dL , IQR −0.03–1.1), whereas those in sinus rhythm had a negative median LA-CS gradient CRP (−0.2, IQR −0.8-[−0.02], p=0.01); femoral artery minus femoral vein gradients in AF versus sinus rhythm failed to show any differences.
AF at the time of the blood draw, rather than a history of AF, was independently associated with inflammation. Differences in trans-cardiac gradients suggest that AF results in sequestration of inflammatory cytokines in the heart.
Atrial fibrillation; CRP; C-Reactive Protein; IL-6; inflammation; coronary sinus; left atrium
Atrial fibrillation (AF) is the commonest of all sustained arrhythmias, and most of the patients seeking medical therapy are in the elderly age group. The management of these patients is particularly difficult due to associated comorbidities. Hypertension, congestive heart failure, left ventricular hypertrophy, and coronary artery disease are often present in the elderly patient population, and therefore, antiarrhythmic drugs often fail due to side effects, proarrhythmia, or poor rhythm control. Recently, radiofrequency catheter ablation has been widely performed as an efficient therapy for recurrent, drug-refractory AF. Nevertheless, patients at old age were underrepresented in prior AF ablation trials, and the current guidelines for catheter ablation of AF recommend a noninvasive approach in the elderly patient group due to the lack of clinical data supporting ablation therapy. However, study results of our group and others are suggesting that catheter ablation is a safe and effective treatment for patients over the age of 65 years with symptomatic, drug-refractory AF, and therefore, patients should not be precluded from catheter ablation only on the basis of age. This paper discusses the pharmacological (rhythm control, rate control, and anticoagulation) and catheter management of AF in the elderly population.
Atrial fibrillation (AF) has been associated with myocardial oxidative stress, and antioxidant agents have demonstrated antiarrhythmic benefit in humans. We compared serum markers of oxidation and associated inflammation in individuals with or without AF.
Serum markers of oxidative stress and inflammation were compared in a cross-sectional, case-control design study of 40 male individuals, with or without persistent or permanent AF, who were matched for age, sex, diabetes, and smoking status, known confounding variables for the measurement of oxidative stress. We used derivatives of reactive oxidative metabolites (DROMs) and ratios of oxidized to reduced glutathione (Eh GSH) and cysteine (Eh CySH) to quantify oxidative stress. We also measured inflammatory markers, including high-sensitivity C-reactive protein, interleukins 1β and 6, and tumor necrosis factor α.
Univariate, conditional logistical regression analysis showed that oxidative stress but not inflammatory markers were statistically associated with AF (P <0.05). The increase in the odds ratios for AF for Eh GSH, Eh CySH, and DROMs were 6.1 (95% CI, 1.3–28.3; P = 0.02), 13.6 (95% CI, 2.5–74.1; P = 0.01), and 15.9 (95% CI, 1.7–153.9; P = 0.02), respectively. There was a stronger correlation between Eh GSH and Eh CySH (r = 0.66) than between Eh GSH and DROMs (r = 0.41). In multivariate analysis corrected for statins and other AF risk factors differing between the groups, the association of AF and oxidative stress remained significant.
These data suggest that oxidative stress markers may have predictive value in AF management.
Atrial fibrillation affects at least 1% of the population and causes marked society-wide morbidity and mortality. Current management of atrial fibrillation including antithrombotic therapy and management of concomitant conditions in all patients, rate control therapy in most patients, and rhythm control therapy in patients with severe atrial fibrillation-related symptoms can alleviate atrial fibrillation-related symptoms but can neither effectively prevent recurrent atrial fibrillation nor suppress atrial fibrillation-related complications. Hence, there is a need for better therapy of atrial fibrillation.
The etiology of atrial fibrillation is complex. Most of the causes of atrial fibrillation which are known at present perpetuate themselves in vicious circles, and presence of the arrhythmia by itself causes marked damage of atrial myocardium. These pathophysiological insights suggest that early diagnosis and comprehensive therapy of atrial fibrillation, including adequate therapy of all atrial fibrillation-causing conditions, rate control, and rhythm control therapy, could help to prevent progression of atrial fibrillation and reduce atrial fibrillation-related complications. Such a therapy should make use of safe and effective therapeutic modalities, some of which have become available recently or will become available in the near future. The hypothesis that early diagnosis and early, comprehensive therapy of atrial fibrillation can improve outcomes requires formal testing in controlled trials.
Atrial fibrillation (AF) has been associated with lung diseases like pneumonia and chronic obstructive pulmonary disease but has only infrequently been associated with inhalational lung injury. We report two cases of resistant AF, which developed in young healthy manual laborers shortly after inhalational lung injury due to massive quantity of pesticides and anhydrous ammonia, respectively. They had no evidence of valvular or structural heart disease and did not have any previous medical problems. The AF was resistant to antiarrhythmic drugs and required pulmonary vein isolation in first patient and possibly the second patient who is currently being evaluated for this procedure. These arrhythmias may reflect direct myocardial injury during and after exposure. Alternatively, multiple mechanisms can cause atrial fibrillation in lung diseases, including hypoxemia, acidemia, inflammatory mediators, and structural changes in the atria and ventricle, and these could lead to AF in inhalational lung injury cases. AF needs to be excluded when patients present with palpitations after inhalational lung injury, especially since, if unrecognized, AF may lead to complications, like thromboembolic phenomenon and tachycardiomyopathy.
Constrictive pericarditis is only diagnosed once in every 10,000 admissions. It is characterized by inflammation and fibrous scarring of the pericardium resulting in a thickened, rigid sac that impairs diastolic filling. Approximately 50% of cases are idiopathic, while post cardiac surgery and post radiation therapy account for 37% and 9% respectively. The scarcity of presenting symptoms and the rarity of diagnosis make it a challenge to recognize.
A 57 year-old man with no past medical history presented to the emergency room with progressing fatigue for two weeks and worsening lower extremity edema for one week, associated with dyspnea on exertion and decreased exercise tolerance. He was noted to be in atrial fibrillation with RVR upon admission to ER. Physical exam was significant for an 8 centimeter elevated JVP, and a Kussmaul's sign, which was noted sitting upright. Mild abdominal distention, hepatomegaly, and 3+ bilateral pitting edema to the upper thigh were also noted. Electrocardiogram showed non-specific low voltage QRS. A lateral chest x-ray showed significantly abundant calcifications along the anterior, inferior aspect of the cardiac silhouette. A subsequent tissue Doppler echocardiogram noted a septal bounce and an elevated early diastolic mitral annular velocity or E'. Cardiac catheterization showed an equalization of pressures, a dip and plateau sign, and ventricular interdependence. A phrenic-to-phrenic nerve pericardectomy was performed, removing a 5 millimeter thick, firm, calcified pericardium. A final diagnosis of idiopathic constrictive pericarditis was diagnosed as tissue pathology showed no abnormalities other than severe calcification. Five days post-operatively, significantly decreased leg edema, heart rate, dyspnea, abdominal distention, and JVP were noted. He was subsequently discharged two weeks post-operative with resolution of his symptoms.
This case illustrates the rarity of having multiple signs and symptoms associated with constrictive pericarditis as well as the new diagnostic capabilities of tissue Doppler. In constrictive pericarditis, elevated JVP is found in 86% of patients, dyspnea on exertion in 78%, edema in 54%, abdominal fullness in 68%, fatigue in 25%, a Kussmaul's sign in 21%, calcifications on chest x-ray in only 20%, and atrial fibrillation in only 10%. Newer data has also shown excellent specificity, 97%, for constrictive pericarditis when an elevated E' of greater than 12 cm/sec is noted. The presence of multiple rare signs and symptoms and the use of new diagnostic tissue Doppler signs make this case extremely unusual. Recognizing these signs and the proper use of cardiac catheterization and tissue Doppler is critical in differentiating constrictive pericarditis from restrictive cardiomyopathy and pericardial tamponade. It is also critical for the initiation of pericardectomy to prevent further deterioration or cardiac death.
PRO-- PCOS is associated with low-grade systemic inflammation as evidenced by elevation of multiple markers of inflammation such as C-reactive protein, interleukin-18, monocyte chemoattractant protein-1 and white blood count as well as endothelial dysfunction and increased oxidative stress.
CON-- The evidence in support of the presence of chronic inflammatory state in the majority of women with PCOS is incontrovertible. It is apparent that PCOS is associated with a significant elevation of multiple markers of inflammation including CRP, IL-18, MCP-1, and white blood count. Furthermore, PCOS is associated with other derangements associated with inflammation such as increased oxidative stress and endothelial dysfunction. While the etiology of systemic inflammation in PCOS remains unclear, recent data raise the intriguing possibility of a link between PCOS, inflammation and chronic low grade infectious agents such as Chlamydia pneumoniae, Helicobacter pylori and pathogens inducing periodontal inflammation.
Atrial fibrillation is the commonest sustained cardiac arrhythmia. It accounts for >35% of all hospital admissions for cardiac arrhythmias in the United States. The presence of atrial fibrillation increases the mortality of a population by up to twofold. The risk of stroke increases from 1.5% in patients with atrial fibrillation from 50–59 years of age to up to 23.5% for such patients aged 80–89 years. Although the diagnosis of atrial fibrillation is usually straightforward, effective treatment is not. This article will discuss how rhythm control of atrial fibrillation can best be achieved, the controversy over the rhythm versus rate control, the maintenance of sinus rhythm with antiarrhythmic drugs after cardioversion, and prevention of thromboembolism. Finally, the recent advances in various non-pharmacological approaches for the treatment of atrial fibrillation will be highlighted.
Atrial arrhythmias are associated with inflammation. The cause and effect of the association is unknown.
To test the hypothesis that atrial tachyarrhythmias contribute to inflammation.
We performed a prospective observational study wherein C-Reactive Protein (CRP) and interleukin-6 (IL-6) levels from the femoral vein and coronary sinus (CS) were compared prior to curative ablation for atrial flutter (AFL, n=59) and paroxysmal supraventricular tachycardia (SVT, n=110). Follow-up levels were obtained at 1 and 6 months.
Peripheral levels of both biomarkers were significantly higher in the AFL group. After multivariate adjustment, only those in the AFL group who presented in AFL or atrial fibrillation (AF) had significantly elevated CRP levels (OR 1.26, p=0.033). Levels of each marker were similar in the CS and peripheral blood in the SVT group; in the AFL group, both CRP and IL-6 were significantly lower in the CS than the periphery (p=0.0076 and p=0.0021, respectively). CRP was significantly lower a median of 47 days after AFL ablation (from a median 6.28 mg/L to 2.92 mg/L, p=0.028) and remained reduced at second follow-up. IL-6 decreased across three time points after AFL ablation (p=0.002). No reduction in inflammatory biomarkers was observed after SVT ablation.
CRP and IL-6 levels are elevated in patients presenting in AFL. Given the lower CS values in these patients, their origin appears to be systemic rather than cardiac. Because these levels significantly fall after ablation of AFL, the atrial tachyarrhythmia appears to be the cause (not the effect) of the inflammation.
Atrial arrhythmias; Atrial flutter; Inflammation; CRP; IL-6; Ablation
Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice with growing prevalence in developed countries. Several medical and interventional therapies, such as atrial specific drugs and pulmonary vein isolation, have demonstrated prevention of recurrences. However, their suboptimal long-term success and significant rate of secondary effects have led to intensive research in the last decade focused on novel alternative and supplemental therapies. One such candidate is polyunsaturated fatty acids (PUFAs). Because of their biological properties, safety, simplicity, and relatively cheap cost, there is a special clinical interest in omega-3 PUFAs as a possible antiarrhythmic agent. Obtained from diets rich in fish, they represent one of the current supplemental therapies. At the cellular level, an increasing body of evidence has shown that n-3 PUFAs exert a variety of effects on cardiac ion channels, membrane dynamic properties, inflammatory cascade, and other targets related to AF prevention. In this article, we review the current basic and clinical evidence pertinent to n-3 PUFAs in AF treatment and prevention. We also discuss controversial outcomes among clinical studies and propose specific subsets of AF patients who will benefit most from n-3 PUFAs.
atrial fibrillation; omega-3 polyunsaturated fatty acids; remodeling; prevention; drug therapy
Increased levels of plasma von Willebrand factor (vWf, an index of endothelial damage/dysfunction) and soluble P‐selectin (sP‐sel, an index of platelet activation) concentrations have been reported as indices of the prothrombotic state in both non‐valvular atrial fibrillation and hypertension separately. However, the effect of hypertension on the levels of these indices in the setting of atrial fibrillation, and whether increasing severity of hypertension presents an additive prothrombotic risk, is unclear.
Plasma concentrations of vWf and sP‐sel were measured by ELISA in 1235 patients with atrial fibrillation, and levels related to a history of hypertension and rising quartiles of systolic, diastolic and pulse pressure in those with and without diabetes mellitus and prior vascular events.
Mean plasma vWf was higher among patients with atrial fibrillation with a history of hypertension (149 vs 145 IU/dl, p = 0.005). Also, an increase in the levels of vWf with increasing quartiles of pulse pressure (p = 0.042) was noticed. However, on multivariate analysis, after adjusting for potential confounders, the effects of both hypertension and pulse pressure became non‐significant (p = 0.261 and p = 0.5, respectively). Levels of sP‐sel were unaffected by a history of hypertension and rising quartiles of systolic and diastolic blood pressure, or pulse pressure.
Among patients with atrial fibrillation, patients with hypertension have higher vWf levels, indicating endothelial damage/dysfunction, which is associated with increasing pulse pressure. However, these associations are probably owing to the presence of other associated cardiovascular disease, rather than hypertension itself. Furthermore, platelet activation (sP‐sel) was unrelated to hypertension or blood pressure in this atrial fibrillation cohort. Hypertension or blood pressure levels do not seem to have an independent additive affect on the prothrombotic state in atrial fibrillation.
The etiology of arrhythmias including atrial fibrillation is multifactorial. Most arrhythmias are associated with comorbid illnesses like hypertension, diabetes, thyroid disease, or advanced age. Although it is tempting to blame a stimulant like caffeine as a trigger for arrhythmias, the literature does not support this idea. There is no real benefit to having patients with arrhythmias limit their caffeine intake. Caffeine is a vasoactive substance that also may promote the release of norepinephrine and epinephrine. However, acute ingestion of caffeine (as coffee or tea) does not cause atrial fibrillation. Even patients suffering a myocardial infarction do not have an increased incidence of ventricular or other arrhythmias after ingesting several cups of coffee. Large epidemiologic studies have also failed to find a connection between the amount of coffee/caffeine used and the development of arrhythmias. As such, it does not make sense to suggest that patients with palpitations, paroxysmal atrial fibrillation, or supraventricular tachycardia, abstain from caffeine use. Energy drinks are a new phenomenon on the beverage market, with 30-50 % of young adults and teens using them regularly. Energy drinks are loaded with caffeine, sugar, and other chemicals that can stimulate the cardiac system. There is an increasing body of mainly anecdotal case reports describing arrhythmias or even sudden death triggered by exercise plus using energy drinks. Clearly, there must be more study in this area, but it is wise to either limit or avoid their use in patients with arrhythmias. Moderate to heavy alcohol use seems to be associated with the development of atrial fibrillation. The term “holiday heart” was coined back in 1978, to describe patients who had atrial fibrillation following binge alcohol use. Thus, it is reasonable to recommend to patients with arrhythmias that they limit their alcohol use, although unfortunately this treatment will likely not completely resolve their arrhythmia.
Arrhythmias; Energy drink; Atrial fibrillation; Alcohol; Caffeine; Sudden death
Atrial fibrillation (AF) is a commonly encountered arrhythmia in our daily practice. Every year a huge bulk of data is published about different management strategies, new antiarrhythmic drugs, anticoagulation protocols and ablation procedures in these patients. In this review article, we discuss different management strategies and new antiarrhythmic drugs as well as those commonly used. We will also have a brief look at anticoagulation in AF.
We try to introduce the most recent publications in this field and we think that this review article may not only give information about the current state of antiarrhythmic therapy of AF, it may also show some progresses that we may anticipate in the near future. New drugs are promising in the management of AF because of better safety profile and also acceptable efficacy. A comparison between the catheter ablation procedure and antiarrhythmic therapy is beyond the scope of this article.
Atrial fibrillation; Anti-arrhythmia agents; Thromboembolism
Fibrin D-dimer levels have been advocated as an useful clinical marker of thrombogenesis.
We hypothesized that i) there is a hyperclotting state after the return of atrial fibrillation to sinus rhythm, ii) the measurement of plasma D-Dimer levels might be a good screening tool of this clotting status, and iii) the duration of arrhythmia influences the haemostasis measured by plasma D-Dimer levels.
Forty-two patients with atrial fibrillation undergoing cardioversion were divided into two groups: in Group A (n = 24,14 male, 56 ± 11 years) the duration of atrial fibrillation was 72 hours or more (142.7 ± 103.8 hours), in Group B (n = 18, 10 male, 61 ± 13 years) the duration of atrial fibrillation was less than 72 hours (25 ± 16 hours). Plasma fibrin D-dimer levels were measured by enzyme immunoassay before, and 36 hours after, cardioversion. The change of plasma D-dimer levels 36 hours after cardioversion was calculated as delta-D-dimer.
There were no significant differences in demographic, clinical, and echocardiographic data, and the success of cardioversion between the two groups. Compared to the control, the baseline D-dimer levels were significantly higher in both groups. The delta D-dimer levels were significantly higher in Group A than in Group B (p < 0.005). Furthermore, plasma D-dimer levels 36 hours after cardioversion (r = 0.52, p = 0.0016) and delta-D-dimer levels (r = 0.73, p < 0.0001) showed significant correlations with the duration of atrial fibrillation.
The longer duration of the atrial fibrillation episode could lead to a more prominent cardiovascular hyperclotting state after cardioversion, and the mean changes of plasma D-Dimer levels could be used as an useful clinical marker of the clotting state after atrial systole return.
Atrial fibrillation; haemostatic markers
Atrial fibrillation (AF) is a common arrhythmia with an estimated clinical prevalence of approximately 1% in the general population and as high as 9% in individuals by the age of 80 years. The aetiology is multifactorial. Systemic disease, e.g., inflammatory processes, sarcoidosis, autoimmune disorders, has also been linked to the development of AF. Myocardial dysfunction observed in sepsis could contribute to arrhythmias and inflammation per se could induce or provoke AF. We describe the successful management of an acute AF in an elderly patient scheduled for emergency laparotomy and closure of hollow viscous perforation.
Acute atrial fibrillation; elderly patient; electrolyte imbalances; sepsis
Atrial fibrillation (AF) is a substantial cause of mortality and morbidity in the Western world. It is a massive burden on health care systems, and its prevalence is expected to double over the next 20 years. Trials evaluating antiarrhythmic drugs or catheter ablation have focused on recurrence of arrhythmia, perhaps neglecting outcomes relevant to patients, such as symptoms, need for antiarrhythmic drugs, need for hospitalization, and rates of stroke and death. An association has been demonstrated between sinus rhythm and survival in several studies, and there is evidence emerging that successful catheter ablation may reduce rates of stroke and death. Similarly, dronedarone has been shown to reduce hospitalizations and death in patients with paroxysmal AF or persistent AF of recent onset, although it may cause adverse events in permanent AF. New antiarrhythmic drugs are a welcome addition to the armamentarium, since there are limitations to current antiarrhythmic drugs. In particular, sotalol, flecainide, and propafenone cannot be used safely in those with structural heart disease, and amiodarone has important adverse reactions that limit long-term use. Indeed, the use of conventional antiarrhythmic drugs may negate any survival benefit derived from maintaining sinus rhythm. Although dronedarone appears promising with respect to hard endpoints such as stroke and death in certain patients, it may not be safe for those with heart failure or those with permanent AF. Furthermore, the trials suggesting that dronedarone may impact on these endpoints were compared with placebo rather than with an active comparator group. Further “head-to-head” comparisons between dronedarone and other antiarrhythmic drugs are needed to determine whether this property is unique to dronedarone alone.
atrial fibrillation; rhythm; antiarrhythmics; ablation; stroke; dronedarone
Atrial fibrillation (AF) is the most common clinical arrhythmia. Recent investigations have suggested that inflammation might have a role in the pathophysiology of AF. In this review, the association between inflammation and AF, and the effects of several agents that have anti-inflammatory actions, such as statins, polyunsaturated fatty acids, corticosteroids and angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, have been investigated.
Atrial fibrillation; Inflammation; Statins
Herein, we describe late complications after the transcatheter device closure of a patent foramen ovale in a patient with migraine headaches. The clinical presentation included acute neurologic symptoms and new-onset atrial fibrillation. A mass on the left atrial side of the occluder was surgically removed. Histologic results showed an inflammatory lesion that consisted predominantly of lymphocytes, plasma cells, and macrophages. Despite complete surgical closure and the termination of atrial fibrillation, the patient continued to experience neurologic events.
Although transcatheter patent foramen ovale closure is associated with low complication rates, a careful risk–benefit evaluation is warranted in view of the potentially severe complications and the current lack of robust pathophysiologic and clinical trial data to support this therapy in the treatment of migraine headaches.
Cardiac surgical procedures/instrumentation; cerebrovascular disorders/etiology; foramen ovale, patent/complications/therapy; heart septal defects, atrial/complications/diagnosis/pathology/ultrasonography; migraine disorders/prevention & control; postoperative complications; prostheses and implants/adverse effects/instrumentation/utilization; risk factors; thrombosis/etiology; treatment outcome