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At least 19 recordsLinked to original sources
PubMed1975

Metabolic studies following thoracotomy for lung cancer with particular reference to postoperative atrial fibrillation.

Atrial fibrillation has proved to be a frequent complication after thoracotomy for lung cancer. In order to study the possibility that metabolic changes are the trigger mechanism of these arrhythmias, free fatty acids (FFA), glycerol, triglycerides, serum insulin and glucose were determined pre- and postoperatively in patients both with and without this postoperative complication. In the primary series of patients, FFA were found to be increased immediately after the start of the atrial fibrillation, partly in relation to the morning values and partly to the 24-hour curve. This is a possible expression of an increased lipolysis in a causal relationship to the arrhythmia. In another series of patients, the degree of lypolysis was demonstrated using the glycerol values. With this method, no signs of increased lipolysis were found in connection with the onset of atrial fibrillation. Thus, changes in the lipoid metabolism were not found to be the trigger mechanism of the postoperative atrial fibrillation. Reduced values of serum insulin and glucose were not demonstrated either during the uncomplicated postoperative period or at the start of atrial fibrillation.

Atrial Fibrillation↗
PubMed1992

Pharmacokinetics and pharmacodynamics of intravenous diltiazem in patients with atrial fibrillation or atrial flutter.

BACKGROUND: Diltiazem, a calcium channel blocker, has been shown to be safe and effective in the treatment of patients in atrial fibrillation and/or atrial flutter. However, there have been no pharmacokinetic/pharmacodynamic studies of diltiazem in these patients. METHODS AND RESULTS: The pharmacokinetics and pharmacodynamics of intravenous diltiazem were determined in 32 patients with atrial fibrillation or atrial flutter (mean +/- SD age, 66 +/- 7 years; mean baseline heart rate, 131 +/- 10 beats per minute) after 20 mg or 20 mg followed by 25-mg bolus doses and a 10 and 15 mg/hr infusion for 24 hours. After the 10 and 15 mg/hr infusions of diltiazem, mean +/- SD elimination half-life was 6.8 +/- 1.8 and 6.9 +/- 1.5 hours, volume of distribution was 411 +/- 151.8 and 299 +/- 70.8 I, and systemic clearance was 42 +/- 12.4 and 31 +/- 8.3 l/hr, respectively. Percentages of the plasma concentrations of the principal metabolites desacetyldiltiazem and N-desmethyldiltiazem to diltiazem were < 15% and < 10%, respectively. Thirty of 32 patients maintained response throughout the 24-hour infusion of diltiazem. Using a sigmoidal Emax pharmacodynamic model, a strong relation (mean +/- SD r2, 0.78 +/- 0.2) was observed between plasma diltiazem concentration and percent heart rate reduction. Mean +/- SD Emax (maximum percent reduction in heart rate from baseline) and EC50 (plasma diltiazem concentration that achieves half Emax) were 52 +/- 17% and 110 +/- 84 ng/ml, respectively. The model predicts that mean plasma diltiazem concentration of 79, 172, and 294 ng/ml are required to produce a 20%, 30%, and 40% reduction in heart rate, respectively. A relation between plasma diltiazem concentration and percent change in systolic blood pressure (SBP) or diastolic blood pressure (DBP) from baseline was not observed (mean +/- SD r2, SBP/DBP: 0.35 +/- 0.24/0.36 +/- 0.2). There were no untoward side effects observed. CONCLUSIONS: First, the pharmacokinetics of diltiazem in patients with atrial fibrillation or atrial flutter is nonlinear with an apparent dose-dependent decrease in systemic clearance with increasing infusion rate. Second, using a sigmoidal Emax model, there is a strong relation between plasma diltiazem concentration and percent heart rate reduction. Third, the plasma concentrations of the principal metabolites desacetyldiltiazem and N-desmethyldiltiazem are low and are not expected to contribute significantly to the pharmacodynamics of intravenous diltiazem in these patients.

Aged↗
PubMed1992

[Drug treatments of atrial fibrillation].

Atrial fibrillation is a daily cardiological problem which poses three types of questions, which, though old, are only partially mastered: anticoagulation, reduction and prevention of recurrence. It is a potent source of embolism. The risk is the greatest in patients with rheumatic valvular disease when the fibrillation is recent and when underlying cardiac disease is uncompensated. Long term anticoagulation is mandatory when the cause is rheumatic heart disease. In other pathologies, though anticoagulation has not been shown to reduce mortality, it significantly reduces the number of cerebrovascular accidents, including in the elderly and with low-dose vitamin K antagonist drugs. The efficacy of anticoagulation in preventing arterial embolism has not been established. Reduction of atrial fibrillation is not essential if the arrhythmia is well tolerated, chronic, especially in elderly patients and when several recurrences have occurred despite preventive therapy. In other cases, medical reduction is to be preferred to cardioversion if the fibrillation is recent and well tolerated. Of the oral and injectable preparations, amiodarone seems to be the drug with best benefit/risk ratio. Prevention of recurrence of fibrillation is unnecessary for many after a first episode, especially when idiopathic. In other cases, there are many available drugs but results are uncertain except in those observed in atrial fibrillation related to the autonomic nervous system. Strictly controlled and statistically exploitable studies show comparable efficacy of quinine and other Class I drugs. Beta-blockers are not very useful and the excellent long term results with amiodarone require confirmation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1976

Lidocaine in Wolff-Parkinson-White syndrome with atrial fibrillation.

Atrial fibrillation in the Wolff-Parkinson-White syndrome may be life-threatening because of the extremely rapid ventricular rates that can occur over the accessory pathway. An 18-year-old man with Wolff-Parkinson-White (type B) syndrome developed episodes of syncope due to atrial fibrillation. In studies during hospitalization the administration of lidocaine immediately slowed the ventricular response by abolishing antegrade conduction over the accessory pathway. The role of lidocaine and other antiarrhythmic drugs in the management of arrhythmias in the Wolff-Parkinson-White syndrome is discussed.

Adolescent↗
PubMed1979

Verapamil in atrial fibrillation and atrial flutter.

A double-blind randomized study was performed to compare the efficacy of intravenous verapamil with saline in 28 patients with a rapid ventricular rate and atrial fibrillation or atrial flutter. Conversion of atrial fibrillation to sinus rhythm occurred in none of 14 patients after saline and in 3 of 20 patients (15%) 7 to 160 min after verapamil. The ventricular rate in atrial fibrillation was slowed greater than or equal to 15% in 2 of 14 patients (14%) by saline, in 17 of 20 patients (85%) by 1 dose of verapamil (p less than 0.001), and in 19 of 20 patients (95%) by 1 or 2 doses of verapamil (p less than 0.001). Conversion of atrial flutter to sinus rhythm occurred in none of 4 patients after saline and in 1 of 7 patients (14%) 105 min after verapamil. The ventricular rate in atrial flutter was slowed greater than or equal to 15% in none of 4 patients by saline, in 4 of 7 patients (57%) by 1 dose of verapamil, and in 7 of 7 patients (100%) by 1 or 2 doses of verapamil (p less than 0.001).

Adult↗
PubMed1992

Redefining the role of digoxin in the treatment of atrial fibrillation.

Atrial fibrillation (AF) encompasses a variety of discrete clinical syndromes, including paroxysmal, chronic, acute, and postoperative. Digoxin, long considered the mainstay of therapy for rate control in all types of AF, appears to have only modest electrophysiologic effects, which are mediated primarily by the autonomic nervous system. Digoxin has less potency than the calcium antagonists or beta-blocking drugs with respect to atrioventricular nodal blockade. Although less potent than calcium antagonists or beta-blocking drugs on the atrioventricular node, digoxin provides positive inotropic support, whereas the other 2 agents can suppress left ventricular function. Thus, digoxin is the agent of choice in patients with AF in the setting of significant left ventricular dysfunction. However, in the absence of left ventricular dysfunction, digoxin should be considered second-line therapy for the treatment of all AF syndromes.

Acute Disease↗
PubMed1977

A new method for quantifying ventricular regularization during atrial fibrillation.

Atrial fibrillation (AF) characteristically results in random variation of the intervals between successive ventricular depolarizations. However, when a patient with AF is treated with excessive amounts of digitalis, regular junctional rhythms may occur. The detection of "regularization" of the ventricular rhythm in patients with AF may signal early digitalis toxicity. In this paper, we describe a new method for quantifying the extent of ventricular regularization by the statistical analysis of the intervals between successive ventricular depolarizations (R-R intervals). This method yields a single index (Z score) which reflects the degree to which a sequence of R-R intervals deviates from a random distribution. Simulation studies demonstrate that our method is sensitive to "regularization" of as little as two to four percent of R-R intervals, even when equal intervals occur in small groups that might easily escape detection by visual electrocardiographic interpretation. Analysis of records from six nondigitalized subjects in AF shows that the sequence of R-R intervals is usually random, or very nearly so. Records obtained from the same patients when digitalized often demonstrate more regularized activity, reflected by an index (Z score) which is higher than expected from chance deviation if a random process is assumed. Preliminary data also suggeest that exercise is associated with substantial regularization of ventricular depolarization.

Atrial Fibrillation↗
PubMed1978

Lidocaine-induced cardiac rate changes in atrial fibrillation and atrial flutter.

To assess atrial and ventricular rate changes after lidocaine injection, 18 atrial flutter patients and 35 atrial fibrillation patients were given intravenous lidocaine, mean dose 100 mg. Continuous electrocardiographic recording for 5 minutes before and at least 10 minutes after lidocaine injection was used to determine rate changes. The atrial flutter rate decreased after lidocaine in 17 of 18 patients (94 per cent), mean maximal decrease 27 beats/minute. The ventricular rate response in atrial flutter was variable but in three patients increased 21, 27, and 47 beats/minute respectively (P less than 0.001). In atrial fibrillation, the mean ventricular rate after rapid lidocaine injection increased six beats/minute (P less than 0.01). In three of 35 atrial fibrillation patients (9 per cent), the ventricular rate increase was greater than 20 beats/minute (P less than 0.001), and in two patients (6 per cent), the ventricular rate increase was associated with potentially serious clinical events. Lidocaine-induced ventricular rate increases are common in atrial flutter and fibrillation, particularly in patients who are also receiving quinidine.

Adult↗
PubMedDate not supplied

Intravenous propafenone for suppression of symptomatic atrial fibrillation and atrial flutter in a first aid hospital.

The efficacy and safety of propafenone (PPF) were prospectively evaluated in 20 patients (13 men and 7 women, age 39 +/- 14 years) with atrial arrhythmias (AA) (atrial fibrillation: n = 13; atrial flutter: n = 7). All patients had arrhythmias from 109 +/- 63 minutes, (iT) without clinical evidence of heart failure. Intravenous PPF was given as a 1 mg/kg bolus over 5 minutes, with a therapeutical possibility of a second bolus (1 mg/kg) after 10 minutes if sinus rhythm was not restored. The conversion time (cT) was 6.4 +/- 2.2 minutes (range 3 to 18 minutes). In 19 patients (95%) sinus rhythm was restored and no serious adverse and proarrhythmic effects were noted in each patient. We conclude that 1) PPF is effective and acted significantly faster in controlling AA; 2) PPF appears to be well tolerated and relative safe with a low incidence of adverse and proarrhythmic effects in patients in a first aid station.

Adult↗
PubMed1992

[Electrophysiologic study of cibenzoline in patients with paroxysmal atrial fibrillation with special reference to atrial fibrillation threshold].

Electrophysiologic effects of cibenzoline were studied in 7 patients (6 males and one female) aged from 40 to 69 years (mean +/- SD; 52 +/- 10) with paroxysmal atrial fibrillation which was documented by 12 leads ECG or by 24 hours Holter monitoring. No organic heart diseases were found except in one patient with dilated cardiomyopathy and sick sinus syndrome (SSS). Cibenzoline (200mg) given orally increased P wave duration, PR interval and QRS duration significantly. The duration of P wave was gradually increased as the pacing frequency was increased. Neither sinus cycle length, nor sinus node recovery time (SRT), nor Wenkebach cycle length, nor atrial effective refractory period, nor QT interval was changed by the drug. One patient with SSS showed increase in SRT from 2,303 msec to 5,150 msec. The minimum current which was required to induce atrial fibrillation by rapid atrial stimulation (50 Hz, 1 sec) lasting more than 30 sec was defined as atrial fibrillation threshold (AFT). The AFT was 4.0 +/- 2.2 mA at the baseline state in 7 patients. After the oral administration of cibenzoline, 5 patients showed increase in AFT, while 1 patient showed decrease and another patient showed no change in AFT. Statistically, AFT was significantly increased to 7.3 +/- 3.4 mA in 7 patients. The results suggest that cibenzoline might be effective to prevent paroxysmal atrial fibrillation in patients without organic heart diseases.

Administration, Oral↗
PubMed1992

Antiarrhythmic drug therapy and cardiac mortality in atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators.

BACKGROUND AND OBJECTIVES: The relation between cardiac mortality and antiarrhythmic drug administration has not been fully determined. This relation was analyzed in 1,330 patients enrolled in the Stroke Prevention in Atrial Fibrillation Study, a randomized clinical trial comparing warfarin, aspirin and placebo for the prevention of ischemic stroke or systemic embolism in patients with nonvalvular atrial fibrillation. METHODS: Patients who received antiarrhythmic drug therapy for atrial fibrillation in this study were compared with patients not receiving antiarrhythmic agents. The relative risk of cardiac mortality, including arrhythmic death, in patients receiving antiarrhythmic drug therapy was determined and adjusted for other cardiac risk factors. RESULTS: In patients receiving antiarrhythmic drug therapy, cardiac mortality was increased 2.5-fold (p = 0.006, 95% confidence interval [CI] 1.3 to 4.9) and arrhythmic death was increased 2.6-fold (p = 0.02, 95% CI 1.2 to 5.6). Among patients with a history of congestive heart failure, those given antiarrhythmic medications had a relative risk of cardiac death of 4.7 (p less than 0.001, 95% CI 1.9 to 11.6) compared with that of patients not so treated; the relative risk of arrhythmic death in the treated group was 3.7 (p = 0.01, 95% CI 1.3 to 10.4). Patients without a history of congestive heart failure had no increased risk of cardiac mortality (relative risk 0.70, 95% CI 0.2 to 3.1) during antiarrhythmic drug therapy. After exclusion of 23 patients with documented ventricular arrhythmias and adjustment for other variables predictive of cardiac death, patients receiving antiarrhythmic drugs were not at increased risk of cardiac death or arrhythmic death. However, in patients with a history of heart failure who received antiarrhythmic drug therapy, the relative risk of cardiac death was 3.3 (p = 0.05, 95% CI 0.99 to 11.1) and that of arrhythmic death was 5.8 (p = 0.009, 95% CI 1.5 to 21.7) compared with the risk in patients not taking antiarrhythmic medications. CONCLUSIONS: Although antiarrhythmic drug therapy was not randomly determined in this trial, the data suggest that in patients with atrial fibrillation and a history of congestive heart failure, the risk of such therapy may outweigh the potential benefit of maintaining sinus rhythm.

Anti-Arrhythmia Agents↗
PubMed1992

Warfarin in the prevention of stroke associated with nonrheumatic atrial fibrillation. Veterans Affairs Stroke Prevention in Nonrheumatic Atrial Fibrillation Investigators.

BACKGROUND: Nonrheumatic atrial fibrillation is common among the elderly and is associated with an increased risk of stroke. We investigated whether anticoagulation with warfarin would reduce this risk. METHODS: We conducted a randomized, double-blind, placebo-controlled study to evaluate low-intensity anticoagulation with warfarin (prothrombin-time ratio, 1.2 to 1.5) in 571 men with chronic nonrheumatic atrial fibrillation; 525 patients had not previously had a cerebral infarction, whereas 46 patients had previously had such an event. The primary end point was cerebral infarction; secondary end points were cerebral hemorrhage and death. RESULTS: Among the patients with no history of stroke, cerebral infarction occurred in 19 of the 265 patients in the placebo group during an average follow-up of 1.7 years (4.3 percent per year) and in 4 of the 260 patients in the warfarin group during an average follow-up of 1.8 years (0.9 percent per year). The reduction in risk with warfarin therapy was 0.79 (95 percent confidence interval, 0.52 to 0.90; P = 0.001). The annual event rate among the 228 patients over 70 years of age was 4.8 percent in the placebo group and 0.9 percent in the warfarin group (risk reduction, 0.79; P = 0.02). The only cerebral hemorrhage occurred in a 73-year-old patient in the warfarin group. Other major hemorrhages, all gastrointestinal, occurred in 10 patients: 4 in the placebo group, for a rate of 0.9 percent per year, and 6 in the warfarin group, for a rate of 1.3 percent per year. There were 37 deaths that were not preceded by a cerebral end point--22 in the placebo group and 15 in the warfarin group (risk reduction, 0.31; P = 0.19). Cerebral infarction was more common among patients with a history of cerebral infarction (9.3 percent per year in the placebo group and 6.1 percent per year in the warfarin group) than among those without such a history. CONCLUSIONS: Low-intensity anticoagulation with warfarin prevented cerebral infarction in patients with nonrheumatic atrial fibrillation without producing an excess risk of major hemorrhage. This benefit extended to patients over 70 years of age.

Aged↗
PubMed1975

Atrial activity during exercise in patients with atrial flutter or atrial fibrillation.

The atrial activity was studied at rest and during exercise in 6 patients with atrial flutter and in 7 patients with atrial fibrillation. In the latter, a special recording technique was used which permitted identification of the f-waves. No increase in the frequency of the atrial waves was found. Thus the increase of the ventricular rate during work in patients with atrial flutter or atrial fibrillation seems to be caused by a change in the atrio-ventricular conduction.

Adult↗
PubMed2026

Histological Determinants of Atrial Dysfunction in Patients With Atrial Fibrillation.

BACKGROUND: Atrial fibrillation (AF) is associated with diverse histological abnormalities, but their contributions to atrial dysfunction and functional recovery remain unclear. METHODS: In a discovery cohort of 375 patients with nonvalvular AF undergoing catheter ablation, atrial biopsy samples were quantitatively analyzed for fibrosis, intercellular space expansion, myofibrillar loss, myocardial nuclear density, and amyloid deposition. Left atrial reservoir strain (LASr) was assessed as a measure of atrial function during sinus rhythm (Group 1) or AF (Group 2) at the time of echocardiography. Functional recovery was defined as the change in LASr 12 months after ablation. Findings were validated in an independent cohort of 191 patients with AF. A subset of samples was additionally analyzed for DNA damage markers, poly(ADP-ribose), and phosphorylated histone H2A.X. RESULTS: LASr improved significantly after ablation in Group 2 but not in Group 1. Multivariable analyses identified greater fibrosis, reduced myocardial nuclear density, and advanced amyloid deposition as significant determinants of impaired atrial function in both groups and of limited postablation functional recovery in Group 2 (all P<0.01). Amyloid deposition was also significantly associated with adverse clinical outcomes. Decision-tree models incorporating LASr accurately identified advanced amyloid deposition in both cohorts (accuracy, 94%-96%). DNA damage markers were inversely associated with myocardial nuclear density and positively associated with cardiomyocyte hypertrophy. CONCLUSIONS: Fibrosis, DNA damage-associated reduction in myocardial nuclear density, and advanced atrial amyloidosis are key determinants of atrial dysfunction and impaired postablation functional recovery in patients with AF. LASr enables noninvasive identification of advanced atrial amyloidosis.

Humans↗
PubMed2025

Contributions of Common, Rare, and Somatic Genetic Variants to Incidence of Atrial Fibrillation.

IMPORTANCE: Atrial fibrillation (AF) has a complex genetic architecture involving common, rare, and somatic variants. The association between these components requires further investigation. OBJECTIVE: To examine the individual and combined contributions of polygenic, monogenic, and somatic genetic variants to AF incidence, and develop an integrated genomic model (IGM-AF) for improved risk prediction. DESIGN, SETTING, AND PARTICIPANTS: This cohort study used whole-genome sequence data from participants of the UK Biobank, with follow-up for AF events through hospital records, death registries, and self-report. The UK Biobank recruited participants aged 40 to 69 years in the UK between 2006 and 2010. Study data were analyzed from August 2022 to November 2024. EXPOSURES: IGM-AF comprising an AF polygenic risk score (PRS), a composite rare variant gene set (AFgeneset), and somatic variants associated with clonal hematopoiesis of indeterminate potential (CHIP). Clinical AF risk was estimated using the Cohorts for Heart and Aging Research in Genomic Epidemiology AF (CHARGE-AF) score. MAIN OUTCOMES AND MEASURES: The primary outcome was hazard ratios (HRs) for 5-year incident AF attributable to PRS, AFgeneset, CHIP, and their interactions. The predictive performance of IGM-AF and its components was quantified using HRs, C statistics, and reclassification indices. RESULTS: A total of 416&#x202f;085 individuals (mean [SD] age, 56.6 [8.0] years; 224&#x202f;642 female [54.0%]) with 30&#x202f;797 AF cases were included. The PRS (HR per 1 SD, 1.65; 95% CI, 1.63-1.67; P&#x2009;<&#x2009;1&#x2009;&#xd7;&#x2009;10-8), AFgeneset (HR, 1.63; 95% CI, 1.52-1.75; P&#x2009;=&#x2009;1.46&#x2009;&#xd7;&#x2009;10-42), and CHIP (HR, 1.26; 95% CI, 1.15-1.38; P&#x2009;=&#x2009;1.41&#x2009;&#xd7;&#x2009;10-6) were associated with incident AF. The 5-year cumulative incidence of AF was at least 2-fold among individuals having all 3 genetic drivers (common, rare, and somatic drivers) compared with those with only 1 driver. Integration of IGM-AF with a clinical risk model (CHARGE-AF) showed higher predictive performance (C statistic, 0.80; 95% CI, 0.80-0.80) compared with IGM-AF and CHARGE-AF alone. The classification of the at-risk population for AF was improved when IGM-AF was added to CHARGE-AF (net reclassification index, 0.08; 95% CI, 0.07-0.09). CONCLUSIONS AND RELEVANCE: Results of this cohort study demonstrated the complementary value of common, rare, and somatic variants in shaping genomic AF risk. Leveraging comprehensive genetic information may enhance screening and preventive interventions for AF.

Humans↗
PubMed1977

Atrial fibrillation in children.

Atrial fibrillation is rare in children. Previous reports associated it with severe rheumatic heart disease and a poor prognosis. This review is of the unique experience of 35 cases of atrial fibrillation in children in the past 22 years; 23 patients were boys. The age of onset ranged from 1 day to 19 years (average, 8 years). Associated cardiac conditions were severe rheumatic mitral regurgitation (3 cases), cardiomyopathy (5), atrial tumors (2), infective endocarditis (1), paroxysmal atrial tachycardia of infants (4), idiopathic paroxysmal atrial fibrillation (1), Marfan's syndrome with mitral regurgitation (1), endocardial fibroelastosis (1), and structural congenital heart malformations (17). Surgical correction of congenital heart lesions was directly related to the development of atrial fibrillation in 14. Varying arrhythmias of the sick-sinus syndrome were observed in five children. The atrial fibrillation was paroxysmal or transient in 21 patients and persistent in 14. Treatment depended on the underlying condition. Digoxin was used in all cases and cardioversion attempted in ten; no patient was given anticoagulants. Three children had cerebral emboli, with residual defects. Eighteen patients are known to be alive, 13 are dead, and 4 are lost to follow-up. Atrial fibrillation in childhood is an indication for complete investigation of the patient and for the institution of treatment appropriate to the underlying disease.

Adolescent↗
PubMed1979

Uncontrolled ventricular rate in atrial fibrillation. A manifestation of dissimilar atrial rhythms.

A patient with coarse atrial fibrillation and a rapid ventricular response developed periods of high grade atrioventricular block interpersed with periods of rapid ventricular conduction after the administration of digitalis and propranolol. Intracardiac atrial recordings showed similar atrial rhythms of high right atrial flutter and left atrial fibrillation. The low right atrial recordings showed flutter during the periods of fast ventricular rates and fibrillation during periods of slower ventricular rates.

Adult↗