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At least 955 records · Page 53Linked to original sources
PubMed2006

Increased propensity for apnea in response to acute elevations in left atrial pressure during sleep in the dog.

Periodic breathing is commonly observed in chronic heart failure (CHF) when pulmonary capillary wedge pressure is abnormally high and there is usually concomitant tachypneic hyperventilation. We hypothesized that acute pulmonary hypertension at pressures encountered in CHF and involving all of the lungs and pulmonary vessels would predispose to apnea/unstable breathing during sleep. We tested this in a chronically instrumented, unanesthetized dog model during non-rapid eye movement (NREM) sleep. Pulmonary hypertension was created by partial occlusion of the left atrium by means of an implanted balloon catheter in the atrial lumen. Raising mean left atrial pressure by 5.7 +/- 1.1 Torr resulted immediately in tachypneic hyperventilation [breathing frequency increased significantly from 13.8 to 19.9 breaths/min; end-tidal P(CO2) (P(ET(CO2))) fell significantly from 38.5 to 35.9 Torr]. This tachypneic hyperventilation was present during wakefulness, NREM sleep, and rapid eye movement sleep. In NREM sleep, this increase in left atrial pressure increased the gain of the ventilatory response to CO2 below eupnea (1.3 to 2.2 l.min(-1).Torr(-1)) and thereby narrowed the CO2 reserve [P(ET(CO2)) (apneic threshold) - P(ET(CO2)) (eupnea)], despite the decreased plant gain resulting from the hyperventilation. We conclude that acute pulmonary hypertension during sleep results in a narrowed CO2 reserve and thus predisposes toward apnea/unstable breathing and may, therefore, contribute to the breathing instability observed in CHF.

Animals↗
PubMed2002

Pulmonary venous systolic flow: influence of gravity on pulmonary venous flow velocities assessed in patients with atrial fibrillation.

The origin of the pulmonary venous (PV) systolic flow wave is still unclear and could be the atrial relaxation and systolic descent of the atrioventricular plane, which decrease atrial pressure (suction) or raised PV pressure. In atrial fibrillation (AF), loss of atrial contraction and relaxation significantly modifies the systolic PV flow wave. The effect of recumbent positional changes on PV, however, has not yet been characterized in AF. The purpose of this study was to evaluate the effect of positional changes on systolic PV flow in patients with AF studied by transesophageal echocardiography. The study group consisted of 45 patients with AF (34 patients with AF, alone, and 11 patients with mitral stenosis [MS]). To assess the influence of left atrial pressure, we included patients with MS and AF. Pulsed wave Doppler transesophageal echocardiography of the left and right upper PV were performed in the left lateral recumbent position in all patients and repeated records were obtained with the subject in the supine position in 25 (AF alone: n = 20, MS: n = 5) of 45 patients. In the left lateral recumbent position, the systolic PV flow velocity and systolic fraction of the left PV, which were recorded on the recumbent subject's lower side, were significantly increased compared with those of the right PV in both AF alone and MS with AF (33.9 +/- 10.8 vs 13.8 +/- 6.4 cm/s, 0.45 +/- 0.09 vs 0.20 +/- 0.10 in AF alone; 30.2 +/- 11.7 vs 14.6 +/- 6.0 cm/s, 0.43 +/- 0.12 vs 0.20 +/- 0.07 in MS, respectively, P < .01). By changing the position from the left lateral to the supine position, systolic PV flow velocity and systolic fraction of the left and right PV became the same (29.3 +/- 8.4 vs 27.9 +/- 8.4 cm/s, 0.39 +/- 0.09 vs 0.36 +/- 0.06 in AF alone, 23.5 +/- 8.8 vs 27.5 +/- 5.0 cm/s, 0.35 +/- 0.08 vs 0.35 +/- 0.09 in MS, respectively). These findings show that the PV volume (hydrostatic pressure) significantly modifies systolic PV flow wave in patients without atrial contraction and relaxation. We should take into consideration the body position on which PV flow is studied.

Aged↗
PubMed1994

Pulmonary congestion enhances responses of lung rapidly adapting receptors to cigarette smoke in rabbit.

We examined the effects of low-nicotine cigarette smoke, pulmonary venous congestion, and their combination on the activity of rapidly (RAR) and slowly adapting receptors (SAR) in anesthetized rabbits. Pulmonary venous congestion was achieved by inflating a balloon in the left atrium to increase left atrial pressure. We examined smoke effects on RARs (averaged over 15 breaths) at baseline left atrial pressure and at subthreshold and suprathreshold increases in left atrial pressure. At baseline, smoke significantly increased RAR activity from 12.1 +/- 4.2 to 16.2 +/- 4.2 impulses/breath (P < 0.05). At subthreshold increases in left atrial pressure (2.9 +/- 0.6 mmHg), smoke produced larger increases in RAR activity (12.3 +/- 3.3 to 22.5 +/- 4.1 impulses/breath; P < 0.05). Suprathreshold increases in left atrial pressure (9.2 +/- 1.1 mmHg) alone increased RAR activity from 10.9 +/- 3.2 to 19.8 +/- 5.9 impulses/breath (P < 0.05). Smoke had no additional effect (22.3 +/- 4.8 impulses/breath; P > 0.05). There was, however, a transient increase in RAR activity (1st 3 breaths of smoke) under all three conditions. Of nine SARs examined, only two were stimulated by smoke. We conclude that in the rabbit smoke-induced stimulation of RARs is augmented by mild pulmonary venous congestion. of RARs is augmented by mild pulmonary venous congestion.

Adaptation, Physiological↗
PubMed2004

Magnitude of left atrial V wave is the determinant of exercise capacity in patients with mitral stenosis.

A large left atrial (LA) V wave can be observed in patients with pure mitral stenosis (MS) due to decreased LA compliance. Based on the hypothesis that exercise capacity may correlate with the magnitude of the LA V wave in patients with MS, symptom-limited exercise testing and right and left heart catheterization were performed in 28 patients. The results show that the magnitude of the LA V wave (p = 0.02) was the strongest predictor of the exercise duration, suggesting that LA compliance may be an important contributing factor in determination of exercise capacity in patients with MS.

Adult↗
PubMed1996

Acute changes in left atrial and left ventricular diameters after physiological pacing.

The present study examined alterations in left atrial diameter (LAD) and diastolic left ventricular diameter (LVDd) in 37 patients (72.2 +/- 9.8 years old) who received physiological pacemakers; 22 with atrioventricular (AV) block and 15 with sick sinus syndrome (SSS). After pacemaker implantation, LAD and LVDd were serially measured using echocardiography, and their diameters were expressed per body surface area (LADI and LVDdI; mm/m2). Pulmonary capillary wedge pressure (PCWP) and cardiac output (CO) were measured in ten patients with SSS and ten with AV block during both right ventricular and AV sequential pacing. After AV sequential pacing, CO increased in 19 of 20 patients (3.2 +/- 0.9 L/min to 3.9 +/- 1.0 L/min; P < 0.001). LADI decreased from 24.9 +/- 4.2 mm/m2 to 21.8 +/- 4.4 mm/m2 (P < 0.001) in 22 patients with AV block and from 24.1 +/- 3.4 mm/m2 to 20.4 +/- 3.8 mm/m2 (P < 0.001) in 15 SSS patients. However, LVDdI did not change significantly in either group of patients. The changes in LAD after the implantation of a physiological pacemaker occurred rapidly, i.e., LAD began to decrease within 1 minute after the procedure, and then reached a plateau. This plateau phase continued for at least 7 days during physiological pacing. There was a positive correlation between the changes in LADI after pacemaker implantation and those in PCWP observed during the AV sequential pacing performed prior to the implantation (r = 0.86; P < 0.001). The reduction in LAD following pacemaker implantation was rapid and seemed to be accompanied by improvement of cardiac function. Thus, it is suggested that the serial measurement of LADI is useful to predict the efficacy of physiological pacemaker implantation.

Aged↗
PubMed2001

Myocardial connections between left atrial myocardium and coronary sinus musculature in man.

INTRODUCTION: Anatomic studies have shown that muscle morphologically identical to that of the atrial myocardium consistently surrounds the coronary sinus (CS). The CS musculature is connected to the left atrial (LA) myocardium in a variable fashion, with fewer connections in its distal portion. The aim of this study was to document the presence of connections between the LA myocardium and the CS musculature, using pacing maneuvers in man, and to study their potential association with natural atrial arrhythmia occurrence. METHODS AND RESULTS: Thirty patients (19 men; mean age 50.5 years) underwent electrophysiologic study, during which a decapolar catheter with 2-mm interelectrode spacing every 10 mm was inserted into the CS, with the proximal electrode pair positioned at the ostium. Associated atrial arrhythmias were paroxysmal atrial fibrillation in 5, typical atrial flutter in 13, LA flutter in 1, and other in 11. Baseline S1 and a single extrastimulus were delivered during distal and proximal CS pacing, while recordings were obtained from the four remaining bipoles. During distal CS pacing, double potentials with increasing interpotential interval from proximal to distal CS as a function of extrastimulus prematurity were detected in nine patients, suggesting block in a discrete local pathway distally connecting the CS to the LA and leading to reversion of low LA activation. Local delay in this pathway without complete CS-LA block resulting in LA activation fusion was observed in eight patients. A single nonfractionated potential at the distal CS, even at the shortest attainable S1-S2 coupling interval, which was interpreted as no block within distal CS-LA connection(s), was observed in the other 13 patients. History of atrial fibrillation or atypical atrial flutter was found in 8 of 9 patients with block at the distal CS-LA connection but in only 3 of 13 patients with no CS-LA connection block (P = 0.004). CONCLUSION: The ability to dissociate the LA from the distal CS suggests the presence of discrete connections between these structures in man. This observation appears to be associated with the clinical occurrence of atrial arrhythmias.

Analysis of Variance↗
PubMed1996

S-(-)-ET 126: a potent and selective M1 antagonist in vitro and in vivo.

The pharmacological profile of the competitive muscarinic antagonist S-(-)-alpha-(hydroxymethyl)benzeneacetic acid 1-methyl-4-piperidinyl ester (S-(-)-ET 126) was evaluated on M1 (rabbit vas deferens; pA2=8.99), M2 (rat left atrium; pA2=8.21) and M3 (rat ileum; pA2=6.84) muscarinic receptors in comparison with pirenzepine. The drug shows a subtype selectivity (M1/M2=8; M1/M3=178; M2/M3=22) that proposes it as a useful pharmacological tool for receptor studies. S-(-)-ET 126, like pirenzepine, prevents the antinociception induced by M1 agonists (McN-A-343 and AF-102B). Unlike pirenzepine and spirotramine, the compound is able to cross the blood brain barrier which makes it useful for in vivo investigations.

Acetylcholine↗
PubMed1989

The mechanism of nitrous oxide-induced changes in pulmonary vascular resistance in a dog model of left atrial outflow obstruction.

Nitrous oxide has been reported to increase pulmonary vascular resistance (PVR) in patients with pulmonary hypertension secondary to mitral stenosis. Additional data suggest this response involves sympathetic stimulation because the increase in PVR can be prevented by alpha-adrenergic and ganglionic blockade. Whether or not active pulmonary vasoconstriction occurs remains unclear. This study was designed to more fully characterize the influence of N2O on pulmonary hemodynamics during left atrial outflow obstruction (LAO). Responses in an in situ blood-perfused lung lobe were compared with those in the remaining intact lung of six dogs anesthetized with pentobarbital, 30 mg/kg, and morphine, 1.5 mg/kg, and prepared for measurement of peak left ventricular (LV) pressure, LV end-diastolic pressure (LVEDP), LV dP/dt, systemic arterial and pulmonary arterial (PA) pressures, and cardiac output (CO). The pulmonary artery branch supplying the left middle lung lobe was cannulated and perfused at a constant rate with warmed blood. LAO was produced by filling the balloon of a Foley catheter positioned in the left atrium (LA) with enough saline to increase PA pressure by 50%; the balloon was subsequently left filled for the entire protocol. Measurements were first obtained during ventilation with 67% N2, and 33% O2. The inspired gas was then changed to 67% N2O and 33% O2 for 10 minutes, and then returned to the N2/O2 mixture. Once baselines had been reestablished (about 10 minutes), phentolamine, 0.75 mg/kg, was administered, and the response to 10 minutes of N2O again observed. N2O did not change vascular resistance in the isolated lobe, but increased intact-lung PVR.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMedDate not supplied

In vitro screening of antitumour agents for cardiotoxicity by means of isolated mouse left atria.

Cardiotoxicity, a side-effect that can occur after treatment with an anticancer drug, has severe clinical implications. Therefore, a model is desired to screen new anticancer drugs or drug combinations for possible cardiotoxic side-effects. In the present study we tested the applicability of the electrically stimulated isolated mouse left atrium model using a wide range of anticancer drugs with known cardiotoxicity. It appeared that the cardiotoxicity observed in our model, i.e. the negative or positive inotropic effects of the drugs on the isolated atrium, corresponded with the observed cardiotoxicity in animals and/or humans. It is therefore concluded that our model can be used to wam for possible cardiotoxic side-effects of anticancer drugs in vivo.

Aminoglycosides↗
PubMed2005

Prenatal cocaine alone and combined with nicotine alters ANG II and IGF-1 induced left atrial contractions in aging male offspring.

Prenatal cocaine or nicotine affects inotropic activity in the hearts of rat offspring. However, the long-term consequence of this exposure on the cardiac response to hormonal challenge is unknown. We assessed the inotropic effects of angiotensin II (ANG II) and insulin-like growth factor 1 (IGF-1) in the left atria of 19.0-24.5 month-old male rats exposed on gestation days 8-21 to 1 of 6 treatments: low cocaine (LC) (20 mg/kg) or high cocaine (HC) (40 mg/kg); 20 mg/kg cocaine and high nicotine (5 mg/kg nicotine) (LC/HN); 40 mg/kg cocaine and low nicotine (2.5 mg/kg nicotine) (HC/LN); pair fed: yoked to HC (PF); saline: injection of 0.9% NaCl (SAL). Isometric contractions were assessed by electrical stimulation of isolated left atria superfused with Tyrode solution (control) to which ANG II (10-7 mol/L, 20 min) and IGF-1 (10-8 mol/L, 20 min) in the presence of ANG II were added sequentially. Offspring in all cocaine groups showed a higher peak tension development (PTD) to ANG II than PF controls. This increase in PTD was attenuated by subsequent addition of IGF-1 in all except HC offspring. However, with the HC/LN combination the IGF-1 effect on PTD was again evident. The velocities of contraction and relaxation were positively affected by ANG II only in the combined prenatal drug groups; IGF-1 reduced only contraction velocity. Our data demonstrate that IGF-1 reverses the positive inotropic effect of ANG-II in atrial muscle of aging rats and that gestational exposure to only high doses of cocaine eliminates this protective response. It appears that combined prenatal exposure to cocaine and nicotine does not exacerbate the decline in cardiac function and responsiveness to inotropic drugs seen in the aging heart.

Aging↗
PubMed1995

Anticholinergic effects of class III antiarrhythmic drugs in guinea pig atrial cells. Different molecular mechanisms.

BACKGROUND: It is well known that vagal stimulation increases the vulnerability to atrial fibrillation via muscarinic receptor-mediated shortening of refractory period. Recently it has been reported that some class III antiarrhythmic drugs effectively terminate or prevent atrial flutter and fibrillation by prolonging atrial effective refractory period. However, effects of class III antiarrhythmic drugs on the muscarinic acetylcholine receptor-operated K+ current (IK.ACh), which is important for the repolarization phase of the action potential in atrial cells, have not been thoroughly examined. METHODS AND RESULTS: Effects of three class III antiarrhythmic drugs, d,l-sotalol, E-4031, and MS-551, on the carbachol (1 mumol/L)-induced action potential shortening and outward K+ current were examined in guinea pig atrial cells by conventional microelectrode and patch clamp techniques. In isolated left atria, d,l-sotalol (100 mumol/L), E-4031 (3 mumol/L), and MS-551 (30 mumol/L) partially reversed the carbachol-induced action potential shortening. In isolated single atrial cells, IK.ACh was activated by extracellular application of carbachol (1 mumol/L) or adenosine (10 mumol/L) or by intracellular loading of GTP gamma S (100 mumol/L). Sotalol (3 to 1000 mumol/L), E-4031 (1 to 100 mumol/L), and MS-551 (1 to 100 mumol/L) inhibited the carbachol-induced IK.ACh in a concentration-dependent manner, and their IC50 (half-maximal inhibition) values were 35.5, 7.8, and 11.4 mumol/L, respectively. However, the GTP gamma S-induced and adenosine-induced IK.ACh were inhibited by high concentrations of E-4031 and MS-551 but not by sotalol. CONCLUSIONS: Sotalol may inhibit IK.ACh by the blockade of the atrial muscarinic receptors, whereas E-4031 and MS-551 may inhibit the current not only by blocking the muscarinic receptors but also by depressing the function of the K+ channel itself and/or G proteins. These drugs may potentially be useful for the prevention and termination of atrial flutter and fibrillation through their inhibitory action on IK.ACh.

Acetylcholine↗
PubMed1993

[Determining factors of successful percutaneous transvenous mitral commissurotomy and eligible indications for the procedure].

The aim of this report is to investigate the factors which influence mean left atrial pressure (LAP) after percutaneous transvenous mitral commissurotomy (PTMC) and the characteristics of patients in whom PTMC is most effective. Fifty one patients with symptomatic mitral stenosis underwent PTMC. The patients included 8 males and 43 females, aged 26-66 years (mean age of 46). These patients were classified into two groups according to LAP after PTMC: 31 cases with LAP after PTMC of 12 mmHg or less (group A) and 20 cases with LAP after PTMC greater than 12 mmHg (group B). The patients of group A were younger (44 +/- 6 vs 48 +/- 6 years, p < 0.05), and had atrial fibrillation (af) less frequently (35 vs 65%, p < 0.05), and had mitral valve calcification less frequently (29 vs 65%, p < 0.01). Before PTMC, LAP (19 +/- 6 vs 23 +/- 5 mmHg, p < 0.01) was lower and mitral valve area (MVA) (0.95 +/- 0.24 vs 0.81 +/- 0.15 cm2, p < 0.05) larger in group A. Symptoms graded according to the New York Heart Association functional classification system were similar in both groups before PTMC. After the procedure, final MVA (1.79 +/- 0.69 vs 1.40 +/- 0.50 cm2, p < 0.05) was larger and systolic pulmonary artery pressure (32 +/- 9 vs 39 +/- 7 mmHg, p < 0.01) lower in group A. Mitral regurgitation > or = 3-grade tended to complicate more frequently (3 vs 20%, NS) in group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Case report: Focal ablation for atrial fibrillation originating from the inferior vena cava and the posterior left atrium.

We identified a case of paroxysmal atrial fibrillation (AF) originating from inferior vena cava (IVC) and the low-posterior left atrium (LA). Both foci, the IVC and the low-posterior LA, simultaneously served not only as trigger but also as driver for maintenance of AF. During AF, the IVC and the low-posterior LA continuously demonstrated the rapid and fractionated potentials that exit into both atria with conduction block. Focal ablation for ectopic beats within the IVC and the low-posterior LA completely eliminated the storm of AF.

Aged, 80 and over↗
PubMed1996

[Spontaneous intracardiac contrast and embolic risk].

Spontaneous contrast in the form of smokey echos in the cardiac chambers is considered to be a risk factor for thromboembolism. The aggregation of red blood cells results in larger target which diffuse a measurable in vitro ultrasonic signal. The phenomenon of erythrocytic aggregation is dependent on the red cells themselves, the plasma fibrinogen and conditions of blood flow. The other constituents of the blood only reflect a small amount of ultrasound, usually undetectable. Transoesophageal echocardiography with high frequency transducers (5 MHz) positioned in close proximity to the cardiac chambers, has become the reference method for detecting spontaneous contrast. This phenomenon is almost exclusively observed in the left atrium and left auricle and rarely in the other cardiac chambers or descending aorta. In pathological situations, spontaneous contrast is essentially implicated in two conditions: mitral valve obstacles and non-valvular atrial fibrillation. Conversely, moderate to severe mitral regurgitation is a negative predictive factor of spontaneous contrast. However, a purely qualitative appreciation of spontaneous contrast which may be influenced by the gain setting and technical specifications of the echocardiograph, and the subjectivity of the operator, is an important limitation. Therefore, the identification of quantitative markers of spontaneous contrats and new therapeutic antithrombotic protocols remain essential.

Atrial Fibrillation↗
PubMed1995

Hemodynamic changes during induction of anesthesia with eltanolone and propofol in dogs.

The purpose of this study was to examine global and regional hemodynamic changes during induction of anesthesia with eltanolone, a new short-acting steroid hypnotic, as compared to propofol, in chronically instrumented dogs. The effects on cardiac performance were assessed in six animals. Renal and hepatic blood flows were examined in a separate study including five animals. Two doses of each drug were investigated: eltanolone 2.5 and 5 mg/kg and propofol 7.5 and 15 mg/kg. Left atrial filling pressures and cardiac output were not affected by either drug. Maximum rate of increase of left ventricular pressures decreased both with eltanolone (-28% and -40% from awake control for the 2.5 and 5 mg/kg doses, respectively) and with propofol (-19% and -30% from awake controls with 7.5 and 15 mg/kg respectively). In contrast to propofol, eltanolone preserved arterial blood pressure. Propofol lowered systemic vascular resistance (-21% and -39% with the low and high dose, respectively), and only slightly decreased left ventricular wall thickening fraction (-16% and -21%). Eltanolone did not affect systemic vascular resistance but reduced the wall-thickening fraction dose-dependently (-28% and -61%). Propofol, but not eltanolone, induced moderate coronary vasodilation. Hepatic arterial blood flow velocity decreased dose-dependently (-21% and -64%) during eltanolone anesthesia whereas, in contrast, it increased after propofol (+59% and +64%). Renal and portal venous blood flows remained essentially unaltered from awake conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed2004

Effect of cardiac resynchronization therapy on left atrial reverse remodeling and spontaneous echo contrast.

Recent studies revealed reverse remodeling in left ventricle with cardiac resynchronization therapy (CRT). However, effects on left atrial remodeling, left atrial total emptying fraction and left atrial spontaneous echo contrast (SEC) have not been adequately evaluated. The aim of this study was to investigate the long-term changes in SEC, left atrial reverse remodeling, and left atrial total emptying fraction after CRT. Twenty patients with systolic heart failure and complete left bundle-branch block underwent implantation of biventricular pacemaker devices. Transthoracic and transesophageal echocardiography were performed one week before and one and six months after pacemaker implantation. After biventricular pacemaker implantation, significant clinical improvement was observed in all patients. Left atrial maximal and minimal volumes showed a significant progressive decline after CRT (reverse remodeling). Left atrial total emptying ejection fraction (LATEF) was 33 +/- 19% at baseline and increased to 37 +/- 10% and 41 +/- 11% at the 1st and 6th months respectively (p = 0.01 and p = 0.04). SEC was detected in 18 of 20 patients (90%) at the beginning of the study. After six months SEC disappeared in 5 patients and frequency of SEC reduced to 45%. Decrease in the intensity of the SEC was also statistically significant (at the 1st and 6th months; p = 0.001 and p < 0.001 respectively). Long-term CRT results in atrial reverse remodeling, increases LATEF, and reduces both frequency and intensity of atrial SEC.

Adult↗
PubMedDate not supplied

Clearance of proteins from the air spaces following cardiogenic edema in sheep.

Studies on the clearance of instilled fluid and protein into the lungs of sheep show that fluid initially clears rapidly from the lungs resulting in an increase in an increase in air space protein concentrations. This is followed by a slower monoexponential clearance of proteins during the next few days. To determine whether the clearance of edema fluid follows the same time course as instilled fluid, alveolar edema was induced in 11 sheep by inflating a balloon in the left atrium for 2 h to increase left atrial pressure 35-40 cm H2O. Protein concentrations in the epithelial lining fluid (ELF) were monitored by performing single-cycle lavages immediately after deflation of the left atrial balloon, and again 3, 21, 48, and 96 h later. During the first 3 h of recovery, 44% of the fluid cleared and ELF protein concentrations rose from 7 +/- 2 to 19 +/- 6 mg/mL in the 7 sheep that recovered well. The ELF protein concentration in these sheep remained elevated for 48 h and then cleared at rates similar to that seen following instillation of proteins. We conclude that insights about mechanisms of clearance of edema fluid obtained from studies of clearance of instilled fluid are valid in cardiogenic edema, but the time course of the clearance differs between the two models.

Animals↗
PubMed2000

Prevention of atrial fibrillation by complete compartmentalization of the left atrium using a catheter technique.

INTRODUCTION: Right atrial compartmentalization has been demonstrated to only reduce the number of atrial fibrillation (AF) episodes; left atrial (LA) fibrillation still occurs. METHODS AND RESULTS: We report successful LA compartmentalization resulting in isolation of all four pulmonary veins in a 51-year-old woman suffering from paroxysmal AF. Deployment of a complete encircling line resulted in dissociation of electrical activation within the isolated area from the remaining LA. Despite attempts at reinduction by pacing maneuvers inside and outside the isolated area, AF was no longer inducible. During 21-week follow-up, the patient remained in stable sinus rhythm with rare atrial extrasystoles. CONCLUSION: If reproducible, this ablation strategy could allow treatment of AF independent of suppression of any triggering event.

Atrial Fibrillation↗