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Left atrial spontaneous echo contrast in patients with permanent pacemakers.

OBJECTIVE: To determine the relations between left atrial appendage function, spontaneous echo contrast, and thromboembolism in patients with different modes of permanent pacemakers. PATIENTS AND METHODS: 88 patients with pacemaker implantation and 25 healthy controls in sinus rhythm had transoesophageal echocardiographic examination of the left atrial appendage. Left atrial size, appendage area, peak filling and emptying velocities of the atrial appendage, and the presence or absence of spontaneous echo contrast and thromboembolism were determined. The results in 63 patients with ventricular pacing (group 1, subdivided into subgroup 1A: 42 patients with sinus rhythm, and subgroup 1B: 21 patients with atrial fibrillation) were compared with those in 25 patients with synchronous pacing (group 2), and 25 normal control subjects (group 3). RESULTS: Patients with ventricular pacing had two distinct appendage flow patterns: well defined biphasic filling and emptying waves in subgroup 1A, and irregular very low filling and emptying waves in subgroup 1B. The ejection fraction of the left atrial appendage in subgroup 1A was significantly better than that in subgroup 1B (mean (SD) 40.6 (12.0)% v 7.6 (5.0)%, P < 0.0001). The spontaneous echo contrast was observed in 90% of subgroup 1B patients but in only 19% in subgroup 1A (P < 0.05) and was not found in groups 2 and 3 (P < 0.0001). There was a trend for increased prevalence of spontaneous echo contrast in subgroup 1A v group 2 (P = 0.053). Thrombi were detected in two cases, and cardiogenic embolism occurred in one case in subgroup 1B. All patients with spontaneous echo contrast had ventricular pacing. Multivariate analysis showed that atrial fibrillation was associated with occurrence of spontaneous echo contrast in patients with ventricular pacing (P = 0.005). CONCLUSIONS: The left atrial appendage ejection fraction was lower with ventricular pacing than with synchronous pacing. With ventricular pacing there was a trend towards increased prevalence of left atrial spontaneous echo contrast in patients in sinus rhythm, and a significantly increased prevalence in patients with atrial fibrillation.

Adult↗

Echocardiographic assessment of left ventricular filling during isoflurane anaesthesia.

PURPOSE: To determine the effect of isoflurane on left ventricular diastolic function, as assessed by Doppler echocardiography. METHODS: Ten patients with normal cardiovascular function were enrolled. Doppler measurements of mitral inflow velocities, and pulmonary venous blood flow velocities were measured preoperatively (transthoracic echocardiography), and intraoperatively (transesophageal echocardiography) at isoflurane MAC 1 and MAC 1.5. Heart rate and blood pressure were measured concomitantly. Variables were compared with repeated measures ANOVA. RESULTS: Isoflurane at both doses caused equal decreases in mitral inflow A(atrial systole) velocity (control: 43 +/- 12.3 cm.sec-1 vs MAC 1: 31 +/- 6.0 cm.sec-1 and MAC 1.5: 31.3 +/- 7.9 cm.sec-1 P < 0.01), the deceleration time of the mitral inflow E (early) velocity (control: 178 +/- 31.7 msec versus MAC 1: 127 +/- 38.3 msec and MAC 1.5: 137 +/- 28.4 msec, P < 0.01), and mean blood pressure (control: 91.1 +/- 15.4 mmHg versus MAC 1: 76.1 +/- 8.8 mmHg and MAC 1.5: 71.9 +/- 6.2 mmHg, P < 0.002). Isoflurane at both doses caused an equal increase in the E/A ratio (control: 1.5 +/- 0.57 vs MAC 1: 2.0 +/- 0.6 and MAC 1.5: 2.2 +/- 0.78, P < 0.01). No changes in mitral inflow E or pulmonary venous velocities were seen. CONCLUSION: The changes in Doppler velocities of mitral inflow and pulmonary venous flow with isoflurane are not consistent with prolonged left ventricular relaxation nor increased myocardial restriction, but are more likely the result of alterations in left ventricular loading conditions and atrial systolic function.

Adolescent↗

Long-term expression of isomyosins and myoendocrine functions in ectopic grafts of atrial tissue.

Tissue fragments of newborn rat atria were transplanted under the dorsal skin or into the bed of the anterior tibial muscle of nude mice. After 5-11 weeks, the grafts, which had reorganized into beating atrium-like structures, were analyzed and compared to ventricular tissue transplanted the same way. As revealed by monoclonal antibodies against alpha- and beta-type myosin heavy chains, atrial grafts retained a typical pattern of myosin expression distinct from that of ventricular grafts. The majority of ectopic atrial myocytes contained specific atrial granules in which cardiodilatin-immunoreactive material has been localized. Specific granules and cardiodilatin immunoreactivity were not found in myocytes of ventricular grafts. We conclude that the long-term maintenance of isomyosin expression and of the myoendocrine function of atrial tissue is largely independent of the anatomical environment.

Animals↗

Role of rate control and regularization through pacing in patients with chronic atrial fibrillation and preserved ventricular function: the VRR study.

AIM: High heart rates in chronic atrial fibrillation (CAF) is one of the factors responsible for hemodynamic alterations and may lead to tachycardiomyopathies. The ventricular rate regulation (VRR) study evaluates the effect of ventricular rate regularization in CAF patients with preserved ventricular function, marked ventricular rate variability, and indications for pacemaker (PM) implantation owing to symptomatic pauses. Rate regularization was achieved using VRR algorithm (INSIGNIA pacemakers, Guidant Corp., St. Paul, MN, USA). METHODS: One month after PM implantation, 58 patients followed two 3-month crossover periods (VRR-OFF; VRR-ON) in which the VRR algorithm was randomized and compared to fixed rate stimulation at 60 ppm. During follow-up visits a 6-minute walk test was performed under partially inhibited conditions (PM at 40 ppm) and ventricular response was recorded. The following parameters were measured: mean ventricular rate (MR), rate variability (RR30), rate recovery after exercise (SLOPE = (R-END - R-REC)/(R-END - 40)), R-END being the rate at end of walk and R-REC the rate 1 minute after exercise. RESULTS: The VRR algorithm decreased rate variability (RR30: -7.36 +/- 8.8; P < 0.01) without increasing ventricular rate (MR: -1.11 +/- 8.3 P = NS), while SLOPE improved significantly (SLOPE: +15.41 +/- 16.8 P < 0.01). CONCLUSIONS: VRR effectively stabilizes rate, without increasing pacing rate above spontaneous rhythm and helps achieve a more favorable autonomic balance, improving rate recovery after exercise.

Atrial Fibrillation↗

Cardiac effects of atrial natriuretic peptide in subjects with normal left ventricular function.

The effects of atrial natriuretic peptide (ANP) infusion were determined in 9 subjects undergoing cardiac catheterization that did not disclose heart disease. Data were obtained at rest and during the steady-state phase of alpha-human-(1-28)-atrial natriuretic peptide infusion (0.5 micrograms/kg bolus, 0.05 micrograms/kg/min intravenously for 10 minutes). Mean blood pressure decreased from 105 +/- 3 to 98 +/- 4 mm Hg (p less than 0.05); pressure measurements and left ventricular (LV) angiograms suitable for analysis were available in 7 of 9 subjects at matched heart rate. The ANP infusion reduced LV end-diastolic and end-systolic volume indexes from 93 +/- 6 to 80 +/- 6 ml/m2 (p less than 0.01) and from 25 +/- 3 to 17 +/- 1 ml/m2 (p less than 0.05), respectively. The LV ejection fraction increased insignificantly from 72 +/- 5 to 77 +/- 4%. End-systolic pressure/volume ratio showed a slight but not significant increase (from 3 +/- 0.4 to 4 +/- 0.8). Initial plasma levels of ANP (48 +/- 12 pg/ml) increased to 1,890 +/- 423 pg/ml (p less than 0.001) during the infusion and individual hemodynamic responses were not related to plasma ANP concentrations. These data suggest that the administration of ANP has no negative effects on LV function and the ANP-induced changes on cardiac performance are related to the reduced cardiac load.

Adult↗

Transcatheter closure of atrial septal defect preserves right ventricular function.

OBJECTIVES: To determine the effects of atrial septal defects (ASD) and their closure on systolic and diastolic right and left ventricular function; and by comparing surgical closure with transcatheter device closure, to establish differences attributable to cardiopulmonary bypass. DESIGN: Cross sectionally guided M mode echocardiographic ventricular long axis function was measured prospectively before and within one week after ASD closure by device in 17 patients and by surgery in 12 patients, and compared with 18 normal subjects. RESULTS: All indices of right ventricular function were impaired after surgery: mean total excursion, -1.89 cm (95% confidence interval (CI), -2.18 to -1.59); peak shortening rate, -9.09 cm/s (-10.82 to -7.35); peak lengthening rate, -9.26 cm/s (-11.09 to -7.43). Total excursion and peak lengthening rate were preserved after device closure, at -0.12 cm (-0.28 to 0.05) and 0.01 cm/s (-2.29 to 2.31), respectively. Left ventricular free wall function was unchanged after closure by either method, while all septal measurements were reduced after closure by either method (changes ranging from -3.51 to -0.32; 95% CI ranging from -4.90 to -0.13). CONCLUSIONS: Left ventricular free wall function is unaffected by ASD closure, whereas septal function is impaired, irrespective of the method of closure. Right ventricular function, both systolic and diastolic, is impaired by cardiopulmonary bypass but preserved after device closure. These findings support the transcatheter approach to ASD closure in anatomically suitable defects.

Balloon Occlusion↗

Atrial ejection force in patients with atrial fibrillation: comparison between DC shock and pharmacological cardioversion.

It is well known that the restoration of sinus rhythm is not always associated with the return of effective atrial contraction. Atrial ejection force (AEF) is a noninvasive Doppler derived parameter that measures the strength of the atrial contraction. The aim of the present study was to use pulsed-Doppler echocardiography to determine if different modalities of cardioversion influence the delay in the return of effective atrial contraction after cardioversion. DC shock and pharmacological therapy were compared. Sixty-eight patients were randomly cardioverted, either using DC shock or i.v. procainamide. The patients who were restored to a sinus rhythm had a complete Doppler echocardiographic examination within 1 hour after the restoration, after 24 hours, after 1 month, and after 3 months. AEF was measured and compared in the two groups of patients and within the same group. AEF was greater immediately and at 24 hours after cardioversion in patients who underwent pharmacological therapy compared to patients treated with DC shock (peak A wave, 60 +/- 9 vs 31 +/- 8 msec, P < 0.001; AEF 11.3 +/- 3 vs 5 +/- 2.9 dynes, P < 0.001). In both groups, AEF increases over time. In conclusion, AEF is a noninvasive parameter that can be easily measured after cardioversion and can give accurate information about the recovery of left atrial mechanical function. This finding may have important implications for guiding the anticoagulant therapy after cardioversion.

Anti-Arrhythmia Agents↗

KCNQ1 gain-of-function mutation in familial atrial fibrillation.

Atrial fibrillation (AF) is a common cardiac arrhythmia whose molecular etiology is poorly understood. We studied a family with hereditary persistent AF and identified the causative mutation (S140G) in the KCNQ1 (KvLQT1) gene on chromosome 11p15.5. The KCNQ1 gene encodes the pore-forming alpha subunit of the cardiac I(Ks) channel (KCNQ1/KCNE1), the KCNQ1/KCNE2 and the KCNQ1/KCNE3 potassium channels. Functional analysis of the S140G mutant revealed a gain-of-function effect on the KCNQ1/KCNE1 and the KCNQ1/KCNE2 currents, which contrasts with the dominant negative or loss-of-function effects of the KCNQ1 mutations previously identified in patients with long QT syndrome. Thus, the S140G mutation is likely to initiate and maintain AF by reducing action potential duration and effective refractory period in atrial myocytes.

Action Potentials↗

Radiofrequency catheter ablation of the atria reduces inducibility and duration of atrial fibrillation in dogs.

BACKGROUND: The purpose of this study was to prevent induction of sustained atrial fibrillation (AF) by radiofrequency catheter ablation (RFCA) of the atria in an open-chest canine model. METHODS AND RESULTS: In dogs randomized to acute studies, RFCA of the atria was performed after reproducible induction of sustained AF (lasting > 30 minutes) with burst stimulation or premature atrial pacing and perpetuation by low level cervical vagal stimulation or IV infusion of methacholine. Additionally, in four dogs, the long-term effectiveness of RFCA was assessed 7 to 21 days after ablation. Continuous discrete transmural lesions were produced with radiofrequency energy pulses (20 to 40 W for 60 seconds) delivered to five atrial epicardial sites and endovascularly to the coronary sinus wall. RFCA electrically isolated regions of the atria that became dissociated from the nonisolated parts. Atrial RFCA markedly attenuated vagally induced shortening of effective refractory period (ERP) at both isolated and nonisolated test sites located in the left and right atria (P < .001, n = 5). RFCA rendered noninducible sustained AF maintained by cervical vagal stimulation. The dose-response curve relating the dose of methacholine required to maintain AF was shifted down and to the right. AF was only inducible with high doses of methacholine. Atrial RFCA reduced the maximal sinus rate and prolonged the corrected sinus-node recovery time (P < .001, n = 6). However, RFCA did not affect atrial contractile function, AV-nodal ERP, or AV-nodal or His-Purkinje conduction times. In dogs in the chronic group, normal sinus rhythm and normal AV conduction were preserved and AF was only inducible with a high dose of methacholine. No atrial perforations resulted. CONCLUSIONS: RFCA in open-chest dogs produces partial vagal denervation and reduces the inducibility of AF.

Animals↗

Regulation of plasma ANF after increases in afterload in conscious dogs.

Although atrial stretch is the primary stimulus for atrial natriuretic factor (ANF) secretion, hormones may directly affect ANF secretion or may indirectly influence ANF by changing left ventricular afterload, thereby altering atrial stretch. To determine whether direct effects are important for the release of ANF in vivo, we measured changes in plasma ANF and in atrial wall function in the conscious dog after the administration of vasopressin, angiotensin II, and phenylephrine and by mechanically increasing left ventricular afterload by partial aortic occlusion. Injections of phenylephrine, angiotensin II, and arginine vasopressin (AVP) that were chosen to cause similar changes in systemic arterial pressure resulted in similar changes in atrial pressure and diameter. Maximum V wave atrial wall stress increased to 283 +/- 12, 311 +/- 41, 327 +/- 24, and 277 +/- 22 g/cm2 for AVP, angiotensin, phenylephrine, and occlusion, respectively, and plasma ANF increased to 242 +/- 81, 248 +/- 62, 299 +/- 95, and 190 +/- 53 pg/ml. There were significant linear correlations between left ventricular afterload and left atrial pressure, and each method for increasing left ventricular afterload shifted the position to the left on an atrial pressure-diameter, compliance curve, by a similar degree. Thus changes in left ventricular afterload result in changes in atrial wall function and similar changes in plasma ANF. No hormonal-specific increase in plasma ANF was found in conscious dogs after increases in afterload.

Angiotensin II↗

Transient atrial dysfunction after conversion of chronic atrial fibrillation to sinus rhythm.

Although conversion of atrial fibrillation (AF) to sinus rhythm can usually be accomplished by electrical or drug therapy, effective atrial systole may not be restored. To investigate the return of atrial transport function and its relation to the duration of the arrhythmia, Doppler echocardiography was performed after conversion in 18 patients with acute AF (less than or equal to 1 week duration), 14 patients with chronic AF (greater than 1 week duration) and 15 control patients. Flow velocities during rapid filling (E wave) and atrial systole (A wave) were measured in both left and right ventricles. Patients in the acute AF group had left ventricular A waves (49 +/- 4 cm/s) and A/E ratios (0.97 +/- 0.1) similar to those of the control patients (55 +/- 7 cm/s, 0.87 +/- 0.08, respectively). In contrast, patients in the chronic AF group had much smaller A waves (19 +/- 5 cm/s) and A/E ratios (0.30 +/- 0.08) than those in the other 2 groups (p less than 0.001). Five patients with chronic AF (36%) had complete left atrial paralysis (A/E = 0) despite normal sinus P waves. Measurements in the right ventricle showed similar differences among the groups. Patients with chronic AF who maintained sinus rhythm showed an increase in A/E ratio to control levels, from 0.45 +/- 0.1 to 0.93 +/- 0.1 (p = 0.003) at 48 days (average) after conversion. Thus, atrial transport function is normal after brief periods of AF, but reduced or absent when conversion is achieved after the arrhythmia has been sustained greater than 1 week.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Improvement of the cardiac function after electrical cardioversion of atrial fibrillation. Echocardiographic study in patients with and without mitral stenosis.

The improvement of the cardiac function after electrical cardioversion of atrial fibrillation has been studied by echocardiography by few authors and only in patients without mitral stenosis. Moreover, discordant results have been obtained. We have studied nine patients with mitral valve disease as well as nine other patients with ischemic heart disease. Both groups were cardioverted within five days of onset of atrial fibrillation, and appropriate echocardiographic measurements were made one hour before and two hours after cardioversion. We found a significant decrease of left atrial diameter in both groups, as well as a significant increase of the end-diastolic diameter and volume of left ventricle and an improvement of the cardiac index. These changes were significantly more pronounced in patients with mitral valve disease and they appear in accordance with the improvement of the cardiac function demonstrated with invasive hemodynamic studies after cardioversion to sinus rhythm. In the group of patients with mitral valve disease and a very dilated left atrium (more than 6 cm. of diameter) atrial fibrillation recurred within the next twelve months. In spite of the limitations of M-mode approach for calculating left ventricular volumes, echocardiography appears to be sensitive and useful for evaluating in the single patient the changes in left ventricular performance after cardioversion of atrial fibrillation to sinus rhythm.

Arteriosclerosis↗

Superior vena cava flow and tricuspid anular motion after cardioversion of atrial fibrillation, and role of right atrial relaxation on systolic venous return.

To determine whether atrial relaxation or systolic descent of the tricuspid anulus is the predominant factor determining systolic venous return, 22 patients with atrial fibrillation were studied. Venous return (i.e., superior vena cava (SVC) flow) was measured using pulsed Doppler echocardiography. Systolic descent of the tricuspid anulus (i.e., total excursion of tricuspid anulus during systole) was also measured using echocardiography. Serial examinations were performed before and after cardioversion of atrial fibrillation in 15 patients. In 11 patients, both the total excursion of the tricuspid anulus and SVC flow were examined in relation to the ratio of the preceding to the pre-preceding RR interval (R2/R1). Systolic forward flow of SVC increased as the ratio of late diastolic to total excursion of the tricuspid anulus (i.e., right atrial systolic function) increased. It correlated significantly with the ratio of late diastolic to total excursion of the tricuspid anulus but not with total excursion. Total excursion of the tricuspid anulus correlated significantly with R2/R1, but systolic forward flow of SVC did not. These results indicate that atrial relaxation rather than systolic descent of the tricuspid anulus was the predominant factor determining systolic forward flow in the SVC.

Atrial Fibrillation↗

Electropharmacodynamics of N-acetylprocainamide in the immature mammalian heart--evidence for a prominent class III effect in the newborn.

The electrophysiologic effects of N-acetylprocainamide (NAPA), a metabolite of procainamide reported to exert significant Class III antiarrhythmic effects in the adult heart, were evaluated in 12 neonatal mongrel canines (ages 7-14 days). Following transvascular placement of quadripolar electrical catheters in the right atrium and ventricle, and a tripolar catheter in the region of the His bundle, electrophysiologic assessments were made of sinus and AV nodal function and atrial and ventricular refractoriness utilizing intracardiac stimulation and recording techniques following cumulative intravenous doses of 20 and 40 mg/kg of NAPA (serum concentrations 13.1 +/- 1.9 and 25.6 +/- 3.4 micrograms/ml). NAPA resulted in an overall increase in sinus cycle length of 18%. No changes were observed in the paced cycle length resulting in AV nodal Wenckebach. Consistent with NAPA's reported Class III action, NAPA increased the effective and functional refractory periods of the ventricle by 35 and 34%, respectively (p less than 0.001). Even larger increases were observed in atrial refractoriness (effective 75%, functional 57%, p less than 0.001). In separate experiments (n = 6), the effects of intravenous NAPA (40 mg/kg) on the duration of the monophasic action potential recorded from the neonatal atrium and ventricle were determined. NAPA increased APD90 of the atrium by approximately 50% and that of the ventricle by 60%, thus confirming a significant effect on myocardial repolarization in the neonate.

Acecainide↗

Excellent results for atrial fibrillation surgery in the presence of giant left atrium and mitral valve disease.

OBJECTIVE: The incidence of sinus conversion in the enlarged left atrium after atrial fibrillation surgery is reported to be low. The purpose of the current study was to investigate the effects of atrial fibrillation surgery on mitral valve disease associated with a giant left atrium (GLA). METHOD: From July of 1997 to February of 2002, 188 patients received mitral valve and atrial fibrillation surgery. The patients were placed in either GLA group (n = 94), or NGLA group (n = 94), based on LA size. The presence and onset of sinus rhythm and the incidence and velocity of transmitral A waves were monitored during the early postoperative period and throughout the follow up period of 42 months. RESULTS: The onset of postoperative sinus rhythm was slightly earlier in the NGLA group than in the GLA group at 1.3+/-0.4 days versus 3.1+/-1.2 days, respectively, (P = 0.008). The sinus conversion rates in the GLA and the NGLA groups were 91.5 and 97.9% in the early postoperative period, and 94.7 and 95.7% at 6 months after surgery, respectively. A wave appearance rates in the early postoperative period in the GLA and the NGLA groups were 62.2 and 71.7%, and continued to improve over time to 94 and 95% by 36 months, respectively. Peak A wave velocities in the early postoperative period in GLA and NGLA groups were 67.4+/-34.0 and 61.1+/-29.5 cm/s without significant change during the follow up. CONCLUSION: The results suggest that atrial fibrillation surgery is effective at inducing sinus rhythm and restoring left atrial contractile function after concomitant mitral valve surgery regardless of LA size.

Atrial Fibrillation↗

Historical perspective of cardiorenal integration.

1. Early research on blood volume as an independent parameter affecting kidney function took the approach that the sensors must be located in the most compliant, that is the reservoir portion, of the cardiovascular system. This encompasses the great veins and the cardiac atria. 2. Small changes in volume were shown not to affect the compliance of this reservoir and messages from the atrial receptor network were shown to travel in the vagus nerve and to control urine volume by antidiuretic hormone. 3. Although greatly affected by the water immersion stimulus, sodium excretion was not as dependent on vagus integrity. The ensuing search for the natriuretic arm of the blood volume mechanism persisted for the next 20 years. 4. Finally, one aspect of the elusive natriuretic factor was found exactly where theory had suggested, namely the most distensible part of the system, in specialized granules in the cardiac atria.

Animals↗

Radiofrequency catheter ablation of the atria eliminates pacing-induced sustained atrial fibrillation and reduces connexin 43 in dogs.

BACKGROUND: We assessed the effects of radiofrequency catheter ablation (RFCA) of the atrial epicardium on pacing-induced sustained atrial fibrillation (AF) and the expression and distribution of the intercellular gap junction protein connexin 43 (Cx43) in dogs. METHODS AND RESULTS: In 12 mongrel dogs, after creation of complete AV block and implantation of a ventricular inhibited pacemaker, a high-rate pulse generator (20 to 30 Hz to induce AF) was implanted in the neck, connected to a right atrial endocardial pacing lead, and used to pace the atrium for 10 to 14 weeks. In group 1 (n=9 dogs), corrected sinus node recovery time (CSNRT), P-wave duration, 24-hour Holter ECG, maximal heart rate (MHR) in response to isoproterenol, and intrinsic heart rate (IHR) after atropine (0.04 mg/kg) and propranolol were measured before and after atrial pacing and RFCA. Group 2 dogs were used to assess the effect of chronic AF alone on Cx43 expression and distribution. All group 1 dogs developed sustained (>24 hours) AF. Right-sided RFCA of the atria eliminated the sustained AF in 5 dogs, but both right and left atrial RFCA was required to abolish sustained AF in the other 4 dogs. After RFCA restored sinus rhythm, CSNRT and P-wave duration were prolonged and MHR and IHR were decreased. Chronic rapid atrial pacing (group 2) increased the expression of Cx43, which was absent in ablated areas and markedly depressed in viable atrial myocytes near the ablation zones (group 1). CONCLUSIONS: Rapid atrial pacing for long time periods induced sustained AF that can be eliminated by linear right and left atrial lesions created with RFCA, with preservation of sinus rhythm and atrial contractile function. Chronic AF increased the expression and distribution of gap junction protein Cx43, which became reduced in ablated and nearby nonablated areas.

Animals↗