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PubMed2006

Alterations in left ventricular structure and function in type-1 diabetics: a focus on left atrial contribution to function.

This study was designed to determine the effects of type 1 diabetes mellitus (T1DM) on left ventricular (LV) and particularly left atrial (LA) structure and function. We evaluated 88 non-obese subjects: 44 with T1DM, 44 age- and gender-matched normal controls (age 39 +/- 11 years). LV and LA structure and function were quantified using two-dimensional echocardiography, pulse-wave Doppler, and tissue Doppler imaging, including early and late diastolic myocardial velocities (Em global and Am global, respectively). The T1DM subjects averaged higher heart rate, relative wall thickness, and ejection fraction, and lower indexed end-systolic volume than normal controls (P < .001, P < .05, P = .01, and P < .05, respectively). T1DM was related to A wave velocity, Am global, A wave integral, LA ejection fraction, and LA systolic ejection fraction (P < .01, P < .05, P < .0005, P < .001, and P < .0005, respectively). In multivariate analyses, T1DM was an independent predictor of the A wave integral, LA ejection fraction, and LA systolic ejection fraction (P < .01, P < .01, and P < .005, respectively). Thus, despite increased relative wall thickness, LV systolic function is increased and early diastolic filling is normal in T1DM subjects; however, they possess changes in LA transport function suggesting increased reliance on LA contribution to LV filling.

Adolescent↗
PubMed2002

Electrical, contractile and structural remodeling during atrial fibrillation.

The natural history of atrial fibrillation (AF) is characterized by a gradual worsening with time. The recent finding that AF itself produces changes in atrial function and structure has provided a possible explanation for the progressive nature of this arrhythmia. Electrical remodeling (shortening of atrial refractoriness) develops within the first days of AF and contributes to an increase in stability of AF. However, 'domestication of AF' must also depend on a 'second factor' since the persistence of AF continues to increase after electrical remodeling has been completed. Atrial contractile remodeling (loss of contractility) leads to a reduced atrial transport function after cardioversion of AF. An important clinical consequence is that during several days after restoration of sinus rhythm, the risk of atrial thrombus formation is still high. In addition, the reduction of atrial contractility during AF may enhance atrial dilatation which may add to the persistence of AF. Tachycardia-induced structural remodeling takes place in a different time domain (weeks to months). Myolysis probably contributes to the loss of atrial contractile force. Although it might explain the loss of efficacy of pharmacological cardioversion and the development of permanent AF, the role of structural remodeling in the progression of AF is still unclear. Atrial structural remodeling also occurs as a result of heart failure and other underlying cardiovascular diseases. The associated atrial fibrosis might explain intra-atrial conduction disturbances and the susceptibility for AF. Thus, both AF itself and the underlying heart disease are responsible for the development of the arrhythmogenic substrate. New strategies for prevention and termination of AF should be build on our knowledge of the mechanisms and time course of AF-induced atrial remodeling.

Animals↗
PubMed1996

Characterization of left atrial appendage Doppler flow in atrial fibrillation and flutter by Fourier analysis.

The aim of this study was to characterize left atrial appendage mechanical function in atrial fibrillation and flutter by Fourier analysis to analyze frequency and regularity of flow. Left atrial appendage function is central to a patient's risk for thromboembolism. Although the function of the appendage can be analyzed by Doppler echocardiography in sinus rhythm, its mechanical function in atrial fibrillation and flutter has not been well characterized. This lack of adequate definition is caused by the complexity and temporal variability of the Doppler flow profiles. We assessed left atrial appendage function in 21 cases of atrial fibrillation (n - 11) and flutter (n = 10) and five in sinus rhythm with transesophageal Doppler echocardiography. Doppler profiles were examined by Fourier analysis, and the power spectra compared and analyzed between patients with atrial fibrillation and flutter. Left atrial appendage Doppler flow in atrial fibrillation produced Fourier spectra over a narrow band of frequencies with a peak frequency of 6.2 +/- 1.0 Hz, significantly higher than in atrial flutter (3.9 +/- 0.6 Hz, p < 0.00001). Additionally, a significant difference in subharmonic modulation (spectral power below the peak frequency) was observed between atrial appendage flow in atrial fibrillation and flutter, because 37% +/- 16% of the total spectral power was achieved before the dominant frequency in atrial fibrillation compared with 20% +/- 14% in atrial flutter (p = 0.02). Conversely, patients in sinus rhythm exhibited broad-banded Fourier spectra with most of the power in discrete frequency spikes at harmonics above the fundamental frequency with very little subharmonic modulation (1% +/- 0.05%). Left atrial appendage function in atrial fibrillation and flutter can be well characterized by Fourier analysis of Doppler flow. Atrial fibrillation has higher dominant frequencies and greater subharmonic modulation compared with flutter. Moreover, atrial fibrillation demonstrated quasiperiodic contraction patterns typically found in chaotic systems. Fourier analysis of left atrial appendage contraction patterns may therefore have significant promise in providing insights into mechanisms of atrial fibrillation and thromboembolism.

Aged↗
PubMed1995

Atrial veins of the human heart.

Modern anatomical description divides the cardiac veins into two groups: tributaries of the greater cardiac vascular system (GCVS) and tributaries of the smaller cardiac vascular system (SCVS), consisting of the Thebesian vessels. Both systems intercommunicate extensively. With the exception of the oblique vein of the left atrium (Marshall's vein), veins draining the walls of both the left and right atrium have not been well illustrated or described in anatomical atlases and textbooks. Consequently, we do not know exactly to which of the two groups (GCVS or SCVS) the atrial veins belong. There are three groups of left atrial veins: (1) tributaries of the left coronary vein and the coronary sinus; (2) special veins draining the right-sided walls of the left atrium that terminate via intramural sinuses in the right atrium, which vessels occur in 92% of cases and belong to the GCVS; (3) in 81% of cases special veins drain the myocardium of the posterior and superior walls of the left atrium. In most cases they empty into the left atrium itself; in almost 40% of the cases they are connected with mediastinal veins. These veins, also belonging to tributaries of the GCVS, constitute a distinctly separate category of cardiac veins and should be designated proper veins of the left atrium. The veins draining the walls of the right atrium fall also into three groups: (1) In most cases there are short or large intramural tunnels or sinuses in the basic walls of the auricle and atrioventricular node area. The generally valveless openings of all the venous tunnels and sinuses are lined up on a circle just above the tricuspid valve and between the openings of both venae cavae. (2) There are also thin veins at the junction of the right atrium with both the superior and inferior vena cava. (3) In addition, there are numerous cardiac veins of the "smallest size" (real Thebesian veins).

Aged↗
PubMed1998

Atrial electrical remodeling by rapid pacing in the isolated rabbit heart: effects of Ca++ and K+ channel blockade.

INTRODUCTION: Electrical remodeling describes atrial electrophysiologic changes that occur following atrial fibrillation. The mechanism(s) responsible for this phenomenon is not well understood. The purpose of this study was to examine the effects of rapid atrial pacing on atrial action potential duration, conduction time and refractoriness in the isolated rabbit heart. The effects of Ca++ and K+ blockade in this model were also studied. METHODS AND RESULTS: Monophasic action potential recordings were made from 12 epicardial atrial sites in 50 isolated perfused rabbit heart preparations. These recordings were analyzed for activation time (AT), 90% action potential duration (APD) and conduction times (CT) measured at a 250 msec cycle length. Atrial effective refractory periods (ERP) were determined at a 200 msec cycle length. All measurements were made at baseline and repeated after 2 hours of biatrial pacing at 250 msec (control group, n = 10) or 2 hours of rapid biatrial pacing (approximately 80 msec) in 4 groups: rapid pacing alone (rapid pacing group); rapid pacing in the presence of 0.1 mM verapamil (verapamil group) for L-type Ca++ channel blockade; rapid pacing with 1 mM 4-aminopyridine (4-AP group) for K+ channel blockade; and rapid pacing with 50 microM nickel chloride (Ni++ group) for T-type Ca++ channel blockade (n = 10 each group). All baseline and post pacing measurements were taken in the presence of Ca++ or K+ blockers for the respective groups. After rapid atrial pacing alone the average APD shortened by 8.2 +/- 10.4 msec compared to 3.6 +/- 12.5 msec shortening for control group (p = 0.002). The shortening of APD was uniform at all recording sites. For the rapid pacing group, CT was unchanged for right to left atrial conduction but shortened significantly for left to right atrial conduction (26.8 +/- 1.9 msec at baseline to 22.3 +/- 4.1 msec post pacing, p = 0.005). Conduction times were unchanged in the control group. The dispersion of repolarization was unchanged by rapid pacing alone. The decrease in APD from baseline to post rapid pacing was similar to the control group for those hearts treated with verapamil and 4-AP (1.5 +/- 12.3 and 4.7 +/- 10.4 msec, respectively, both p > or = 0.18 vs control group). The decrease in APD was significantly greater for the Ni++ group (11.8 +/- 14.3 msec) than for either the control group or rapid pacing group (both p < or = 0.023). The dispersion of repolarization was increased only in the 4-AP group post rapid pacing (41.7 +/- 6.2 msec at baseline to 53.5 +/- 9.6 msec post pacing, p = 0.01). ERPs were unchanged in any of the 5 groups except for a decrease in left atrial ERP in the Ni++ group after rapid pacing (98 +/- 14 msec at baseline to 88 +/- 8 msec post rapid pacing, p = 0.005). CONCLUSIONS: In the isolated rabbit heart model: 1) atrial APD is shortened after rapid pacing; 2) the shortening of APD is attenuated by verapamil and 4-AP but exaggerated by Ni++; 3) atrial conduction times are shortened in a direction specific manner after rapid pacing; and 4) shortening of ERP in this model is measured only in the presence of Ni++. These findings suggest that both L-type Ca++ and 4-AP sensitive channels may participate in atrial electrical remodeling.

4-Aminopyridine↗
PubMed1996

A new method for analysis of atrial activation during chronic atrial fibrillation in man.

To further clarify the mechanisms maintaining chronic atrial fibrillation (CAF), a method identifying preferable activation patterns of the atria during fibrillation, by time averaging of multiple discrete excitation vectors, was developed. Repeated recordings, each of 56 atrial bipolar electrograms simultaneously acquired during 8 s, were made at multiple sites in the right atrial free wall and the left atrial appendage in 16 patients with CAF using a 2.17 x 3.54 cm electrode array. The local activation times (LAT's) in each recording were estimated as the median activation time at the respective measurement point. By calculating the time difference between the LAT's at adjacent measurement points in two spatial dimensions, a direction vector was created for each activation wave passing each set of measurement points, a total of 42 sets. By time averaging of the individual direction vectors (typically n = 55) at each set of measurement points, preferable activation patterns were determined. Three types of activation patterns were found: 1) inconsistent activation (n = 5), 2) consistent activation with preferential propagation directions (n = 7) and 3) consistent activation with impulses originating from a localizable site within the recording area (n = 4). All activation patterns were reproducible and the two latter patterns were proven significant using statistical tests. We conclude that this new method is useful in further clarification of the mechanisms involved in the maintenance of atrial fibrillation.

Aged↗
PubMed1996

Exercise induced sympathetic influences do not change interatrial conduction times in VDD and DDD pacing.

Using telemetry, right atrial electrogram (RA), and marker channel of atrial sense events (MA) in combination with the left atrial electrogram (LA), recorded by a filtered bipolar esophageal lead, interatrial conduction during submaximal exercise and at rest was examined in 46 DDD pacemaker patients. The RA-LA and MA-LA conduction times measured in the presence of atrial sensing (VDD) as well as the conduction time SA-LA from atrial stimulus (SA) to LA, determined during atrial pacing (DDD) were found to be individual constants independent of exercise induced sympathetic influences. Thus, having determined an optimal mechanical interval (LA-LV)mech/opt from left atrium to ventricle by other methods, the optimal AV delay for DDD as well as for VDD operation can be calculated by the sum of the appropriate interatrial conduction time (SA-LA, respectively MA-LA) and the (LA-LV)mech/opt interval. Due to the constant SA-LA and MA-LA, the difference between these two values (AV delay correction interval) is a constant as well, which remains unchanged during exercise. Therefore, in selecting the rate responsive AV delay, only hemodynamic and not electrophysiological measurements need to be considered.

Aged↗
PubMed2002

Comparison of left ventricular geometry and left atrial size and function in patients with aortic stenosis versus those with pure aortic regurgitation.

Chronic aortic valve disease can result in distinct adaptive left ventricular (LV) geometric patterns, which has different effects on LV function and left atrial (LA) performance. In this study we assessed the effect of LV geometry on LA size and function, and we verified the relation between LA size and LV mass in patients with distinct LV overload subsets. We analyzed 183 patients with aortic valve disease who underwent a complete echocardiographic evaluation. Based on the type of valvular dysfunction, patients were classified into 2 groups: 141 patients with aortic stenosis (group AS) and 42 patients with pure aortic regurgitation (group AR). Each of these 2 groups were then divided into those with a concentric LV pattern and those with an eccentric pattern. Both LA size and LA ejection force were significantly greater in group AS than group AR, particularly in patients with a concentric LV pattern. The degree of LA enlargement depended on LV mass in the patients with a concentric LV pattern (group AS r = 0.61, p <0.00001; group AR r = 0.38, p = 0.04). In contrast, no relation was found between LA size and LV mass in the patients with an eccentric pattern, independently of the type of valve dysfunction. Our results indicate that the influence of LV geometry on LA size and function in patients with aortic valve disease is relevant. A concentric LV pattern is associated with greater LA size and higher ejection than an eccentric pattern, suggesting that chronic LV pressure overload more than volume overload has a greater effect on stimulating increases in LA performance. The degree of LA enlargement depends on LV mass in patients with a concentric LV pattern, whereas it was unpredictable in those with an eccentric LV pattern.

Adult↗
PubMedDate not supplied

Electrical and structural remodeling: role in the genesis and maintenance of atrial fibrillation.

Atrial fibrillation (AF) and congestive heart failure (CHF) are 2 frequently encountered conditions in clinical practice. Both lead to changes in atrial function and structure, an array of processes known as atrial remodeling. This review provides an overview of ionic, electrical, contractile, neurohumoral, and structural atrial changes responsible for initiation and maintenance of AF. In the last decade, many studies have evaluated atrial remodeling due to AF or CHF. Both conditions often coexist, which makes it difficult to distinguish the contribution of each. Because of atrial stretch in the setting of hypertension or CHF, atrial remodeling frequently occurs long before AF arises. Alternatively, AF may lead to electrical remodeling, that is, shortening of refractoriness due to the high atrial rate itself. In many experimental AF or rapid atrial pacing studies, the ventricular rate was uncontrolled. In those studies, atrial stretch due to CHF may have interfered with the high atrial rate to produce a mixed type of electrical and structural remodeling. Other studies have dissected the individual role of AF or atrial tachycardia from the role CHF plays in atrial remodeling. Atrial fibrillation itself does not lead to structural remodeling, whereas this is frequently produced by hypertension or CHF, even in the absence of AF. Primary and secondary prevention programs should tailor treatment to the various types of remodeling.

Action Potentials↗
PubMedDate not supplied

[Atrial natriuretic hormone and endocrine functions].

The atrial natriuretic hormone (ANP) is a cardiac hormone which gene and receptors are widely present in the body. Its main function is to lower blood pressure and to control electrolyte homeostasis. Its main targets are the kidney and the cardiovascular system but ANP interacts with many other hormones in order to regulate their secretion. The adrenal glands are the first endocrine target. Steroidogenesis, especially mineralocorticoid synthesis, is inhibited by ANP, but glucocorticoid production seems to be depressed too. As ANP synthesis is enhanced by the latter, it suggests a regulatory loop. Moreover ANP inhibits the thyroid synthesis whereas its production is enhanced by thyroid hormone. The hypothalamo-hypophyseal axis is another important target. ANP inhibits ACTH release and arginine vasopressin secretion. Vasopressin enhances ANP synthesis while GH decreases it. Finally the endocrine effects of ANP strengthen the cardiovascular and renal effects of the hormone, antagonizing the salt and water retention due to aldosterone and AVP. Because of a local production, ANP may also act as a paracrine hormone that influences the function of many endocrine systems (ovarian function for instance). In the central nervous system, ANP acts as a neurotransmitter in order to regulate pituitary and vegetative functions. Plasma ANP levels are impaired in several endocrine diseases : the plasma hormone levels increase in hypercortisolism, hyperaldosteronism, thyrotoxicosis and inappropriate antidiuretic hormone secretion; it decreases in hypothyroidism. In case of Addison's disease, ANP may be used to assess the quality of mineralocorticoid treatment, in association with the other biological criteria.

Adrenal Glands↗
PubMed1992

[Left atrial booster pump function in patients with hypertrophic cardiomyopathy and essential hypertension: evaluations based on left atrial pressure-volume relationship].

In patients with hypertrophic cardiomyopathy (HCM) and essential hypertension (HT), left ventricular dysfunction in early diastole which is associated with left atrial contraction plays an important role in left ventricular filling. To evaluate left atrial booster pump function, we analyzed left atrial preload (left atrial pressure at the end of diastasis; LAPd, left atrial volume index at the end of diastasis; LAVd), left atrial afterload (left ventricular end-diastolic pressure; LVEDP, left ventricular chamber stiffness constant; K), and left atrial ejection indices (left atrial ejection fraction during atrial contraction; LAEF, left atrial ejection volume index during atrial contraction; ACVI). The study subjects consisted of control subjects (n = 5), HT patients (n = 6), and HCM patients (n = 11). The left ventricular wall was significantly thicker in the HT and HCM groups. The left ventricular rapid filling volume index was less in the HT group, and significantly less in the HCM than in the control group. LAPd and LAVd were greater in the HT group than in the control group, and greater in the HCM group than in the HT group. LVEDP and K were greater in the HT group than in the control group, and significantly greater in the HCM group than in the other 2 groups. ACVI was greater in the HT group than in the control group, but in the HCM group, ACVI was significantly less than in the HT group and did not differ significantly from that in the control group. LAEF was significantly less in the HCM group than in the other 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Improved left atrial transport and function with orthotopic heart transplantation by bicaval and pulmonary venous anastomoses.

Orthotopic heart transplantation (OHT) with bicaval and pulmonary venous anastomoses avoids the large atrial anastomoses of the standard biatrial technique. To determine whether the bicaval technique improves atrial performance, we used Doppler echocardiography to study 13 patients with bicaval OHT, 15 with biatrial OHT, and 8 normal subjects. All were in sinus rhythm and free of rejection. Left atrial size, transmitral (M) and late diastolic (A) mitral flow velocity integrals were measured. Atrial transport (A/M, %) and atrial ejection force (kilodynes, calculated from peak A-wave velocity and mitral orifice area) were assessed. Left atrial dimensions in the bicaval (4.3 +/- 0.5 cm) and biatrial groups (4.9 +/- 0.9 cm) were larger than in controls (3.3 +/- 0.8 cm, p < 0.05). Left atrial transport (37% +/- 12% and 35% +/- 12%) and ejection force (14.1 +/- 6.9 kdyne and 10.2 +/- 7.8 kdyne) were similar in the bicaval group and controls (p not significant) but were significantly lower in the biatrial group (20% +/- 19% and 3.6 +/- 4.0 kdynes, p < 0.05). The bicaval and pulmonary venous technique of OHT produces more physiologic atrial function compared with the biatrial technique as evidenced by greater atrial ejection force and more normal atrial transport.

Adult↗
PubMed1991

Right atrial ischemia exacerbates hemodynamic compromise associated with experimental right ventricular dysfunction.

To determine the importance of right atrial function with acute right ventricular dysfunction, sequential right ventricular and right atrial ischemia were induced in 15 dogs. Right ventricular ischemia resulted in right ventricular free wall dyskinesia, right ventricular dilation by ultrasound, elevated right ventricular filling pressure and paradoxic septal motion. There were decrements in right ventricular systolic pressure (28.9 +/- 5.5 to 25.5 +/- 4.6 mm Hg) (p less than 0.05 for these and all subsequent values) and stroke work (5.66 +/- 0.94 to 2.66 +/- 0.62 g.m/m2), resulting in reductions in left ventricular preload, systolic pressure (123 +/- 11 to 97 +/- 12 mm Hg) and stroke volume (24.2 +/- 4.3 to 19.1 +/- 5.2 ml). Right atrial contractility was augmented, as indicated by increases in peak A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.22 +/- 0.02 to 1.46 +/- 0.3) and right atrial stroke work (0.11 +/- 0.02 to 0.25 +/- 0.05 g.m/m2). Right atrial ischemia depressed right atrial contraction, as indicated by decreased A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.46 +/- 0.3 to 1.04 +/- 0.2) and stroke work (0.25 +/- 0.05 to 0.04 +/- 0.01 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Effect of left ventricular contractile performance on passive left atrial filling--clinical study using radionuclide angiography.

Many invasive and noninvasive methods have been used to study the cardiac atria; however, few allow quantitative measurement of atrial function. To determine the interaction between left ventricular (LV) contraction and left atrial (LA) filling, gated radionuclide angiography was conducted in 30 normal subjects (24 men and 6 women, mean age 58 +/- 10 years, range 26-68). LV and LA time-activity curves and their first-derivative curves were obtained simultaneously by using the method of Bough et al. The LV ejection fraction (64 +/- 18%) and LV peak ejection rate (LVPER; 3.42 +/- 0.27 EDV/s) were computed from these curves. As indices of LA filling, LA fractional emptying (38 +/- 12%) and LA peak filling rate (LAPFR; 2.86 +/- 0.17 LAVmax/s)--the latter being defined as the peak rate of LA filling during the LA filling phase--were also computed from these curves. In all subjects, the timing of the LVPER coincided with the occurrence of LAPFR, and there was a significant positive correlation between the LVPER and LAPFR (r = 0.81, p < 0.001), indicating that the LAPFR was strongly affected by the degree of LVPER. Thus, these results indicate that LV contractile performance plays an important role in determining LA passive filling during ventricular systole.

Adult↗
PubMed1996

Evaluation of left atrial appendage anatomy and function in recent-onset atrial fibrillation by transesophageal echocardiography.

Data regarding left atrial (LA) and LA appendage anatomy and function among patients with newly recognized atrial fibrillation (AF) who have not received long-term warfarin are currently unknown. To identify echocardiographic indexes which characterize those at increased risk for thrombus formation, we analyzed transesophageal echocardiographic studies in 100 consecutive patients with newly recognized AF (duration 2.6 +/- 0.3 week) who had not received long-term warfarin. Fourteen percent of patients had LA thrombi. LA thrombi were associated with larger LA appendages, more depressed LA appendage outflow velocities, and a higher prevalence of severe spontaneous LA contrast. Patients with spontaneous contrast had larger LA and LA appendage anatomy and lower LA appendage ejection velocity. Among patients presenting with their first episode of AF, greater LA appendage ejection and filling velocities and smaller LA and LA appendage sizes were seen among those with AF of <2 weeks duration compared with those with AF of >2 weeks. Thus, patients with recent onset AF and LA thrombi or spontaneous echo contrast have more dilated LA and LA appendage anatomy, and more depressed LA appendage systolic function. Data from patients with their first episode of AF suggests that AF is associated with rapid LA remodeling.

Adult↗
PubMed1997

Electrophysiological properties in patients undergoing atrial compartment operation for chronic atrial fibrillation with mitral valve disease.

AIMS: Surgical treatment for atrial fibrillation is now feasible in selective cases. The aim of this study was to assess the electrophysiological properties of patients undergoing atrial compartment operation for chronic atrial fibrillation. METHODS AND RESULTS: Electrophysiological studies were performed in 20 mitral valve patients with atrial fibrillation who had been maintained in sinus rhythm for more than 1 year after atrial compartment operation. Intra-cardiac recording and programmed electrical stimulation were performed in various atrial compartments. The parameters studied included sinus node function, atrial conduction and refractoriness, atrioventricular conduction function and inducible arrhythmias if any. Intra-cardiac recordings showed that the rhythm was of sinus origin in all cases, with the earliest atrial activity located in the high right atrium. The mean sinus cycle length was 750 +/- 110 ms, AH time 106 +/- 29 ms, and HV time 53 +/- 7 ms. The sinus node function was normal in 18 patients (90%), and only two patients had prolonged sinus node recovery and sino-atrial conduction. The right atrial appendage compartment was driven by the sinus node in all patients. However, the conduction time from the high right atrium to the right atrial appendage compartment was markedly prolonged in 12 of 15 patients (80%) undergoing the three-compartment operation in which an incision was placed between the high right atrium and right atrial appendage compartments. On the other hand, the electrical activities in the left atrial compartment were much more varied. In 13 of 20 patients (65%), the left atrial compartment was driven by the sinus node; 11 of the 13 patients had a normal or mildly prolonged conduction time (ranged 75 to 146 ms), whereas two patients had a marked delay in conduction (200 ms and 266 ms, respectively). In the remaining seven patients, the left atrial compartments were dissociated from the rest of the heart; five of them had a quiescent left atrium, one a fluttering left atrial rhythm, and one a slow left atrial rhythm. The effective refractory period was longer in the left atrial compartment (242 +/- 47 ms) as compared to that of the high right atrium (224 +/- 26 ms, P < 0.01) and right atrial appendage compartments (219 +/- 25 ms, P < 0.01). Programmed electrical stimulation could not induce atrial fibrillation in any patient, whereas two patients had inducible atrial flutter and three repetitive atrial responses. CONCLUSIONS: (1) Atrial compartment operation does not impair sinus node function in most cases. (2) Elimination of atrial fibrillation while maintaining the electrical connection between different atrial compartments is feasible.

Adolescent↗
PubMed2004

P-wave dispersion for predicting maintenance of sinus rhythm after cardioversion of atrial fibrillation.

P-wave measurements and left atrial function were investigated to predict the maintenance of sinus rhythm after cardioversion of atrial fibrillation. Left atrial dimension <45 mm (p = 0.02) and P-wave dispersion <46 ms (p <0.001) were independent predictors of sinus rhythm maintenance, with a sensitivity of 89% and 96%, respectively. Duration of atrial fibrillation, maximum P-wave duration, and no spontaneous echocardiographic contrast were also univariate predictors.

Aged↗
PubMed1983

[Considerations on the therapy with physiologic pacemakers].

Physiologic pacemakers offer hemodynamic benefits in comparison to conventional pacing, but demand more detailed diagnosis of the arrhythmia in need of treatment. In order to prevent endless loop tachycardias, ventriculoatrial conduction must be analyzed. Normal sinus node and atrial function should be confirmed in atrial triggered ventricular stimulation. The techniques and values of preimplantation investigations, including intracardiac electrophysiological procedures, are discussed.

Atropine↗