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At least 73 records · Page 4Linked to original sources
PubMed1989

Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation.

Full recovery of atrial mechanical activity may not occur immediately after successful electrical cardioversion of atrial fibrillation to sinus rhythm. To examine the time course of recovery of left atrial mechanical function, serial two-dimensional, M-mode and transmitral pulsed Doppler echocardiographic studies were performed in 21 patients after elective direct current cardioversion of atrial fibrillation of 3 weeks' to 24 months' duration (mean 5 months). Over 3 months of follow-up, there were significant increases in both peak A wave velocity (p less than 0.005) and percent atrial contribution to total left ventricular filling (p less than 0.005). Compared with values in a normal control population, peak A wave velocity and percent atrial contribution to total left ventricular filling did not return to normal until 3 weeks after cardioversion in patients who remained in sinus rhythm. Left atrial dimension also decreased over the follow-up period (p less than 0.05) in patients with persistent sinus rhythm. These results may have important implications in guiding the appropriate duration of anticoagulant therapy after cardioversion, and in clinically assessing the hemodynamic benefit of restoring sinus rhythm in an individual patient.

Aged↗
PubMed1981

Left atrial transport function.

These studies show that the left atrial booster pump action serves as a supercharger which can increase left ventricular stroke volume in the range of 25 percent; and in patients with aortic stenosis, stroke work in the range of 50 percent (4). These changes can occur in the face of increased resistance to left ventricular filling in clinical conditions such as aortic stenosis where there is diminished left ventricular compliance and in mitral stenosis where there is stenotic resistance to left ventricular filling from the atrium. In spite of this fact, assessment of left atrial function by measurement of cardiac output changes occurring after return from atrial fibrillation to normal sinus rhythm yields erratic and confusing results. The reason for this is that atrial function, per se, is not a primary determinant of steady state cardiac output. Sequential A-V pacing may temporarily increase stroke volume in an acute setting like myocardial infarction. Nevertheless, one cannot infer from such observations that the use of permanent transvenous A-V sequential pacing will augment steady state cardiac output over a period of time. This is an important point to remember when considering the use of sequential A-V pacing, since it requires insertion of more complicated pacing and sensing wires as well as a more complex circuitry. All of these features lead to an increased risk of pacemaker malfunction. This increased risk of malfunction is not justified unless there is good evidence that atrial contribution is important in a given patient.

Aortic Valve Stenosis↗
PubMed1992

Effect of the pericardium on atrial systolic function.

The effect of pericardial constraint on atrial systolic function was investigated in nine acutely instrumented anesthetized dogs. Left and right atrial pressures were recorded by high-fidelity catheters; auricular diameters and free wall segment lengths were measured by sonomicrometry. Atrial function curves were constructed by relating atrial systolic dimensional shortening to atrial end-diastolic pressure during progressive volume loading. With the pericardium closed, the function curves were shifted markedly downward and rightward, such that atrial systolic shortening was reduced at any given pressure. There was a concomitant leftward and upward shift of the atrial end-diastolic pressure-dimension relationship. The relationship between atrial systolic shortening and atrial end-diastolic dimension was not shifted. These results suggest that the apparent depression of atrial systolic function with the pericardium closed is due to a restrictive effect of the pericardium on atrial filling. In conclusion, in the acutely dilated heart, the pericardium restricts atrial filling and thus causes a reduction in atrial systolic contribution to ventricular filling.

Animals↗
PubMed1986

[Left ventricular function during atrial fibrillation assessed by left ventricular function curve using ECG-gated blood pool scintigraphy].

Cardiac function is difficult to assess in patients with atrial fibrillation due to the widely fluctuating cycle lengths resulting in variable ventricular hemodynamics. With respect to ECG-gated blood pool scintigraphy, distortion of the time activity curve occurs due to a summation of irregular cycle lengths. Therefore, performing such a study has been regarded meaningless. To evaluate left ventricular function during atrial fibrillation using scintigraphic technique, a new processing algorithm was devised to make multiple gated images which are discriminated by the preceding R-R interval, and left ventricular filling and function curves were established. The left ventricular filling curve, obtained by plotting end-diastolic volume against the preceding R-R intervals demonstrated an impairment of blood filling in cases of mitral stenosis and constrictive pericarditis, which resolved after mitral commissurotomy in case of mitral stenosis. The left ventricular function curve, established by plotting stroke volume against end-diastolic volume, was analyzed according to indices such as "slope" and "position". Both of these indices were significantly reduced in relation to the severity of heart failure according to the NYHA's functional classification and cardiomegaly on chest radiography. On individual comparisons of underlying diseases, the indices decreased in the following order; lone atrial fibrillation, hyperthyroidism, aging, hypertension, mitral valve disease, ischemic heart disease, dilated cardiomyopathy and aortic regurgitation. The indices correlated closely with ejection fraction. In cases of mitral regurgitation, however, the function curves were situated to the right and above those of lone atrial fibrillation and decreased in slope despite the fairly well-maintained ejection fraction. After treatment with digitalis and/or diuretics, the function curves shifted to the left and upward. In conclusion, left ventricular filling and function curves based on a newly-devised algorithm of ECG-gated blood pool scintigraphy are of considerable clinical value in evaluating cardiac performance in patients with atrial fibrillation. They are widely applicable to the assessment of therapeutic and interventional effects.

Atrial Fibrillation↗
PubMed1991

Echo-Doppler evaluation of the effects of heart rate increments on left atrial pump function in normal human subjects.

It is commonly believed that the atrial contribution to left ventricular filling increases during heart rate increments. However, the relative contribution of the pump function (atrial systole) and of the passive role (diastasis and reservoir) of the atrium to end-diastolic left ventricular filling is not well known. In order to investigate this problem, we performed a two-dimensional echo-Doppler study during right atrial pacing. Transmitral flow velocity curves were obtained by means of pulsed Doppler. Pacing was performed (1) at the lowest heart rate at which it was possible to obtain a stable capture of the atria, (2) at the heart rate at which the early and late Doppler filling waves almost completely overlapped. In both stages pacing was interrupted for a few seconds to obtain some post-pacing beats. Doppler tracing recorded at rest, during pacing and in the immediate post-pacing beats were analysed to obtain well-known parameters of atrial contribution; atrial peak flow velocity, early to atrial peak flow velocity ratio, and time-velocity integral of the atrial wave. Furthermore, in order to distinguish end-diastolic passive flow from the active contribution of atrial systole to filling, we superimposed the envelope of the last Doppler curve obtained during atrial pacing over the envelope of the first post-pacing curve. In this way the area of the atrial wave of the paced beat was divided by the mid-diastolic part of the post-pacing one into two areas, the integrals of which correspond to the active and passive atrial contribution respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Electrocardiographic signs of atrial overload in hypertensive patients: indexes of abnormality of atrial morphology or function?

Left atrial electrocardiographic (ECG) abnormalities have been reported as common findings in hypertension; however, their relationships with atrial anatomy are still uncertain. In addition, in arterial hypertension several studies demonstrated an abnormal left ventricular filling. The aim of this study was to investigate the relationships of the ECG signs of left atrial abnormality to atrial anatomy and left ventricular filling as evaluated by pulsed-wave (PW) Doppler in a group of patients with uncomplicated essential hypertension. To this end, 53 untreated essential hypertensive patients (age 44 +/- 8 years; blood pressure 160.5 +/- 21.5/104.7 +/- 13.5 mm Hg) underwent a complete 12-lead ECG and a PW Doppler study of the transmitral flow velocities. The ECG criteria of left atrial abnormality were: P wave wider than 0.12 (or 0.10) second or higher than 0.25 mV in lead II; P wave/PR segment ratio (Macruz index) greater than 1.6 in lead II; and P wave terminal forces in lead V1 equal to or more negative than 0.04. Echocardiographic measurements were made according to American Society of Echocardiography (ASE) convention. Doppler parameters of left ventricular filling were measured as E and A peak velocity, A/E ratio, and the ratio between the velocity-time integral under the E peak and that of the whole diastolic flow, which represents the rapid filling fraction (RFF). At least one ECG sign of atrial abnormality was present in 34 patients (64%); the Macruz index gave the most common ECG index of atrial abnormality (31 patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Mechanism of augmented left atrial pump function in myocardial infarction and essential hypertension evaluated by left atrial pressure-dimension relation.

To analyze left atrial (LA) pump function in normal subjects, in patients with essential hypertension and in patients with a healed myocardial infarction, LA dimension (aortic-root echogram) and pressure (catheter-tip manometer) were simultaneously recorded in 25 patients (8 normal subjects, 7 with hypertension and 10 with myocardial infarction). The pressure-dimension relation of the left atrium was composed of 2 loops: the A loop (expressing the pump function of the left atrium) and the V loop. LA dimension at the beginning of active LA shortening was significantly greater in hypertensive subjects (33 +/- 3 mm) and in those with myocardial infarction (32 +/- 4 mm) than in normal subjects (28 +/- 3 mm) (p less than 0.01, p less than 0.05, respectively). The area of the A loop significantly increased in subjects with hypertension (48 +/- 3 mm Hg.mm, p less than 0.01) and in subjects with myocardial infarction (29 +/- 10 mm Hg.mm, p less than 0.05), compared with normal subjects (20 +/- 8 mm Hg.mm). The mean fractional shortening velocity of the left atrium significantly increased in subjects with hypertension, compared with normal subjects and those with myocardial infarction (p less than 0.05 for both). LA peak wall tension during the LA active contraction period significantly increased with hypertension and with myocardial infarction, compared with normal subjects (p less than 0.01, p less than 0.05, respectively). The area of the A loop was directly proportional to the LA dimension at the beginning of active LA shortening (r = 0.53), p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Endocrine function of the heart. Structure and biological properties of peptides secreted by the heart atrium].

Apart from the generally known functions, the heart has also an endocrine function. Atrial cardiocytes, being typical secretory cells, release peptide hormones into the blood stream: atrial natriuretic peptide containing 28 amino acids and cardiodilatin. The structure of atrial peptides was determined. It was shown that both peptides were derived from their common precursor, a protein containing 151 amino acids. The presence of specific receptors is demonstrated on plasmatic membranes of cells of kidney epithelium, arterial smooth muscle, arterial endothelium, kidney cortex and hypophysis. The interaction of atrial peptides with these receptors activates the guanylate cyclase system. The biological action of atrial peptides manifests itself in the quick, massive and instantaneous increase of diuresis and electrolyte excretion, elevated clearance of creatinine, decrease of kidney vascular resistance, intensification of glomerular filtration, inhibition of stimulated secretion of aldosterone, relaxation of blood vessels, elimination of arterial and intestinal spasm induced by various endogenous and exogenous vasoconstrictors and in correction of kidney hypertension. Various radioimmunoassays for the presence of atrial peptides in human plasma were developed; it was shown that in patients with congestive heart failure the content of atrial peptides is increased.

Amino Acid Sequence↗
PubMed1985

The role of the atria in fluid volume control.

Neural reflexes from the heart, in particular the atria, are well documented and are involved in sodium and water excretion. Current work also indicates that the atria have an important endocrine function. Atrial peptides, which have been recently characterized and synthesized, may play a significant role in the homeostasis of body fluids.

Animals↗
PubMed1989

Atrial wall function and plasma atriopeptin during volume expansion in conscious dogs.

Mean left atrial pressure is believed to be an accurate estimate of atrial stretch in vivo and is used to assess the stimulus for atriopeptin release in both animals and humans. However, for a number of years it has been known that atrial stretch receptor discharge occurs during specific phases of the atrial cycle and that B-receptor discharge correlates with the passive filling of the atrium, which occurs during the V wave. The purpose of this study was to develop the concept that phase-specific changes in atrial wall stress are responsible for atriopeptin secretion. In chronically instrumented conscious dogs, volume expansion (1,000 ml of saline in 5 min) increased left atrial pressure and dimensions and caused a 663 +/- 189% increase in plasma immunoreactive atriopeptin from 44 pg/ml. At this time, mean left atrial pressure increased only 202 +/- 36% (mean +/- SE), whereas A wave pressure increased 146 +/- 19% and V wave pressure increased 290 +/- 67%. A and V wave dimensions increased only a few percent. After developing atrial wall thickness constants for diastole (KCl fixation) and systole (BaCl2 fixation), calculated atrial A wave wall stress increased 163 +/- 25%, and V wave wall stress increased 346 +/- 85%. Minute wall stress (wall stress times heart rate) gave an even better correlation with changes in plasma atriopeptin. V wave minute wall stress increased 690 +/- 168%, whereas A wave wall stress increased 366 +/- 56%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Mechanical hyperventilation: effect on specialized atrioventricular conduction, supraventricular refractoriness, and experimental atrial arrhythmias in dogs anesthetized with pentobarbital or pentobarbital-halothane.

The effect of hypocapnia (PCO2ET 25 vs 40 torr) on specialized atrioventricular (AV) conduction, supraventricular refractory periods, and experimental atrial arrhythmias provoked by premature atrial stimulation (atrial echoes-echoes, repetitive atrial firing (RAF)) was assessed in dogs anesthetized with pentobarbital or pentobarbital-halothane (1.0% end-tidal). Catheter His bundle electrocardiography was used. Both hypocapnia and halothane prolonged AV nodal conduction, but the effect of halothane was more pronounced. Halothane prolonged the atrial functional (AtFRP), atrial effective (AtERP), and AV nodal functional refractory (AVFRP) periods. These effects of halothane were linked to an increased incidence of RAF but not to echoes. Hypocapnia prolonged the AVFRP (less than halothane), had no effect on the AtFRP and shortened the AtERP. These effects of hypocapnia were associated with an increased incidence of echoes, but not with RAF. Echoes and RAF are thought to be caused by reentry within the sinus node, atria, and AV node. The differing effects of halothane and hypocapnia on the incidence of these arrhythmias may be due to differning effects on supraventricular refractoriness.

Anesthesia↗
PubMed1985

Fast algorithms for the analysis of sino-atrial node function.

The calculations of parameters of the sino-atrial node function have previously required the application of a non-linear least squares curve-fitting algorithm. We have compared five algorithms, three of which eliminate the need for direct non-linear least squares routines. The fast algorithms can provide greater accuracy while using less than 10% of the computing time. They make it feasible to provide real-time analysis during clinical electrophysiological studies.

Arrhythmias, Cardiac↗
PubMed1992

Functional capacity of patients with atrial fibrillation and controlled heart rate before and after cardioversion.

OBJECTIVE: To measure exercise duration (which frequently is diminished by atrial fibrillation) and to compare the gain in exercise duration achieved by heart rate control with the gain after cardioversion. METHODS AND RESULTS: Eighteen patients (10 with structural heart condition and eight with lone atrial fibrillation) did the treadmill exercise stress test using the Bruce protocol. Resting supine heart rate was lowered below 100 beats/min by verapamil (initial exercise stress test). An exercise stress test was then repeated as often as needed to achieve 'heart rate control' (less than 130 beats/min at the end of a 3 min walk at 10 degrees elevation and 2.74 km/h speed). This heart rate control was obtained by gradual increases in verapamil dose. Subsequently, the patients were converted to normal sinus rhythm chemically (seven patients) or electrically (11 patients) and an exercise stress test was repeated. At cardioversion, patients were on antiarrhythmic therapy and verapamil was discontinued in most. All patients had left atrial size measured by echocardiogram before and after cardioversion, and all were followed for four months. Upon achieving controlled heart rate, exercise duration increased in 16 patients (average gain was 164 s). After cardioversion to normal sinus rhythm, exercise duration further increased in 13 cases with an average additional gain of 90 s. The total increase in exercise duration after cardioversion was 254 s. Post cardioversion, all patients with lone atrial fibrillation improved. A decline in exercise performance occurred in four patients with fixed cardiac output. Average gain in exercise duration was independent of drugs used. Left atrial size remained increased post cardioversion (50.4 mm before and 52 mm after). During four months of follow-up, only eight patients could continue on the same medication given for cardioversion. Three patients did not maintain normal sinus rhythm. CONCLUSIONS: Conversion to normal sinus rhythm in patients with atrial fibrillation is associated with improved exercise tolerance except in cases with fixed cardiac output. Restoration of mechanical atrial function appears to be responsible for improved exercise performance following cardioversion.

Aged↗
PubMed1970

Left atrial booster function in valvular heart disease.

This study was designed to assess atrial booster pump action in valvular heart disease and to dissect booster pump from reservoir-conduit functions. In five patients with aortic stenosis and six with mitral stenosis, sequential atrioventricular (A-V) pacing was instituted during the course of diagnostic cardiac catheterization. Continuous recording of valvular gradient allowed estimation of flow for each cardiac cycle by transposition of the Gorlin formula. Left ventricular ejection time and left ventricular stroke work in aortic stenosis or left ventricular mean systolic pressure in mitral stenosis were also determined. Control observations were recorded during sequential A-V pacing with well-timed atrial systole. Cardiac cycles were then produced with no atrial contraction but undisturbed atrial reservoir function by intermittently interrupting the atrial pacing stimulus during sequential A-V pacing. This intervention significantly reduced valvular gradient, flow, left ventricular ejection time, and left ventricular mean systolic pressure or stroke work. Cardiac cycles were then produced with atrial booster action eliminated by instituting synchronous A-V pacing. The resultant simultaneous contraction of the atrium and ventricle not only eliminated effective atrial systole but also placed atrial systole during the normal period of atrial reservoir function. This also significantly reduced all the hemodynamic measurements. However, comparison of the magnitude of change from these two different pacing interventions showed no greater impairment of hemodynamic state when both booster pump action and reservoir function were impaired than when booster pump action alone was impaired. The study confirms the potential benefit of well placed atrial booster pump action in valvular heart disease in man.

Adolescent↗
PubMed1983

Function of atrial preferential conduction routes under normal and abnormal conditions.

The function of the atrial preferential conduction routes was examined by the microelectrode technique under normal and abnormal conditions in excised rabbit hearts. The sinus impulse during normal conditions traveled faster along the left and the right branch of the crista terminalis (anterior and posterior preferential routes, respectively) in the atrium toward the A-V node. Cutting of either route caused a delay of the impulse arrival in the zone beyond the lesion. The internodal conduction time was delayed 12 msec upon cutting of the posterior route, but there was no conduction delay after cutting the anterior route. This indicates that the posterior path is the dominant conduction route under normal conditions. When both routes were cut, the internodal conduction time was delayed 33 msec from the control value. During abnormal conditions, an ectopic pacemaker was found to occur mainly in the regions of two routes, as well as in the coronary sinus region. The cutting of either route, combined with the application of acetylcholine or high external K+, resulted in easier provocation of re-entrant arrhythmias in response to premature-stimuli than before the cutting.

Animals↗