Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Atrial Function, Left”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources

Relation of atrial natriuretic peptides to left ventricular systolic and diastolic function in heart failure.

BACKGROUND: Plasma concentrations of atrial natriuretic peptides are correlated with atrial pressures, as are left ventricular ejection fraction and left ventricular filling abnormalities. AIMS: This study investigated the relation of atrial natriuretic peptides to both left ventricular systolic and diastolic function in heart failure. METHODS: Plasma concentrations of atrial natriuretic peptide and N-terminal pro-atrial natriuretic peptide were measured in 63 patients with chronic heart failure and left ventricular systolic dysfunction. According to Doppler transmitral flow measurements, 19 patients had a restrictive and 44 patients had a non-restrictive left ventricular filling pattern. RESULTS: Plasma concentrations of atrial natriuretic peptide and N-terminal pro-atrial natriuretic peptide were higher in patients with a restrictive filling pattern than in patients with a non-restrictive filling pattern (197 vs. 75 pmol/l, P<0.0001 and 1.14 vs. 0.45 nmol/l, P<0.0001). In univariate analysis, atrial natriuretic peptide and N-terminal pro-atrial natriuretic peptide correlated with deceleration time, E/A ratio and left ventricular ejection fraction. In multivariate analysis, both peptides appeared independently related to left ventricular ejection fraction and left ventricular filling pattern. CONCLUSION: In patients with chronic heart failure, atrial natriuretic peptides provide information on left ventricular systolic as well as diastolic function.

Aged↗

Echocardiographic evaluation of left ventricular filling in mitral stenosis. Role of atrial contraction.

Echocardiographic evaluation of left ventricular volume change during rapid and atrial filling periods was made in patients with mital stenosis. The significant reduction of rapid filling volume was observed and the rate of rapid filling was approximately the half of normal in mitral stenosis. The rapid filling period showed a good correlation to the mitral valve area measured at operation. After surgical treatment, the rate of rapid filling was significantly increased but was still significantly smaller than normal. It was suggested that the remained structural abnormality of mitral apparatus depressed the inflow through the mitral valve in early diastole despite successful mitral valvotomy. Left ventricular filling during atrial contraction (atrial filling) was augmented twice as much as normal in patients with milder mitral stenosis, compensating the decreased early diastolic filling. In contrast, the atrial filling did not increase in severe mitral stenosis, resulting in the decreased cardiac output. Following mitral commissurotomy, the atrial filling in milder mitral stenosis was reduced but remained significantly larger than normal. There was no change of atrial filling in severe mitral stenosis postoperatively. This fact suggested the existence of impaired contraction of left atrium in cases with severe mitral stenosis. Our results show that the altered left atrial transport function plays an important role in the left ventricular filling in mitral stenosis.

Adult↗

[A case of tricuspid pouch associated with ventricular septal defect and functional left ventricular-right atrial communication].

We reported a 60-year-old woman with tricuspid pouch associated with ventricular septal defect and subsequent left ventricular-right atrial communication. Preoperative angiographic findings suggested the presence of membranous septal aneurysm, ventricular and atrial septal defects, and tricuspid insufficiency. However, at operation, besides perimembranous inlet type ventricular septal defect, a pouch, 1.5 cm in diameter was found in the adjacent part to the septal leaflet within the anterior one of the tricuspid valve. The ventricular septal defect was closed with a patch. From these findings, it is speculated that the tricuspid pouch was formed by the effect of jet stream through the ventricular septal defect.

Diagnosis, Differential↗

[Interatrial defect functionally cancelled by a left atrial myxoma within the framework of embolizing mitral stenosis and insufficiency].

The case is presented by a 54 year-old woman, studied because of a clinical diagnosis of mitral valve disease, in which echocardiographic and angiocardiographic examination afforded the diagnosis of left atrial tumor. The surgical finding was of a large myxoma implanted on the atrial septum and prolapsing into the mitral opening and engaging with a branch into an atrial septal defect of the cavalis superior type. Some considerations are made on the times of possible origin and growth of the tumor; the complete absence of the increased pulmonary flow in the presence of a large interatrial communication suggested an early beginning of the tumor that, obstructing the defect, might have hindered the hemodynamic derangement.

Diagnosis, Differential↗

Effects of volume loading, propranolol, and heart rate changes on pump function and systolic time intervals of the left atrium in open-chest dogs.

Left atrial (LA) pressure-dimension curve was constructed and the area of A-loop (AAL, in mm.mmHg) which reflected LA stroke work was measured in 14 open-chest dogs before and after saline infusion, in 14 dogs before and after propranolol administration under fixed heart rate and in 12 dogs while atrial pacing rate was increased stepwise. The peak +dP/dt of LA systolic pressure (LA +dP/dt, in mm Hg/s) and LA percent fraction shortening (LA %FS) were obtained as indices of LA pump function. The peak -dP/dt of X descent in LA pressure (LA -dP/dt, in mm Hg/s) was measured as an index of LA relaxation. From pulsed Doppler mitral flow velocities, A-wave acceleration (AC, in cm/s2), LA pre-ejection period corrected by P-wave duration (LA PEPc), and LA ejection time (LA ET) were measured. AAL, LA +dP/dt, AC, LA %FS, and LA -dP/dt increased after saline infusion (AAL; 2.2 +/- 1.6 to 5.1 +/- 3.3 (p < 0.05), LA +dP/dt; 34 +/- 16 to 52 +/- 23 (p < 0.05), AC; 320 +/- 90 to 472 +/- 98 (p < 0.05), LA %FS; 9 +/- 4 to 12 +/- 4 (p < 0.05), and LA -dP/dt; 38 +/- 28 to 60 +/- 32 (p < 0.05)) and decreased after propranolol administration (AAL; 2.9 +/- 1.9 to 1.2 +/- 0.7 (p < 0.05), and LA +dP/dt; 42 +/- 19 to 28 +/- 11 (p < 0.05), AC; 332 +/- 92 to 254 +/- 102 (p < 0.05), LA %FS; 14 +/- 5 to 8 +/- 5 (p < 0.05), and LA -dP/dt; 36 +/- 19 to 26 +/- 18 (p < 0.05)), but did not change significantly during heart rate increments. LA PEPc decreased after saline infusion (114 +/- 11 to 104 +/- 14 (p < 0.05)) and increased after propranolol administration (108 +/- 8 to 129 +/- 13 (p < 0.05)). As pacing rate was increased, LA PEPc and LA ET showed no significant changes. Both AAL and LA +dP/dt correlated significantly with LA PEPc (r = -0.76 and -0.66), but not with LA ET (r = -0.08 and -0.04). In conclusions, LA pump function was augmented by volume loading and decreased by propranolol, but unchanged by heart rate increments. These changes in LA pump function were reflected by LA PEPc, but not by LA ET. LA PEPc is a useful index of LA pump function which is not heart rate dependent.

Animals↗

Epinephrine increases mortality after brief asphyxial cardiac arrest in an in vivo rat model.

Epinephrine may be detrimental in cardiac arrest. In this laboratory study we sought to characterize the effect of epinephrine and concomitant calcium channel blockade on postresuscitation myocardial performance after brief asphyxial cardiac arrest. Anesthesized rats were disconnected from mechanical ventilation, resulting in cardiac arrest. Resuscitation was attempted after 1 min with mechanical ventilation, oxygen, chest compressions, and IV medication. In experimental series 1 and 2, animals were allocated to 10 or 30 microg/kg epinephrine or 0.9% saline. In series 3, animals received 30 microg/kg of epinephrine and were randomized to 0.1 mg/kg of verapamil or to 0.9% saline. In series 1 and 3, left ventricular function was assessed using transthoracic echocardiography. In series 2, left atrial pressure was measured. Epinephrine was associated with increased mortality (0/8 [0%] in controls, 4/12 [33.3%] in 10 microg/kg animals, and 16/22 [72.8%] in 30 microg/kg animals; P < 0.05), hypertension (P < 0.001), tachycardia (P = 0.004), early transient left atrial hypertension, and dose-related reduction in left ventricular end diastolic diameter (P < 0.05). Verapamil prevented mortality associated with large-dose epinephrine (0% versus 100%) and attenuated early diastolic dysfunction and postresuscitation hypertension (P = 0.001) without systolic dysfunction. Epinephrine appears to be harmful in the setting of brief cardiac arrest after asphyxia.

Animals↗

Patient with atrioventricular node reentrant tachycardia with eccentric retrograde left-sided activation: treatment with radiofrequency catheter ablation.

We describe a patient with supraventricular tachycardia with triple atrioventricular (AV) node pathway physiology. A discontinuous curve was present in the antegrade AV nodal function curves. During right ventricular pacing, the earliest retrograde atrial activation was recorded at the left-sided coronary sinus electrode. The retrograde ventricular-atrial interval was long and had decremental conduction. We induced a slow-slow AV node reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation. After slow pathway ablation, dual AV nodal pathway physiology was present. AVNRT with eccentric retrograde left-sided activation is relatively rare, and our findings suggest that eccentric retrograde left-sided atrial inputs consist partially of a slow pathway and disappear with slow pathway ablation.

Atrial Function, Left↗

Late improvement in ventricular performance following internal cardioversion for persistent atrial fibrillation: an argument in support of concealed cardiomyopathy.

The aim of the study was to evaluate the time course of atrial and ventricular function improvement following internal atrial cardioversion in patients with structural heart disease. Twenty-nine patients with chronic persistent atrial fibrillation (AF) and underlying structural heart disease were followed by serial echocardiograms performed at 1 and 6 hours, 1 day, 1, 2, and 3 weeks, and 1, 2, 3, and 6 months after successful cardioversion. Sinus rhythm was maintained at 6 months in 24 patients. Following cardioversion the time course of left atrial mechanical function (peak A wave, percent A wave filling) differed from that of left ventricular ejection fraction: peak A wave values (cm/s) increased significantly at 1 week (51 +/- 23 vs 35 +/- 15 at 1 hour, P < 0.05), percent A wave filling (%) increased significantly at 2 weeks (34 +/- 12 vs 22 +/- 9 at 1 hour, P < 0.05), whereas left ventricular ejection fraction (%) increased later (at 1 month 60 +/- 14 vs 55 +/- 14 at baseline, P < 0.05 and at 2 months 60 +/- 14 vs 56 +/- 14 at 1 hour, P < 0.05). In conclusion, restoration of sinus rhythm results in an improvement in left ventricular ejection fraction during follow-up, even in patients with structural heart disease without fast ventricular rates at baseline. The dissociation between the time course of atrial and ventricular function improvement suggests that the latter was partly due to regression of a concealed form of cardiomyopathy and/or of a ventricular dysfunction due to chronic AF.

Analysis of Variance↗

Selective aldosterone blockade suppresses atrial tachyarrhythmias in heart failure.

INTRODUCTION: Renin-angiotensin-aldosterone system activation may be involved in the pathogenesis of atrial arrhythmias in congestive heart failure (CHF). The effects of aldosterone blockade on atrial tachyarrhythmias have not been evaluated. This study's aim was to determine whether selective aldosterone blockade suppresses atrial tachyarrhythmia inducibility and modifies atrial electrical and/or structural remodeling in a canine model of rapid ventricular pacing (RVP)-induced CHF. METHODS AND RESULTS: Dogs were assigned randomly to treatment with oral placebo or eplerenone (50 mg/day) and divided into four groups: two sham-operated (no RVP) and two RVP groups. After 5 weeks of no RVP or RVP at 230 beats/min along with concurrent placebo or eplerenone treatment, dogs underwent electrophysiologic and echocardiographic studies. Sustained atrial tachyarrhythmia inducibility (>10-minute duration), atrial effective refractory periods (ERPs), systolic and diastolic function, and left atrial and left ventricular (LV) chamber sizes were assessed. Placebo-treated RVP dogs developed CHF with LV systolic and diastolic dysfunction, left atrial and LV enlargement, increased atrial ERPs, and inducible sustained atrial tachyarrhythmias. Eplerenone treatment in RVP dogs significantly suppressed sustained atrial tachyarrhythmia inducibility, nonuniformly prolonged atrial ERPs and attenuated LV diastolic dysfunction without modifying left atrial or LV dilation or ejection fractions in CHF. Isoproterenol (2-4 microg/min) reversed eplerenone's atrial antiarrhythmic and ERP prolonging effects in CHF. Eplerenone did not alter atrial ERPs in sham (no RVP) dogs without CHF. CONCLUSIONS: Eplerenone suppresses inducibility of sustained atrial tachyarrhythmias, selectively prolongs atrial ERPs, and attenuates LV diastolic remodeling in RVP-induced CHF. Aldosterone blockade may be a promising new approach for atrial tachyarrhythmia prevention in CHF.

Administration, Oral↗

Dimensional characteristics of left ventricular function after coronary artery bypass grafting.

During coronary artery bypass grafting, 20 patients underwent epicardial placement of miniature ultrasonic dimension transducers across the minor-axis diameter of the left ventricle to monitor cardiac function postoperatively. Left atrial or left ventricular pressure was measured in all patients, and thermodilution cardiac outputs were obtained routinely. Data from 1, 6, 12 and 20 hours postoperatively were analyzed. Directional changes in systolic shortening of the left ventricular diameter correlated well with stroke volume measured by thermodilution techniques and could be used as an on-line index of cardiac output. In five patients who had preoperative abnormalities in wall motion, systolic bulging of the minor-axis diameter was seen initially after revascularization and then gradually resolved over the next 12 hours. Systolic bulging that did not resolve was the earliest indication of a perioperative myocardial infarction in another patient. The end-diastolic diameter increased progressively in all patients in the first 12 hours postoperatively and was associated with stabilization of cardiac function. This improvement in diastolic left ventricular filling was not reflected (p greater than 0.2) by changes in mean left atrial pressure. Therefore, ultrasonic assessment of left ventricular diameter is a simple, precise and safe method of monitoring systolic and diastolic ventricular function postoperatively.

Adult↗

Impact of congestive heart failure and left ventricular systolic function on the prognostic significance of atrial fibrillation and atrial flutter following acute myocardial infarction.

BACKGROUND: Reports on the prognostic importance of atrial fibrillation following myocardial infarction have provided considerable variation in results. Thus, this study examined the impact of left ventricular systolic function and congestive heart failure on the prognostic importance of atrial fibrillation in acute myocardial infarction patients that might explain previous discrepancies. METHODS: The study population was 6676 patients consecutively admitted to hospital with acute myocardial infarction. Information on the presence of atrial fibrillation/flutter, left ventricular systolic function and congestive heart failure were prospectively collected. Mortality was followed for 5 years. RESULTS: In patients with left ventricular ejection fraction<0.25, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.8 (1.1-3.2); p<0.05) but not an increased 30-day mortality. In patients with 0.25 0.35. In patients with congestive heart failure, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.5 (1.2-1.9); p<0.001) and increased 30-day mortality (OR=1.4 (1.1-1.7); p<0.001) but not in patients without congestive heart failure. In hospital survivors, atrial fibrillation/atrial flutter was associated with an increased long-term mortality in all subgroups except those with left ventricular ejection fraction<0.25. CONCLUSIONS: Atrial fibrillation/atrial flutter is primarily associated with increased in-hospital mortality in heart failure patients. Long-term mortality is increased in all subgroups except those with left ventricular ejection fraction<25%.

Aged↗

Non-invasive detection of left atrial mechanical failure in patients with left ventricular disease.

OBJECTIVE: To define patients with left atrial mechanical failure and identify its echocardiographic, physiological, and clinical associations. DESIGN: Prospective study with cross sectionally guided M mode and Doppler echocardiograms, and with apexcardiograms, electrocardiograms, and phonocardiograms. SETTING: Tertiary cardiac referral centre. PATIENTS: 10 patients with left atrial mechanical failure and 20 healthy controls of similar age. RESULTS: 10 patients with left atrial mechanical paralysis were identified among 4036 adults over a 1 year interval. Nine were in sinus rhythm and one had a DDD pacemaker. Left atrial mechanical activity was absent on M mode echocardiograms of the left sided atrioventricular ring and the aortic root. A Doppler A wave on transmitral flow and a clearly defined A wave on the left ventricular apexcardiogram were also absent, though evidence of right atrial mechanical movement was present in nine patients. Mean (SD) age was 63 (19) years and six were men. Nine had left ventricular disease and one had undergone extensive resection of the left atrium. Abnormal measurements of left ventricular end diastolic dimension (62 (13) mm), fractional shortening (15 (6)%), isovolumic relaxation time (19 (12) ms), left atrial size (45 (10) mm), and transmitral Doppler E wave deceleration time (110 (35) ms) were recorded. CONCLUSION: Left atrial mechanical failure may be present in patients with left ventricular disease despite normal sinus rhythm. Normal atrial activation on 12 lead electrocardiogram suggests it is primarily mechanical in origin. The possibility of left atrial mechanical failure must be considered when Doppler patterns of transmitral flow are used to assess left ventricular diastolic function.

Adult↗

Dual site right atrial pacing can improve the impact of standard dual chamber pacing on atrial and ventricular mechanical function in patients with symptomatic atrial fibrillation: further observations from the dual site atrial pacing for prevention of atrial fibrillation trial.

BACKGROUND: The effects of atrial pacing mode on atrial and ventricular function in patients with atrial fibrillation (AF) and bradycardia have not been evaluated. We evaluated atrial and ventricular function during randomization to support pacing (SP), high right atrial pacing (HRA), and dual site right atrial pacing (DAP). METHODS: Seventy-nine patients (66 +/- 12 yr, 46 male) with standard pacing indications and symptomatic AF were randomized to each of three pacing modes (DAP, HRA, SP) for 6 months in a crossover design. Echocardiographic studies were performed at enrollment and the end of each mode. Paired comparisons of atrial and ventricular function parameters were performed between each pacing mode and baseline. RESULTS: HRA pacing in DDDR mode resulted in increased left ventricular (LV) end systolic volume (78 +/- 42 vs. 60 +/- 31 ml, p = 0.001) and reduced LV ejection fraction (44 +/- 14 vs. 50 +/- 11%, p = 0.007) compared to baseline. These parameters did not change during DAP. DAP resulted in increased peak A wave velocity (75 +/- 19 vs. 63 +/- 23 cm/s, p = 0.003) and atrial filling fraction compared to baseline (0.47 +/- 0.15 vs. 0.38 +/- 0.13, p = 0.005). Atrial and ventricular function were similar between control and SP. CONCLUSION: DAP, but not HRA or SP, improved left atrial (LA) function in patients with AF and bradycardia. HRA pacing in DDDR mode resulted in LA dilatation and deterioration of LV function which was not observed with DAP.

Aged↗