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 739 records · Page 41Linked to original sources
PubMed1995

Left atrial mechanical and biochemical adaptation to pacing induced heart failure.

OBJECTIVE: To determine the left atrial mechanical and biochemical adaptations to congestive heart failure, 10 dogs with rapid atrial and ventricular pacing and seven control dogs were studied. METHODS: Animals were instrumented with left atrial sonomicrometers and micromanometers and left atrial pressure-volume relationships were generated by phenylephrine boluses for maximum elastance (Emax) and end systolic elastance (Ees) calculations. Left atrial maximum volume, ejection fraction, and mean circumferential fibre shortening (Vcf) were compared at matched left atrial pressure. At necropsy, myosin heavy chain (MHC) isoforms from the left atrial body and appendage were separated with SDS-PAGE, stained with monoclonal antibodies to alpha and beta MHC, and quantified with laser densitometry. RESULTS: Left atrial ejection fraction and Vcf were significantly lower and maximum atrial volume and atrial systolic stroke volume were significantly greater in heart failure than in control. Emax was not significantly altered in heart failure, at 5.9(SD 2.9) v 4.5(1.6) mm Hg.ml-1 in controls. However, Vcf was lower (P < 0.05) and the A loop pressure-volume area (an index of eternal mechanical work performed by the left atrium) was greater (P < 0.05) in heart failure than in control dogs. The percent beta MHC in the left atrial body was greater in dogs with heart failure than in controls, at 42.6(9.8) v 17.3(9.0)%, P < 0.05. By contrast there was no significant beta MHC isoform switch in the left atrial appendage [14.4(7.6) v 17.9(9.7)%]. CONCLUSIONS: In this model of left atrial pressure and volume overload, there is significant upregulation of beta MHC in the left atrial body but not in the appendage and this isoform switch is associated with decreased velocity of left atrial contraction, increased atrial mechanical work, and unchanged force generation.

Animals↗
PubMed1992

[Rhythmogenic cardiomyopathies of atrial origin in children. Myth or reality?].

Incessant, rapid, supraventricular tachycardia may be complicated by cardiac failure with ventricular dilatation and hypokinetic wall motion on echocardiography: so-called tachycardia-induced cardiomyopathy. The diagnosis is simple when the cardiac rhythm is not sinus rhythm. The authors report the cases of 4 children aged 7 months to 12 years, referred for diagnosis and treatment of apparently primary cardiomyopathy. The findings of spontaneous or vagally-induced atrioventricular conduction defects, a permanently rapid atrial rhythm though influenced by 24 hour variations, or periodic abnormal rate increases, suggested myocardial dysfunction due to an ectopic atrial tachycardia. This was an essential step in management as the control of the tachycardia by amiodarone or betablocker therapy resulted in regression of symptoms and normalisation of left ventricular function. However, some atrial tachycardias are very resistant to medical treatment and, in such cases, there should be no hesitation in using more radical approaches, surgery or ablation, even and especially in patients with severe cardiac failure. In conclusion, apparently primary dilated cardiomyopathy in children may be due to chronic atrial arrhythmia and it is essential to perform at least Holter monitoring in order not to miss this diagnosis.

Adrenergic beta-Antagonists↗
PubMed1979

Spinal cord ischemia and left atrial myxoma.

A 62-year-old man had an acute, transient, flaccid paraplegia. Examination showed a primary cardiac tumor with emboli to major branches of the aorta. A myxoma was removed from the left atrium, and normal function returned. Left atrial myxoma should be suspected as a cause for embolism to the CNS.

Embolism↗
PubMed1996

F-amplitude, left atrial appendage velocity, and thromboembolic risk in nonrheumatic atrial fibrillation. Stroke Prevention in Atrial Fibrillation Investigators.

BACKGROUND: Reduced left atrial appendage velocity (LAAV) has been identified as a marker for thromboembolism in patients with atrial fibrillation. HYPOTHESIS: It was postulated that electrocardiographic (ECG) F-wave amplitude would correlate with LAAV, and inversely with the risk of thromboembolism in patients with atrial fibrillation. METHODS: In all, 53 patients with nonrheumatic (NRAF) and 7 patients with rheumatic (RAF) atrial fibrillation underwent assessment of maximum LAAV, which was correlated to the maximum ECG F-wave voltage from lead V1 (F(max)). In 450 NRAF patients on neither aspirin nor warfarin, the relationship between F(max) and thromboembolic risk was assessed over an average follow-up of 1.3 years. RESULTS: F(max) did not correlate with LAAV (r = 0.2, p = 0.07). Patients with intermittent atrial fibrillation (n = 123) had smaller F(max) amplitude than patients with constant atrial fibrillation (n = 327) (mean 0.73 vs. 0.88 mV-1, p = 0.001). F(max) amplitude was not related to a history of hypertension, systolic blood pressure, duration of NRAF, abnormal transthoracic echocardiographic left ventricular (LV) systolic function or left atrial (LA) diameter. There was a strong trend for increased LV mass being related to smaller F(max) amplitude after adjusting for body surface area (p = 0.06). F(max) amplitude was not correlated with risk of embolic events, including only those events presumed by a panel of case-blinded neurologists to be cardioembolic. CONCLUSIONS: F(max) amplitude in NRAF is smaller in patients with intermittent versus constant AF. It does not correlate with LAAV, LA size, increased LV mass, or systolic dysfunction, hypertension, or risk of embolism. Therefore, F(max) amplitude may not be used as a surrogate for LAAV, or as a measure of thromboembolic risk in NRAF.

Aged↗
PubMedDate not supplied

Influence of left atrial pressure on left atrial appendage flow velocity patterns in patients in sinus rhythm.

To examine changes in left atrial appendage flow velocity patterns in relation to left atrial pressures during sinus rhythm, transesophageal echocardiography and cardiac catheterization were performed in 31 patients with myocardial diseases in sinus rhythm and 20 control subjects without cardiovascular disease. The 31 patients were divided into two groups according to mean pulmonary capillary wedge pressure: the group with high wedge pressure (19.9 +/- 5.8 mmHg) and the group with low wedge pressure (8.6 +/- 2.9 mmHg). The left atrial appendage peak early emptying velocity was decreased significantly in the groups with both high and low wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity was significantly greater in the group with low wedge pressure compared with the control group, whereas it was decreased significantly in the group, with high wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity had a significant negative correlation with wedge pressure. The maximum left atrial appendage area at end systole in the group with high wedge pressure was significantly greater than that in both the group with low wedge pressure and the control group. There was a significant positive correlation between the maximum left atrial appendage area and the wedge pressure, as well as a significant negative correlation between the left atrial appendage ejection fraction during atrial contraction and the wedge pressure. In the group with high wedge pressure, one patient had evidence of left atrial appendage thrombi and two had spontaneous echo contrast. These results suggest that even in patients in sinus rhythm, a marked elevation in the left atrial pressure is likely to reduce the left atrial appendage peak early and late emptying velocities. These changes may be accompanied by an increased incidence of thrombus formation in the left atrial appendage compared with individuals with normal or only slightly elevated left atrial pressures.

Atrial Function↗
PubMed1997

Influence of nighttime blood pressure on left atrial size in uncomplicated arterial systemic hypertension.

The aim of the study was to determine the relations of 24-h blood pressure (BP) and its different phases with left atrial size. A total of 130 subjects (mean age 46 years) not taking cardiac drugs were studied by M-mode and Doppler echocardiography and ambulatory BP recording. Subjects (excluding those with coronary artery or valvular heart disease, heart failure, or diabetes) were classified into two groups: 25 normotensives and 105 hypertensives (history of antihypertensive treatment and office diastolic BP > 90 mm Hg). The two groups were comparable in terms of sex, age, and heart rate, whereas body mass index, (P < .01), office BP, average 24-h BP, and average daytime and nighttime BP (all P < .00001) were higher in hypertensives. Hypertensives also had increased left atrial dimension, left atrial dimension/aortic root ratio (both P < .001), and left ventricular mass (LV) indexed for height (P < .0001). Positive correlations of left atrial dimension were found with office BP, average 24-h, average daytime and nighttime systolic and diastolic BP, LV mass index, and Doppler-derived E/A ratio. In a multivariate model that included potentially confounding factors, only body mass index (standardized beta coefficient = 0.41, P < .00001), average nighttime diastolic BP (beta = 0.33, P < .00001), and male sex (beta = 0.18, P < .01) were independent predictors of left atrial size in the pooled population. In conclusion, left atrial size is more closely related to ambulatory, rather than office, BP measurements, and high average nighttime BP is a powerful marker of left atrial enlargement in arterial hypertension.

Adult↗
PubMed1993

Pulmonary venous flow pattern studied by transoesophageal pulsed Doppler echocardiography in mitral stenosis in sinus rhythm: effect of atrial systole.

In 13 patients with isolated mitral stenosis in sinus rhythm the pulmonary venous flow was evaluated by transoesophageal pulsed Doppler echocardiography. The patients were divided into two groups according to their mitral valve area (MVA); Group I (MVA < 1.5 cm2, n = 7 patients); and Group II (MVA > 1.5 cm2, n = 6). The patients in group I with haemodynamically significant mitral stenosis had lower velocities of systolic (S), diastolic (D) and atrial retrograde (A) waves of pulmonary venous flow (PVF) compared to milder stenosis (P < 0.05). The peak velocity of pulmonary retrograde venous flow at atrial contraction (A) primarily depends on the relative amplitude of the atrial transmitral wave (RA), which is measured from the onset of atrial systole to its peak velocity. We found a highly positive correlation between RA of mitral valve flow (MVF) and A wave of PVF (r = 0.87, P < 0.0001). There was also a highly negative correlation (r = 0.80, P < 0.001) between A of PVF and ratio of early (PE) to late (PA) velocities of MVF. Therefore, the retrograde A wave of PVF is related to the pressure generated in the left atrium during atrial systole. Use of pulmonary vein velocities in conjunction with mitral flow velocities can increase our understanding of the haemodynamics of mitral stenosis and provide a new insight into left atrial performance.

Adult↗
PubMed1992

Left atrial contribution to ventricular filling during the course of evolving heart failure.

BACKGROUND: Abnormal left ventricular (LV) filling has been observed in patients with heart failure and is characterized by marked heterogeneity of mitral inflow velocity. In the present study, the contribution of the left atrium to LV filling was examined in eight dogs during the course of evolving heart failure. METHODS AND RESULTS: Heart failure was produced by multiple sequential intracoronary embolizations with microspheres. Pulsed Doppler echocardiography was used to measure mitral inflow velocity at baseline, before embolization, and at 3, 8, 15, 23, and 33 weeks after initiation of microembolization. The early rapid LV filling (Ei) and late left atrial filling (Ai) components were quantitated based on the time-velocity integral of the early and late mitral inflow velocity waveforms, respectively. Ei decreased progressively from 7.6 +/- 1.5 cm at baseline to 4.0 +/- 0.4 cm at 33 weeks (p less than 0.01). In contrast, Ai initially increased from 1.8 +/- 0.9 cm at baseline to 2.7 +/- 0.4 cm at 3 weeks (p less than 0.01) and subsequently decreased gradually to below baseline values reaching 0.8 +/- 0.4 cm at 33 weeks (p less than 0.01). These temporal changes of Ei and Ai were accompanied by a gradual reduction of LV ejection fraction (56 +/- 5% versus 22 +/- 2%) (p less than 0.01) (baseline versus 33 weeks) and by a gradual increase of LV end-diastolic wall stress (24 +/- 7 versus 92 +/- 8 g/cm2) (p less than 0.01), left atrial dimension (2.4 +/- 0.2 cm to 3.3 +/- 0.3 cm) (p less than 0.01), and left atrial fractional shortening (22 +/- 3% versus 15 +/- 2%) (p less than 0.01). CONCLUSIONS: The initial rise in left atrium contribution to LV filling may represent a compensatory response to the diminution of the rapid early component of LV filling. With further progression of LV dysfunction, the left atrium contribution to LV filling gradually decreased. This reduction may be mediated by increased workload imposed on the left atrial myocardium due to increased LV diastolic wall stress, which, over time, may have lead to intrinsic left atrium dysfunction.

Animals↗
PubMed1995

[Cardioversion in atrial fibrillation. Results and complications in 1,152 prospective patients. Study Group of the Working Society of Leading Cardiologic Hospital Physicians].

BACKGROUND: Pharmacological and direct-current cardioversion of atrial fibrillation are often performed interventions. Little is known about results and complications of cardioversion in daily practise. PATIENTS AND METHODS: Demographic, procedural and outcome data from patients with cardioversion of atrial fibrillation were collected in a prospective, multicenter registry of 61 hospitals. RESULTS: Between July 1994 and December 1994 1152 patients with a mean age of 64 +/- 11 years were registered on an intention-to-treat basis. 62% were male. The most prevalent underlying disorders were coronary artery disease (34.7%), valvular heart disease (18.1%), and cardiomyopathy (6.9%). 16.4% of patients had lone atrial fibrillation. New onset atrial fibrillation was reported in 21%, paroxysmal in 32% and chronic in 47% of patients. The mean duration of atrial fibrillation was 7 +/- 26 weeks (range 1 day to 7 years, median 5 days). In 3.8% of patients no cardioversion attempt was made and follow-up was not possible in another 5.5%. 19.2% of patients cardioverted spontaneously. Direct current cardioversion was attempted in 39.7% and pharmacological cardioversion in 31.8% of patients. Cardioversion was successful (sinus rhythm at discharge) in 96.4% of spontaneous cardioversion, in 73.1% of direct current cardioversion and in 84.4% of pharmacological cardioversion. Success of cardioversion was significantly related to duration of atrial fibrillation, NYHA functional class and left atrial diameter (p < 0.001). In 55 (4.8%) cases complications were reported of which 14 were fatal. Five cases of sudden death occurred, all of which were related to quinidine therapy for pharmacological cardioversion. Five cases of embolism were reported. Two were not associated with cardioversion attempts and 3 occurred within 24 hours after successful direct current cardioversion. Two of these patients were effectively anticoagulated at the time of cardioversion. A total of only 62% of patients with atrial fibrillation of more than 48 hours duration were anticoagulated for cardioversion with coumadine or i.v. heparin. CONCLUSIONS: The main risks of cardioversion are fatal proarrhythmic events in pharmacological attempts to restore sinus rhythm. The risk of embolism is despite low rates of effective anticoagulation low.

Aged↗
PubMed1998

Use of intraventricular dispersion of the peak diastolic flow velocity as a marker of left ventricular diastolic dysfunction in patients with atrial fibrillation.

The aim of this study was to evaluate the use of intraventricular dispersion of the peak diastolic flow velocity as a marker of left ventricular diastolic dysfunction in patients with atrial fibrillation. Regional diastolic flow velocity patterns at 1, 2, and 3 cm away from the mitral tip toward the apex were simultaneously recorded with the mitral flow velocity pattern by using pulsed Doppler echocardiography in 24 patients with atrial fibrillation before electrical or medical cardioversion. Echocardiographic examination was repeated after 10 to 30 days (ie, at the time of recovery of left atrial mechanical functions) after cardioversion of atrial fibrillation in all patients. Thirteen patients were found to have diastolic dysfunction; the remaining 11 patients with a normal E/A ratio constituted the control group. Afterward, the data recorded before the cardioversion were analyzed for each patient. In subjects with normal diastolic function, the peak diastolic flow velocity (PDFV) at the mitral tips also was maintained at the positions 1 to 3 cm away from the tip in the left ventricular cavity (PDFV at the mitral tips: 0.84 m/s, PDFV at 3 cm: 0.85 m/s; P =.34). In contrast, the regional PDFV progressively decreased toward the apex in patients with diastolic dysfunction (PDFV at the mitral tips: 0.82 m/s, PDFV at 3 cm: 0.63 m/s; P =.0004). Only 77% of the initial velocity was maintained at 3 cm away from the mitral tips in patients with diastolic dysfunction, whereas almost 100% of the initial velocity was preserved in patients with normal diastolic function (P <.001). These findings suggest that the assessment of the intraventricular decrease in mitral PDFV may be used as a reliable marker of diastolic dysfunction in patients with atrial fibrillation.

Atrial Fibrillation↗
PubMed1988

Interventricular septal motion and left ventricular function in patients with atrial septal defect.

In order to assess whether the paradoxical motion of the interventricular septum seen in patients with atrial septal defect (ASD) is due to a true abnormality in septal contraction, eight patients with ASD (age, 1.6-17 years) and eight age-matched control patients were studied using qualitative and quantitative two-dimensional (2D) and M-mode echocardiography. 2-D-echocardiographic images recorded from the parasternal short-axis projection at the level of the papillary muscles and 2D-directed M-mode tracings at this level were obtained. Comprehensive wall motion analysis of the left ventricular (LV) endocardial and epicardial borders was performed using both fixed reference and center of mass (floating reference) models. Our results indicate that interventricular septal wall motion and function are normal in patients with ASD. The apparent "paradoxical" motion is due to excessive anterior motion of the entire left ventricle, and is present only when a fixed reference system is used to assess myocardial motion, but is not present when a center of mass (floating reference system) is employed. Left ventricular function assessed by % area and perimeter change, mean radial shortening fraction, and mean radial wall thickening (2D) as well as LV shortening fraction and septal and posterior wall thickening (M-mode) was not significantly different between the two groups. Standard M-mode tracings can therefore be used to assess LV function despite this apparent abnormal septal motion.

Adolescent↗
PubMed1992

Simultaneous measurement of left atrial pressure by Doppler echocardiography and catheterization.

Simultaneous, continuous wave Doppler echocardiography, left ventricular systolic and mean pulmonary capillary wedge pressure measurements were performed during cardiac catheterization in 54 patients with mitral regurgitation. Doppler-derived left atrial pressure, which was calculated by subtracting mitral regurgitant gradient from brachial artery systolic pressure, correlated well with mean pulmonary capillary wedge pressure by catheter (r = 0.933, SEE = 2.9 mmHg, P < 0.001); a comparison between non-invasive and invasive systolic gradients across the mitral valve yielded a high correlation (r = 0.91, SEE = 6.0 mmHg, P < 0.001); and there was also a high correlation between brachial artery and left ventricular systolic pressures (r = 0.93, SEE = 4.9 mmHg, P < 0.01). It is concluded that Doppler echocardiography provides a reliable and accurate method for complete non-invasive assessment of left atrial pressure in patients with mitral regurgitation.

Adolescent↗
PubMed1995

High incidence of left atrial thrombus detected by transoesophageal echocardiography in heart transplant recipients.

The aim of the study was the detection of spontaneous echo contrast (SEC) and left atrial thrombus by transoesophageal echocardiography (TEE) in patients who had undergone orthotopic heart transplantation. TEE was prospectively performed in 64 heart transplant recipients (53 males, 11 females, mean age 51 years). Since surgery (mean time: 31 months), all heart transplant recipients had received either aspirin (39), or dipyridamole (22), or both (3). Despite the antiplatelet treatment, an acute arterial embolism (two strokes, one popliteal and one mesenteric ischaemia) occurred in four patients who subsequently received an oral anticoagulant therapy. TEE was performed with a biplane high-frequency transducer after lidocaine pharyngeal anaesthesia, midazolam intravenous injection and antibiotic prophylaxis. Mean ejection fraction was 63 +/- 10%. None had evidence of rejection at endomyocardial biopsy performed on the same day as TEE and analysed in a blinded fashion. All were in sinus rhythm. Left atrial SEC was found in 35 patients (55%) and was associated with left atrial thrombus in 18 patients (28%). These thrombi were localized in the donor left atrial appendage in 10 cases, on the posterior wall of the left atrium in six cases, on the donor part of inter-atrial septum in one case and on the suture line in one case. They were not detected by transthoracic echocardiography (TTE). When compared with patients without thrombus, no difference was found concerning left atrial size, left ventricular ejection fraction, pulmonary artery pressure and number of previous episodes of rejection. However, cardiac index was significantly lower in patients with left atrial thrombus.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Function, Left↗
PubMed1994

Assessment of ductus arteriosus shunt in preterm infants supported by mechanical ventilation: effect of interatrial shunting.

We studied 51 preterm infants (< 1500 gm) with serial color Doppler echocardiography to determine the impact of incompetence of the foramen ovale on the hemodynamic implications of shunting through a patent ductus arteriosus. Doppler and two-dimensional echocardiographic measures included left atrial/aortic root ratio, right (RVSV) and left ventricular stroke volumes (LVSV), and outputs to determine relative ventricular outputs (RVSV/LVSV) and to calculate the pulmonary/systemic flow ratio (Qp/Qs), the diameter of the color flow Doppler mapping of interatrial and ductal shunts, pulsed Doppler pattern, and velocity of those shunts. The dominant direction of shunting at the ductal and atrial levels was left to right. In studies with minimal atrial shunting, there was a weak but significant correlation between RVSV/LVSV (1/(Qp/Qs)) and the left atrial/aortic root ratio, LVSV, and output index, but there was a close correlation with the diameter of the color flow Doppler of the shunt within the ductus (r = -0.8). With this diameter used as a constant, increasing color flow Doppler diameter of atrial shunt significantly reduced LVSV and increased RVSV/LVSV (1/(Qp/QS)). In infants with large ductal and atrial shunts, right ventricular output was often greater than left ventricular output. We conclude that atrial shunting has a significant impact on the hemodynamic implications of ductal shunting in many very preterm infants. This renders use of the relative ventricular outputs to calculate Qp/Qs inaccurate as a single measure of shunt size in patent ductus arteriosus. If the shunt is predominantly left to right, the most accurate assessment is provided by color flow ductal shunt diameter.

Atrial Function, Left↗
PubMed1997

Left ventricular diastolic filling dynamics during isometric exertion in syndrome X assessed with Doppler flowmetry.

To study left ventricular diastolic properties in syndrome X, we analyzed transmitral filling dynamics during handgrip exertion. In 14 normal subjects (N), 17 with syndrome X (Syn X), 16 with single-vessel disease (SVD), and 8 with multiple-vessel disease (MVD), transmitral inflow was recorded at baseline and during handgrip (50% of maximal effort for one minute) using pulsed Doppler echocardiography. We measured early diastolic (E) and late atrial (A) inflow velocities, A/E ratio and percent change of A/E from baseline (%A/E). Blood pressure and heart rate increased to the same degree in each group during handgrip. In normal subjects, E did not change with handgrip; A (51 +/- 10 vs 54 +/- 11 cm/sec, P < 0.05) and A/E (1.16 +/- 0.22 vs 1.25 +/- 0.33, P < 0.05) increased minimally. In Syn X subjects, E decreased (51 +/- 10 vs 38 +/- 10 cm/sec, P < 0.0001), A increased (52 +/- 11 vs 60 +/- 14 cm/sec, P < 0.005), and A/E increased markedly (1.07 +/- 0.31 vs 1.68 +/- 0.51, P < 0.0001). The %A/E in Syn X and MVD were significantly larger than that in SVD and N (Syn X: 58 +/- 29%; MVD: 45 +/- 25%; SVD: 22 +/- 21%; N: 8 +/- 13%). Handgrip-induced changes in diastolic filling in syndrome X and are similar to those in MVD and more marked than in SVD. These changes are consistent with impaired ventricular relaxation and support a generalized left ventricular (LV) abnormality in syndrome X.

Adult↗