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At least 1,225 records · Page 68Linked to original sources
PubMed2005

Right atrial pacing impairs cardiac function during resynchronization therapy: acute effects of DDD pacing compared to VDD pacing.

OBJECTIVES: We aimed to compare the hemodynamic effects of right-atrial-paced (DDD) and right-atrial-sensed (VDD) biventricular paced rhythm on cardiac resynchronization therapy (CRT). BACKGROUND: Cardiac resynchronization therapy improves hemodynamics in patients with severe heart failure and left ventricular (LV) dyssynchrony. However, the impact of active right atrial pacing on resynchronization therapy is unknown. METHODS: Seventeen CRT patients were studied 10 months (range: 1 to 46 months) after implantation. At baseline, the programmed atrioventricular delay was optimized by timing LV contraction properly at the end of atrial contraction. In both modes the acute hemodynamic effects were assessed by multiple Doppler echocardiographic parameters. RESULTS: Compared to DDD pacing, VDD pacing resulted in much better improvement of intraventricular dyssynchrony assessed by the septal-to-posterior wall motion delay (VDD 106 +/- 83 ms vs. DDD 145 +/- 95 ms; p = 0.001), whereas the interventricular mechanical delay (difference between onset of pulmonary and aortic outflow) did not differ (VDD 20 +/- 21 ms vs. DDD 18 +/- 17 ms; p = NS). Furthermore, VDD pacing significantly prolonged the rate-corrected LV filling period (VDD 458 +/- 123 ms vs. DDD 371 +/- 94 ms; p = 0.0001) and improved the myocardial performance index (VDD 0.60 +/- 0.18 vs. DDD 0.71 +/- 0.23; p < 0.01). CONCLUSIONS: Our findings suggest that avoidance of right atrial pacing results in a higher degree of LV resynchronization, in a substantial prolongation of the LV filling period, and in an improved myocardial performance. Thus, the VDD mode seems to be superior to the DDD mode in CRT patients.

Atrial Fibrillation↗
PubMed1998

[Sotalol--atrial fibrillation, reduced renal function and sudden death].

Sotalol is a betablocker with additional antiarrythmic properties. Its pharmacokinetic properties may lead to increased serum levels of the drug in patients with reduced kidney function. We report on a case in which kidney failure in a patient using sotalol for paroxysmal atrial fibrillation gave rise to torsade de pointes ventricular tachycardia and, eventually, sudden death. Gradual prolongation of the QT interval suggested an overdose of sotalol. Sotalol has been commonly used in cases of angina pectoris and hypertension. The recently published SWORD study has, however, changed the indications for its use, and sotalol should now only be used in cases of severe supraventricular and ventricular arrythmias.

Acute Kidney Injury↗
PubMed2004

Comparison of transthoracic echocardiography versus cardiovascular magnetic resonance imaging for the assessment of ventricular function in adults after atrial switch procedures for complete transposition of the great arteries.

Adult patients with a history of transposition of the great arteries and atrial switch operation were studied with transthoracic echocardiography and cardiovascular magnetic resonance imaging. Measurements of ventricular dimensions and function by these 2 techniques in 18 consecutive patients were well correlated.

Adult↗
PubMed1995

The role of the left atrial appendage. A volume loading study in open-chest dogs.

Although the left atrial appendage has a quite unique structure, its function remains unclear. To clarify the function of the left atrial appendage, changes in its anteroposterior, transverse and longitudinal dimensions, and in the anteroposterior dimension of the left atrial body were measured by a sonomicrometer during volume loading in open chest dogs. In the control state, fractional shortening of the transverse dimension of the appendage was greater than that of the atrial body. After dextran infusion, each dimension of the appendage and body, measured just before atrial contraction, increased curvilinearly. The percent increase in appendage dimensions was greater than that of the atrial body dimension (p < 0.05). Systolic shortenings of the appendage increased until mean left atrial pressure reached approximately 15 mmHg but after further pressure elevation, it decreased. In postmortem isolated hearts, the appendage volume was 17.2 +/- 4.4% of the whole left atrial volume. These findings indicate that the appendage has a considerable volume with a greater compliance and assists left ventricular filling during atrial contraction by a Frank-Starling mechanism.

Animals↗
PubMed2005

Effect of acute changes in load on left ventricular diastolic function during device closure of atrial septal defects.

Echocardiographic indexes of left ventricular (LV) diastolic function were assessed in 18 patients before and after device closure of secundum atrial septal defects. The tissue Doppler early diastolic peak annular velocity (Ea) and color M-mode velocity of propagation (Vp), indexes of relaxation, seemed to be load independent and were not affected by the change in LV filling hemodynamics, whereas the mitral inflow peak E-wave velocity and E/Ea ratio were more load dependent, with a resultant increase after the closure of large atrial shunts.

Adolescent↗
PubMed1997

Capacitive function of the heart: influence of acute changes in heart volume on mean right atrial pressure.

Net transfer of blood volume into or out of the cardiac chambers should have the same effect on central venous pressure as does transfer of an equal volume of blood to or from peripheral organs (e.g., spleen, or liver). We studied five pentobarbital sodium-anesthetized open-chest pigs (20-23 kg) to determine whether a reduction in the time-averaged volume of blood contained in the heart, induced by rapid atrial pacing, can raise right atrial pressure. A central premise of our study is that the mean value of right atrial pressure is acutely governed by the volume of blood that distends the central veins, and that atrial contractions primarily determine how atrial pressure varies about its mean value. To prevent changes in cardiac output from altering central blood volume and pressure, cardiac output during rapid pacing (2.36 +/- 0.18 l/min) was made to equal the resting output (2.35 +/- 0.16 l/min). This was achieved by selecting a rate of pacing at which the tendency for more frequent cardiac contractions to raise cardiac output was counterbalanced by the decrease in stroke volume induced by rapid pacing. Autonomic reflex mechanisms were attenuated by pharmacological blockade. Mean arterial pressure was minimally affected in the transition from a normal sinus rhythm (89 +/- 6 beats/min) to rapid atrial pacing (165 +/- 7 beats/min) in four pigs. Mean right atrial pressure rose abruptly from 2.8 +/- 0.5 mmHg during normal sinus rhythm to 3.5 +/- 0.5 mmHg (P = 0.015) at the onset of rapid pacing in these four pigs, presumably owing to decreased cardiac blood volume and a reciprocal expansion of central venous volume. In the fifth pig, a reduction in cardiac output induced by tachycardia led to a larger rise in mean right atrial pressure than did a reduction in cardiac output induced by bradycardia, presumably because tachycardia reduces cardiac blood volume whereas bradycardia raises cardiac volume. We conclude that the heart may play an important role in maintaining or raising its own filling pressure when heart rate rises.

Animals↗
PubMed1976

Sinus node function in children. Factors influencing its evaluation.

Overdrive atrial stimulation was performed in 20 electrophysiologically normal children at the time of routine diagnostic cardiac catheterization, for the determination of the sinus node recovery time (SNRT). Measurements were made at pacing rates of 120, 150, 180, and 200 beats/min. The absolute recovery times demonstrated wide range of values (420-1280 msec). Expressed as a percent of the resting P-P interval, values at pacing rates of 120 and 150 beats/min were 109-166%, with significantly less overdrive suppression (P less than 0.001) occurring at the two faster pacing rates. Atropine diminished the maximum SNRT in all patients tested. This study reports normal values for the SNRT in children. Factors which influence the SNRT are the resting heart rate, the rate of overdrive, and the autonomic tone. In children, the sinus node recovery time should be expressed in terms of the resting sinus interval.

Adolescent↗
PubMed1986

Effect of human alpha-atrial natriuretic polypeptide on adrenocortical function in man.

To determine the effects of atrial natriuretic polypeptide (ANP) on plasma levels of ACTH, cortisol, aldosterone and dehydroepiandrosterone (DHEA), synthetic human alpha-ANP (h alpha-ANP) was infused i.v. into eight normotensive, disease-free volunteers, at a dose and duration previously found to be sufficient to produce apparent cardiovascular and renal effects. The mean basal concentration of plasma ACTH determined by radioimmunoassay was 18.2 +/- 3.1 ng/l. Plasma ACTH concentrations tended to be decreased during the infusion in all subjects. However, the change in plasma ACTH concentrations during infusion of h alpha-ANP was essentially the same as that during the infusion of saline. The mean plasma cortisol concentration was significantly suppressed from 25 to 40 min after the end of synthetic h alpha-ANP infusion. At 90 min after infusion, the mean plasma level of cortisol reverted to the pretreatment level. There was a non-significant increase in plasma renin activity following the infusion. The mean plasma aldosterone concentration was reduced by 15% (P less than 0.05) during the infusion and returned to preinfusion levels 10 min after termination of the infusion, after which the mean plasma concentration declined to the level seen during infusion. Administration of h alpha-ANP had no significant influence on plasma DHEA concentrations, but there was a tendency to decrease during the infusion. Our data suggest that synthetic h alpha-ANP inhibits adrenocortical steroidogenesis in man.

Adrenal Cortex↗
PubMed2003

Atrial stunning: determinants and cellular mechanisms.

BACKGROUND: Atrial stunning is a transient depression of atrial and atrial-appendage mechanical function after successful cardioversion of atrial fibrillation compared with its precardioversion state. METHOD: Atrial stunning associated with different methods of cardioversion of atrial fibrillation and the determinants and cellular mechanisms of atrial stunning were elaborated by thoroughly examining the studies on the subject identified through a comprehensive literature search. RESULTS AND CONCLUSION: Atrial stunning has been reported with all methods of cardioversion of atrial fibrillation, including transthoracic electrical, low-energy internal electrical, pharmacological, and spontaneous. It is a function of the underlying atrial fibrillation becoming apparent at the restoration of sinus rhythm, regardless of the method used for conversion. Unsuccessful cardioversion does not result in atrial stunning. The duration of the preceding atrial fibrillation, atrial size, and underlying structural heart disease are the determinants of atrial stunning. A shorter duration of atrial fibrillation and smaller atrial diameters are associated with a relatively less severe stunning, lasting for a shorter duration. Atrial stunning after cardioversion of atrial fibrillation of <1 week usually resolves within 24 hours, and atrial stunning after cardioversion of chronic atrial fibrillation usually resolves within 4 weeks. Tachycardia-induced atrial cardiomyopathy, atrial cytosolic calcium alterations with down-regulation of the L-type Ca2+ channels and up-regulation of the Na+/Ca2+ exchanger, atrial hibernation with myocyte dedifferentiation and myolysis, and atrial fibrosis are the suggested mechanisms underlying atrial stunning. Atrial stunning determines the risk of postcardioversion thrombus formation in atria and atrial appendages, the duration of postcardioversion anticoagulation therapy, the recovery of the atrial contribution to the ventricular function, and the functional recovery of the patients after successful cardioversion of atrial fibrillation.

Animals↗
PubMed1985

Effects of atrial natriuretic factor on human platelet function.

We examined the hypothesis that atrial natriuretic factor (ANF), a substance with known vasorelaxant activities, shares with other vasodilators the property of inhibiting platelet function. Aggregation of citrated platelet-rich plasma (PRP) from 23 healthy volunteers induced by ADP, adrenaline, arachidonic acid, collagen, gamma-thrombin, the endoperoxide analogue U-44069, serotonin, the calcium ionophore A-23187 or platelet aggregating factor was measured after incubation of PRP with ANF for 3 minutes at concentrations of 4 X 10(-9), 4 X 10(-8) and 4 X 10(-7) M or vehicle as control. ANF decreased ADP-induced aggregation significantly (P less than 0.02), but only at the highest concentration used and to a minor extent (control: 73.6 +/- 11.2%; after ANF 4 X 10(-7) M: 60.0 +/- 17.1%, mean +/- S.D., n = 39) by a selective inhibitory effect on the secondary wave; neither aggregation by all other agents tested nor thromboxane B2 generation induced by ADP and adrenaline was altered by incubation with ANF. Although ANF thus has detectable effects on ADP-induced platelet aggregation in vitro, these data suggest that ANF is unlikely to be a physiologically significant modulator of platelet function.

Adenosine Diphosphate↗
PubMed1994

Relations between left atrial appendage blood flow velocity, spontaneous echocardiographic contrast and thromboembolic risk in vivo.

OBJECTIVES: The aim of this study was to determine the relations between spontaneous echo contrast, left atrial appendage blood flow velocity and thromboembolism. BACKGROUND: Left atrial thrombus and spontaneous echo contrast, a putative marker of thromboembolic risk, are frequently located in the left atrial appendage. Measurement of left atrial appendage outflow Doppler velocity by transesophageal echocardiography is a recent technique for assessment of left atrial appendage function, which may be important in thrombus formation. METHODS: Transthoracic and transesophageal echocardiographic studies were performed in 140 patients with atrial fibrillation (chronic in 80 patients, paroxysmal in 50 patients, first episode < 2 weeks in 10 patients). The left atrium and appendage were inspected for thrombus and spontaneous echo contrast, which was graded from 0 (none) to 4+ (severe). Outflow velocity profiles were obtained by pulsed wave Doppler at the orifice of the left atrial appendage. RESULTS: Left atrial spontaneous echo contrast was present in 78 patients (56%). In multivariate logistic regression analysis, spontaneous echo contrast was the only significant correlate of left atrial thrombus and was present in 14 (93%) of 15 patients. Spontaneous echo contrast and age were associated positively, and anticoagulant therapy was associated negatively, with previous thromboembolic events. Increasing grades of spontaneous echo contrast were associated with decreasing left atrial appendage blood velocity. The velocity in patients with thrombus was not significantly different from that in patients with 4+ spontaneous echo contrast. In multivariate linear regression analysis, the grade of spontaneous echo contrast was significantly and negatively associated with left atrial appendage velocity (p = -0.0001) and mitral regurgitation (p = -0.0002) and significantly and positively associated with left atrial area (p = 0.0005). The odds ratio for spontaneous echo contrast was 28:1 for low left atrial appendage blood flow velocity (< 35 cm/s) and 96:1 for low velocity and the absence of mitral regurgitation. CONCLUSIONS: Spontaneous echo contrast is the cardiac factor most strongly associated with left atrial appendage thrombus and embolic events. Spontaneous echo contrast formation is promoted by reduced blood flow velocity and increased left atrial size but is diminished by mitral regurgitation.

Adult↗
PubMed1993

Heterogeneity and time course of improvement in cardiac function after cardioversion of chronic atrial fibrillation: assessment of serial echocardiographic indices.

OBJECTIVE: To assess the clinical characteristics of patients in whom cardiac function improved after cardioversion of atrial fibrillation and the time course of the improvement. DESIGN: A prospective serial study of echocardiograms recorded before cardioversion and one day, seven days, one month, and three months after cardioversion. SETTING: Echocardiography laboratory of a university hospital. PATIENTS: 23 patients with chronic atrial fibrillation in whom cardioversion was successful. MAIN OUTCOME MEASURES: M mode indices of the left ventricular wall motion and pulsed Doppler indices of the left ventricular inflow. RESULTS: Three months after cardioversion percentage fractional shortening had increased by more than 5% in 14 patients (improved group) and by less than 5% in nine patients (non-improved group). Those in whom cardiac function improved had significantly higher heart rates and a greater reduction in ventricular filling during atrial fibrillation and a more prominent atrial filling wave three months after cardioversion than those patients in the non-improved group. Over the three months of follow up the mean (1SD) percentage fractional shortening increased from 22 (3)% to 30 (4)% in the improved group and in this group heart rate fell one day after cardioversion. A month after cardioversion the percentage fractional shortening had increased to 35 (5)% and the atrial systolic contribution to left ventricular filling increased from 30 (9)% on day 1 to 47 (12)%. CONCLUSIONS: Cardioversion improved cardiac function in patients with tachycardia and reduced ventricular filling during atrial fibrillation. Because both an immediate reduction of heart rate and a delayed recovery of atrial booster pump function played an important part in the improvement of cardiac function the long-term effects of cardioversion should be assessed at least a month after cardioversion.

Adult↗
PubMed1995

Functional explanation for increased atrial natriuretic peptide in systemic sclerosis.

We related atrial natriuretic peptide (ANP) among 30 consecutive patients with systemic sclerosis (SScl) and 48 gender- and age-matched controls to the measurements of left ventricular (LV) function as evaluated by echocardiography and external pulse curves to determine possible causative factors for an increased level of plasma ANP. The patients had a markedly elevated plasma ANP level (239.4 +/- 59 vs. 178.2 +/- 36 pmol/l, p < 0.0005), which was not related to LV systolic function, heart rate, or blood pressure. Patients had LV hypertrophy and plasma ANP correlated directly to interventricular septal thickness (r = 0.41, p < 0.005), LV posterior wall thickness (r = 0.32, p < 0.01), and wall thickness to cavity dimension (r = 0.44, p < 0.0005), LV mass index (r = 0.40, p < 0.005). LV early filling properties were impaired, with reduction of atrial emptying index (p < 0.0005) and increased contribution of atrial contraction to LV filling. Plasma ANP correlated to atrial emptying index (r = 0.41, p < 0.0005) and to apex-cardiographic a wave (r = 0.28, p < 0.05). Plasma ANP was also related to left atrial dimension index (r = 0.27, p < 0.05), and was still related to atrial emptying index, but not to left atrial dimension, when considering the degree of LV hypertrophy in multivariate analysis. We conclude that ANP is elevated in patients with SScl. Reduced LV compliance, probably due to increased fibrosis, may cause changes in atrial pressure sufficient to stimulate ANP production without systolic dysfunction as a prerequisite.

Adult↗
PubMed1997

Effects of atrial dilatation on refractory period and vulnerability to atrial fibrillation in the isolated Langendorff-perfused rabbit heart.

BACKGROUND: Atrial fibrillation (AF) is frequently observed under conditions that are associated with atrial dilatation. The aim of this study was to investigate the effects of atrial dilatation on the substrate of AF. METHODS AND RESULTS: In 15 Langendorff-perfused rabbit hearts, the interatrial septum was perforated, and after occlusion of the caval and pulmonary veins, biatrial pressure was increased by raising the level of an outflow cannula in the pulmonary artery. Right and left atrial effective refractory periods (AERPs), monophasic action potentials (MAPs), and inducibility of AF by single premature stimuli were measured as a function of atrial pressure. Increasing the atrial pressure from 0.5+/-0.7 to 16.2+/-2.2 cm H2O resulted in a progressive shortening of the right AERP from 82.2+/-9.8 to 48.0+/-5.1 ms. In the left atrium, an increase in pressure up to 7.4+/-0.3 cm H2O had no effect on the AERP. At higher pressures, however, the left AERP also shortened, from 67.5+/-7.5 to 49.3+/-2.0 ms. The duration of MAPs also decreased by an increase in atrial pressure, showing a high correlation with the shortening in AERP (r=.94, P<.01). All these changes were completely reversible within 3 minutes after release of the atrial stretch. Dilatation of the atria was a major determinant for the vulnerability to AF. The inducibility of AF increased from 0% at low pressures to 100% when the atrial pressure was >10 cm H2O. Release of the atrial wall stress resulted in prompt cardioversion of AF. The increased vulnerability for AF was highly correlated with the shortening in AERP (logistic regression r=.97). No correlation was found with the spatial dispersion between right and left AERPs. CONCLUSIONS: Increased atrial pressure in the isolated rabbit heart resulted in a significant increase in vulnerability to AF that was closely correlated to shortening of the AERP. These changes were completely reversible within 3 minutes after release of the atrial stretch, resulting in prompt termination of AF.

Animals↗
PubMed1996

Atrial natriuretic peptide inhibits mineralocorticoid receptor function in rat colonic surface cells.

Atrial natriuretic peptide (ANP) inhibits and aldosterone (ALDO) stimulates Na conductive transport. Therefore, the effects of ANP and its second messenger cGMP on mineralocorticoid receptor (MR) function in rat colon surface and crypt cells were examined. 100 nM 8-Br-cGMP decreased surface [3H]ALDO binding by 42 +/- 4% but increased crypt [3HvALDO binding by 52+/-16%. ANP decreased surface [3H]ALDO binding by approximately 50% after a 2.5-h lag period but had no effect on crypt ALDO binding. ANP and cGMP rapidly (< 15 min) inhibited surface cell ALDO-induced MR nuclear translocation but did not affect crypt MR nuclear translocation. Inhibition of cGMP-dependent protein kinase with KT5823 blocked the inhibitory effects of ANP and 8-Br-cGMP on surface cell ALDO binding and MR nuclear translocation. In crypt, KT5823 increased baseline [3H]ALDO binding but did not inhibit the stimulatory effect of exogenous cGMP. DEAE-cellulose chromatography and gel mobility shift assay showed that ANP did not inhibit surface MR activation. ANP inhibited ALDO stimulated short circuit current in distal colon. These data demonstrate cell-specific regulation of MR function. In surface cells, ANP rapidly inhibits MR nuclear translocation and ALDO-induced short circuit current. ANP inhibition of MR function may be an additional mechanism of ANP antagonism of Na reabsorption.

Aldosterone↗