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PubMed1995

Prevalence of residual left atrial thrombi among patients with acute thromboembolism and newly recognized atrial fibrillation.

BACKGROUND: Thromboembolism related to atrial fibrillation (AF) is a major cause of morbidity and mortality. Patients with acute thromboembolism and AF are at high risk for early recurrent events. OBJECTIVE: To determine the prevalence of left atrial thrombi in patients who had acute thromboembolism and newly diagnosed AF. PATIENTS AND METHODS: Adult inpatients with AF were screened to identify those with acute (< 36 hours) systemic thromboembolism and newly recognized AF. Of 41 qualifying patients, 31 (76%) agreed to undergo transesophageal echocardiographic study, including 24 with acute neurologic events and seven with peripheral thromboembolism. A control population consisted of 88 adults with newly recognized AF without clinical thromboembolism. RESULTS: Transesophageal echocardiography identified left atrial thrombi in 13 (43%) of the 30 study patients who underwent transesophageal echocardiography compared with nine (10%) of 87 controls (P < .001). Spontaneous echo contrast was identified in 27 (87%) of the study population vs 42 (48%) of controls (P < .001). The prevalence of this marker of blood stasis did not differ between patients with left atrial thrombi without thromboembolism (P = .69). Duration of AF, prevalence of abnormal left ventricular function, left atrial size, and mitral regurgitation were similar in both groups. CONCLUSIONS: Left atrial thrombi were identified in more than 40% of patients with acute thromboembolism and newly recognized AF. These data suggest that a major source of recurrent thromboembolism in this group may be residual thrombus migration. Among patients with AF and atrial thrombi, clinical thromboembolism seems to occur randomly, or is related to an unidentified process.

Acute Disease↗
PubMed1995

Lung function in relation to haemodynamic status after atrial redirection for transposition of the great arteries.

To assess the interplay between haemodynamic sequelae and lung function after atrial redirection for transposition of the great arteries, we investigated 15 Mustard (age 12.0-22.0 years), and 15 Senning patients (age 7.2-12.1 years). As diagnosed at cardiac catheterization and ultracardiography, 16 (11 Mustard) had major haemodynamic sequelae, including systemic ventricle dysfunction, pulmonary hypertension, pulmonary venous obstruction, systemic venous obstruction and atrial septal defects. Static and dynamic lung volumes, ventilation distribution and diffusion capacity were assessed by body plethysmography, spirometry, the single-breath nitrogen test (N2slope) and the single-breath method for diffusion capacity (DLCO) respectively. Apart from DLCO, our own reference values were used for comparison. We found small lung volumes, a high functional residual capacity, a high N2slope and a low DLCO. Tests of > 2SD in the abnormal direction were more prevalent in the Mustard group (P = 0.06) and significantly more prevalent in patients with pulmonary hypertension. Six had normal lung function tests, 15 had unclassified abnormalities, three had small lungs and three had central airway obstruction. Peripheral airway obstruction was only present in three of four subjects with moderate or severe pulmonary hypertension. The study confirms some previous reports indicating a high frequency of lung function abnormalities in these patient groups and discusses a possible relationship to haemodynamic status.

Adolescent↗
PubMed2003

[Hemodynamic consequences of atrial fibrillation].

Beside supraventricular extra beats, atrial fibrillation is the most common cardiac arrhythmia. Atrial fibrillation according to Douglas P. Zipes definition is an arrhythmia characterised by complete asynchronous atrial depolarisation, without following hemodynamic effective contraction. Atrial electric activity can be detected during electrocardiography as irregular oscillation of the isoelectric line of low and variable amplitude 350-600/min waves. Atrial fibrillation previously considered as a benign arrhythmia is associated with severe clinical complications as hemodynamic disturbances and closely connected with it cerebral embolization. In the present study we focused on left ventricle function during atrial fibrillation. We evaluate a deterious effect of high, irregular heart rate which stimulates left ventricle systolic dysfunction, so called "tachycardiomyopathy". Deterioration of left ventricle systolic function usually coexists with diastolic impairment, which is difficult to treat even if sinus rhythm is restored. We also analysed the pathophysiologic mechanism of left ventricle impairment during atrial fibrillation at cellular level. In second part of this paper we discussed dependence between size and function of left atrium and its appendage and atrial fibrillation induction. One must take into account of vicious circle mechanism induction during atrial fibrillation, which promotes arrhythmia stabilization, as well as after sinus rhythm restoration--may provoke recurrence of arrhythmia. Intracellular changes followed by electrophysiological alteration are regarded as causes of the mentioned mechanism. Accordingly to the newest studies, gene expression plays a role in arrhythmia induction and stabilization. This means that the problem is very complicated and also gives hope to effective treatment of atrial fibrillation including gene modification.

Atrial Fibrillation↗
PubMed2000

Immediate effect of balloon valvuloplasty on hemostatic changes in mitral stenosis.

This study was conducted to assess right and left atrial hemostatic function in patients with mitral stenosis (MS) and to investigate the immediate effect of balloon mitral valvuloplasty (BMV) on hemostatic function. BMV was performed in 28 patients with MS (age 29 +/- 8 years) who had sinus rhythm and no left atrial (LA) thrombus. Right and left atrial biochemical markers of platelet activity (platelet factor 4 [PF4] and B thromboglobulin [BTG]), coagulation (thrombin-antithrombin III complex [TAT]), and fibrinolytic activity (D-dimer) were measured before and 30 minutes after BMV. Right atrial levels of these markers were also measured in 20 control subjects. Compared with control subjects, patients with MS had higher right atrial levels of PF4 (30 +/- 15 vs 5 +/- 2 IU/ml), BTG (231 +/- 53 vs 30 +/- 8 IU/ml), TAT (7 +/- 4 vs 2 +/- 0.3 microg/L), and D-dimer (380 +/- 145 vs 160 +/- 35 ng/ml, p < 0.0001 in all). TAT levels were higher in the left atrium than in the right atrium of patients before BMV (8 +/- 4 vs 7 +/- 4 microg/L, p < 0.0001). BMV was successful (final mitral valve area > or = 1.5 cm2 and > or = 50% increase of the initial valve area) in all patients. There was a significant reduction of LA levels of PF4 (35 +/- 8 to 26 +/- 9 IU/ml, p < 0.0001), BTG (225 +/- 41 to 196 +/- 28 IU/ml, p < 0.001), and TAT (10 +/- 5 to 7 +/- 1 microg/L, p < 0.05) in the 16 patients with LA pressure < 10 mm Hg after BMV, whereas these markers were not reduced in the 12 patients with left atrial pressure > or = 10 mm Hg after BMV. These data indicate that platelet function, coagulation status, and fibrinolytic activity are increased regionally in the left atrium and in the systemic circulation in patients with MS and sinus rhythm in the absence of LA thrombus. Successful BMV induces a significant reduction of prethrombotic status in patients with low LA pressure after the procedure. Patients with high LA pressure after BMV maintain a high prethrombotic state and may be considered at an increased risk of thromboembolism after the procedure.

Adolescent↗
PubMed1976

Effect of chagasic sera on the rat isolated atrial preparation: immunological, morphological and function aspects.

An antibody reacting with the plasma membrane of working myocardial cells, skeletal muscle fibres, and endothelial cells (EVI antibody) has been described in the sera of patients with Chagas' disease. In the present study of rat isolated atrial preparations beating in ddifferent media, direct immunofluorescence and ultrastructural immunohistochemical procedures indicate that the antibody can interact with the living tissue, becoming fixed to the plasma membranes. Transmission electronmicroscopy studies also showed the presence of sarcolemmal alterations. These observations suggest a possible pathogenic effect of the EVI antibody. The presence of EVI-positive sera in the beating medium leads to a significant increase in the frequency of contractions; no significant effects of EVI-positive sera in contractile force were seen. The increase in frequency could be prevented by previous treatment with a b-adrenergic blocking agent (MJ-1999), but not by an x-blocker (phentolamine) or by an anti-histamine compound (cyproheptadine). The changes described were observed only in those atrial preparations which were beating in media containing EVI-positive sera. In those atria beating in control media (KR,KR plus normal human serum, KR plus EVI-negative chagasic serum), neither immunological nor morphological or functional changes wersence of EVI-positive chagasic serum diminished atrial stimulation after added norepinephrine. These results suggest the possibility that the EVI antibody may act as a b-adrenergic agonist at the cell plasma membrane level. Such an effect might account for some of the clinical features of chronic Chagas' heart disease.

Animals↗
PubMed2001

Impact of atrial fibrillation on clinical status, atrial size and hemodynamics in patients after mitral valve replacement.

BACKGROUND AND AIM OF THE STUDY: The association between mitral valve disease and atrial fibrillation (AF) is well known, but few data exist regarding the impact of AF after mitral valve replacement (MVR) on NYHA functional class, atrial size and hemodynamic parameters. The present study was conducted to evaluate these issues. METHODS: Eighty-six patients (26 men, 60 women) who underwent MVR were evaluated by transthoracic echocardiography. Fifty-nine patients had chronic AF (AF group), and 27 were in sinus rhythm (sinus group). Variables analyzed included end-systolic left atrial and right atrial areas, tricuspid regurgitation, and presence and duration of AF. Peak and mean transprosthetic mitral valve gradients and pulmonary pressure were estimated by Doppler echocardiography. RESULTS: Groups were matched for age, sex and time from MVR (mean 6.6 years). Sixty-four patients (77%) had rheumatic heart disease, 18 (21%) had mitral valve disease, and two (2%) had mitral valve prolapse. Mean duration of AF was 11+/-12 years (range: 8-50 years). Preoperatively, AF patients had a worse NYHA class than sinus patients (2.8+/-0.8 versus 1.1+/-0.7, p = 0.001), but both had similar fractional shortening of the left ventricle and preserved prosthetic mitral valve function. Multivariate analysis identified AF as a single predictor of NYHA class after MVR. Although left and right atrial areas were larger in AF patients (47+/-25 versus 27+/-7 cm2, p = 0.0001 and 30+/-12 versus 17+/-5 cm2, p = 0.0001, respectively), the left:right atrial size ratio was not significantly different between groups. Multivariate analysis identified mean transmitral gradient and duration of AF as independent predictors of left atrial size after MVR (p = 0.01 and p = 0.0001, respectively). Tricuspid regurgitation and duration of AF were independent predictors of right atrial size (p = 0.003 and p = 0.0001, respectively). CONCLUSION: The presence of AF after MVR is associated with a worse NYHA functional class, increased transmitral gradients, and larger areas of both atria, when compared with sinus rhythm. Hence, a special effort should be made to correct arrhythmia during surgery, and in case of paroxysmal arrhythmia, earlier surgery should be considered before the condition becomes chronic.

Aged↗
PubMedDate not supplied

[Atrial natriuretic factor and pulmonary function].

The aim of this review is to provide a critical and concise discussion of present knowledge on the role of atrial natriuretic factor (ANF) in physiological as well as pathological pulmonary conditions. The lung contributes only to a small extent to the production of circulating ANF; on the other hand, the lung represents the major degrading site of the protein. Plasmatic ANF concentration increment during lung disease may therefore be due to a reduction in ANF plasma removal enzyme rather than to increased ANF production. Lung tissue shows more ANF receptor sites than any other organ. The effect of ANF on bronchial and pulmonary artery muscle lining is particularly evident. In fact ANF administration in asthmatic patients leads to bronchodilation comparable to dilation induced by salbutamol. Furthermore, elevated levels of circulating ANF seem to influence fluid redistribution through alveolar-capillary membrane leading to protein mobilization through the alveolar space. On the contrary, in the cardiomyopathic hamster ANF induces relevant guanylate cyclase activation before the animal has developed hemodynamic changes. Guanylate-cyclase activation may protect the lung through counteracting pulmonary edema formation, as shown by fluid reduction in alveolar spaces following pneumotoxic agents administration. This effect seems independent of natriuretic and hypotensive ANF effects.

Animals↗
PubMed1986

Effects of atrial natriuretic factor on renal function and cyclic GMP production.

Anesthetized beagle dogs received increasing doses of continuous infusions of a 26-amino-acid synthetic atrial natriuretic factor (ANF). Urinary sodium excretion rose in a dose-dependent manner to a maximum level similar to that seen after hydrochlorothiazide administration. Mean arterial blood pressure decreased, but only modestly, and not in a dose-dependent fashion. Dogs chronically retaining NaCl secondary to constriction of the thoracic inferior vena cava showed only modestly enhanced natriuresis when infused with similar levels of ANF. When ANF was infused directly into the renal artery of anesthetized beagles, a dose-dependent natriuresis and calciuresis were observed with maximal fractional sodium excretion averaging approximately 8%. Although glomerular filtration tended to increase, the average dose-related changes were not significant. Cyclic GMP excretion was increased during intra-renal-arterial infusion of ANF. Excretion of cyclic GMP by both the infused and noninfused kidneys was equal, which suggests that urinary cyclic GMP was not nephrogenous but derived from the elevated circulating levels. These and other data from rats dissociate changes in urinary cyclic GMP excretion and sodium excretion.

Animals↗
PubMed1992

Effects of atrial natriuretic peptide on myocardial contractile and diastolic function in patients with heart failure.

Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside. Mean arterial pressure decreased with atrial natriuretic peptide (89 +/- 3 to 80 +/- 2 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (90 +/- 4 to 73 +/- 3 mm Hg, p less than 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 +/- 2 to 16 +/- 3 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (24 +/- 2 to 13 +/- 3 mm Hg, p less than 0.05). Cardiac index increased during infusion of each agent from 2.0 +/- 0.2 to 2.4 +/- 0.2 liters/min per m2 (p less than 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Left ventricular systolic and diastolic function after two-stage anatomic correction of transposition of the great arteries.

Anatomic repair of transposition of the great arteries (TGA) has been developed because of concerns about right ventricular function after atrial repair by the Mustard or the Senning technique. This study assessed left ventricular systolic and diastolic function in three patients after two-stage anatomic repair. Two patients had a ventricular septal defect (one with coarctation), and the third patient had right ventricular dysfunction precluding atrial repair. All had pulmonary artery banding. The mean ages at the time of repair and catheterization were 2.75 and 4.9 years, respectively. The control group included 10 patients with insignificant or no cardiac disease. At cardiac catheterization the group with TGA had a higher mean end-diastolic volume index (110.9 +/- 4.74 ml/m2) compared to normal subjects (79.1 +/- 14.55; p less than 0.001), mean end-systolic volume index (37.3 +/- 3.69 vs 22.7 +/- 4.42; p less than 0.001), mass index (101.0 +/- 16.9 vs 68.2 +/- 12.34; p = 0.038), and stroke volume index (73.6 +/- 3.52 vs 56.5 +/- 12.1; p = 0.0027). The ejection fractions, end-diastolic and peak systolic pressures, and stresses were not different. There was no difference in the relationship between the mean rate-corrected velocity of circumferential fiber shortening and end-systolic stress for the group with TGA, but myocardial stiffness was markedly elevated (29.5 +/- 1.84 vs 10.8 +/- 2.20; p less than 0.001). Thus, this study found abnormalities of left ventricular size after two-stage anatomic repair of TGA in this group of patients with TGA.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1987

Effect of atrial natriuretic factor on renal function in rats with papillary necrosis.

The current study was designed to evaluate whether the renal papilla participates in the natriuretic and diuretic response to atrial natriuretic factor (ANF). Papillary necrosis was induced in female rats by intravenous infusion of 2-bromoethylamine hydrobromide (BEA) 48 h prior to clearance experiments; untreated (UNT) animals served as controls. Rats were anesthetized with pentobarbital sodium, tracheotomized, and catheters placed in a femoral artery and vein and in the bladder. At the time of surgery, the bladder urine was collected and its osmolality used as an indication of papillary destruction. Mean urine osmolalities (+/- SE) of BEA rats were significantly lower than those of UNT rats (443 +/- 10 vs. 1,229 +/- 57 mosmol/kg, respectively), indicating that BEA caused papillary necrosis. Synthetic ANF (rat 8-33) was given as a bolus intravenously (1.25, 2.5, 5.0 micrograms/kg). The ANF-induced increases in sodium excretion were not significantly different between UNT and BEA rats at any ANF dose. These results demonstrate that a functional papilla is not required for the action of ANF in the rat.

Animals↗
PubMed1999

Stimulation of L-type Ca2+ current in human atrial myocytes by insulin.

OBJECTIVE: The L-type calcium current (ICa,L) in isolated human atrial myocytes was investigated as a possible target of insulin in the regulation of cardiac function. METHODS: Atrial myocytes were obtained from patients undergoing cardiac surgery. Using the whole-cell configuration of the patch-clamp technique, we investigated the stimulation of ICa,L by insulin in single human atrial myocytes. RESULTS: We found a dose-dependent stimulation of ICa,L by insulin at concentrations of 100 nM, 1 microM and 10 microM. Maximum stimulation of ICa,L over basal ICa,L was 140 +/- 12% (n = 11) at 10 microM insulin. The maximum conductance of ICa,L was increased by 10 microM insulin from 4.0 +/- 0.3 nS to 8.3 +/- 1.0 nS (n = 6). The stimulation of ICa,L by insulin was dose-dependent and reversible. Isoproterenol (10 nM) that stimulates ICa,L by 271 +/- 48% (n = 10) over basal ICa,L acted faster than insulin. The half-maximum stimulation of ICa,L by isoproterenol and insulin (10 microM) was reached after 31 +/- 2 s and 52 +/- 5 s, respectively. The insulin effect shown was totally reversed by acetylcholine (3 microM) which is known to inhibit adenylyl cyclase activity/cAMP-production via Gi-proteins. Also, the selective insulin receptor tyrosine kinase inhibitor (hydroxy-2-naphthanelyl-methyl)phosphonic acid completely inhibited the insulin induced effect. CONCLUSION: Our data show that insulin stimulates the L-type calcium current in isolated human atrial myocytes in a dose-dependent and reversible manner which appears to involve the insulin receptor tyrosine kinase. Insulin regulation of ICa,L in human atrial myocytes may be an interesting system for the analysis of the metabolic syndrome in man.

Acetylcholine↗
PubMed1994

Histamine H3-receptor signaling in the heart: possible involvement of Gi/Go proteins and N-type Ca++ channels.

Discovered as inhibitory autoreceptors in central histaminergic pathways, histamine H3-receptors may also modulate peripheral cholinergic and central adrenergic function. Recently, H3-receptors were reported to inhibit adrenergic inotropic responses in guinea pig atria, possibly at prejunctional sites. We have assessed whether the H3-mediated modulation of cardiac adrenergic activities results from a reduction in norepinephrine release. We have found that (R) alpha-methylhistamine, the selective histamine H3-receptor agonist, attenuates the inotropic and chronotropic response of isolated guinea pig atria to transmural stimulation of adrenergic nerve endings. This attenuation was associated with a marked reduction in endogenous norepinephrine release. In contrast (R) alpha-methylhistamine did not modify the chronotropic effect of exogenous norepinephrine. The attenuation of adrenergic responses by (R) alpha-methylhistamine was 1) prevented by thioperamide, the selective H3-receptor antagonist; 2) attenuated by pertussis-toxin pretreatment and 3) potentiated by the N-type Ca(++)-channel blocker omega-conotoxin, which also potentiated the sympathetic modulatory effects of adrenergic-alpha 2 and adenosine-A1 receptor agonists. Our findings indicate that prejunctional histamine H3-receptors modulate the depolarization-dependent norepinephrine release from sympathetic nerve endings in the guinea pig myocardium. These receptors are probably coupled to a pertussis-toxin-sensitive Gi/Go protein and probably effect a reduction in Ca++ current. We have previously reported that sympathetic stimulation elicits a frequency-dependent release of cardiac histamine, whereas others had found that adrenergic activity regulates histamine's rapid turnover pool. Accordingly, presynaptic H3-receptors are likely to serve a modulatory role in cardiac adrenergic function.

Adrenergic Fibers↗