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PubMed1986

Electrophysiologic cardiac function before and after surgery in children with atrioventricular canal.

Thirty-two children with atrioventricular (AV) canal underwent electrophysiologic studies: 18 underwent preoperative studies at a median age of 3 years (range 6 months to 16 years); 14 underwent postoperative studies at a median age of 4 years (range 2 to 19); and 2 underwent both preoperative and postoperative matched studies. In the preoperative group the following abnormalities were observed: first-degree AV block in 5 patients (due to internodal conduction delay in 1, AV nodal conduction delay in 2 and normal intracardiac intervals in 2); internodal conduction delay but normal PR interval in 4; and disease of the sinus node in only 1. In the postoperative group the following abnormalities were observed: first-degree AV block in 9 (due to AV nodal conduction delay in 2, His-Purkinje system conduction delay in 1, upper normal intracardiac intervals in 3 and unidentified in 3); prolongation of the right ventricular apical activation time in 11 of 13 with right bundle branch block; abnormal sinus node function in 3; and abnormal AV nodal function in 4 (1 of whom had associated sinus node disease). Atrial and ventricular functions were normal in all preoperative and postoperative patients. Electrophysiologic dysfunction is rare in preoperative patients with AV canal; in postoperative patients electrophysiologic abnormalities occur in 38% and involve the sinus and AV nodes in 19 and 25%, respectively.

Adolescent↗
PubMed1990

Emulation of conduction system functions in the hearts of early mammalian embryos.

The conduction system functions of atrioventricular sequential contractions, atrioventricular delay, and coordination of ventricular contraction were examined in rat embryos at the earliest functional stage of cardiac development (before cardiac looping, n = 6) and shortly after looping (n = 15). Atrioventricular sequential contractions were observed in all embryos, and contractions appeared to originate in the left sinus horn. Atrioventricular delay was present in both prelooped (132 +/- 32 ms) and looped (141 +/- 15 ms) hearts. Before looping, contractions traveled from proximal ventricle to bulbus cordis, a distance of 253 +/- 27 microns, in 72 +/- 22 ms. After looping, contractions crossed an increased intraventricular distance (520 +/- 28 microns, p less than 0.005) in substantially less time (16 +/- 7 ms, p less than 0.005). Sinoatrial and atrioventricular nodal functions are emulated in both prelooped and looped hearts of early mammalian embryos, and His-Purkinje system function is emulated in looped hearts.

Animals↗
PubMed1999

Maze procedure and homograft replacement of a rheumatic mitral valve.

A 64-year-old woman presented with congestive heart failure due to severe mitral valve stenosis and chronic atrial fibrillation. A Maze III procedure was performed, and the mitral valve replaced with a mitral homograft. Postoperatively, the patient regained normal sinus rhythm, had trivial mitral regurgitation, regained her atrial transport function, and had improved myocardial function.

Atrial Fibrillation↗
PubMed1997

Effects of atrial fibrillation on left ventricular function and geometry in mitral stenosis.

This study shows that patients with mitral stenosis have depressed left ventricular ejection performance and spherical remodeling of the left ventricular cavity, which is more marked in those with atrial fibrillation. These changes have important clinical implications regarding treatment strategy in patients with mitral stenosis and chronic atrial fibrillation.

Atrial Fibrillation↗
PubMed1984

Occult thyrotoxicosis in patients with chronic and paroxysmal isolated atrial fibrillation.

Thyroid function tests, including thyrotropin releasing hormone administration (TRH), were performed in 40 consecutive patients with isolated atrial fibrillation (IAF) (i.e., without any other evidence of cardiac disease). The arrhythmia was chronic in 5 and paroxysmal in 35 patients. Thyrotoxicosis could not be diagnosed either clinically or by abnormal serum levels of T4, T3, T3 BC, and thyroid stimulating hormone (TSH). Thyroid stimulating hormone response to TRH, which was normal in 35 patients, was absent in 5 (12.5%) who were considered to have occult thyrotoxicosis. One had chronic and the other 4 had paroxysmal IAF. The arrhythmia did not recur after antithyroid treatment in these four patients who were in sinus rhythm after a mean follow-up period of 21 months. Full exploration of the thyroid function therefore seems useful not only in patients with chronic IAF, but also in those affected by the paroxysmal form.

Adult↗
PubMed1989

Characteristics and specific localization of receptors for atrial natriuretic peptides at non-neuronal cells in cultured mouse spinal cord cells.

Characteristics of atrial natriuretic peptide receptors were determined in cultured mouse spinal cord cells. Saturation and competition experiments demonstrated the presence of a single class of atrial natriuretic peptide binding sites with high affinity (KD = 0.054 nM) and a density of 1.92 fmoles/10(6) cells. A similar affinity (KD = 0.070 nM) was observed in rat spinal cord membrane preparations. These atrial natriuretic peptide binding sites were functional receptors since the treatment of cells with atrial natriuretic peptide increased cyclic guanosine monophosphate levels within these cells in a classical time-dependent manner. When atrial natriuretic peptide was applied onto the cell body of intracellularly recorded spinal cord neurons, this peptide did not evoke a change of the input resistance or of the resting membrane potential value. Light-microscopic autoradiography studies showed that no atrial natriuretic peptide binding could be detected on typical birefringent neurons but it could be located on astroglial and epithelial cells as identified by immunocytochemical markers. These results show that functional atrial natriuretic peptide receptors with high affinity exist in cultured mouse spinal cord cells and are not located on neurons. The presence of atrial natriuretic peptide receptors on astrocytes suggests that this neuropeptide might be a good candidate for neuron-glial communication. As the atrial natriuretic peptide binding sites previously shown in epithelia responsible for maintaining fluid and electrolyte gradients, the atrial natriuretic peptide receptors on epithelial cells in these spinal cord cultures may be involved in vivo in the control of water balance in the central nervous system.

Animals↗
PubMedDate not supplied

Pulmonary venous velocity patterns in mitral stenosis.

Pulmonary venous (PV) velocities obtained by transthoracic echocardiography are used to assess diastolic function. The systolic/diastolic (S/D) PV velocity ratio is increased with impaired early diastolic filling and decreased with elevated mean left atrial pressure (LAP). Mitral stenosis (MS) is characterized by impaired filling and elevated LAP. We hypothesized that the S/D ratio would be increased in MS except in severe MS with high LAP, in which the S/D ratio would be decreased. Patients with isolated MS who underwent transthoracic echocardiography were studied. The PV S/D ratio was compared in mild (n = 18), moderate (n = 16), and severe (n = 7) MS. There was no characteristic PV pattern, with each category showing a wide range of S/D ratios (mild, S/D ratio = 1.42 +/- 0.56; moderate, S/D ratio = 1.19 +/- 0.59, and severe, S/D ratio = 1.33 +/- 0.53) (mean +/- SD). Furthermore, there was no relationship between the S/D ratio and any index of severity of MS. There is no characteristic PV velocity pattern in MS.

Atrial Function, Left↗
PubMed2002

Human cardiac inwardly-rectifying K+ channel Kir(2.1b) is inhibited by direct protein kinase C-dependent regulation in human isolated cardiomyocytes and in an expression system.

BACKGROUND: Protein kinases A (PKA) and C (PKC) are activated in ischemic preconditioning and heart failure, conditions in which patients develop arrhythmias. The native inward rectifier potassium current (IK1) plays a central role in the stabilization of the resting membrane potential and the process of arrhythmogenesis. This study investigates the functional relationship between PKC and IK1. METHODS AND RESULTS: In whole-cell patch-clamp experiments with isolated human atrial cardiomyocytes, the IK1 was reduced by 41% when the nonspecific activator of PKC phorbol 12 myristate 13-acetate (PMA; 100 nmol/L) was applied. To investigate the effects of PKC on cloned channel underlying parts of the native IK1, we expressed Kir(2.1b) heterologously in Xenopus oocytes and measured currents with the double-electrode voltage-clamp technique. PMA decreased the current by an average of 68%, with an IC50 of 0.68 nmol/L. The inactive compound 4-alpha-PMA was ineffective. Thymeleatoxin and 1-oleolyl-2-acetyl-sn-glycerol, 2 specific activators of PKC, produced effects similar to those of PMA. Inhibitors of PKC, ie, staurosporine and chelerytrine, could inhibit the PMA effect (1 nmol/L) significantly. After mutation of the PKC phosphorylation sites (especially S64A and T353A), PMA became ineffective. CONCLUSIONS: The human IK1 in atrial cardiomyocytes and one of its underlying ion channels, the Kir(2.1b) channel, is inhibited by PKC-dependent signal transduction pathways, possibly contributing to arrhythmogenesis in patients with structural heart disease in which PKC is activated.

Amino Acid Sequence↗
PubMed1986

[Sinus node function of ischemic heart disease patients with chronotropic incompetence].

Forty-five (17.6%) of 256 coronary patients showed inadequately small heart rate augmentation in response to rationed exercise ("chronotropic incompetence"). To assess their sinoatrial node function, esophageal atrial stimulation was done in all patients before and after drug-induced vegetative block, and the adjusted sinoatrial node function time and sinoatrial conduction time were determined. Electrophysiological evidence suggests that "chronotropic incompetence" is in most cases determined by abnormal sinoatrial rhythm. Rationed exercise testing can be used as a screening test for latent weak sinoatrial node syndrome in coronary patients.

Angina Pectoris↗
PubMed1994

[Cor triatriatum sinistrum and atrial septal defect].

The cor triatriatum sinistrum is a rare congenital malformation. Frequently, the patients become symptomatic in infancy with clinical signs of severe congestive heart failure. We report on an adult patient with only mild symptoms with cor triatriatum sinistrum and atrial septal defect. The embryological basis of the disorder and the hemodynamic conditions which permitted this patient to remain symptom free for a long period are discussed.

Atrial Function, Left↗
PubMed1991

An atrial natriuretic factor analogue at low doses attenuates forearm reflex vasoconstriction to cardiopulmonary receptor deactivation in patients with hypertension.

Contrasting data exist about a possible modulation of the autonomic function by atrial natriuretic factor (ANF) in human beings, particularly at low, biologically, significant concentrations. We have evaluated that possibility by increasing plasma ANF levels through the infusion of a synthetic analogue (WY-47,663, anaritide) in five male patients with mild to moderate uncomplicated hypertension. Nonhypotensive lower body negative pressure (-10 mm Hg x 5 min) was used to selectively deactivate cardiopulmonary receptors and to stimulate sympathetic efferent tone reflexogenically. ANF was given at either a low rate (0.005 micrograms/kg/min x 60 min, which was previously shown to increase plasma ANF in a range compatible with physiologic stimuli) or at a high rate (0.05 micrograms/kg/min x 60 min, each). Administration of ANF was preceded and followed by vehicle infusion (Haemacell x 30 min). Forearm blood flow (venous plethysmography), intraarterial blood pressure, and heart rate were monitored continuously, and venous immunoreactive ANF, plasma renin activity, aldosterone level, and venous hematocrit were measured at the end of both control and infusion periods. Arterial norepinephrine values, an indirect index of sympathetic discharge, were measured at rest and during lower body negative pressure conditions. Graded systemic ANF infusion increased immunoreactive ANF and venous hematocrit, decreased aldosterone level and plasma renin activity, whereas resting norepinephrine levels, blood pressure, and heart rate did not change. Lower body negative pressure decreased forearm blood flow during vehicle infusion, but it lost its vasoconstrictor effect during infusion of ANF. To identify the site of that inhibitory action, ANF was also infused into the brachial artery at rates that raised local but not systemic levels of immunoreactive ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Effects of exercise on natriuretic peptides and cardiac function in man.

We evaluated cardiac function and the plasma levels of atrial (ANP) and brain (BNP) natriuretic peptides during bicycle (B) and hand-grip (HG) exercises in eight healthy males. Each test was preceded by a control protocol in resting conditions. Left ventricular (LV) function (echocardiography) was evaluated during both exercises. Atrial function was assessed only during HG. Plasma ANP significantly increased during B (+236%) and HG (+77%), while there was a significant trend towards higher plasma BNP levels during B (+41%) and HG (+30%) than during the corresponding control tests. Plasma ANP correlated with heart rate in both tests, with left atrial volume, pulmonary vein flow systolic fraction and mitral flow E/A ratio in HG; BNP in both test correlated with LV dimensions and function. These data suggest that during exercise the cardiac release of ANP and BNP is differently regulated and related to changes in left atrial and LV function, respectively.

Adult↗
PubMed2005

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↗
PubMed1994

Functional beta-adrenoceptors in the left atrium of normotensive and hypertensive rats.

1. The aim of the study was to characterize the functional beta 1-and beta 2-adrenoceptors of the rat left atrium and to investigate how these functional beta-adrenoceptor responses were altered in hypertension. The contractile responses of the left atrium from Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rats to isoprenaline, T-0509 and procaterol were characterized. Subsequently, the effects of selective beta 1-(bisoprolol) and beta 2 (ICI 118,551)-adrenoceptor antagonists were investigated on these responses. 2. The maximal combined contractile responses of the rat left atrium to cardiac stimulation and CaCl2, isoprenaline, T-0509 or procaterol were not altered by hypertension. 3. The sensitivities to CaCl2 (pD2 on WKY left atrium = 2.99), isoprenaline (8.82) and T-0509 (8.84) were not altered by hypertension. There was an increase in sensitivity to procaterol from a pD2 value of 7.21 to 7.61 in the left atrium of the SH rat. 4. The basal tension induced by cardiac stimulation alone was inhibited by bisoprolol at > or = 10(-8) M and by ICI 118,551 at > or = 10(-7) M and this inhibitory effect is probably due to membrane stabilizing activity. 5. The pKB values for bisoprolol against isoprenaline, T-0509 and procaterol on the WKY were 8.43, 8.68 and 8.18, respectively, and were not different from SH rat left atrium. 6. The pKB value for ICI 118,551 against isoprenaline was increased from 7.06 on the WKY to 7.44 on the SH rat left atrium. The pKB values for ICI 118,551 against T-0509 and procaterol on the WKY were 7.18 and 8.14, respectively and were not significantly different from the SH rat left atrium values. 7. These results suggest that: (a) procaterol stimulates the beta 1-, in addition to, the beta 2-adrenoceptors of the rat left atrium; (b) functional beta 1-adrenoceptors are not altered in hypertension, and (c) there is probably an increase in the affinity of procaterol and isoprenaline for the beta 2-adrenoceptors which underlies the small increase in the functional beta 2-adrenoceptor response in hypertension.

Animals↗
PubMed1998

First experience with an automatic sensing algorithm in single-lead VDD stimulation.

UNLABELLED: An "Autosensing" algorithm available in SSI(R) and DDR(R) pacemakers automatically adapts the device's sensitivity to changing intracardiac signals. The atrial sensing function of this algorithm was tested for the first time with a VDD pacing system in which large variations of the atrial signal may occur because the atrial electrodes float in the atrial blood pool. METHODS: 15 patients with a VDD pacing system were studied (Unity 292-07, lead 425; Sulzer Intermedics). The atrial sensing threshold was measured, and the atrial sensitivity was programmed with a 2:1 safety margin. The autosensing algorithm and sensitivity profile were temporarily activated, and an ambulatory ECG with continuous marker annotation was recorded. All patients underwent a 30-minute daily life activities protocol. A beat-to-beat analysis of the ambulatory ECG was correlated with the changes in atrial sensitivity. RESULTS: The algorithm changed the baseline sensitivity from 0.57 +/- 0.23 mV during the test to 0.39 +/- 0.20 mV after the final rest period (P < 0.05). During the test 12.6 +/- 10.2 adaptations of the sensitivity occurred (range 0-33). In eight patients atrial undersensing occurred in 4.4% +/- 7.5% of the cycles (4-458 unsensed P waves). In these patients, the algorithm continuously adjusted the sensitivity towards more sensitive values, operating 19.1 +/- 18.3 changes compared with 5.4 +/- 7.3 changes in patients without undersensing (P = 0.009). Oversensing did not occur. CONCLUSION: The autosensing algorithm effectively optimized atrial sensitivity in VDD pacing. In patients with atrial undersensing the algorithm continuously remained near the most sensitive settings, thus reacting as intended. A faster sensitivity adjustment of the system would be desirable.

Activities of Daily Living↗