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PubMed2005

Closure of atrial septal defect in the adult. Cardiac remodeling is an early event.

BACKGROUND: Study aimed to describe the extent and the temporal profile of cardiac remodeling after atrial septal defect closure in the adult. METHODS: Prospective and longitudinal echocardiographic assessment of right and left heart size before and after (1 day-1 week/1/4/12 months) surgical or catheter-based atrial septal closure in 39 adults (age 54+/-15 years). RESULTS: Right ventricular and atrial sizes were markedly reduced, left ventricular size increased and left atrial size remained unchanged after closure. Older age and a history of atrial fibrillation reduced the potential to normalize right and left atrial size after closure. The greater part of the changes occurred very early, in the 1st day/1st week. From then on the speed of change gradually diminished and after 4 months no important changes were observed. The mode of closure did not influence the degree or the pace of the remodeling. CONCLUSION: Cardiac remodeling after atrial septal closure in the adult is a common and early event that seems by and large completed within the first half year after closure. The ventricles seem to have a higher capacity of remodeling than the atria in this setting. The mode of closure does not seem to significantly impact remodeling.

Adult↗
PubMed2003

Intrinsic cardiac nervous system in tachycardia induced heart failure.

The purpose of this study was to test the hypothesis that early-stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiac function. After 2 wk of rapid ventricular pacing in nine anesthetized canines, cardiac and right atrial neuronal function were evaluated in situ in response to enhanced cardiac sensory inputs, stimulation of extracardiac autonomic efferent neuronal inputs, and close coronary arterial administration of neurochemicals that included nicotine. Right atrial neuronal intracellular electrophysiological properties were then evaluated in vitro in response to synaptic activation and nicotine. Intrinsic cardiac nicotine-sensitive, neuronally induced cardiac responses were also evaluated in eight sham-operated, unpaced animals. Two weeks of rapid ventricular pacing reduced the cardiac index by 54%. Intrinsic cardiac neurons of paced hearts maintained their cardiac mechano- and chemosensory transduction properties in vivo. They also responded normally to sympathetic and parasympathetic preganglionic efferent neuronal inputs, as well as to locally administered alpha-or beta-adrenergic agonists or angiotensin II. The dose of nicotine needed to modify intrinsic cardiac neurons was 50 times greater in failure compared with normal preparations. That dose failed to alter monitored cardiovascular indexes in failing preparations. Phasic and accommodating neurons identified in vitro displayed altered intracellular membrane properties compared with control, including decreased membrane resistance, indicative of reduced excitability. Early-stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiodynamics. While maintaining its capacity to transduce cardiac mechano- and chemosensory inputs, as well as inputs from extracardiac autonomic efferent neurons, intrinsic cardiac nicotine-sensitive, local-circuit neurons differentially remodel such that their capacity to influence cardiodynamics becomes obtunded.

Animals↗
PubMed1990

Modulation of electrophysiological properties of neonatal canine heart by tonic parasympathetic stimulation.

The effects of tonic right and left vagal stimulation (RVS and LVS) on electrophysiological properties of the immature myocardium and specialized conduction system were evaluated in 11 neonatal canines pretreated with propranolol (1 mg/kg iv). Electrophysiological studies were performed by recording intracardiac electrograms from multiple endocardial catheters during programmed electrical stimulation. Assessments were made of sinus node function, intra-atrial, atrioventricular (AV) nodal and His-Purkinje conduction, and atrial and ventricular refractoriness in the control state and during RVS and LVS at 4-12 Hz. Vagal stimulation prolonged the sinus cycle length; RVS produced a 38% increase and LVS a 25% increase at 8 Hz (P less than 0.01). There were no changes in the intra-atrial or His-Purkinje conduction times. Comparable increases occurred during RVS and LVS in the paced cycle length resulting in AV nodal Wenckebach, the AV nodal conduction time at a paced cycle length of 340 ms, and the effective and functional refractory periods of the AV node, suggesting symmetrical influences of the right and left vagus on neonatal AV nodal function. Right atrial effective and functional refractory periods shortened significantly during vagal stimulation (ERP, 36% RVS and 23% LVS; FRP, 27% RVS and 15% LVS), and in 5 of 11 neonates, a sustained regular atrial tachyarrhythmia was induced during atrial extra-stimulation. Small yet significant increases were observed in the right ventricular ERP and FRP during vagal stimulation. This study provides information regarding the functional integrity of the parasympathetic nervous system and its potential role as a modulator of the electrophysiological properties of the newborn heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Doppler tissue imaging analysis of ventricular function after surgical and transcatheter closure of atrial septal defect.

The long-term ventricular function of children after surgical and transcatheter closure of secundum atrial septal defects was assessed by Doppler tissue imaging and compared with that of age-matched controls. Long-term right ventricular function was impaired in patients after surgical repair, as reflected by decreased systolic and diastolic tricuspid annular velocities and an increased Tei index. In contrast, right ventricular function was preserved after transcatheter device closure.

Adolescent↗
PubMed1990

[Left ventricular function (based on two-dimensional echocardiographic data) during bicycle ergometry and transesophageal electrical stimulation of the atria in patients with hypertrophic cardiomyopathy].

The central hemodynamics was studied and compared in 20 patients with hypertrophic cardiomyopathy (HCMP) at rest, during bicycle ergometry (BEM) and transesophageal pacing of the atria (TEPA). According to the BEM readings, HCMP patients did not show any material differences from normals' reaction to exercise on the part of the volumetric and hemodynamic parameters as well as left ventricle contractile function. At the same time as revealed by TEPA, HCMP patients did manifest differences from normals' response in the hemodynamics and myocardial contractility. Alterations that occur in HCMP patients undergoing TEPA in response to an isolated increase of frequency of the cardiac rhythm are likely to reflect latent disorders of systolic function of the asymmetric hypertrophied left ventricle which is not capable of making adequate volumetric and functional restructure.

Adult↗
PubMed1983

The relationship of human atrial cellular electrophysiology to clinical function and ultrastructure.

Although previous studies have described the electrophysiological and ultrastructural characteristics of human cardiac fibers, no attempt has been made as yet to describe quantitatively the relationship between the ultrastructural and cellular electrophysiological derangements occurring with cardiac disease, and their clinical manifestations. In this study, we used standard microelectrode techniques to record the action potential characteristics of human atrial fibers obtained during cardiac surgery and correlated the electrophysiological parameters with clinical and ultrastructural data. Ultrastructure was studied by optical and electron microscopy. We found a multiple linear regression among maximum diastolic potential, atrial size and pressure, P wave duration and ultrastructure changes. Proliferations of Z band material, widening of intercalated discs, and degenerative changes were quantified and correlated with electrophysiological and clinical data. These studies emphasize the relationship between hemodynamic anomalies and resultant changes in both human atrial fiber structure and electrical function. Finally, the likelihood of occurrence of arrhythmias can be predicted using the analytic method described.

Adolescent↗
PubMed1986

The effect of bicycle exercise and atrial pacing on left ventricular volume and function in healthy persons and in patients with coronary artery disease. An echocardiographic study.

The haemodynamic response to submaximal exercise and atrial pacing in 30 healthy subjects and in 30 patients with coronary artery disease was investigated by M-mode echocardiography. In healthy subjects, the cardiovascular function after atrial pacing was not altered substantially. Exercise, however, caused a marked improvement in haemodynamics, which was due to increased myocardial contractility and diminished afterload. On the other hand, in patients with coronary artery disease, both after exercise and after atrial pacing a significant deterioration of left ventricular function was observed.

Adult↗
PubMed2003

Abnormal sinus node function in clinical arrhythmias.

To understand abnormal sinus node function in clinical atrial arrhythmias, it is essential to understand the normal function of the sinus node. Much of our understanding of the sinus node comes from work done in rabbits. In small animals, the node is a thin structure and can be modeled in two dimensions. However, in canines and humans, the node is a more complex structure completely surrounded by myocytes. Recent data suggest that the node may be insulated from the surrounding atrial myocytes, except at a limited number of exit sites. A model of the node with discrete exit sites explains how atrial activation can be initiated from multiple sites simultaneously. Within the node there may exist specialized pathways that explain the complex conduction within the node. Multiple cell types, with different intrinsic rates, combined with the nonuniform distribution of autonomic receptors, provide a basis for understanding the dynamics of heart rate control and the initiation of atrial activation. In addition, this model of the sinus node provides a framework to propose novel mechanisms underlying various atrial arrhythmias, such as atrial premature depolarizations or sinus node reentry.

Action Potentials↗
PubMed2001

Reversible impairment of left and right ventricular systolic and diastolic function during short-lasting atrial fibrillation in patients with an implantable atrial defibrillator: a tissue Doppler imaging study.

AF with a fast ventricular response may cause ventricular mechanical impairment, though whether short-lasting AF with satisfactory rate control may affect ventricular function is unknown. This study investigated if prompt cardioversion by an implantable atrial defibrillator (IAD) may prevent left (LV) and right ventricular (RV) systolic and diastolic dysfunction. Ten patients (mean age 61 +/- 9 years, 8 men) with paroxysmal AF without structural heart disease who received an IAD were studied by echocardiography and tissue Doppler imaging (TDI) for both ventricles. Measurements were made during baseline sinus rhythm and at 1-minute, 20-minute, 4-hour, and 1-week postcardioversion of an episode of spontaneous AF. The occurrence of AF and the ventricular rate were monitored at 2-hour intervals by the device. There were 50 episodes of AF with a mean duration of 8.8 +/- 8.9 days (2 hours to 37 days). There was no difference in M-mode measured LV fractional shortening and ejection fraction between baseline sinus rhythm and after cardioversion. However, the TDI derived myocardial systolic velocity (TDI-S) was significantly lower at 1-minute postcardioversion and was normalized at 1 week in both LVs (baseline: 5.7 +/- 1.8, 1 minute: 4.2 +/- 1.0, 20 minutes: 4.3 +/- 0.9, 4 hours: 4.8 +/- 1.0, 1 week: 5.5 +/- 1.8 cm/s; P < 0.005 when comparing 1 minute and 20 minutes to baseline; P < 0.05 when comparing 4 hour to baseline) and RV (baseline: 10.4 +/- 2.1, 1 minute: 7.8 +/- 1.4, 20 minutes: 8.1 +/- 1.2, 4 hours: 9.2 +/- 1.5, 1 week: 10.0 +/- 2.0 cm/s; P < 0.005 when comparing 1 minute, 20 minutes, and 4 hours to baseline). For diastolic function, transmitral Doppler study showed a decrease in early filling velocity at 1 minute (P < 0.05) and 20 minutes (P < 0.005), which was normalized at 4 hours. There was no change in transtricuspid Doppler flow. However, TDI derived myocardial early filling velocity was decreased in the LV (baseline: 6.0 +/- 2.8, 1 minute: 5.4 +/- 2.3, 20 minutes: 5.4 +/- 2.1, 4 hours: 6.1 +/- 2.2, 1 week: 5.8 +/- 1.7 cm/s; P < 0.05 when comparing 1 minute and 20 minutes to baseline) and RV (baseline: 8.9 +/- 3.5, 1 minute: 7.9 +/- 3.3, 20 minutes: 8.1 +/- 3.3, 4 hours: 8.5 +/- 2.9, 1 week: 8.4 +/- 3.5 cm/s; P < 0.05 when comparing 1 minute to baseline). AF of a longer duration (> 48 hours) resulted in a more depressed TDI-S in LV (> 48 hours: 4.2 +/- 1.0, < or = 48 hours: 5.3 +/- 1.3 cm/s; P < 0.01). Shocks in sinus rhythm did not affect any of the above echocardiographic parameters. Therefore, despite adequate rate control, short-lasting AF impairs systolic and diastolic function in both ventricles, which improves gradually after cardioversion. Early restoration of sinus rhythm by an IAD minimizes ventricular dysfunction. TDI is a sensitive tool to assess early systolic and diastolic dysfunction.

Atrial Fibrillation↗
PubMed1988

Effect of low dose infusion of atrial natriuretic peptide on renal function in man.

1. The effects of the infusion of a low dose (2 pmol min-1 kg-1 for 3 h) of human atrial natriuretic peptide (hANP) were studied in seven healthy volunteers undergoing a water diuresis. Lithium clearance was used to monitor proximal tubular function. 2. hANP increased urine flow rate, sodium, calcium and magnesium excretion without significant changes in potassium and phosphate excretion, heart rate or blood pressure. 3. hANP caused a small change in fractional lithium clearance, and larger changes in distal nephron handling of sodium and water. 4. Plasma renin activity tended to decrease during the infusion of hANP, while plasma aldosterone concentration decreased during and increased after stopping the infusion of hANP. 5. The data suggest that hANP inhibits the reabsorption of sodium and water by an action on distal segments of the nephron and perhaps the proximal tubule. Inhibition of renin and aldosterone secretion may contribute to the natriuresis.

Adult↗
PubMed1982

Left atrial size and left ventricular function in coronary artery disease: an echocardiographic-angiographic correlative study.

M-mode echocardiography was used to determine left atrial size in 100 patients with coronary artery disease undergoing cardiac catheterization. Patients were divided in two groups on the basis of left atrial diameter (greater than or equal to 40 mm in 40 patients and less than 40 mm in 60). Patients with larger left atria had a higher frequency of electrocardiographic evidence of left atrial abnormality (p less than 0.01) and myocardial infarction (p less than 0.001). Pulmonary capillary wedge and left ventricular end-diastolic pressures were higher (p less than 0.005) in patients with larger left atria. An abnormal end-diastolic volume (greater than 100 ml/M2) was observed in 13 patients with enlarged left atria compared to none with normal left atrial size (p less than 0.001). Triple vessel disease was more frequent (63% vs 32%) and single vessel disease less frequent (10% vs 37%) in patients with larger left atria (p less than 0.005). Abnormal left ventricular contractile patterns were noted in 45% of patients with normal left atrial diameters compared to 80% in those with an enlarged left atrium (p less than 0.001). An abnormally low ejection fraction (less than 0.5) was observed in 25% and 80%, respectively, in patients with normal and enlarged left atria (p less than 0.001). Of 58 patients with normal ejection fractions, only 17% had left atrial diameters greater than or equal to 40 mm compared to 71% of 42 patients with abnormally low ejection fractions (p less than 0.001). Of 18 patients with left atrial diameters greater than 42 mm, only two had normal ejection fractions. The mean ejection fraction for patients with left atrial diameters less than 40 mm was 0.63 +/- 0.13 compared to 0.41 +/- 0.18 for those with diameters greater than or equal to 40 mm (p less than 0.001). The sensitivity, specificity, and predictive value for an enlarged left atrium in identifying an abnormal ejection fraction were, respectively, 71, 83, and 75%. These findings indicate that M-mode echocardiographic left atrial enlargement is a useful marker of advanced hemodynamic and angiographic abnormality in patients with coronary artery disease.

Adult↗
PubMed2001

Intracellular calcium changes and tachycardia-induced contractile dysfunction in canine atrial myocytes.

OBJECTIVES: Indirect evidence suggests a role for Ca(2+)-overload in electrical and mechanical alterations caused by atrial tachycardia. The present study assessed the alterations in cellular [Ca(2+)] and contractile function caused by rapid atrial cellular activation. METHODS: Intracellular Ca(2+) transients (CaT) and cell shortening (CS) were measured by microfluorometry (Indo-1 AM) and video edge-detection in isolated, field-stimulated canine atrial myocytes (37 degrees C). RESULTS: Abrupt increases in frequency (0.3-3 Hz) caused rapid increases in diastolic [Ca(2+)]i (DCa) that were maintained during rapid-pacing for up to 50 min. When short-term (3-min) rapid-pacing was imposed, CaT and CS increased initially upon returning to 0.3 Hz, but then declined rapidly to 64+/-5 and 49+/-7%, respectively, of pre-tachycardia values, returning to control after approximately 15 min. Post-tachycardia CaT and CS reductions were prevented by decreasing [Ca(2+)]o during tachycardia to prevent Ca(2+)-overload. CS reductions correlated with indices of Ca(2+) loading during tachycardia. Restoration of CaT to normal during post-tachycardia contractile dysfunction (by increasing [Ca(2+)]o) returned CS to normal, indicating that reduced Ca(2+) release, not reduced myofilament Ca(2+)-sensitivity, caused post-tachycardia contractile failure. Estimation of sarcoplasmic-reticulum Ca(2+)-stores (caffeine-induced Ca(2+)-release) confirmed tachycardia-induced Ca(2+)-loading and suggested that reduced Ca(2+)-stores decreased Ca(2+)-release post-tachycardia. CONCLUSIONS: Atrial tachycardia increases cellular Ca(2+)-loading, leading to post-tachycardia abnormalities in Ca(2+)-handling that produce contractile dysfunction. These findings are the first direct evidence for the frequently-postulated role of Ca(2+)-overload in tachycardia-induced abnormalities of atrial function.

Animals↗
PubMed1995

The effect of pathophysiology on the surgical treatment of ischemic mitral regurgitation: operative and late risks of repair versus replacement.

Operative correction of ischemic mitral regurgitation (IMR) is associated with high risk approach. The objective of this retrospective study was to examine the interaction between the various underlying pathophysiologic mechanisms, the operative procedure, and their influence on short- and long-term outcomes. Over a 10-year period starting January 1984, mitral valve repair or replacement was performed on 150 patients with IMR. The age range was 42-86, mean 67, years; 71 (47%) were females; 139 (93%) were in NYHA functional class III or IV; 23 (15%) were reoperations; and 30 (20%) were in atrial fibrillation. Functional IMR due to annular dilatation or restrictive leaflet motion was present in 106 (71%), and structural IMR due to ruptured chordae or papillary muscle in 44 (29%). Mitral valve repair was performed in 94 (63%) with an annuloplasty ring employed in 80 (85%) patients. Mitral valve replacement was performed in 56 (37%), with 40 (71%) receiving a bioprosthesis (32 Hancock and 8 Carpentier-Edwards valves) and 16 (29%) a St. Jude valve. Coronary artery bypass graft surgery was performed in 139 (93%) patients. The overall operative mortality (OM) was 14/150 (9.3%). The OM for repair was 9.5% compared to 8.9% for replacement (P = NS). There was higher OM in the elderly, particularly in the repair group (P = 0.053), and a trend towards reduced OM in the recent years of the study (P = NS). No predictors of OM were identified by multivariate logistic regression analysis. Long-term follow-up was 98% complete and ranged from 2-120, mean 31.2, months for a total of 935 patient-years. The overall 5-year survival rate was 71 +/- 6%, with 91 +/- 5% for the replacement group compared to 56% +/- 10% for the repair group (P = 0.01). The functional subset of IMR who had a repair had the worse long-term survival (43 +/- 13%) compared to the structural/repair (76 +/- 13%) and structural/replacement groups (89 +/- 8%), and 92 +/- 7% for the functional/replacement group ((P = 0.0049). Multivariate logistic regression analysis identified the functional/repair group (hazards ratio 4.4; +/- 95%, confidence interval 1.6, 11, (P = 0.0031); and earlier years of surgery (hazards ratio 4.7; +/- 95% confidence interval 1.021; (P = 0.046) to be predictors of worse long-term survival. These results suggest that, in IMR, the underlying responsible pathophysiologic mechanisms appear to be the major determinants of survival, rather than the choice of the operative procedure.

Adult↗
PubMedDate not supplied

The effects of verapamil on the electrophysiology of the intact immature mammalian heart.

The electrophysiologic effects of intravenous verapamil were compared in six intact neonatal puppies ages 3-15 days and in adult dogs. Utilizing standard intracardiac recording and programmed stimulation techniques, sinus and AV nodal function and atrial and ventricular refractory periods were determined following incremental intravenous doses of 0.075 mg/kg, 0.15 mg/kg, and 0.30 mg/kg of verapamil. In the neonate, intravenous verapamil resulted in a significant increase of the sinus cycle length (37 +/- 6%) but no changes occurred in either the percent sinus node recovery time or the corrected sinus node recovery time. The atrial effective refractory period was prolonged by verapamil (32 +/- 12%). Concerning atrioventricular (AV) nodal function, verapamil produced a small but significant prolongation of resting AH interval (50.5 +/- 2.4 ms (control) versus 57.3 +/- 4.7 ms post 0.30 mg/kg) and a dose-related prolongation of the paced cycle length resulting in AV nodal Wenckebach (170 +/- 12.8 ms control, 190 +/- 10.3 ms post 0.075 mg/kg, 215.8 +/- 13.0 ms post 0.15 mg/kg and 246.7 +/- 22.8 ms post 0.30 mg/kg). The effective refractory period (ERP) and functional refractory period (FRP) of the atrioventricular node (AVN) were prolonged in a dose-dependent fashion (ERP-AVN: 75 +/- 19% increase, FRP-AVN: 42 +/- 14% increase). Retrograde conduction, present in all six neonates, was completely abolished in four of six subjects and significantly prolonged in one other puppy by verapamil. No changes in ventricular refractory periods were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Labelling with [125I]-SB 207710 of a small 5-HT4 receptor population in piglet right atrium: functional relevance.

1. We investigated the affinity of SB 207710 for sinoatrial 5-HT4 receptors and the density of right atrial 5-HT4 receptors with [125I]-SB 207710 in right atria of new-born piglets. 2. SB 207710 (1-100 nM) antagonized the 5-HT-evoked tachycardia surmountably with a pKB of 9.8. 3. [125I]-SB 207710 (5-1500 pM) labelled a small population of saturable binding sites with a pKD of 10.1 and with 5-HT4 receptor characteristics. The density of atrial binding sites with 5-HT4 receptor characteristics was 174 and 22 times lower respectively than those of atrial beta 1- and beta 2-adrenoceptors, labelled with (-)-[125I]-cyanopindolol. 4. We suggest that the small 5-HT4 receptor population may in part explain why the maximal tachycardia caused by 5-HT is smaller than that caused by catecholamines.

Animals↗
PubMed2005

The role of the implantable atrial cardioverter-defibrillator.

Atrial and dual-chamber defibrillators with atrial antitachycardia functions represent an emerging option for the treatment of patients with drug-refractory atrial fibrillation. Atrial cardioversion has been demonstrated to be highly effective in treating spontaneous tachyarrhythmias and may reduce atrial fibrillation burden by preventing atrial remodeling. Device implantation has been associated with an improved quality of life and a reduced hospitalization rate. Patient selection and tailored device programming are critical as regards clinical outcome. The individual psychological profile analysis as well as the underlying heart disease and clinical patterns of atrial fibrillation represent the main drivers for the right strategy. Controlled studies are needed in order to define the subset of patients who can benefit more from device implantation.

Atrial Fibrillation↗
PubMed1987

Relationship of plasma concentrations of human atrial natriuretic peptide to renal function and blood pressure in patients with progressive chronic renal failure.

Recent experimental and clinical findings indicate that immunoreactive human Atrial Natriuretic Peptide (alpha-hANP) is involved in the regulation of blood volume and arterial blood pressure (BP). Whereas the potential regulatory role of alpha-hANP in acute changes of extracellular fluid volume (ECFV) and in the modulation of BP has been demonstrated in various studies, their involvement in the chronic maintenance of sodium and water homeostasis is still equivocal. Moreover the role of alpha-hANP is of particular interest in chronic renal failure, since in this pathological condition increased sodium and water retention plays a major pathogenetic role in the development of hypertension and altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. To evaluate the relationship between the degree of renal insufficiency, BP and circulating alpha hANP we determined plasma alpha-hANP concentrations in 16 nondialyzed patients with progressive chronic renal failure (CRF) of various degree. Serum creatinine concentrations ranged from 127 to 1187 (435 +/- 76) mumol/l, systolic BP from 135 to 200 (158 +/- 4) and diastolic BP from 80 to 110 (94 +/- 2) mm Hg respectively. Plasma alpha-hANP concentrations ranged from 49 to 753 with a mean of 228 +/- 42 pg/ml which was thus significantly higher as compared to 90.0 +/- 16.2 pg/ml found in healthy volunteers (p less than 0.05). A highly significant linear correlation between plasma alpha-hANP and serum creatinine concentrations (r = 0.92) was observed; a weaker correlation was found between mean arterial pressure and alpha-hANP (r = 0.66) and serum creatinine concentration (r = 0.59), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗