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Electrophysiologic effects of atropine on sinus node and atrium in patients with sinus nodal dysfunction.

Electrophysiologic studies were conducted in 21 patients with sinus nodal dysfunction before and after intravenous administration of 1 to 2 mg of atropine. The mean sinus cycle length (+/- standard error of the mean) was 1,171 +/- 35 msec before and 806 +/- 29 msec after administration of atropine (P less than 0.001). Mean sinus nodal recovery time determined at a aced rate of 130/min and maximal recovery time were, respectively, 1,426 +/- 75 and 1,690 +/- 100 msec before and 1,169 +/- 90 and 1,311 +/- 111 msec after atropine (P less than 0.001 and less than 0.001). Mean calculated sinoatrial conduction time, measured in 16 patients, was 113 +/- 8 msec before and 105 +/- 9.7 msec after atropine (difference not significant). Mean atrial effective refractory period, measured at an equivalent driven cycle length, was 262 +/- 11.1 msec before and 256 +/- 10.3 msec after atropine (not significant). Mean atrial functional refractory period was 302 +/- 12.5 msec before and 295 +/- 11.3 msec after atropine (not significant). The shortening of sinus cycle length and sinus recovery time with atropine was similar to that noted in patients without sinus nodal dysfunction. In contrast, atropine had insignificant effects on sinoatrial conduction and atrial refractoriness in this group whereas it shortens both in normal subjects. This finding may reflect altered perinodal and atrial electrophysiologic properties in patients with sinus node disease.

Adult↗

Regulation of atrial natriuretic factor receptors in portal hypertensive rabbits.

BACKGROUND/AIMS: Portal hypertension is characterized by a marked splanchnic hyperemia due to a reduction in mesenteric vascular resistance. Possible mediators of this decreased resistance include an increased amount of and/or responsiveness to vasodilatory substances. Previous studies have demonstrated an enhanced hypotensive effect of exogenous atrial natriuretic factor in portal hypertension. We hypothesized that changes in the atrial natriuretic factor hormone receptor system may contribute to this response and hence underlie the marked hyperemia of portal hypertension. METHODS: We used a portal-vein-ligated rabbit model of portal hypertension to study the integrity of the atrial natriuretic factor receptor system within the hyperemic vasculature. RESULTS: There was no significant difference in the serum concentrations of sodium, potassium, atrial natriuretic factor, ANG-II, cGMP, serum osmolality, or hematocrit between normal and portal hypertensive rabbits. Superior mesenteric artery, thoracic aorta and portal vein atrial natriuretic factor receptor number and affinity were determined using [125I]-rANF99-126 binding analysis and affinity cross-linking studies. Receptor classification using specific atrial natriuretic factor-C receptor ligands, along with affinity cross-linking studies revealed two receptor subtypes present on these vessels. There was a significant decrease in the number of atrial natriuretic factor receptors in the portal vein and a significant increase in the superior mesenteric artery in portal hypertension without any significant change in affinity. Thoracic aortic atrial natriuretic factor receptors were increased with a concurrent decrease in affinity in portal hypertension. There was a concomitant increase in tissue cGMP levels within the superior mesenteric artery and thoracic aorta of portal hypertensive animals but not the portal vein. CONCLUSION: These data suggest the increased number of functional atrial natriuretic factor receptors may in part contribute to the hyperdynamic splanchnic circulation peculiar to portal hypertension.

Animals↗

Clinical, adrenergic and heart endocrine measures in chronic atrial fibrillation as predictors of conversion and maintenance of sinus rhythm after direct current cardioversion.

The aim of this study was to evaluate clinical, adrenergic and endocrine factors that could predict sinus rhythm maintenance after direct current cardioversion in chronic atrial fibrillation. Nineteen patients with chronic non-rheumatic atrial fibrillation (mean duration 6 +/- 5 months) were studied. They were exercised 24 h before cardioversion at maximum effort with the Naughton protocol. Heart rate and blood pressure at rest and exercise were recorded and blood samples were taken for the assessment of adrenergic activity, by measuring cyclic adenosine monophosphate, heart endocrine function, atrial natriuretic peptide and its second messenger, cyclic guanosine monophosphate. Fifteen of the 19 patients were initially converted to sinus rhythm (eight patients with external and seven patients with internal DC shocks). After 3 months eight patients remained in sinus rhythm and 11 had relapsed, most of them within the first month. On exercise the chronotropic response was lower in the group who remained in sinus rhythm than in the group in atrial fibrillation (peak heart rate 147 +/- 11 beats.min-1 vs 165 +/- 24 beats.min-1 P = 0.02). During exercise, the systolic blood pressure in the sinus group reached higher values than in the group who relapsed (192 +/- 17 mmHg vs 176 +/- 18 mmHg, P = 0.03). Cyclic adenosine monophosphate increased significantly from rest to peak exercise in the sinus rhythm group (from 23 +/- 9 pmol.ml-1 to 31 +/- 15 mol.ml-1, P = 0.02) while it remained unchanged in the atrial fibrillation group (25 +/- 10 pmol.ml-1 to 24 +/- 8 pmol.ml-1, P = 0.02). For all 19 patients the difference in cyclic adenosine monophosphate between rest and exercise was negatively correlated with maximum heart rate (r = 0.58, P = 0.009). Atrial natriuretic peptide increased from rest to peak exercise in the sinus rhythm group (from 129 +/- 58 fmol.ml-1 to 140 +/- 66 fmol.ml-1) while it remained unchanged in the group in which atrial fibrillation persisted or recurred (from 112 +/- 58 fmol.ml-1 to 111 +/- 53 fmol.ml-1, P = 0.002). A significant correlation between atrial natriuretic peptide and cyclic guanosine monophosphate levels at exercise before cardioversion was found for the sinus rhythm group only (r = 0.76, P = 0.02). In patients with non-rheumatic chronic atrial fibrillation evaluation of clinical parameters such as heart rate and blood pressure changes during maximal exercise can be useful in the choice of suitable therapy. An inadequate increase in plasma cyclic-adenosine monophosphate and atrial natriuretic peptide on exercise could predict patients with more severe underlying disease, where cardioversion should not be recommended.

Aged↗

Systemic embolism in chronic sinoatrial disorder.

We attempted to estimate the prevalence of systemic embolism in patients with chronic sino-atrial disorder. In a group of 100 patients, evidence of embolism was found in 16, of whom 15 had the bradycardia-tachycardia syndrome. In 712 controls with chronic complete heart block, who were matched for age and sex, embolism had occurred in only 1.3 per cent (P less than 0.001). A second group of 41 patients with chronic ventricular bradycardia and atrial flutter or fibrillation had an embolic prevalence of 7.3 per cent, which was also greater than that in the controls (P less than 0.05). All patients with sinoatrial disorder in whom systemic embolism developed were over 54 years of age; multiple episodes occurred in six. The risk of embolization remains even if the bradycardia-tachycardia syndrome is replaced by stable atrial fibrillation. Impaired atrial function appears to be a key factor in predisposing to intracardiac thrombosis, and paroxysmal supraventricular tachycardia increases the risk of subsequent embolization.

Age Factors↗

Diastolic heart failure: old story, new concepts.

Diastolic heart failure refers to a clinical syndrome characterised by symptoms and signs of congestive heart failure, with a normal or subnormal left ventricular (LV) systolic function associated with alterations in LV diastolic function. Diastolic dysfunction is a pathological condition during which the LV is unable to accept a volume of blood coming back from the lungs appropriate to maintain its stroke volume under normal filling pressure. Three eventually associated mechanisms are responsible for such dysfunction: impaired LV relaxation, increased LV stiffness and loss of normal atrial function. Prevention of LV hypertrophic remodelling should decrease the incidence of diastolic heart failure.

Heart Failure↗

Hemodynamic and electrophysiologic effects of combined infusion of lidocaine and propafenone in humans.

The hemodynamic and electrophysiologic effect of a combined intravenous infusion of lidocaine (100 mg bolus followed by 2 mg/min infusion) and propafenone (1 or 2 mg/kg) in patients with a history of ventricular arrhythmia was studied. Lidocaine infusion alone significantly increased the mean pulmonary artery (+28%) and pulmonary capillary wedge (+17%) pressure, with no effect on cardiac index. Lidocaine alone produced no consistent change in any measured electrophysiologic parameter, except slight QTc shortening (-2%, P less than .05). Propafenone alone, particularly at the higher dose (2 mg/kg), produced significant increases in mean blood pressure (+14%), right atrial pressure (+78%), pulmonary artery pressure (+50%), pulmonary capillary wedge pressure (+65%), systemic vascular resistance (+29%), and pulmonary vascular resistance (+61%) and a decrease in cardiac index (-12%). Significant prolongation of PR (+9%), AH (+29%), and HV (+23%) intervals, atrial functional refractory period (+12%), ventricular effective (+7%) and functional (+6%) refractory period, and Wenckebach cycle length (+13%) also occurred after the administration of propafenone alone. Only the effects on atrioventricular (AV) node were observed at the lower dose of propafenone (1 mg/kg). Combined infusion of lidocaine with propafenone produced a mild, statistically insignificant additional negative inotropic effect but reversed the prolongation in atrial and ventricular refractoriness produced by propafenone alone. Thus, the data show that lidocaine attenuates certain electrophysiologic effects of propafenone, which might alter its antiarrhythmic efficacy, while producing mild additive negative inotropic effects that may be of hemodynamic significance.

Adult↗

Regulation of atrial natriuretic peptide release in normal humans.

Atrial volume, pressure, and heart rate are considered the most important modulators of atrial natriuretic peptide (ANP) release, although their relative role is unknown. Continuous positive-pressure breathing in normal humans may cause atrial pressure and atrial volume to go in opposite directions (increase and decrease, respectively). We utilized this maneuver to differentially manipulate atrial volume and atrial pressure and evaluate the effect on ANP release. Effective filling pressure (atrial pressure minus pericardial pressure) was also monitored, because this variable has been proposed as another modulator of ANP secretion. We measured right atrial (RA) pressure, RA area, esophageal pressure (reflection of pericardial pressure), and RA and peripheral venous ANP in seven healthy adult males at rest and during continuous positive-pressure breathing (19 mmHg for 15 min). Continuous positive-pressure breathing decreased RA area (mean +/- SE, *P less than 0.05) 13.6 +/- 1.1 to 10.5 +/- 0.8* cm2, increased RA pressure 4 +/- 1 to 16 +/- 1* mmHg, increased esophageal pressure 2 +/- 1 to 12 +/- 1* mmHg, and increased effective filling pressure 2 +/- 0 to 4 +/- 1* mmHg. RA ANP increased from 67 +/- 17 to 91 +/- 18* pmol/l and peripheral venous ANP from 43 +/- 4 to 58 +/- 6* pmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The assessment of autonomic function in chronic atrial fibrillation: description of a non-invasive technique based on circadian rhythm of atrioventricular nodal functional refractory periods.

AIMS: Heart rate variability (HRV) parameters can be used to assess autonomic function and to predict outcome, but this has been done exclusively in patients with sinus rhythm. Atrial fibrillation (AF) is the commonest sustained arrhythmia and is particularly prevalent in heart failure. We have developed a simple index to assess autonomic function in patients with chronic AF. METHODS AND RESULTS: Forty patients with chronic AF (>1 month) and symptoms of heart failure underwent ambulatory 24 h electrocardiography recording as well as evaluation of symptoms, exercise capacity (6 min walk distance), ventricular function (echocardiography and radionuclide ventriculography), and neuroendocrine activation. A number of standard HRV parameters shown to have prognostic significance in sinus rhythm were also determined. A modified in-house HRV statistical programme was used to filter labelled QRS intervals and to compute the 5th percentile RR interval in each hour. This parameter has been shown to approximate the functional refractory period (FRP) of the atrioventricular node (AVN). A cosine curve was fitted to hourly 5th percentile RR intervals for each patient and from this was estimated the diurnal change in hourly 5th percentile RR interval (approximating DeltaFRP of the AVN) and, by inference, diurnal variation in sympathovagal input to the AVN. Digoxin was the sole agent permitted for control of ventricular rate. DeltaFRP of the AVN varied and revealed a significant correlation, on multivariate analysis, with mean RR interval (P<0.001), SDARR (SD of 5-min average RR intervals during 24 h, P<0.001), and NYHA class of heart failure (classes III and IV heart failure vs. classes I and II, P=0.02). SDARR has previously been shown independently to predict mortality in patients with chronic AF and heart failure. CONCLUSION: This analysis describes a novel non-invasive method for assessing autonomic function in chronic AF. Whether DeltaFRP in chronic AF patients can independently predict adverse prognosis or sudden death requires further study.

Aged↗

Prucalopride is a partial agonist through human and porcine atrial 5-HT4 receptors: comparison with recombinant human 5-HT4 splice variants.

Prucalopride is a gastrointestinal prokinetic drug that acts through 5-HT4 receptors, but its potential effects on cardiac atrial function are unknown. We investigated the effects of prucalopride on human right atrium, piglet left atrium, and piglet sinoatrial node. The effects of prucalopride on 5-HT4 receptor splice variants a, b, g and i, known to be expressed in human atrium, were studied for comparison. Prucalopride was an inotropic partial agonist, compared with 5-HT, on paced human atrial trabeculae (-logEC50M=7.4) and porcine left atria (-logEC50M=7.2), with intrinsic activity of 0.77 and 0.63 respectively. Prucalopride (1 microM) surmountably antagonized the positive inotropic effects of 5-HT on human (pK(P)=7.2) and porcine (pK(P)=7.1) atrium. Prucalopride was also a chronotropic partial agonist (-logEC50M=7.4, intrinsic activity=0.72 with respect to 5-HT) on spontaneously beating piglet atria. The cardiostimulant effects of prucalopride were prevented by GR113808 (1 microM), consistent with mediation through 5-HT4 receptors. Prucalopride bound to recombinant 5-HT4(a), 5-HT4(b), 5-HT4(g), and 5-HT4(i) receptors, labeled by [3H]GR113808, with pKi values of 7.6, 7.5, 7.4, and 7.8 respectively. Prucalopride stimulated adenylyl cyclase as a partial agonist on 5-HT4(a), 5-HT4(b), and 5-HT4(i) receptors with intrinsic activities of 0.82, 0.86, and 0.78 and -logEC50 values of 7.2, 7.3, and 7.2 respectively. At the 5-HT4(g) receptor prucalopride acted as a full agonist (-logEC50M=8.0) compared with 5-HT in the cell line tested, which was probably due to high receptor expression levels. We conclude that prucalopride is a cardiostimulatory partial agonist through human and porcine 5-HT4 receptors. Since prucalopride acts similarly through 5-HT4(a), 5-HT4(b), 5-HT4(g), and 5-HT4(i) receptors, any of these variants could be involved in the mediation of cardiostimulation.

Adenylyl Cyclases↗

Dynamic nature of atrial fibrillation substrate during development and reversal of heart failure in dogs.

BACKGROUND: Clinical atrial fibrillation (AF) often results from pathologies that cause atrial structural remodeling. The reversibility of arrhythmogenic structural remodeling on removal of the underlying stimulus has not been studied systematically. METHODS AND RESULTS: Chronically instrumented dogs were subjected to 4 to 6 weeks of ventricular tachypacing (VTP; 220 to 240 bpm) to induce congestive heart failure (CHF), followed by a 5-week recovery period leading to hemodynamic normalization at 5-week recovery (Wk5(rec)). The duration of burst pacing-induced AF under ketamine/diazepam/isoflurane anesthesia increased progressively during VTP and recovered toward baseline during the recovery period, paralleling changes in atrial dimensions. However, even at full recovery, sustained AF could still be induced under relatively vagotonic morphine/chloralose anesthesia. Wk5(rec) dogs showed no recovery of CHF-induced atrial fibrosis (3.1+/-0.3% for controls versus 10.7+/-1.0% for CHF and 12.0+/-0.8% for Wk5(rec) dogs) or local conduction abnormalities (conduction heterogeneity index 1.8+/-0.1 in controls versus 2.3+/-0.1 in CHF and 2.2+/-0.2 in Wk5(rec) dogs). One week of atrial tachypacing failed to affect the right atrial effective refractory period significantly in CHF dogs but caused highly significant effective refractory period reductions and atrial vulnerability increases in Wk5(rec) dogs. CONCLUSIONS: Reversal of CHF is followed by normalized atrial function and decreased duration of AF; however, fibrosis and conduction abnormalities are not reversible, and a substrate that can support prolonged AF remains. Early intervention to prevent fixed structural abnormalities may be important in patients with conditions that predispose to the arrhythmia.

Animals↗

Hemodynamic determinants of exercise capacity in chronic atrial fibrillation.

To evaluate the response of patients with chronic atrial fibrillation (AF) to exercise, 79 male patients (mean age 64 +/- 1 years) with AF underwent resting two-dimensional and M-mode echocardiography and symptom-limited treadmill testing with ventilatory gas exchange analysis. Patients were classified by underlying disease into five subgroups: no underlying disease (LONE: n = 17), hypertension (HT: n = 11), ischemic heart disease (n = 13), cardiomyopathy or history of congestive heart failure (CHF: n = 26), and valvular disease (n = 12). A higher maximal heart rate than expected for age was observed (175 vs 157 beats/min), which was most notable in the LONE and HT subgroups. Maximal oxygen uptake (VO2 max) was lower than expected for age in all groups. Patients with CHF had a lower resting ejection fraction than all other patients (p < 0.001), a lower VO2 max, and a lower maximal heart rate than LONE and HT patients (p < 0.001). Stepwise regression analysis demonstrated that echocardiographic measurements at rest were poor predictors of VO2 max and VO2 at the ventilatory threshold. Among clinical, morphologic, and exercise variables, maximal systolic blood pressure accounted for the greatest variance in exercise capacity, but it explained only 35%. In patients with AF the higher than predicted maximal heart rates may be a compensatory mechanism for maintaining exercise capacity after the loss of normal atrial function. However, even in the absence of underlying disease, it does not appear to compensate fully for a compromised exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Atrial natriuretic factor in the freshwater turtle Pseudemys scripta: a partial characterization.

The presence of natriuretic and vasorelaxant materials in the atria and ventricles of a Chelonian reptile, the freshwater turtle Pseudemys scripta, was verified and the active substance partially characterized. Crude atrial and ventricular extracts were acutely natriuretic and diuretic when administered to anesthetized rats increasing sodium excretion 23.5 +/- 7.9 and 5.11 +/- 18 microM Na/10 min/mg extract, respectively. Although atrial extracts were relatively more natriuretic than ventricular extracts, the total natriuretic content of ventricular extracts was approximately twofold greater. Moreover, partially purified atrial extracts were found to relax precontracted isolated rat aortic ring segments and exhibited immunoreactivity to mammalian ANP antisera. Also, the natriuretic and immunoreactive substance was purified further by size exclusion chromatography and a molecular weight of 3-5 kDa was determined. Using the bovine adrenal glomerulosa ANP receptor, this partially purified natriuretic substance displayed an apparent binding affinity similar to that of mammalian ANP. Finally, in order to demonstrate that this reptile is physiologically responsive to ANP, synthetic rat ANP (10 micrograms/kg) was shown to decrease arterial pressure in conscious turtles from a control value of 37.2 +/- 5.2 to 30.3 +/- 2.7 mm Hg. These data demonstrate that unlike other non-Chelonian reptiles, both the atria and the ventricles of this Chelonian reptile synthesize and store substantial levels of biologically active ANP-like materials, and further, that ANP is a highly conserved and primitive cardiac hormone.

Animals↗

Effects of long-term diabetes and treatment with gangliosides on cardiac sympathetic innervation: a biochemical and functional study in mice.

The effect of long-term diabetes on cardiac sympathetic innervation was investigated in genetically obese diabetic mice (db/db). Previous studies have shown the presence of a peripheral neuropathy starting a few months after birth, and we recently reported a significant reduction of myocardial norepinephrine (NE) levels in the hearts of diabetic mice at the age of 6 months. In the present study, histofluorescence analysis of comparable sections of cardiac tissue of both control and diabetic animals confirmed the picture of a sympathetic denervated heart in this experimental model. Furthermore, functional studies in isolated atria revealed a difference between the two groups of animals: in fact heart rate increases induced by transmural stimulation were significantly lower in diabetic mice. Since a bovine brain ganglioside mixture (Cronassial) has been extensively studied for its effect on peripheral diabetic neuropathy, a group of diabetic mice was treated throughout the sixth month with this drug (10 mg/kg/day i.p.). The ganglioside treated animals showed a marked recovery of atrial function and cardiac NE concentration. The above results clearly indicate sympathetic neural damage in db/db animals, likely related to an autonomic diabetic neuropathy and a possible protection by ganglioside of adrenergic nerves from this alteration.

Animals↗

Percutaneous extraction of a fractured, exposed atrial "J" lead retention wire.

The recent identification of fracturing of the retention wire in the Telectronics atrial lead, models 329-701 and 330-801, and the report of death due to cardiac tamponade caused by aortic puncture resulting from protrusion of the retention wire, necessitates fluoroscopic screening of these patients and the explantation of all leads identified to have the component failure. We present in this paper a percutaneous alternative to lead explantation in patients with protrusion of the retention wire through the polyurethane insulation and with an otherwise properly functioning atrial lead.

Electrodes, Implanted↗

[Doppler echocardiography and double chamber pacing].

Doppler-echocardiography is playing an increasing role in cardiac pacing: 1) Before implantation, to determine any cardiac disease possibly accompanying the conduction disturbance, and the quality of atrial function in order to identify the appropriate indications for the type of pacing which will restore normal AV synchronism. Alongside morphometric data (size of atria, etc.), this analysis is based above all on the evaluation of LV filling flows and ejection, if necessary during provisional pacing in DRV mode. It is important to be aware of and prevent certain problems: 1st degree AV block with very long PR, high degree interatrial conduction disturbances, etc. 2) To evaluate the possible benefits of pacing in certain new indications, e.g. obstructive hypertrophic cardiomyopathy (measurement of intra-LV gradient in sinus rhythm and with DRV pacing with total ventricular capture). 3) After implantation, to optimise the programming of double-chamber pacemakers and in particular AV intervals (base-line AV interval with paced atrial cycle, AV interval with detected atrial cycle, hysteresis of AV interval corresponding to the difference between the two previous values, slope of automatic variation in AV interval during exercise, etc.). Individual programming of these parameters based upon analysis of transmitral and ejection flow rates, at rest and, if necessary, during exercise, enables the optimisation of cardiac function (which is above all useful in the presence of concomitant organic heart disease) while at the same time improving the electrophysiological behaviour of the pacemaker at high frequencies.

Cardiac Pacing, Artificial↗

Abnormal maternal cardiac function precedes the clinical manifestation of fetal growth restriction.

OBJECTIVE: To compare maternal hemodynamics in women whose fetuses are small-for-gestational age (SGA) with those in women with fetal growth restriction (FGR) before manifestation of the clinical disease. METHODS: Thirty-five normotensive pregnant women with fetal abdominal circumference < 10th centile, normal fetal anatomy and normal umbilical artery pulsatility index (PI) underwent maternal echocardiographic examinations between 27 and 30 weeks of gestation. Pregnancies were followed until delivery and fetuses were retrospectively classified as either SGA or FGR and the maternal hemodynamic data were compared. RESULTS: Nineteen SGA and 16 FGR patients were retrospectively identified after delivery. Heart rate, stroke volume, cardiac output, left atrial function and left ventricular mass index were higher, while mean blood pressure and total vascular resistance were lower in the SGA group compared with the FGR group. A significant inverse linear correlation was found between total vascular resistance and weight centile (r = 0.83; P < 0.0001). CONCLUSIONS: Mothers of SGA fetuses show hemodynamic features similar to those with physiological pregnancies suggesting that their fetuses are likely to be constitutionally small and not pathologically growth-restricted.

Adult↗

Radionuclide left ventricular function curve during atrial pacing in normal subjects and in patients with coronary artery disease.

We used radionuclide angiography during right atrial pacing to assess left ventricular function in 7 normal subjects and 20 patients with coronary artery disease. A left ventricular function curve relating stroke volume to end-diastolic volume was plotted for each patient. The normal pacing ventricular function curve was a straight line passing through the origin of axes. The pacing ventricular function curve was abnormal in 18 of the 20 patients with coronary artery disease, and three different shaped curves were obtained, reflecting decreased contractile force for the same end-diastolic volume during ischemia. Cardiac output and blood pressure do not change during atrial pacing, thus the Frank-Starling relationship is evaluated by this method during almost experimentally controlled conditions. Relating stroke volume to end-diastolic volume, and not end-diastolic pressure, distinguishes between overall left ventricular systolic function and left ventricular compliance.

Adult↗

Late functional deterioration after atrial correction for transposition of the great arteries.

Late anatomic and functional results were evaluated in 220 consecutive survivors who underwent surgery in 1964-1984 for atrial correction of transposition of the great arteries (TGA). Actuarial survival was 87% at 10 years and 83% at 20 years and was higher in patients with simple than in those with complex TGA (92% vs. 84% at 10 years). Although 83% of simple TGA and 78% of complex TGA survivors belong to the oligosymptomatic or asymptomatic group, failure of the systemic ventricle occurred in 17 (7.7%) patients. This failure was more common in patients with complex than in those with simple TGA (12.1% vs. 4.1%, p less than 0.05); actuarial incidence of such failure was 3% at 5 years and 11% at 15 years, and it caused 10 of 25 (40%) of late deaths. Late dysrhythmias necessitating pacemaker implantation had an incidence of 9.8% at 10 years. Reoperations were performed in 20 (9.1%) patients, with 12 of 23 (52%) reoperations occurring in the first 2 years after correction. Stenosis of caval inflow (eight patients), or residual atrial or ventricular septal defects (eight patients) were the most common causes of reoperation. Systemic atrioventricular valve incompetence necessitating surgery occurred in only three patients. Atrial correction gives good late results, but late functional deterioration occurs in some patients.

Child↗