Work stress and the long QT syndrome: high job strain and effort-reward imbalance at work associated with arrhythmic risk in the long QT syndrome.

OBJECTIVES: To examine whether work stress is associated with a symptomatic status of the long QT syndrome (LQTS). METHODS: The sample comprised 173 KCNQ1, KCNH2, or SCN5A gene mutation carriers (70 symptomatic) and control groups of 203 relatives without the family mutation, and of 1209 population-based young Finns control subjects. Work stress was assessed using the Job Content Questionnaire and Occupational Stress Questionnaire. RESULTS: We found an association between the occurrence of symptoms in the LQTS and high work stress, higher job demands/effort, lower job control, and lower rewards compared with control subjects. We also found that symptomatic LQTS mutation carriers had higher work stress than asymptomatic LQTS mutation carriers. CONCLUSIONS: Higher work stress is related to arrhythmic risk in the LQTS. It may be useful to incorporate assessment of work conditions and stress interventions into management of high-risk patients.

Common candidate gene variants are associated with QT interval duration in the general population.

OBJECTIVES: QT interval prolongation is associated with increased risk of sudden cardiac death at the population level. As 30-40% of the QT-interval variability is heritable, we tested the association of common LQTS and NOS1AP gene variants with QT interval in a Finnish population-based sample. METHODS: We genotyped 12 common LQTS and NOS1AP genetic variants in Health 2000, an epidemiological sample of 5043 Finnish individuals, using Sequenom MALDI-TOF mass spectrometry. ECG parameters were measured from digital 12-lead ECGs and QT intervals were adjusted for age, gender and heart rate with a nomogram (Nc) method derived from the present study population. RESULTS: The KCNE1 D85N minor allele (frequency 1.4%) was associated with a 10.5 ms (SE 1.6) or 0.57 SD prolongation of the adjusted QT(Nc) interval (P=3.6 x 10(-11)) in gender-pooled analysis. In agreement with previous studies, we replicated the association with QT(Nc) interval with minor alleles of KCNH2 intronic SNP rs3807375 [1.6 ms (SE 0.4) or 0.08 SD, P=4.7 x 10(-5)], KCNH2 K897T [-2.6 ms (SE 0.5) or -0.14 SD, P=2.1 x 10(-7)] and NOSA1P variants including rs2880058 [4.0 ms (SE 0.4) or 0.22 SD, P=3.2 x 10(-24)] under additive models. CONCLUSIONS: We demonstrate that each additional copy of the KCNE1 D85N minor allele is associated with a considerable 10.5 ms prolongation of the age-, gender- and heart rate-adjusted QT interval and could thus modulate repolarization-related arrhythmia susceptibility at the population level. In addition, we robustly confirm the previous findings that three independent KCNH2 and NOSA1P variants are associated with adjusted QT interval.

[Effect of aluminum and iron on lipid metabolism in aquatic invertebrates].

Methods of thin-layer, gas-liquid, and liquid chromatography were applied to the study of the effect of various concentrations of aluminum and iron salts on the contents of phospholipids, cholesterol, and fatty acids in the aquatic invertebrate Hydropsyche contubernalis L. (Trichoptera). It was found that the effect of the metals under study on lipid contents in living organisms depended on the composition of the aqueous medium and concentrations of the metals. Aluminum and iron altered the value of the cholesterol-to-phospholipid molar ratio. In the absence of lethal effects, this was indicative of attempts to switch adaptational biochemical mechanisms to stabilize cellular structures.

Repolarization abnormalities detected by magnetocardiography in patients with dilated cardiomyopathy and ventricular arrhythmias.

INTRODUCTION: Abnormal repolarization is one of the acknowledged mechanisms leading to malignant ventricular arrhythmias. We used a novel magnetocardiographic technique to investigate the role of inhomogeneous repolarization in patients with nonischemic dilated cardiomyopathy prone to sustained ventricular arrhythmias. METHODS AND RESULTS: Forty-nine dilated cardiomyopathy patients were studied, 18 with a history of sustained ventricular tachycardia (n = 6) or ventricular fibrillation (n = 12) and 31 with no ventricular arrhythmias. The magnetocardiogram was registered and QT apex and QT end intervals were determined by a computer algorithm. Inhomogeneity of repolarization was characterized with indices describing QT apex and QT end dispersion, and T wave end duration. In addition, time-domain late fields of the QRS complex in magnetocardiography and QT dispersion in 12-lead ECG were determined. T wave end was longer in the arrhythmia group in patients with sinus rhythm (87 +/- 15 msec vs 73 +/- 12 msec; P = 0.005) and in those not having bundle branch block. Magnetocardiographic late fields of the QRS complex were not different between groups. QT apex and end dispersion on magnetocardiography or 12-lead ECG showed no difference. CONCLUSION: Prolongation of the end part of the T wave revealed by magnetocardiography is related to malignant ventricular arrhythmias in dilated cardiomyopathy. The results suggest that abnormal repolarization rather than delayed conduction underlies the arrhythmias in this disease.

Plasma and pericardial fluid natriuretic peptide levels in postinfarction ventricular dysfunction.

AIMS: In the present study we examined plasma and pericardial fluid ANP and BNP concentrations in postinfarction ventricular dysfunction. The association of peptide levels to left ventricular (LV) dysfunction and to the localization of the myocardial infarction (MI) was studied. METHODS AND RESULTS: Plasma and pericardial fluid samples were obtained from 37 patients undergoing coronary bypass surgery. According to the ECG and preceding coronary angiography, the patients were divided into three groups: previous anterior myocardial infarction (MI) (n=12), previous inferior/posterior MI (n=15) and no history of MI (n=10). When compared to the control group with no MI, the patients with anterior MI had elevated plasma ANP and BNP (134+/-13 vs. 81+/-15 pg/ml, P<0.01 and 95+/-10 pg/ml vs. 26+/-8 pg/ml, P<0.01, respectively) and pericardial fluid BNP (473+/-60 pg/ml vs. 57+/-8 pg/ml, P<0.001) levels. The plasma natriuretic peptide concentrations were not increased in the patients with inferior/posterior MI, but the pericardial fluid BNP concentrations were greater than in the patients with no history of MI (129+/-35 pg/ml vs. 57+/-8 pg/ml, P<0.05). Six of the 12 patients with previous anterior MI had LVEF> or =45%. Despite their normal LV systolic function, these patients had increased plasma and pericardial fluid BNP levels when compared to the group with no history of MI (68+/-18 pg/ml vs. 26+/-8 pg/ml, P<0.05 and 534+/-258 pg/ml vs. 57+/-8 pg/ml, P<0.01, respectively). CONCLUSIONS: Previous anterior myocardial infarction was associated with increased cardiac BNP production even if the LV systolic function was normal (LVEF> or =45%). The high pericardial fluid BNP concentrations in postinfarction patients suggest that the BNP synthesis and release are augmented in the ventricular myocardium independent from the LVEF.

Multimodality MR imaging assessment of myocardial viability: combination of first-pass and late contrast enhancement to wall motion dynamics and comparison with FDG PET-initial experience.

PURPOSE: To combine three magnetic resonance (MR) imaging modalities-dobutamine stress cine, first pass, and late contrast material-enhanced T1-weighted imaging-and to compare the results with 2-[fluorine 18]fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) in the assessment of unviable myocardium in coronary artery disease. MATERIALS AND METHODS: Ten patients with multivessel coronary artery disease underwent MR imaging before and 6 months after bypass surgery. Left ventricular cine MR imaging was performed at rest and during dobutamine infusion. Inversion-recovery gradient-echo images were obtained to study myocardial contrast enhancement at first pass and 5 minutes later. FDG PET was performed with orally administered acipimox before surgery. RESULTS: With dobutamine cine MR imaging, unviable myocardium was detected with a sensitivity of 79% and a specificity of 93%; postoperative wall thickening was the standard. First-pass analysis increased these values to 97% and 96%; analysis of late enhancement with T1-weighted imaging, to 62% and 98%. FDG PET had a sensitivity of 81% and a specificity of 86%. CONCLUSION: The combination of first-pass enhancement analysis and wall motion assessment with stress significantly increases the specificity of MR imaging in the detection of unviable sectors.

Survey of the coding region of the HERG gene in long QT syndrome reveals six novel mutations and an amino acid polymorphism with possible phenotypic effects.

Analysis of the entire coding region of the HERG gene of 39 Finnish LQTS patients revealed eight mutations, six of which are hitherto unreported. All these mutations are located in the evolutionarily conserved regions of HERG, including the transmembrane domains (P451L, Y569H, 1631delAG, G584S, G601S, T613M) and the cytoplasmic N-terminus (453delC, R176W) of the channel. Our present and earlier results suggest that the LQT2 subtype accounts for approximately 20-30% of LQTS cases in Finland. We also report the first common amino acid polymorphism (K897T) of the HERG channel, with allele frequencies of 0.84 and 0.16. Investigation of 170 genetically homogenous LQT1 patients suggests that this polymorphism may influence QT interval in female individuals.

Homozygosity for a HERG potassium channel mutation causes a severe form of long QT syndrome: identification of an apparent founder mutation in the Finns.

OBJECTIVES: We studied the clinical characteristics and molecular background underlying a severe phenotype of long QT syndrome (LQTS). BACKGROUND: Mutations of cardiac ion channel genes cause LQTS, manifesting as increased risk of ventricular tachycardia and sudden death. METHODS: We studied two siblings showing prolonged QT intervals corrected for heart rate (QTc), their asymptomatic parents with only marginally prolonged QTc intervals and their family members. The potassium channel gene HERG was screened for mutations by deoxyribonucleic acid sequencing, and the electrophysiologic consequences of the mutation were studied in vitro using the whole-cell patch-clamp technique. RESULTS: A novel missense mutation (L552S) in the HERG channel, present in the homozygous state in the affected siblings and in the heterozygous state in their parents, as well as in 38 additional subjects from six LQTS families, was identified. One of the homozygous siblings had 2:1 atrioventricular block immediately after birth, and died at the age of four years after experiencing unexplained hypoglycemia. The other sibling had an episode of torsade de pointes at the age of two years. The mean QTc interval differed significantly (p < 0.001) between heterozygous symptomatic mutation carriers (500 +/- 59 ms), asymptomatic mutation carriers (452 +/- 34 ms) and noncarriers (412 +/- 23 ms). When expressed in vitro, the HERG-L552S formed functional channels with increased activation and deactivation rates. CONCLUSIONS: Our data demonstrate that homozygosity for a HERG mutation can cause a severe cardiac repolarization disorder without other phenotypic abnormalities. Absence of functional HERG channels appears to be one cause for intrauterine and neonatal bradycardia and 2:1 atrioventricular block.

Arrhythmic disorder mapped to chromosome 1q42-q43 causes malignant polymorphic ventricular tachycardia in structurally normal hearts.

OBJECTIVES: The purpose of this study was to provide clinical and anatomical characteristics as well as genetic background of a malignant arrhythmogenic disorder. BACKGROUND: An inherited autosomally dominant cardiac syndrome causing stress-induced polymorphic ventricular tachycardia and syncope in the absence of structural myocardial changes was detected in two families. METHODS: Two unrelated families with six victims of sudden death and 51 living members were evaluated. Resting and exercise electrocardiograms (ECG), echocardiography, magnetic resonance imaging (MRI), cineangiography, microscopic examination of endomyocardial biopsies and a drug testing with a class IC antiarrhythmic agent flecainide were performed. A genetic linkage analysis was carried out to map the gene locus. RESULTS: Of the 24 affected individuals, 10 had succumbed with six cases of sudden death, and 14 survivors showed evidence of disease. Exercise stress test induced ventricular bigeminy or polymorphic ventricular tachycardia in affected individuals. Three children initially examined before 10 years of age developed arrhythmias during a four-year follow-up. Resting ECGs were normal in affected subjects except a slight prolongation of the QT intervals adjusted for heart rate (QTc) (430 +/- 18 vs. 409 +/- 19 ms, affected vs. nonaffected, p < 0.01). Administration of flecainide did not induce ECG abnormalities encountered in familial idiopathic ventricular fibrillation. Ventricular volumes, contractility and wall measurements were normal by echocardiography, right ventricular cineangiography and MRI. Histopathological examination showed no fibrosis or fatty infiltration. The cumulative cardiac mortality by the age of 30 years was 31%. The disease locus was assigned to chromosome 1q42-q43, with a maximal pairwise lod score of 4.74 in the two families combined. Only one heterozygous carrier was clinically unaffected suggesting high disease penetrance in adulthood. CONCLUSIONS: A distinct cardiac disorder linked to chromosome 1q42-q43 causes exercise-induced polymorphic ventricular tachycardia in structurally normal hearts and is highly malignant. Delayed clinical manifestation necessitates repeated exercise electrocardiography to assure diagnosis in young individuals of the families.

Ventricular Arrhythmia Suppression by Magnesium Treatment after Coronary Artery Bypass Surgery.

Ventricular arrhythmias occur frequently shortly after coronary artery bypass grafting (CABG), and their occurrence coincides with the postoperative decline in serum magnesium (Mg) levels. To examine if this decline causes ventricular arrhythmias and if their appearance could be reduced by intravenous Mg administration, 140 consecutive CABG patients were randomized to receive 70 mmol of Mg sulphate (N = 69) or placebo (N = 71) over two days. Serum Mg concentration fell to 0.77 mmol/l in the control group but rose to 1.09 mmol/l in the Mg group (p < 0.001). On 48 h Holter, the number of ventricular premature complexes (VPC) on the third postoperative day was reduced in the Mg group (4 +/- 5 vs 12 +/- 21 VPCs/h; p < 0.05) and the incidence of complex ventricular arrhythmias (Lown grade 2-5) was significantly diminished (19% vs 41% of the patients; p < 0.05). In multivariate analysis, high risk ventricular arrhythmias (repetitive polymorphic ventricular complexes, couplets, R-on-T complexes or operative tachycardia) were independently predicted by high number of bypassed vessels (p = 0.01), poor NYHA functional class (p = 0.06), preoperative diuretic use (p = 0.07), and low postoperative Mg levels (p = 0.08). In conclusion, correction of the postoperative decline in serum Mg concentration decreases the occurrence of early VPCs and complex ventricular arrhythmias. Patients with extensive underlying coronary artery disease and prior diuretic therapy appear to benefit greatest from Mg treatment.http://link.springer-ny.com/link/service/journals/00547/bibs/8n3p165.html

Hemodynamic and neuroendocrine effects for candoxatril and frusemide in mild stable chronic heart failure.

OBJECTIVES: The study aimed to assess the hemodynamic and neuroendocrine effects of candoxatril and frusemide compared with placebo in patients with mild chronic heart failure. BACKGROUND: Candoxatril is an atriopeptidase inhibitor. It increases circulating levels of atrial natriuretic peptide leading to natriuresis and diuresis, which alleviate the symptoms of a failing heart. METHODS: This was a multicenter, randomized, double-blind study. Forty-seven patients with mild stable chronic heart failure received candoxatril 400 mg/day, frusemide 40 mg/day or placebo for up to six weeks. Cardiac indices were determined at rest and during exercise, and blood samples were taken for laboratory analysis. Assessments were performed at baseline (day 0) and after six weeks (day 42). RESULTS: In comparison with placebo, both drugs significantly reduced mean pulmonary capillary wedge pressure following the first dose administration. Only candoxatril significantly reduced pulmonary capillary wedge pressure during exercise on day 0, while both drugs significantly reduced this parameter on day 42. Changes in the remaining hemodynamic parameters were comparable for both drugs relative to placebo. Frusemide significantly increased mean plasma renin activity (days 0 and 42), and the mean aldosterone concentration (day 42) in comparison with placebo, whereas candoxatril caused no significant changes in any of the hormonal parameters assessed. CONCLUSIONS: These results show that candoxatril, 400 mg/day, has a similar hemodynamic profile to frusemide, 40 mg/day, but it does not induce adverse neuroendocrine effects. Candoxatril therefore appears to offer a clinically significant advantage over frusemide, providing an alternative therapeutic approach to the treatment of patients with mild stable chronic heart failure.

Sinus node function and ventricular repolarization during exercise stress test in long QT syndrome patients with KvLQT1 and HERG potassium channel defects.

OBJECTIVES: This study was performed to evaluate the QT interval and heart rate responses to exercise and recovery in gene and mutation type-specific subgroups of long QT syndrome (LQTS) patients. BACKGROUND: Reduced heart rate and repolarization abnormalities are encountered among long QT syndrome (LQTS) patients. The most common types of LQTS are LQT1 and LQT2. METHODS: An exercise stress test was performed in 23 patients with a pore region mutation and in 22 patients with a C-terminal end mutation of the cardiac potassium channel gene causing LQT1 type of long QT syndrome (KVLQT1 gene), as well as in 20 patients with mutations of the cardiac potassium channel gene causing LQT2 type of long QT syndrome (HERG gene) and in 33 healthy relatives. The QT intervals were measured on electrocardiograms at rest and during and after exercise. QT intervals were compared at similar heart rates, and rate adaptation of QT was studied as QT/heart rate slopes. RESULTS: In contrast to the LQT2 patients, achieved maximum heart rate was decreased in both LQT1 patient groups, being only 76 +/- 5% of predicted in patients with pore region mutation of KvLQT1. The QT/heart rate slopes were significantly steeper in LQT2 patients than in controls during exercise. During recovery, the QT/heart rate slopes were steeper in all LQTS groups than in controls, signifying that QT intervals lengthened excessively when heart rate decreased. At heart rates of 110 or 100 beats/min during recovery, all LQT1 patients and 89% of LQT2 patients had QT intervals longer than any of the controls. CONCLUSIONS: LQT1 is associated with diminished chronotropic response and exaggerated prolongation of QT interval after exercise. LQT2 patients differ from LQT1 patients by having marked QT interval shortening and normal heart rate response to exercise. Observing QT duration during recovery enhances the clinical diagnosis of these LQTS types.

Changes in heart rate variability in elderly patients undergoing major noncardiac surgery under spinal or general anesthesia.

BACKGROUND AND OBJECTIVES: Heart rate variability (HRV), widely used as an indicator of activity of the autonomic nervous system, has been reported to decrease during and after both spinal and general anesthesia in patients without cardiovascular disease. We evaluated the changes in HRV bands in 40 patients with a high risk of ischemic heart disease. METHODS: The patients were randomly assigned to receive either spinal (SA) or general anesthesia (GA) for elective total hip arthroplasty or peripheral vascular surgery. Anesthetic techniques and perioperative fluid administration were standardized. Holter monitoring was started preoperatively and continued until the third postoperative day. Three HRV frequency bands were analyzed. RESULTS: A significant decrease was seen in very low frequency (VLF) and low frequency (LF) bands during GA but not during SA. Also the LF/high frequency (HF) ratio decreased during GA but not during SA. A decrease in all HRV frequency bands was seen after both types of anesthesia. None of the frequency bands returned back to the preoperative level during the 3-day trial. Postoperatively circadian variation was found only in the VLF band after SA. CONCLUSIONS: The sympathovagal balance (LF/HF) is more stable during SA than during GA in patients with a high risk of ischemic heart disease. The postoperative decrease in HRV bands, however, is independent of the anesthetic technique.

Factors associated with post-operative myocardial ischaemia in elderly patients undergoing major non-cardiac surgery.

Forty patients (> 65 years) undergoing hip arthroplasty or peripheral vascular surgery both associated with high risk for post-operative myocardial ischaemia were randomized to receive either spinal or general anaesthesia. Ambulatory ECG recording (Holter) until the third post-operative morning, a daily 12-lead ECG and serum creatine kinase and troponine concentraItions were obtained. The number of ischaemic episodes, total duration of ischaemia and ischaemic minutes per hour were noted for each patient peri-operatively. Sixteen of the patients (40%) had post-operative myocardial ischaemia. An intra-operative increase in the plasma concentration of norepinephrine but not epinephrine was detected in the patients who later developed post-operative myocardial ischaemia. The increase in plasma norepinIephrine concentrations correlated with the decrease in core temperature. The type of anaesthesia had no effect on the incidence of myocardial ischaemia during or after surgery. Our results suggests that intra-operatively decreased core temperature and the increase in plasma concentration of norepinephrine probably caused peripheral vasoconstriction leading to latent cardiac dysfunction. These events should be avoided in the patients at risk of post-operative cardiac ischaemia.

Effect of ethanol drinking, hangover, and exercise on adrenergic activity and heart rate variability in patients with a history of alcohol-induced atrial fibrillation.

To elucidate the mechanism of alcohol-induced atrial fibrillation (AF) we studied the heart rate variability and parameters of the adrenergic system during alcohol intake, hangover, and exercise in 6 men (mean age 43 years) prone to alcohol-induced AF, together with 6 age-matched controls. The ambulatory (15 hour) electrocardiogram was recorded and blood samples were taken for lymphocytic beta adrenoceptor, plasma catecholamine, and cyclic adenosine monophosphate (cAMP) measurements before and after alcohol intake (blood alcohol 1.5 per thousand), during hangover, and after a standardized bicycle exercise test. The beta-adrenoceptor density in lymphocytes was unchanged in the control group after alcohol intake or during hangover. Each of the AF patients had an increase in beta-adrenoceptor density after ethanol drinking (mean increase 29%, p <0.05). The hangover or exercise beta-receptor values did not differ from those in corresponding controls. Plasma adrenaline concentration tended to decrease and noradrenaline to increase after drinking and during hangover in both groups. Plasma cAMP levels were lower in patients after drinking than in controls (p <0.05). The exercise values of the adrenergic parameters were very similar in AF patients whether or not preceded by alcohol. Analysis of ambulatory electrocardiography showed a very low rate of ectopic beats in both AF patients and controls. Analysis of heart rate variability revealed a tendency toward an increase in sympathetic/parasympathetic component ratio (low-frequency/high-frequency ratio) in AF patients, but not in controls, after ethanol drinking. In conclusion, no signs of arrhythmogenic cardiac disease were detected in patients with AF to explain the tendency toward AF. Increases in beta-adrenoceptor density and low-frequency/high-frequency ratio during ethanol intoxication in patients with AF suggest an exaggerated sympathetic reaction.

Comparison of sotalol and metoprolol in the prevention of atrial fibrillation after coronary artery bypass surgery.

New-onset atrial fibrillation (AF) is frequent after coronary artery bypass grafting (CABG), and beta-blockers decrease its incidence. To examine whether a beta-blocker with class III properties is superior to a pure one, 191 consecutive patients undergoing CABG were randomized to receive oral sotalol, 120 mg daily (n = 93), or metoprolol, 75 mg daily (n = 98), postoperatively. The doses were adjusted if beta-blockade was inadequate or excessive. AF occurred in 16 (16%) of 98 sotalol patients and in 30 (32%) of 93 metoprolol patients (p < 0.01). Symptoms related to beta-blockade or proarrhythmia did not appear. After CABG, sinus heart rate increased in both groups (p < 0.001) but less in the sotalol patients (p < 0.001) throughout the postoperative period. Corrected QT duration (by the Bazett equation) was prolonged after the operation in both groups (p < 0.001), whereas uncorrected QT duration at similar heart-rate levels were prolonged only in sotalol patients (mean increase, 31 ms; 95% confidence interval, 2042 ms; p < 0.01). Uncorrected QT durations at similar heart-rate levels were longer during sotalol (compared with metoprolol) treatment (p < 0.05). Heart rates or QT durations did not differ between the patients with or without AF. In conclusion, sotalol significantly reduces the incidence of AF after CABG. Although a marked class III effect is demonstrated with relatively low doses (as prolonged ventricular repolarization) in direct comparison unbiased by any rate correction, its contribution as an enhanced antifibrillatory mechanism in the postoperative state remains unconfirmed.

Later potentials on signal-averaged electrocardiograms in children after right ventriculotomy.

After corrective surgery for congenital heart defects, scars may create fractionation and delay of the electrical signals in the heart muscle, providing a substrate for arrhythmias. Signal-averaged electrocardiograms (SAECGs) were obtained from 33 children after right ventriculotomy, on average 6 years after surgery, and from 38 healthy controls of the same age. The duration of the filtered QRS complex (fQRS), the duration of the low amplitude signal (< 40 microV) in the terminal QRS complex (LAS40), and the root mean square amplitude of the terminal 40 ms of the QRS complex (RMS40) were determined. The values of fQRS > or = 117 ms, RMS40 < or = 25 microV, and LAS40 > or = 35 ms, which were beyond the mean +/- 2 SD of the healthy controls, were considered abnormal. Most patients had right bundle branch block and therefore a prolonged fQRS. Late potentials were defined as present if both the RMS40 and LAS40 were abnormal. Altogether nine patients (27%) had late potentials. In the patients with late potentials the incidence of serious ventricular arrhythmias was 44% (4 of 9) and in the patients without late potentials 0% (0 of 24). In seven patients with enlargement of the right ventricle, the incidence of arrhythmias was 57% (4 of 7) when late potentials were present and 0% (0 of 7) when they were absent. In the present study late potentials were associated with a history of arrhythmias, especially when the right ventricle was enlarged. Therefore the SAECG may be useful for determining the risk of serious arrhythmia events in children operated for congenital heart defects.

The influence of intravenous magnesium sulphate on the occurrence of atrial fibrillation after coronary artery by-pass operation.

To examine the influence of magnesium (Mg) on hypomagnesaemia and atrial fibrillation (AF) following coronary artery by-pass surgery, 140 consecutive patients were randomized to receive 70 mmol of magnesium sulphate intravenously (n = 69) or placebo (n = 71). Serum magnesium concentrations fell to 0.77 +/- 0.10 mmol.l-1 in the control group but rose to 1.09 +/- 0.17 mmol.l-1 in the Mg group (P < 0.001). The incidence of AF was 29% in the Mg group and 26% in the placebo group (NS). The AF patients were older, more of them had had prior AF episodes, their sinus rates (SR) were slower (78 +/- 10 vs 86 +/- 12 beats.min-1; P < 0.01) and serum Mg concentrations higher (0.89 +/- 0.21 vs 0.80 +/- 0.11 mmol.l-1; P < 0.05). The incidence of AF was 43% in the highest quartile of serum Mg and 23% among the rest (P = 0.056). In patients experiencing AF during the first three post-operative days, serum Mg concentrations were higher and SR slower on each day compared with non-AF patients. SR increased post-operatively less with high Mg levels (P = 0.044). In the Mg group, serum Mg and SR were the only independent predictors of AF. In conclusion, the incidence of post-operative AF is not decreased with magnesium. High Mg levels are likely to provoke AF probably by mechanisms that modify SR.