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Biomedical subjects

L Toivonen

Publications and source records attributed to L Toivonen.

At least 55 records · Page 3Linked to original sources
PubMed1999

Bioelectromagnetic localization of a pacing catheter in the heart.

The accuracy of localizing source currents within the human heart by non-invasive magneto- and electrocardiographic methods was investigated in 10 patients. A non-magnetic stimulation catheter inside the heart served as a reference current source. Biplane fluoroscopic imaging with lead ball markers was used to record the catheter position. Simultaneous multichannel magnetocardiographic (MCG) and body surface potential mapping (BSPM) recordings were performed during catheter pacing. Equivalent current dipole localizations were computed from MCG and BSPM data, employing standard and patient-specific boundary element torso models. Using individual models with the lungs included, the average MCG localization error was 7+/-3 mm, whereas the average BSPM localization error was 25+/-4 mm. In the simplified case of a single homogeneous standard torso model, an average error of 9+/-3 mm was obtained from MCG recordings. The MCG localization accuracies obtained in this study imply that the capability of multichannel MCG to locate dipolar sources is sufficient for clinical purposes, even without constructing individual torso models from x-ray or from magnetic resonance images.

Body Surface Potential Mapping↗
PubMed1999

Nonfluoroscopic localization of an amagnetic stimulation catheter by multichannel magnetocardiography.

This study was performed to: (1) evaluate the accuracy of noninvasive magnetocardiographic (MCG) localization of an amagnetic stimulation catheter; (2) validate the feasibility of this multipurpose catheter; and (3) study the characteristics of cardiac evoked fields. A stimulation catheter specially designed to produce no magnetic disturbances was inserted into the heart of five patients after routine electrophysiological studies. The catheter position was documented on biplane cine x-ray images. MCG signals were then recorded in a magnetically shielded room during cardiac pacing. Noninvasive localization of the catheter's tip and stimulated depolarization was computed from measured MCG data using a moving equivalent current-dipole source in patient-specific boundary element torso models. In all five patients, the MCG localizations were anatomically in good agreement with the catheter positions defined from the x-ray images. The mean distance between the position of the tip of the catheter defined from x-ray fluoroscopy and the MCG localization was 11 +/- 4 mm. The mean three-dimensional difference between the MCG localization at the peak stimulus and the MCG localization, during the ventricular evoked response about 3 ms later, was 4 +/- 1 mm calculated from signal-averaged data. The 95% confidence interval of beat-to-beat localization of the tip of the stimulation catheter from ten consecutive beats in the patients was 4 +/- 2 mm. The propagation velocity of the equivalent current dipole between 5 and 10 ms after the peak stimulus was 0.9 +/- 0.2 m/s. The results show that the use of the amagnetic catheter is technically feasible and reliable in clinical studies. The accurate three-dimensional localization of this multipurpose catheter by multichannel MCG suggests that the method could be developed toward a useful clinical tool during electrophysiological studies.

Adult↗
PubMed1998

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.

Adrenergic beta-Agonists↗
PubMed1998

Autonomic modulation of QT intervals in post-myocardial infarction patients with and without ventricular fibrillation.

The autonomic nervous system plays an important role in the genesis of sudden cardiac death. The aim of this study was to evaluate spatial autonomic QT interval modulation at the myocardial level. Circadian patterns of QT intervals and heart rate variability (HRV) components and their hourly linear correlations were determined by Holter recordings in 15 healthy subjects (controls), in 15 post-myocardial infarction (MI) patients resuscitated from ventricular fibrillation (VF) (VF group), and in 15 matched infarction patients without a history of arrhythmia events (MI group). QT intervals were measured in modified leads V1 and V5 individually at same stable heart rates during each hour and related to hourly measures of HRV. Controls had highly significant correlations between QT intervals and the high-frequency component of HRV (parasympathetic modulation), and between QT intervals and low- to high-frequency ratio (sympathetic modulation) uniformly in both leads (r from 0.62 to 0.81, p <0.001). The MI group had impaired sympathetic modulation in V5 (r = 0.34, p = NS), but had uniform and exaggerated sensitivity to parasympathetic modulation. In the VF group the QT difference between V1 and V5 leads correlated with parasympathetic modulation (r = 0.401, p <0.05) and sympathetic modulation (r = 0.446, p <0.05). Thus, normal subjects exhibit spatially uniform autonomic QT modulation. Myocardial damage can result in abolished, exaggerated, or regionally discordant QT modulation, and this may generate arrhythmic vulnerability.

Adult↗
PubMed1998

Dispersions of the QT interval in postmyocardial infarction patients presenting with ventricular tachycardia or with ventricular fibrillation.

Increased QT interval dispersion is associated with ventricular arrhythmias. The aim of this study was to examine if in postmyocardial infarction patients with impaired left ventricular function, increased QT dispersion is associated with ventricular tachycardia (VT) and ventricular fibrillation (VF). Measures of QT dispersion, calculated as maximum-minimum (D) and standard deviation (SD) of QTend, QTapex, JTend, JTapex, and Tend intervals in the 12-lead electrocardiogram, were compared in patients who late after myocardial infarction experienced sustained VT (VT group) only, VF (VF group) only, or had no ventricular arrhythmias (controls). The 25 patients in each group were individually matched for age, gender, number of diseased coronary vessels, location of the previous myocardial infarction, and left ventricular ejection fraction. Dispersion measures of QTend, QTapex, and JTapex intervals separated VT group from controls, but none of the measures separated the VF group from controls. QTendD was 49+/-18 ms in controls, 57+/-18 ms in the VF group (controls vs VF group, p = NS), and 65+/-29 ms in the VT group (controls vs VT group, p <0.05). VT group had increased QTapexSD, JTapexSD, and JTapexD compared with the VF group. The cycle length of induced sustained monomorphic VT, present in 19 VT and 19 VF patients, correlated with several dispersion indexes in the VT group, but not with those in the VF group. Thus, in postmyocardial infarction patients with a severely damaged left ventricle, increased QT dispersion is associated with susceptibility to sustained VT, but not to VF.

Aged↗
PubMed1998

Molecular genetics of the long QT syndrome: two novel mutations of the KVLQT1 gene and phenotypic expression of the mutant gene in a large kindred.

At least three different gene loci were recently shown to account for the long QT syndrome (LQTS), a monogenic disorder with altered myocardial repolarization and occurrence of life-threatening cardiac arrhythmias. We screened 44 unrelated probands for mutations of the gene encoding the cardiac potassium channel KVLQT1 using single-strand conformational polymorphism (SSCP) and subsequent DNA sequencing. Two different mutations, T182I and D188N, were identified in two separate pedigrees. Cosegregation of the mutation with the disease phenotype was evident in both families. No mutations were identified at codon 212, previously suggested to represent a mutational hot spot of the KVLQT1 channel, in any of the 44 probands. The large pedigree with the D188N mutation (30 affected and 43 nonaffected individuals) permitted an analysis of expression of the mutant gene in its documented carriers. Although the mean (+/-SD) QTc interval was markedly longer in affected (484+/-38 ms) than in nonaffected individuals (406+/-27 ms, P < 0.001), there was a marked overlapping of individual values in these two groups. QTc values in symptomatic and asymptomatic carriers of the mutant gene were not significantly different. In conclusion, we have identified two novel mutations of the KVLQT1 component of a cardiac potassium channel. Our data support the functional significance of the pore-S6 domain of this membrane protein and emphasize the diagnostic usefulness of DNA analyses in families with LQTS.

DNA Mutational Analysis↗
PubMed1998

Effects of epinephrine and phenylephrine on QT interval dispersion in congenital long QT syndrome.

OBJECTIVES: Measurement of QT interval dispersion during pharmacologic adrenergic stimulation was used to assess the effect of alpha- and beta-adrenergic stimulation on arrhythmic vulnerability in familial long QT syndrome (LQTS). BACKGROUND: Nonhomogeneity in the ventricular action potential duration causes electrical instability leading to life-threatening ventricular arrhythmias and is markedly increased in LQTS. QT interval dispersion measured from the electrocardiogram (ECG) can be used as an index of nonhomogeneous ventricular repolarization. METHODS: Sixteen symptomatic patients with LQTS and nine healthy control subjects were examined at baseline and during epinephrine (mainly beta-adrenergic agonist, 0.05 microg/kg body weight per min) and phenylephrine infusions (alpha-adrenergic agonist, mean 1.4 microg/kg per min). QT interval dispersion was determined from a 12-lead ECG as interlead range and coefficient of variation measured to the end (QTend) and apex (QTapex) of the T wave. RESULTS: At baseline QTend dispersion was greater in patients with LQTS compared with control subjects (mean [+/-SD] 68+/-34 vs. 36+/-7 ms, p=0.001). QTend dispersion was markedly increased in patients with LQTS by use of epinephrine (from 68+/-34 to 90+/-36 ms, p=0.002), but remained unchanged in control subjects. Phenylephrine did not affect QT dispersion in either group (all p=NS). Atrial pacing to achieve comparable heart rates during baseline and epinephrine and phenylephrine infusions did not influence the magnitude of QT dispersion in either group. QTapex dispersion analysis gave congruent results. CONCLUSIONS: Epinephrine but not phenylephrine increased QT dispersion, suggesting that beta-adrenergic stimulation provokes arrhythmias in patients with LQTS by aggravating nonhomogeneity of ventricular repolarization, whereas alpha-adrenergic stimulation is less important for arrhythmic vulnerability. The results also suggest that rapid pacing may not reduce vulnerability to arrhythmias in congenital LQTS.

Action Potentials↗
PubMed1998

Evaluation of QT interval duration and dispersion and proposed clinical criteria in diagnosis of long QT syndrome in patients with a genetically uniform type of LQT1.

OBJECTIVES: This study investigated the ability of QT duration, QT dispersion (QTD) and clinical diagnostic criteria to correctly identify genetically documented LQT1 type long QT syndrome (LQTS) patients, and to separate symptomatic and asymptomatic LQT1 patients. BACKGROUND: Ventricular repolarization has played an essential role both in diagnosis and risk assessment of LQTS. Today, molecular genetic techniques permit unequivocal identification of many LQTS patients. METHODS: QT interval and QTD in 12 symptomatic and 18 asymptomatic LQT1 patients and their 43 healthy relatives were evaluated. The sensitivity and specificity of upper normal limits of QT interval, two QT interval adjustment methods (Bazett's and Fridericia's formulas), and the proposed clinical criteria for LQTS were assessed. Occurrence of a mutant (D188N) KVLQT1 gene was considered as the basis of classification into affected and nonaffected individuals. RESULTS: Diagnostic sensitivity and specificity values were 90% and 88% using Bazett's formula, and 80% and 100% using Fridericia's cubic root formula or upper normal limits for QT interval. Suggested diagnostic criteria for LQTS reached 100% specificity, but 47% of the DNA-documented LQT1 patients were classified into the category of low or intermediate probability of LQTS. QT interval and heart rate did not differ between symptomatic (464 +/- 47 ms, 70 +/- 9 min(-1)) and asymptomatic 460 +/- 41 ms, 65 +/- 13 min(-1)) LQT1 patients. QTD was increased in symptomatic LQT1 patients compared to unaffected relatives (66 +/- 48 vs. 37 +/- 15 ms, p = 0.02), but symptomatic patients LQT1 did not differ from asymptomatic (45 +/- 19 ms). CONCLUSIONS: Not all LQT1 patients can be distinguished from healthy relatives by assessment of QT duration or clinical criteria. Presence of LQT1 gene can carry the risk of cardiac events even with no or only marginal prolongation of QT interval.

Adolescent↗
PubMed1998

Rate adaptation of QT intervals during and after exercise in children with congenital long QT syndrome.

OBJECTIVES: To improve the diagnostic criteria of the congenital long QT syndrome in borderline cases we examined rate adaptation of ventricular repolarization phases during exercise and subsequent recovery in children with the long QT syndrome and controls. METHODS: Nineteen children with definite long QT syndrome and 19 healthy controls underwent exercise testing. QT intervals were measured to the apex (early QT), to the end (total QT) and from apex to the end of the T wave (late QT) at heart rates from 90 by steps of 10 to 150 beats, min-1. RESULTS: In 11/19 long QT syndrome patients (61%) and 2/19 controls (12%) the total QT lengthened during the recovery phase compared with exercise (P = 0.005) at the lowest comparable heart rate. No difference was found between the groups during exercise. The sensitivity of rate adaptation of repolarization intervals was analysed by calculating linear regression slopes relating the QT intervals to the heart rates. During recovery, slopes relating the total QT to heart rate were steeper in long QT syndrome patients than those in controls (-2.50 +/- 0.82 vs -1.79 +/- 0.47, P = 0.003). Total QT/heart rate slopes differed between exercise and recovery phases in the long QT syndrome group only (-1.77 +/- 0.71 vs 2.50 +/- 0.82, P = 0.009). In long QT syndrome patients, the difference in total QT/heart rate slopes was mainly because the late QT/heart rate slopes indicating inhomogeneity of repolarization were steeper during recovery (-1.27 +/- 0.74) than during exercise (-0.46 +/- 0.29, P < 0.0001). CONCLUSIONS: After exercise in long QT syndrome children the QT interval lengthens abnormally and inhomogeneity of repolarization increases. Evaluation of the QT interval, and especially its late portion after exercise, may help in establishing the diagnosis of long QT syndrome.

Adaptation, Physiological↗
PubMed1998

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.

Anti-Arrhythmia Agents↗
PubMed1998

Magnetocardiographic QT interval dispersion in postmyocardial infarction patients with sustained ventricular tachycardia: validation of automated QT measurements.

QT dispersion is a measure of heterogeneity in ventricular repolarization. Increased ECG QT dispersion is associated with life-threatening ventricular arrhythmias. We studied if magnetocardiographic (MCG) measures of QT dispersion can separate postmyocardial infarction patients with and without susceptibility to sustained VT. Manual dispersion measurements were compared to a newly adapted automatic QT interval analysis method. Ten patients with a history of sustained VT (VT group) and eight patients without ventricular arrhythmias (Controls) were studied after a remote myocardial infarction. Single-channel MCGs were recorded from 42 locations over the frontal chest area and the signals were averaged. QT dispersion was defined as maximum-minimum or standard deviation of measured QT intervals. VT group showed significantly more QT and JT dispersion than Controls. QTapex dispersions were 127 +/- 26 versus 83 +/- 21 ms (P = 0.004) and QTend dispersions 130 +/- 37 versus 82 +/- 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QTapex and 27% for QTend dispersion on average. In conclusion, increased MCG QT interval dispersion seems to be associated with a susceptibility to VT in postmyocardial infarction patients. MCG mapping with automated QT interval analysis may provide a user independent method to detect nonhomogeneity in ventricular repolarization.

Algorithms↗
PubMed1998

Extensive variation in the signal amplitude of the atrial floating VDD pacing electrode.

The dependence of atrial signal amplitude on the site of the atrial sensing dipole of a single-pass lead was examined in 29 patients. The vertical location of the dipole was documented in supine fluoroscopy during quiescent and deep breathing and in upright chest roentgenogram, and was expressed as a proportion of the right atrial height. As the group average, the atrial signal amplitude was equal when tested in supine, sitting, standing, and right- or left-side positions in follow-up determinations. The signal amplitude varied markedly between postures, showing a coefficient of variation of 45% +/- 24% within the group. Coefficient of variation within the 6-month follow-up period in each tested position ranged from 31%-44%. Correlation between postures was weak (range of r = 0.53-0.81). Vertical location of the atrial dipole had no relationship to the signal amplitude. At least in one posture or test occasion the atrial signal amplitude was very low, < or = 0.35 mV in 20 patients, and below detection limit (0.25 mV) in 5 patients. Programmed to high sensitivity, atrial undersensing was rare in ambulatory electrocardiography, ranging from 0-9,000 missed atrial beats (0%-8%), with a median of 100 beats/24 hours. In conclusion, temporary variation in atrial signal amplitude is extensive. Despite occasionally measured large signal amplitudes atrial sensitivity in single lead VDD pacemakers should be programmed high, and if poor atrial tracking is suspected, other methods besides routine sensitivity testing should be adapted.

Aged↗
PubMed1998

Magnetocardiographic pacemapping for nonfluoroscopic localization of intracardiac electrophysiology catheters.

The purpose of the study was to validate, in patients, the accuracy of magnetocardiography (MCG) for three-dimensional localization of an amagnetic catheter (AC) for multiple monophasic action potential (MAP) with a spatial resolution of 4 mm2. The AC was inserted in five patients after routine electrophysiological study. Four MAPs were simultaneously recorded to monitor the stability of endocardial contact of the AC during the MCG localization. MAP signals were band-pass filtered DC-500 Hz and digitized at 2 KHz. The position of the AC was also imaged by biplane fluoroscopy (XR), along with lead markers. MCG studies were performed with a multichannel SQUID system in the Helsinki BioMag shielded room. Current dipoles (5 mm; 10 mA), activated at the tip of the AC, were localized using the equivalent current dipole (ECD) model in patient-specific boundary element torso. The accuracy of the MCG localizations was evaluated by: (1) anatomic location of ECD in the MRI, (2) mismatch with XR. The AC was correctly localized in the right ventricle of all patients using MRI. The mean three-dimensional mismatch between XR and MCG localizations was 6 +/- 2 mm (beat-to-beat analysis). The co efficient of variation of three-dimensional localization of the AC was 1.37% and the coefficient of reproducibility was 2.6 mm. In patients, in the absence of arrhythmias, average local variation coefficients of right ventricular MAP duration at 50% and 90% of repolarization, were 7.4% and 3.1%, respectively. This study demonstrates that with adequate signal-to-noise ratio, MCG three-dimensional localizations are accurate and reproducible enough to provide nonfluoroscopy dependant multimodal imaging for high resolution endocardial mapping of monophasic action potentials.

Action Potentials↗
PubMed1998

Electrocardiographic measures of ventricular repolarisation dispersion in patients with coronary artery disease susceptible to ventricular fibrillation.

OBJECTIVE: To study electrocardiographic measures of ventricular repolarisation dispersion in patients prone to ventricular fibrillation compared with controls matched for the extent of coronary heart disease and the use of beta blockers. DESIGN: A case-control study. SETTING: Cardiovascular laboratory of a tertiary referral centre. PATIENTS: Fifty patients with documented ventricular fibrillation not associated with acute myocardial infarction, and their controls matched for sex, age, number of diseased coronary vessels, left ventricular ejection fraction, previous myocardial infarction and its location, and the use of beta blockers. MAIN OUTCOME MEASURES: Electrocardiographic measures of QT, JT, and Tend interval dispersions in a 12 lead electrocardiogram. RESULTS: The ventricular fibrillation patients compared to controls showed increased mean (SD) QTapex dispersion (53 (18) ms v 44 (18) ms, respectively; p < 0.01) and mean (SD) Tend dispersion (46 (17) ms v 38 (15) ms, respectively; p < 0.05). CONCLUSIONS: Increased QTapex and Tend dispersions are associated with a susceptibility to ventricular fibrillation even when the extent of the coronary heart disease and use of beta blockers are taken into consideration. However, because of a considerable overlap between the groups, measures of QT dispersion assessed from a 12 lead electrocardiogram do not provide clinically useful information for identification of patients at risk of sudden cardiac death.

Case-Control Studies↗
PubMed1997

Cardiac repolarization interval in end-stage diabetic and nondiabetic renal disease.

BACKGROUND AND HYPOTHESIS: QT interval length is influenced by autonomic nervous activity. In patients with diabetic autonomic neuropathy, both prolongation and shortening of ventricular repolarization has been reported. We studied diabetic and nondiabetic uremic patients to assess the effects of autonomic neuropathy on QT interval length. METHODS: 24-hour electrocardiogram recordings were performed in 12 diabetic and 11 nondiabetic renal transplantation patients, and in 12 control patients. Mean and corrected QT interval (QTc) during the 24-h period and intervals at predetermined heart rates at day and night periods were determined. The degree of autonomic neuropathy was assessed with cardiovascular autonomic function tests and measurement of heart rate variability. RESULTS: In the diabetic group, severe autonomic neuropathy was present; in nondiabetic uremic patients, abnormalities were less severe. Mean QTc interval during 24 h was 444 +/- 24, 447 +/- 21, and 442 +/- 19 ms in the diabetic and nondiabetic uremic patients, and in the control groups, respectively, without any between-group difference. QT and QTc interval length did not differ among the groups when measured at heart rates of 70, 80, 90, or 100 beats/min. CONCLUSIONS: In patients with autonomic failure caused by diabetes and/or uremia, QT interval length cannot be used as a diagnostic indicator of cardiac autonomic neuropathy.

Adult↗
PubMed1997

Electrocardiographic repolarization during stress from awakening on alarm call.

OBJECTIVES: The present study aimed to characterize the electrocardiographic features of cardiac repolarization during an arousal reaction in healthy subjects. BACKGROUND: Electrocardiographic ST segments and T waves may indicate the activity of cardiac autonomic nervous control. Abnormal dynamics of repolarization are considered to reveal susceptibility to cardiac arrhythmias. Responses in normal subjects may help to understand the effects on patients' arrhythmias. METHODS: Ambulatory electrocardiography was performed in 30 healthy physicians during emergency calls while they were on duty in the hospital. Samples were taken before and during the 1st 30 s after the calls. Polarity of the T wave and ST segment depression were determined. The QT interval and the cardiac cycle length (CL) were measured, and their relation (QT/CL slope) was calculated. For comparison, the QT interval was also measured in stable conditions at specified heart rates of 60 to 110 beats/min. RESULTS: During arousal, the T wave was inverted in 19 subjects (63%) and the ST segment depressed > or = 0.1 mV in 10 (33%). The proportional duration of the terminal T wave also varied. The time course of these alterations followed the change in heart rate. During the strongest arousal reaction, the heart rate increased from 55 +/- 7 to 112 +/- 18 beats/min (mean +/-SD) and reached maximum at 17s on average. The QT interval shortened only slightly and was on average 59 to 67 ms longer (p < 0.001) than that at similar heart rates during stable conditions. The QT/CL slope was almost horizontal, 0.085 +/- 0.061, during arousal and much steeper, 0.168 +/- 0.055 (p < 0.001), during stable conditions. CONCLUSIONS: Derangements in the T wave and ST segment as signs of sympathetic overactivity are common during arousal and are associated with marked inertia in QT interval adaptation. These modifications of ventricular repolarization may mediate the generation of stress-provoked arrhythmias in electrically unstable hearts.

Adult↗
PubMed1997

Abnormal ambulatory electrocardiographic findings in patients with the Marfan syndrome.

OBJECTIVES: The aim of this study was to assess the prevalence of cardiac dysrhythmias and abnormalities of conduction and repolarization in the Marfan-syndrome (MFS). SUBJECTS AND METHODS: Forty-five adult MFS patients (25 men) and healthy age and sex matched controls. A 24-h ambulatory electrocardiogram was recorded. RESULTS: There was no difference in heart rates between the two groups. Two MFS patients had atrial fibrillation. The median number of premature atrial beats was 12/24 h in the MFS group vs. 6/24 h in the controls (P < 0.05), and the respective medians of premature ventricular beats were 17/24 h vs. 1/24 h (P < 0.001). Five patients but no healthy person had salvos of > or = 3 premature ventricular complexes (P < 0.05). Ventricular premature beats with R on T configuration were recorded in nine patients but in none of the control subjects (P < 0.05). Both PQ and QT intervals at heart rates of 60, 80 and 100 beats min-1 were longer in the MFS group compared with healthy persons (P < 0.005). Also ST segment depression was seen more often in the MFS group (17/43 vs. 6/45; P < 0.05). In patients with MFS, the findings at ambulatory electrocardiography showed no association with echocardiographically determined aortic root diameter, left atrial diameter or left ventricular diameters, wall thickness and systolic function. Nor did the electrocardiographic findings correlate with the presence of mitral or tricuspid valve prolapse. CONCLUSIONS: Patients with MFS have a higher prevalence of cardiac dysrhythmias than healthy persons. Likewise they have prolonged atrio-ventricular conduction time and disturbed depolarization as suggested by longer QT intervals and more common ST segment depression.

Adult↗