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Biomedical subjects

M Viitasalo

Publications and source records attributed to M Viitasalo.

At least 37 records · Page 2Linked to original sources
PubMed1999

QT interval and QT dispersion in endurance athletes and in power athletes using large doses of anabolic steroids.

We measured electrocardiographic repolarization indexes in athletes. Physiologic adaptive cardiac hypertrophy did not increase QT dispersion in endurance athletes despite long QT intervals due to increased vagal tone. In contrast, power athletes taking large doses of anabolic steroids had increased QT dispersion despite short QT intervals, which seems to reflect altered myocardium in the hypertrophied heart.

Adrenal Cortex Hormones↗
PubMed1999

Effects of acute alcohol infusion on duration and dispersion of QT interval in male patients with coronary artery disease and in healthy controls.

BACKGROUND AND HYPOTHESIS: Alcohol consumption may have advantageous epidemiologic effects but ethanol also increases the risk of sudden coronary death. Prolongation of QT interval has been reported in chronic alcoholics. Long QT period predisposes to serious arrhythmias, and therefore we studied whether acute alcohol intoxication prolongs repolarization in patients with stable coronary artery disease (CAD). METHODS: The effects of acute ethanol steady-state intravenous infusion (0.72 g/kg body weight within 60 min) on QT interval and QT dispersion, assessed by 12-lead electrocardiograms (ECG), were studied in 22 men with stable CAD and in 10 controls. Heart rate variability was measured by Holter recordings. RESULTS: Mean blood alcohol rose to 26.1 +/- 4.3 mmol/l(1.2 +/- 0.2/1000), and was maintained for 2 h. Heart rate was 56 +/- 7 beats/min before and 54 +/- 8 beats/min during ethanol infusion (NS). The heart rate-adjusted QT interval increased on the average 13-23 ms over the 12-lead ECG (p < 0.005). The QT dispersion remained unaltered. The was no difference in the repolarization response in the patients with CAD compared with the controls. The high- and low-frequency components of heart rate variability remained unaltered. CONCLUSIONS: In middle aged men, regardless of the presence of CAD, moderate amounts of alcohol cause prolongation of ventricular repolarization. Changes in the activity of the autonomic nervous system do not seem to explain the observed phenomenon.

Adult↗
PubMed1999

Angiotensinogen gene M235T polymorphism predicts left ventricular hypertrophy in endurance athletes.

OBJECTIVES: We studied whether left ventricular mass in athletes associates with polymorphisms in genes encoding components of the renin-angiotensin system. BACKGROUND: Adaptive left ventricular hypertrophy is a feature of the athlete's heart. However, similarly training athletes develop left ventricular mass to a different extent, suggesting that genetic factors may modulate heart size. METHODS: We measured left ventricular mass by echocardiography in 50 male and 30 female elite endurance athletes aged 25 +/- 4 (mean +/- SD) years. Deoxyribonucleic acid samples were prepared for genotyping of angiotensinogen (AGT) gene M235T polymorphism, angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and angiotensin II type 1 receptor (AT1) gene A1166C polymorphism. RESULTS: The AGT gene M235T genotypes were significantly associated with left ventricular mass independently of blood pressure in both genders (p = 0.0036 for pooled data). TT homozygotes had greater mass compared with MM homozygotes in both men (147 +/- 12 g/m vs. 132 +/- 15 g/m, p = 0.032) and women (121 +/- 12 g/m vs. 101 +/- 13 g/m, p = 0.019). There was a gender difference in the relation between myocardial mass and AGT genotype, MT heterozygotes resembling MM homozygotes among women and TT homozygotes among men. The other studied gene polymorphisms were not associated with left ventricular mass. CONCLUSIONS: Angiotensinogen gene M235T polymorphism is associated with the variability in left ventricular hypertrophy induced by endurance training, with athletes homozygous for the T allele having the largest hearts. We found no association between ACE gene I/D or AT1 gene A1166C polymorphisms and left ventricular mass.

Adaptation, Physiological↗
PubMed1999

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.

Adolescent↗
PubMed1999

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.

Adolescent↗
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

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

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

Effects of acute alcohol ingestion on heart rate variability in patients with documented coronary artery disease and stable angina pectoris.

The effects of acute alcohol intake (ethanol blood concentration 1.3 +/- 0.4%) on heart rate variability were evaluated with 24-hour Holter recordings in 20 patients with stable coronary artery disease in a juice-controlled experiment. In the frequency domain analysis, the high-, low-, and very low frequency components were significantly decreased after alcohol: these changes last longer than the elimination of alcohol.

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↗
PubMed1997

Electrocardiographic findings in female endurance athletes.

OBJECTIVE: To determine the prevalence of aberrations in the resting electrocardiogram (ECG) in female athletes. DESIGN: Case-control study. PARTICIPANTS: Thirty female endurance athletes and 30 age-matched nonobese nonathletic control subjects. MAIN OUTCOME MEASURES: Different measurements based on resting ECGs. MAIN RESULTS: The athletes had lower heart rate (mean 53 +/- SD 7) than the controls (67 +/- 11; p < 0.0001), but no group difference was found in atrioventricular conduction (PQ interval). Cornell voltage (RaVl + SV3) reflecting left ventricular mass was higher in athletes (1.18 +/- 0.58 mV vs. 0.78 +/- 0.41 mV; p = 0.0030), but the deviations from normal limits were small. The index reflecting right ventricular mass (RV1 + SV5) was higher in athletes (0.58 +/- 0.23 mV) than controls (0.45 +/- 0.23 mV; P = 0.036) but did not exceed the criterion for right side hypertrophy. QRS duration was slightly prolonged in athletes (99 +/- 10 ms vs. 92 +/- 9 ms; p = 0.010), as were rate-adjusted QT intervals (p < 0.05). J-point elevations (p = 0.0062) and ST-segment elevations (p = 0.013) were seen more frequently in athletes, but were usually small. CONCLUSIONS: The female athlete's ECG differs less from control subjects than has been reported in male athletes. Extrathoracal anatomic considerations may explain some of the sex differences. However, when clear-cut ECG abnormalities are observed in female athletes, organic heart disease must be carefully excluded.

Adult↗