Prevalence of abnormal ECGs in male soccer players decreases with the Seattle criteria, but is still high.

Electrocardiogram (ECG) and echocardiography are mandatory in preparticipation cardiac screening in soccer players. Abnormal ECG findings usually require follow-up investigations. The main aim of this study was to compare the prevalence of abnormal ECG findings in male professional soccer players according to European Society of Cardiology's (ESC) recommendations and the Seattle criteria, and to assess the need for echocardiography. ECGs from 587 of 595 (99%) players were recorded with ClickECG, and measurements were derived with visually adjusted on-screen calipers on the computer-based averaged PQRST complex. Echocardiographic recordings were performed with Vivid 7/i and categorized according to reference values for athlete's heart. After the initial screening, 32 (5.5%) players were recommended for follow-up. The prevalence of abnormal ECGs was 29.3% vs 11.2% according to the ESC's recommendations and the Seattle criteria, respectively. None of the players with abnormal ECGs only according to the ESC's recommendations had abnormal echocardiograms. Echocardiography alone detected one player with abnormalities (athlete's heart). The Seattle criteria reduced the number of athletes with abnormal ECGs considerably compared with the ESC recommendations. Based on echocardiographic evaluations, this increased the specificity of the Seattle criteria, without increasing the number of false-negative ECGs. The need for mandatory echocardiography in soccer players seems limited.

Visual or computer-based measurements: important for interpretation of athletes' ECG.

BACKGROUND: ECG is recommended for preparticipation health examination in athletes. Owing to a lack of consensus on how to read and interpret athletes' ECGs, different criteria for abnormality are used. AIMS: To compare the prevalence of abnormal ECGs and test the correlation between visual and computer-based measurements. METHODS: In a preparticipation cardiac screening examination of 595 male professional soccer players aged 18-38 years, ECGs were categorised according to the European Society of Cardiology's (ESC) recommendations and the Seattle criteria, respectively. Visual measurements were conducted with callipers on-screen on the averaged PQRST complex in each lead, calculated by the trimmed mean. Computer-based measurements were derived from the medium beat. Heart rhythm and conduction were scored visually by a cardiologist. Categorical variables were compared by κ statistics (K) and continuous variables by intraclass correlation. RESULTS: ECGs of good quality were available from 579 players. According to the ESC's recommendations and Seattle criteria, respectively, ECGs were categorised as abnormal in 171 (29.5%) vs 64 (11.1%) players after visual assessment, and in 293 (50.6%; K=0.395) vs 127 (21.9%; K=0.564) after computer-based measurements. Intraclass correlation was very good for measurements of R and S wave amplitudes and moderate to very good for intervals. K was very good for pathological Q wave amplitudes and moderate for T wave inversions. CONCLUSIONS: Abnormal ECGs were more than twice as common after computer-based than after visual measurements. Such a difference will markedly influence the number of athletes who need further examinations. Reference values may need adjustments dependent on measurement methods.

Low-grade systolic murmurs in healthy middle-aged individuals: innocent or clinically significant? A 35-year follow-up study of 2014 Norwegian men.

OBJECTIVE: To determine whether a low-grade systolic murmur, found at heart auscultation, in middle-aged healthy men influences the long-term risk of aortic valve replacement (AVR) and death from cardiovascular disease (CVD). Setting and subjects. During 1972-1975, 2014 apparently healthy men aged 40-59 years underwent an examination programme including case history, clinical examination, blood tests and a symptom-limited exercise ECG test. Heart auscultation was performed under standardized conditions, and murmurs were graded on a scale from I to VI. No men were found to have grade V/VI murmurs. Participants were followed for up to 35 years. RESULTS: A total of 1541 men had no systolic murmur; 441 had low-grade murmurs (grade I/II) and 32 had moderate-grade murmurs (grade III/IV). Men with low-grade murmurs had a 4.7-fold [95% confidence interval (CI) 2.1-11.1] increased age-adjusted risk of AVR, but no increase in risk of CVD death. Men with moderate-grade murmurs had an 89.3-fold (95% CI 39.2-211.2) age-adjusted risk of AVR and a 1.5-fold (95% CI 0.8-2.5) age-adjusted increased risk of CVD death. CONCLUSIONS: Low-grade systolic murmur was detected at heart auscultation in 21.9% of apparently healthy middle-aged men. Men with low-grade murmur had an increased risk of AVR, but no increase in risk of CVD death. Only 1.6% of men had moderate-grade murmur; these men had a very high risk of AVR and a 1.5-fold albeit non-significant increase in risk of CVD death.

Percentiles of intrauterine placental volume and placental volume relative to fetal volume: A prospective magnetic resonance imaging study.

INTRODUCTION: We aimed to provide percentiles of intrauterine placental growth and placental growth relative to fetal growth (placental to fetal ratio) by measuring placental and fetal volumes by magnetic resonance imaging (MRI). METHODS: In this prospective study, 107 unselected singleton pregnancies were examined by MRI at gestational week 27 and 37. Based on the estimated volumes of the placenta and the fetus, we calculated median and percentiles at gestational weeks 27 and 37. RESULTS: Median placental volume at gestational week 27 was 513 cm3 (Inter Quartile Range (IQR) 182 cm3), and 831 cm3 (IQR 252 cm3) at week 37. The 10th - 90th percentiles included placental volumes between 392 and 717 cm3 at gestational week 27, and 631-1087 cm3 at week 37. The placental to fetal ratio was significantly higher at gestational week 27 than at week 37, with a median ratio of 0.54 (IQR 0.18) and 0.31 (IQR 0.08), respectively (p < 0.001). The 10th-90th percentiles included placental to fetal ratios between 0.43 and 0.73 at gestational week 27 and 0.25-0.39 at week 37. DISCUSSION: At gestational week 27, the placental volume was about half the size of the fetal volume, whereas at week 37, the placental volume was about one third of the fetal volume. This finding suggests that placental growth was less prominent than fetal growth after gestational week 27. Knowledge about the distribution of intrauterine placental size in the general population of pregnancies are prerequisites for diagnosing abnormal placental size.

Magnetic resonance-assisted imaging of slow flow in the pancreatic and common bile duct in healthy volunteers.

BACKGROUND: Magnetic resonance cholangiopancreaticography (MRCP) is commonly used to evaluate the pancreatic (PD) and common bile duct (CBD), and the addition of secretin is used to obtain functional information (S-MRCP). Neither method gives any information on flow velocities within the ducts. PURPOSE: To evaluate a new, MRI diffusion-based, slow-flow-sensitive sequence for the detection of slow flow changes in the PD and CBD. MATERIAL AND METHODS: Seven healthy volunteers were examined. A modified single-shot turbo spin-echo sequence was used to detect slow flow changes. Three b factors (0, 6, and 12 s/mm(2)) were used. The flow sensitivity was applied in two directions, vertically and horizontally. Scanning was performed before and after glucagon was given, and again after an intravenous injection of secretin. The sequence gives signal loss from a duct when flow increases, and such changes were recorded. RESULTS: All images showed the PD with b = 0 (no flow sensitization). After administration of glucagon, artifacts from bowel movements were reduced and visibility of the PD was improved at both b = 6 and b = 12. Significant reduction of the visibility of the PD, indicating increased flow, was recorded both at b = 6 and b = 12 after the administration of secretin. There were no changes in the visibility of the CBD. CONCLUSION: This study shows that MRI-based detection of slow flow changes inside the PD is possible. Due to the sequence's high sensitivity to any motion, further studies are required before adopting the method for clinical use.

Vitamin E restores endothelium dependent vasodilatation in cholesterol fed rabbits: in vivo measurements by photoplethysmography.

OBJECTIVE: Pulse curve plethysmography was used to examine the effect of vitamin E on endothelium dependent and independent vasodilatation in unanaesthetised cholesterol fed rabbits in vivo. The height of the dicrotic notch was used as an index of general arterial vasodilatation. METHODS: Twenty eight rabbits were divided into three study groups; a control group (group 1, n = 8), a group fed 1% cholesterol (group 2, n = 10), and a group fed 1% cholesterol with the addition of 0.2% vitamin E after four weeks (group 3, n = 10). After six weeks on diet the vasodilator responses to acetylcholine and glyceryl trinitrate were measured by photoplethysmography of the rabbit ear. Recordings were made during light sedation at baseline and during infusion of acetylcholine (1.5, 3.0, 6.0, and 12 micrograms.min-1) and glyceryl trinitrate (3.75, 7.5, and 15.0 micrograms.min-1). In a second set of experiments with control fed rabbits (n = 5), acetylcholine infusions were given before and after infusion of L-nitro-arginine (15 mg). RESULTS: The relative height of the dicrotic notch (which predominantly indicates arterial tone in the larger vessels) was reduced by acetylcholine in a dose dependent manner, but in cholesterol fed rabbits (group 2) this response was significantly decreased. Rabbits receiving concomitant dietary vitamin E responded in a similar manner to controls. The difference was most prominent using acetylcholine at a dose of 3.0 micrograms.min-1, where the mean change from baseline was 11(SEM 4)% in group 2, compared to 31(6)% in group 1 (p = 0.01), and to 26(5)% in group 3 (p = 0.02). Similar differences between the groups were observed for the increase in heart rate during acetylcholine infusions. In contrast, the responses to glyceryl trinitrate were similar in all groups. After infusions of L-nitro-arginine, the responses to acetylcholine were blunted. CONCLUSIONS: Supplementation with vitamin E restored the otherwise reduced vascular response to acetylcholine in cholesterol fed rabbits. Analysis of photoplethysmographic pulse curves is a simple non-invasive method of evaluating arterial vasodilator effects. However, the nature of the measured dilator response needs to be characterised further.

Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

The catecholamine content in blood platelets is considerably higher than that in plasma, and platelet catecholamines must be taken up from plasma, since blood platelets lack enzymes for catecholamine synthesis. However, it is unknown whether platelets take up and store catecholamines during physiological in vivo increments in plasma catecholamines. Previously untreated 50-year-old men (n = 17) with mild to moderate essential hypertension were given a low sodium diet for 2 weeks. Urinary excretion of sodium decreased from 201 +/- 11 (SE) to 24 +/- 5 and 19 +/- 4 mmol/24 hr after 1 and 2 weeks, respectively. During the first week, the blood platelet concentration of norepinephrine increased from 27.2 +/- 2.9 to 39.6 +/- 4.7 pg/mg (p less than 0.005) and venous plasma norepinephrine increased from 3.7 +/- 0.4 to 5.6 +/- 0.5 pg/ml (p less than 0.005), and venous plasma dopamine increased from 26 +/- 4 to 41 +/- 5 pg/ml (p less than 0.05). During the second week, both plasma and platelet norepinephrine and dopamine remained elevated. Platelet epinephrine showed a small increase from baseline to the second week (p less than 0.05), but no concomitant increase in plasma epinephrine occurred. Thus, sodium depletion increases both platelet and plasma catecholamines and blood platelets may take up catecholamines in vivo. Platelet catecholamine content may be an integrated measure of plasma catecholamine concentrations during variations caused by sodium depletion.

Increased platelet and vascular smooth muscle reactivity to low-dose adrenaline infusion in mild essential hypertension.

During low-dose adrenaline infusion, platelet count, platelet size, plasma beta-thromboglobulin (BTG) and forearm vascular resistance (FVR) were measured in twelve 40-year-old men with mild, untreated hypertension. The average platelet count increased from 195 to 226 X 10(9)/l (P less than 0.001), platelet size from 7.31 to 7.53 X 10(-15)/l (P less than 0.01), BTG from 0.61 to 1.08 nmol/l (P less than 0.02) and FVR decreased from 97 to 58 (arbitrary units; P less than 0.001) during the infusion. The change in platelet count reflects splenic release of platelets, the change in plasma BTG reflects platelet release reaction, while the reduced FVR reflects vascular smooth muscle cell relaxation. In 11 normotensive men aged 40 years, platelet count increased from 187 to 201 X 10 g/l (P less than 0.01) during an equal low-dose adrenaline infusion. This increase in platelet count is significantly less than in the hypertensive group (P less than 0.01). There was statistically no significant change in platelet size, BTG or FVR in the normotensive group. Arterial adrenaline rose from 0.5 to 2.5 nmol/l in the hypertensive and from 0.5 to 2.4 nmol/l in the normotensive group. A third group of 12 normotensive men received saline infusion: neither platelet parameters nor FVR changed in this group. Thus, a small and equal dose of adrenaline elicited a greater increase in platelet count, an enhanced platelet release reaction and a more pronounced forearm vasodilation in hypertensive than in normotensive subjects.

Increased platelet size and release reaction in essential hypertension.

Basal platelet function was measured in 35 40-year-old men with untreated mild essential hypertension and compared with 44 age-matched normotensive men. The groups differed significantly with respect to platelet size in venous blood (hypertensive, 7.46 +/- 0.10 X 10(-15) l versus normotensive, 7.11 +/- 0.09 X 10(-15) l; P = 0.01) and arterial concentration of the platelet-specific protein beta-thromboglobulin (hypertensive, 1.11 +/- 0.23 nmol/l versus normotensive, 0.59 +/- 0.04 nmol/l; P = 0.02). The normotensive subjects had significantly higher beta-thromboglobulin (BTG) in venous than in arterial blood (P less than 0.01). The hypertensive men showed no such difference. In contrast to the normotensive subjects, the hypertensive group had reduced arterial compared with venous platelet count (P less than 0.01). This may reflect an increased liability in the hypertensive subjects to lose platelets through adherence to the cannula during arterial blood sampling. The above findings point to increased platelet activity in essential hypertension, particularly in arterial blood.

Half-life of platelet factor 4 (PF-4) in plasma and platelets from macaca mulatta.

Human platelet factor 4 (PF-4) showed a reaction of complete identity with PF-4 from Macaca mulatta when tested against rabbit anti-human-PF-4. Such immunoglobulin was used for quantitative precipitation of in vivo labelled PF-4 in monkey serum. The results suggest that the active protein had an intra-platelet half-life of about 21 hours. In vitro 125I-labelled human PF-4 was injected intravenously into two monkeys and isolated by immuno-precipitation from platelet-poor plasma and from platelets disrupted after gel-filtration. Plasma PF-4 was found to have a half-life of 7 to 11 hours. Some of the labelled PF-4 was associated with platelets and this fraction had a rapid initial disappearance rate and a subsequent half-life close to that of plasma PF-4. The results are compatible with the hypothesis that granular PF-4 belongs to a separate compartment, whereas membrane-bound PF-4 and plasma PF-4 may interchange.

Decreased platelet-free dopamine and unchanged noradrenaline and adrenaline in essential hypertension.

The content of free-catecholamines in blood platelets is much higher than in plasma and platelet catecholamines must be taken up from plasma, since platelets lack the enzymes for catecholamine synthesis. There is some evidence that platelet catecholamine content under certain circumstances may be an integrated measure of plasma catecholamine concentrations over time. Platelet-free catecholamines were therefore assayed in 18 untreated patients with essential hypertension and in 16 normotensive control subjects. Mean platelet-free dopamine in the hypertensive group was 3.7 +/- 0.4 pg/mg platelet weight, i.e. significantly less than the 6.5 +/- 0.9 pg/mg found in the normotensive (p less than 0.005). Platelet contents of noradrenaline and adrenaline did not differ. Decreased platelet-free dopamine and unchanged platelet noradrenaline and adrenaline persisted after adjustment for increased body weight in the hypertensive group. Although the reasons for decreased platelet-free dopamine in the hypertensive group remain unknown, this finding may add to previous result showing facilitated release of granular contents from blood platelets in patients with essential hypertension. Our data do not support platelet levels of free-catecholamines to be a marker of increased sympathetic tone in essential hypertension.

Effects of adrenaline infusion on platelet number, volume and release reaction.

At the end of a diagnostic right heart catheterization ten patients received an intravenous infusion of l-adrenaline which gradually increased the arterial plasma adrenaline concentration from resting physiological values to high values as seen during myocardial infarction, pheochromocytoma and hypoglycemia. Blood was sampled from the brachial artery, femoral vein and hepatic vein. During the adrenaline infusion venous beta-thromboglobulin concentrations increased 23% from 61 +/- 5 to 80 +/- 7 micrograms/l (mean +/- SE), arterial platelet counts 20% from 212 +/- 17 to 253 +/- 25 X 10(9)/l and arterial platelet volume 4% from 7.25 +/- 0.20 to 7.56 +/- 0.21 femtoliter. All changes were significant at the 5% level. Thus, acute increments of arterial plasma adrenaline significantly stimulated the blood platelet parameters studied.

Does increased platelet release normalize during anti-hypertensive treatment?

Blood platelet function was evaluated in 10 men, all 50 years old, with untreated, mild hypertension. Each patient was examined four times: At the beginning of the study, after 5 weeks on placebo treatment, after the following 5 weeks on propranolol 160 mg daily, and finally after a second period of 5 weeks on placebo. At baseline the plasma level of the platelet release product beta-thromboglobulin (BTG) was 41.6 (30.5-57.0) micrograms/l (median and 95% confidence interval). During the first placebo period BTG was normalized to 21.0 (14.1-25.9) micrograms/l. While systolic blood pressure and heart rate fell during beta-adrenergic receptor blockade, BTG remained unchanged throughout the rest of the observation periods. Platelet size increased significantly during treatment with beta-blocker. The present study indicates that the normalization of elevated platelet function which previously has been reported to occur during anti-hypertensive drug therapy, may be explained by patient adaptation to the blood sampling procedure.

Effects of fasting on plasma and platelet-free fatty acids and platelet function in healthy males.

10 healthy male volunteers fasted for 72 hours. Their plasma concentration of free fatty acid increased more than two-fold, to 1.8 mmol/l. The number of reversible venous "in vivo" platelet aggregates increased significantly (p less than 0.01); this figure correlated with the concentration of long-chain saturated free fatty acid in plasma (p less than 0.02). The correlation with the amount of long-chain saturated free fatty acid plus oleic acid (18:1) was even better (p less than 0.01). Plasma PF-4 concentration increased, suggesting increased platelet release reaction. In spite of the plasma increase, total platelet FFA concentration was reduced and there was a change in the distribution of platelet free fatty acid which correlated with the degree of aggregation.

Awareness of high blood pressure stimulates platelet release reaction.

The present study aimed at testing the hypothesis of a link between mental stress and blood platelet function. Twenty-nine 19-year-old men were recruited from the 98th percentile of mean blood pressure (116 mmHg) at a routine medical screening. They were not informed about their elevated blood pressures at the time of the screening. One year later they were randomized into two groups. Group 1 (n = 16) was exposed to mental stress by a letter informing them about their high blood pressure, while group 2 (n = 13) was sent a neutral letter. At an examination 2 weeks later, heart rate (p less than 0.05) and plasma adrenaline (p less than 0.05) responses to a cold pressor test were exaggerated in the informed group. The plasma beta-thromboglobulin (beta TG) concentration was elevated in the informed group (p less than 0.05) as was mean blood pressure (p less than 0.05). beta TG correlated positively with hematocrit (r = 0.59, p less than 0.005) and mean blood pressure (r = 0.43, p less than 0.05), and negatively with plasma HDL (r = -0.61, p = 0.001). The study shows that awareness of hypertension induces a hyperadrenergic state which is associated with the platelet release reaction. Under these circumstances platelet release seems to be correlated to established coronary heart disease risk factors.

Increased plasma noradrenaline during severe sodium restriction does not stimulate platelet release in essential hypertension.

Seventeen 50-year old hypertensive men, previously untreated with blood pressure 157 +/- 4/110 +/- 2 mmHg (means +/- SE) were given a low sodium diet for 2 weeks. During the second week, the diet was supplemented with potassium. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:4 and 1:11, respectively. Sympathetic noradrenergic tone increased considerably during the first week. Thus, venous plasma noradrenaline increased from 254 +/- 22 to 347 +/- 28 pg/ml (p less than 0.001) and arterial concentration from 253 +/- 36 to 317 +/- 42 pg/ml (n = 10, p less than 0.001). No significant change was observed in sympathetic adrenal tone as reflected by normal plasma adrenaline in venous (42 +/- 5 vs 43 +/- 6 pg/ml, ns) or arterial blood (71 +/- 10 vs 82 +/- 15 pg/ml, n = 10, ns) or in venous plasma concentration of the blood platelet release product beta-thromboglobulin (BTG) (50 +/- 8 vs 43 +/- 5 ng/ml, ns). During the second week sympathetic noradrenergic tone remained highly significantly elevated compared to baseline but still no change in plasma adrenaline or plasma BTG was found. Thus, whereas sodium depletion did increase plasma noradrenaline concentration markedly in these hypertensive men, no change in adrenaline concentration was observed, and blood platelet release reaction was unchanged. Plasma noradrenaline within the physiological concentration range does not seem to serve as a regulator of in vivo platelet function.

Acute effects of cigarette smoking on platelet function and plasma catecholamines in hypertensive and normotensive men.

In this randomized controlled crossover study essential hypertensive men (n = 13) and matched normotensive controls (n = 18) were examined before and during cigarette and sham smoking to assess the acute effects of smoking on platelets and plasma catecholamines. Platelet activity in vivo was determined by measurements of the released alpha-granule constituent beta-thromboglobulin (beta-TG) in plasma and in urine. Urinary high molecular weight beta-TG and venous plasma epinephrine increased significantly during smoking in the hypertensive group, but not among the normotensive men. Thus, cigarette smoking induces a mild platelet release reaction and also elicits a significantly higher epinephrine response in hypertensive men compared to normotensive controls.

Beta-thromboglobulin in urine and plasma: influence of coronary risk factors.

Blood platelet activation in vivo was evaluated by measuring beta-thromboglobulin in plasma and high molecular weight beta-thromboglobulin in urine in hypertensive smoking and nonsmoking middle-aged men (n=36) and in normotensive age-matched controls (n=40). We found no significant linear relationships between nocturnal or resting urinary high molecular weight beta-thromboglobulin and plasma beta-thromboglobulin in the combined hypertensive and normotensive groups. The excretion of high molecular weight beta-thromboglobulin correlated significantly with diastolic blood pressure when all subjects were pooled. After 60 minutes supine rest, nonsmokers had higher excretion of high molecular weight beta-thromboglobulin than smokers. Plasma beta-thromboglobulin levels tended to be higher in hypertensives. In multivariate analyses, resting high molecular weight beta-thromboglobulin excretion was positively related to diastolic blood pressure and negatively related to smoking, whereas plasma beta-thromboglobulin was positively related to diastolic blood pressure and inversely related to apolipoprotein A1 and B. We conclude that urinary high molecular weight beta-thromboglobulin and plasma beta-thromboglobulin are not closely related, but are complementary analyses, as there are methodological confounders for both variables.

Radiofrequency catheter ablation of two right Mahaïm-like accessory pathways in a patient with Ebstein's anomaly.

A 17-year-old woman with Ebstein's anomaly and recurrent episodes of antidromic tachycardia with two distinct morphologies is described. The tachycardias were produced by two separate Mahaïm-like accessory pathways. These were localized by their activation potentials at the anterolateral ventricular margin of the tricuspid annulus and ablated in a single session using radiofrequency current.