Cardiovascular health in former elite male athletes.

To increase our knowledge on the effects of previous and current physical activity on cardiovascular health, we studied a group of Finnish male former elite athletes (endurance, n = 49; power, n = 50) and their 49 age and area-matched controls, aged 64-89 years. Body mass index (BMI), fasting serum glucose, lipids, blood pressure, and ultrasonography of cardiac and carotid artery structure and function were measured. Former endurance athletes smoked less, had lower prevalence of hypertension, and had higher intensity and volume of leisure time physical activity (LTPA) than the controls. No difference was detected in cardiac or carotid artery structure and function between these groups. Former athletes performing high-intensity LTPA were slightly younger (possible selection bias), had lower BMI and waist circumference, lower use of antihypertensives, lower prevalence of diabetes, lower pulse wave velocity, and higher carotid artery elasticity than former athletes not performing high-intensity LTPA. In conclusion, former athletes had a higher intensity and volume of LTPA than the controls. Athletes performing vigorous LTPA had more elastic arteries than athletes performing moderately or no LTPA. Vigorous LTPA through the whole lifetime associates with good cardiovascular health, although the previous medical history may play an important role.

Fish consumption, omega-3 fatty acids, and environmental contaminants in relation to low-grade inflammation and early atherosclerosis.

BACKGROUND: Fish consumption and omega-3 polyunsaturated fatty acid (PUFA) intake are shown to protect from cardiovascular diseases (CVD). However, most fish contain environmental contaminants such as dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), polychlorinated biphenyls (PCBs), and methylmercury (MeHg) that may have adverse effects on cardiovascular health. OBJECTIVE: Our aim was to elucidate the associations of fish consumption, omega-3 PUFAs, environmental contaminants with low-grade inflammation, early atherosclerosis, and traditional CVD risk factors. METHODS: The Health 2000 survey participants (n=1173) represented the general Finnish population and the Fishermen study participants (n=255) represented a population with high fish consumption and high exposure to environmental contaminants. Model-adjusted geometric means and tests for linear trend were calculated for CVD risk factors by tertiles of fish consumption and serum omega-3 PUFAs, and additionally in the Fishermen study only, by tertiles of serum PCDD/F+PCB, and blood MeHg. RESULTS: Serum triglyceride decreased across omega-3 PUFA tertiles in both sexes and studies. Insulin resistance, C-reactive protein, tumour necrosis factor α, and interleukin 6 decreased across omega-3 PUFA tertiles among the Health 2000 survey participants. Among the Fishermen study men, insulin resistance and arterial stiffness indicated by ß-stiffness index tended to increase and the RR estimate for carotid artery plaque tended to decrease across tertiles of PCDD/F+PCB and MeHg. CONCLUSION: Previously established hypotriglyceridemic and anti-inflammatory effects of omega-3 PUFAs were seen also in this study. The hypothesised favourable effect on insulin sensitivity and arterial elasticity was suggested to be counteracted by high exposure to environmental contaminants but the effect on plaque prevalence appeared not to be harmful.

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.

Home-measured blood pressure is more strongly associated with electrocardiographic left ventricular hypertrophy than is clinic blood pressure: the Finn-HOME study.

Electrocardiographic evidence of left ventricular hypertrophy (ECG-LVH) has a grave prognostic significance in hypertensive patients. The purpose of our study was to assess whether ECG-LVH is more strongly associated with home-measured blood pressure (BP) than with clinic BP, and whether the correlation between home BP and ECG-LVH increases with the number of home measurements performed. We studied a representative sample of the general adult population (1989 subjects 45-74 years of age) in Finland. Subjects included in the study underwent a clinical interview, electrocardiography and measurement of clinic BP (mean of two clinic measurements) and home BP (mean of 14 duplicate home measurements performed during 1 week). Home BP correlated significantly better than clinic BP with the Sokolow-Lyon voltage (home/clinic systolic: r=0.23/0.22, P=0.60; diastolic: r=0.17/0.12, P=0.009), Cornell voltage (systolic: r=0.30/0.25, P=0.004; diastolic: r=0.21/0.12, P<0.001) and Cornell product (systolic: r=0.30/0.24, P=0.001; diastolic r=0.22/0.14, P<0.001) criteria of ECG-LVH. The correlation between home BP and ECG-LVH increased slightly with the number of home measurements, but even the mean of the initial two home BP measurements correlated equally well (systolic BP), or better (diastolic BP) with ECG-LVH than did clinic BP. In conclusion, home BP measurement allows us to obtain a large number of measurements that have a strong association with ECG-LVH. Our data support the application of home BP measurement in clinical practice.

Exercise capacity, disability and leisure physical activity of subjects with multiple sclerosis.

The purpose of the present study was to examine exercise capacity and its relationship to neurological disability as measured using the Expanded Disability Status Scale (EDSS) and to leisure physical activity in subjects with multiple sclerosis (MS). Thirty-four men and 61 women (mean age 44 +/- 6.7 years, mean disease duration 5.7 +/- 6.4 years) with mild to moderate disability (EDSS range 1.0-5.5) participated. They underwent an incremental exercise test on a leg cycling ergometer. Leisure physical activity was measured using a questionnaire. Peak oxygen uptake (VO2peak) in men was 27.0 +/- 5.2 mL/kg/min, and in women 21.7 +/- 5.5 mL/kg/min. The disability correlated inversely with the VO2peak both in men (r = - 0.50, P = 0.004) and in women (r = - 0.25, P = 0.05). No correlation between disease duration and VO2peak was found. In a multivariate regression analysis, neurological disability was confirmed as a predictor of VO2peak. No evidence of a relationship between leisure physical activity and VO2peak was found. A main finding was that disability and exercise capacity are inter-related, even in subjects who are not severely handicapped (84% had an EDSS of < 4.0). The level of disability should be taken into account in the planning of aerobic exercise programs for fully ambulatory MS subjects.

Multiple clinic and home blood pressure measurements versus ambulatory blood pressure monitoring.

To compare multiple clinic and home blood pressure (BP) measurements and ambulatory BP monitoring in the clinical evaluation of hypertension, we studied 239 middle-aged pharmacologically untreated hypertensive men and women who were referred to the study from the primary healthcare provider. Ambulatory BP monitoring was successfully completed for 233 patients. Clinic BP was measured by a trained nurse with a mercury sphygmomanometer and averaged over 4 duplicate measures. Self-recorded home BP was measured with a semiautomatic oscillometric device twice every morning and twice every evening on 7 consecutive days. Ambulatory BP was recorded with an auscultatory device. Two-dimensionally controlled M-mode echocardiography was successfully performed on 232 patients. Twenty-four-hour urinary albumin was determined by nephelometry. Clinic BP was 144.5+/-12.6/94.5+/-7.4 mm Hg, home BP (the mean of 14 self-recorded measures) was 138.9+/-13.1/92.9+/-8.6 mm Hg, home morning BP (the mean of the first 4 duplicate morning measures) was 137.1+/-13.7/92.4+/-9.2 mm Hg, daytime ambulatory BP was 148.3+/-13. 9/91.9+/-7.8 mm Hg, nighttime ambulatory BP was 125.5+/-16.4/75. 6+/-8.9 mm Hg, and 24-hour ambulatory BP was 141.7+/-14.0/87.2+/-7.6 mm Hg. Pearson correlation coefficients of clinic, home, home morning, and daytime ambulatory BPs to albuminuria and to the characteristics of the left ventricle were nearly equal. In multivariate regression analyses, 36% (P<0.0001) of the cross-sectional variation in left ventricular mass index was attributed to gender and home morning systolic BP in models that originally included age, gender, and clinic, self-measured home morning, and ambulatory daytime, nighttime, and 24-hour systolic and diastolic BPs. We concluded that carefully controlled nonphysician-measured clinic and self-measured home BPs, when averaged over 4 duplicate measurements, are as reliable as ambulatory BP monitoring in the clinical evaluation of untreated hypertension.

Effects on left ventricular hypertrophy of long-term nonpharmacological treatment with sodium restriction in mild-to-moderate essential hypertension.

BACKGROUND: Cross-sectional studies on human hypertension have suggested an association between sodium intake and left ventricular hypertrophy (LVH). METHODS AND RESULTS: The effects on LVH of a nonpharmacological treatment program based mainly on sodium restriction were examined by serial echocardiography in a 12-month controlled, randomized study that included 76 previously untreated subjects with uncomplicated mild-to-moderate hypertension. The mean daily sodium excretion of 38 subjects randomized into the treatment group decreased from 195 +/- 95 to 94 +/- 73 mmol (P < .001) at 6 months and to 109 +/- 74 mmol (P < .001) at 12 months. This was accompanied by a weight decrease from 81.4 +/- 18.0 to 79.2 +/- 17.4 kg (P < .001) at 6 months and to 80.6 +/- 17.5 kg (NS) at 12 months. The net blood pressure decrease (difference in change from baseline between the treatment and control groups) was 8.9 mm Hg (P < .001) in systolic blood pressure and 6.5 mm Hg (P < .001) in diastolic blood pressure during the first 6 months and 6.7 mm Hg (P < .01) in systolic blood pressure and 3.8 mm Hg (P < .01) in diastolic blood pressure during the last 6 months. After 12 months of sodium restriction, left ventricular mass (LVM) had decreased by 5.4% (from 238 +/- 63 to 225 +/- 51 g, P < .01), and LVM index (LVMI) had decreased by 4.7% (from 123 +/- 26 to 117 +/- 22 g/m2, P < .05), whereas no changes occurred in these parameters in the control group. In treated subjects with baseline LVMI of more than the median value of 133 g/m2 in men and 107 g/m2 in women, LVM decreased by 8.6% (from 272 +/- 62 to 249 +/- 51 g, P < .01), and LVMI decreased by 7.1% (from 140 +/- 23 to 130 +/- 22 g/m2, P < .01). LVM and LVMI remained unchanged in treated subjects with LVMI values equal to or less than the median. CONCLUSIONS: Our data suggest that long-term nonpharmacological treatment with moderate sodium restriction decreases LVH.

Responses of atrial natriuretic factor to long-term sodium restriction in mild to moderate hypertension.

The effects of long-term sodium restriction on plasma atrial natriuretic factor (ANF) concentrations, and the role of baseline plasma ANF concentration as an indicator of changes in haemodynamics and left ventricular hypertrophy during this treatment were studied in 40 middle-aged previously untreated mildly to moderately hypertensive men and women in a 6-month controlled randomized study. The main emphasis of the treatment programme was to reduce daily sodium intake to less than 70 mmol. Mean sodium excretion decreased from 148 +/- 74 mmol 24 h-1 to 79 +/- 71 mmol 24 h-1 in the treatment group, but remained unchanged in the control group (173 +/- 68 mmol 24 h-1 vs. 186 +/- 62 mmol 24 h-1; P less than 0.01 for the difference in changes between the groups). Mean plasma ANF concentrations in the treatment group were 52.4 +/- 20.7 (median 50) pg ml-1 at baseline and 38.7 +/- 26.3 (median 42) pg ml-1 at 6 months, and the corresponding values in the control group were 55.5 +/- 20.5 (median 50) pg ml-1 and 46.1 +/- 32.4 (median 50) pg ml-1, respectively (P = NS for the difference in changes). The ANF concentration decreased from 70 +/- 14 pg ml-1 to 32 +/- 26 pg ml-1 in treated subjects with a high baseline plasma ANF concentration (greater than 50 pg ml-1), but increased from 37 +/- 11 pg ml-1 to 45 +/- 27 pg ml-1 in subjects with a low baseline plasma ANF concentration (less than or equal to 50 pg ml-1) (difference in changes P less than 0.001). Compared with treated subjects with low baseline plasma ANF levels and with controls, treated subjects with high baseline plasma ANF levels showed a decrease (P less than 0.05) in interventricular septal and left posterior wall thicknesses, in relative wall thickness, and in peripheral resistance. These results suggest that in mildly to moderately hypertensive subjects long-term sodium restriction decreases high plasma ANF concentrations concomitantly with regression of concentric left ventricular hypertrophy, probably as a result of changes in haemodynamics.

Hormone response of diabetic patients to exercise at cool and warm temperatures.

Both exercise and high ambient temperatures stimulate the secretion of counterregulatory hormones which can change glucose homeostasis. We studied whether in diabetic patients there are any differences in the hormonal response to exercise performed at cool or warm ambient temperatures. A study was performed on eight male insulin-dependent patients at rest and during exercise at +10 degrees C and +30 degrees C. Exercise consisted of three consecutive 15-min periods at 60% of maximal aerobic capacity. The concentrations of plasma lactate and counterregulatory hormones at rest were similar at warm and cool temperature, whereas prolactin concentration was higher (P less than 0.01) at +30 degrees C. Exercise resulted in an increase in noradrenaline, growth hormone and prolactin (P less than 0.01), prevented the diurnal decrease in cortisol, but had no effect on glucagon. Hormone responses to exercise were similar at +10 degrees C and at +30 degrees C, except for cortisol and noradrenaline which showed greater responses at warm than at cool temperatures. This may have been due to the higher relative work load at warm compared to cool temperatures as suggested by the higher heart rate and greater increase of lactate at +30 degrees C. These data indicate that within a range of ambient temperatures commonly occurring in sports, the response of counterregulatory hormones is largely independent of ambient temperature in insulin-dependent diabetic patients.