Obstructive sleep apnea and hypertension--double trouble?
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Biomedical subjects
Publications and source records attributed to S Jern.
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BACKGROUND: The relation between QRS changes during exercise and ischemic heart disease is controversial. The present investigation addressed whether exercise QRS changes are related 1) to myocardial ischemia or necrosis, 2) to possibly confounding factors such as baseline QRS size and changes in heart rate and ST magnitude during exercise, and 3) to the location of scintigraphic defects. METHODS: Advanced computerized vectorcardiography (MIDA1000, Ortivus Medical AB, Sweden) was recorded in 71 consecutive patients referred for 201TI exercise myocardial scintigraphy. Maximal exercise tests were performed in the sitting position on a bicycle ergometer. Planar scintigraphic images were obtained immediately after exercise and 4 hours later in three projections, and were evaluated blindly. RESULTS: Exercise QRS changes correlated to baseline QRS size (X, Y, and Z leads; P < 0.005), change in heart rate (X and Y leads; P < 0.01), and ST change at J + 20 ms (X, Y, and Z leads; P < 0.0001). Increased QRS magnitudes in the Y and Z leads correlated to late perfusion defects (P < 0.0001). These correlations remained after correction for baseline QRS size and changes in heart rate and ST magnitude at J+20 ms during exercise (P < 0.0001). No consistent relationships were observed between the location of myocardial perfusion defects and the stress-induced alterations in QRS. CONCLUSIONS: Baseline QRS size and changes in heart rate and ST magnitude may have important confounding effects on the QRS response to exercise. However, even after consideration of these factors, the QRS response to exercise was related to late (4 h) scintigraphic myocardial perfusion defects. The findings suggest that the presence of myocardial infarctions or long-lasting ischemia after exercise is associated with increased QRS magnitudes during exercise.
The treatment of hypertension is based on an assessment of the balance between the effects of therapy on survival on the one hand and effects of the patient's symptoms and well-being on the other. The concept of quality of life is used to summarise the latter effects. Preservation of quality of life involves both the prevention of hypertensive complications and detrimental effects on well-being induced by drugs. However, scientific accumulation of data in this area has been severely hampered by the lack of consensus as to how quality of life should be defined and measured. The scientific power of the quality of life concept has also yet to be proven. Although recent studies indicate that specific aspects of quality of life could be adequately assessed the relative importance of minor shifts in questionnaire or test scores remains an unresolved scientific and clinical issue. Despite these shortcomings a series of studies now available suggests that there are only minor differences between the first-line antihypertensive drugs (e.g. beta-blockers and ACE inhibitors) regarding their effect on quality of life.
Urinary cortisol output and serum cortisol concentrations were measured in the steady state, under "field" conditions, and during standardized inhibitory and stimulatory tests in premenopausal, obese women, and were analyzed in relation to adipose tissue distribution. Urinary cortisol output was increased under field conditions in women with an elevated waist to hip circumference ratio (WHR) and, in particular, in women with a large abdominal sagittal diameter, indicating visceral fat accumulation. However, dexamethasone inhibition of cortisol secretion was normal. Stimulation with corticotropin analogue and with physical (cold-pressor test) or mental (color-word or mathematic) stress tests also showed elevated responses of serum cortisol, but not of prolactin or growth hormone concentrations. It is suggested that women with visceral fat accumulation have elevated cortisol secretion due to an increased sensitivity along the hypothalamic-pituitary-adrenal axis, and that this may be causing their abnormal fat depot distribution.
Changes in the QRS segment during exercise have repeatedly been suggested to provide diagnostic information with respect to ischaemic heart disease, but the subject is controversial. In order to study the possibly confounding effects of gender, age, resting ECG and exercise performance, 50 healthy subjects were investigated with computerized vectorcardiography during a maximal ergometer exercise test. The overall change in the QRS complex decreased significantly with age and female gender (P < 0.001). However, these responses were better explained by baseline QRS size, change in heart rate and systolic blood pressure (adjusted r2 > 0.70, vs adjusted r2 > 0.41). Effects of age were seen in the Y-lead, and gender effects in the X- and Z-leads (P < 0.0001). In multivariate analyses, X- and Y-lead alterations correlated negatively to change in heart rate and resting QRS size (X-lead; adjusted r2 > 0.50, Y-lead; r2 > 0.44). Z-lead alterations correlated negatively with female gender and resting Z-lead QRS size (adjusted r2 > 0.31). ST changes correlated with QRS changes in the X- and Y-leads (P < 0.05). QRS changes immediately after exercise correlated with alterations during exercise (P < 0.004), maximal load (P < 0.01) and time to hypotension post-exercise (X- and Z-lead; P < 0.02). In conclusion, QRS changes appear to be related to baseline QRS size, change in heart rate and ST change, factors which may have important confounding effects. Consideration of these factors may help in resolving the controversy surrounding QRS changes.
In order to find new ischaemic parameters, the spatial changes of the Frank vectorcardiogram were continuously analysed with a new, highly precise vectorcardiographic method during, and immediately after a maximal exercise test. This was done in 18 young healthy males, and 18 patients with scintigraphic reversible ischaemia. During exercise, different patterns between the groups were noted for the changes in the mean QRS magnitude in the Y-lead (P less than 0.005), the QRS-integral (P less than 0.05), and the QRS-duration (P less than 0.05). Immediately after exercise, several QRS parameters in the normal group continued to change according to the same pattern as during exercise (P less than 0.05), which was in contrast with the patterns of the ischaemic group (P less than 0.01). The spatial ST difference at J+20 ms discriminated well between the groups, especially when corrected for QRS-magnitudes at rest and heart rate (P less than 0.0005). In short, this pilot study supports previous findings in that changes in amplitude and duration of the QRS complex during exercise discriminated between healthy young males and patients with ischaemic heart disease. Moreover, rapid discriminating changes were seen in the QRS segment during cessation of exercise. These changes deserve attention since they may be of importance for the conflicting results on the diagnostic value of QRS changes during exercise.
Central obesity increases the risk for cardiovascular disease, but little is known about its hemodynamic effects. The aims were to investigate the influence of obesity (as defined by body mass index) and abdominal fat accumulation (as defined by the waist/hip ratio) on hemodynamics at rest and during mental stress. Invasive hemodynamic studies were performed in 20 healthy, normotensive young men (aged 18-22 years) recruited from an unbiased population sample. Their body mass index and waist/hip ratio ranged between 18.5 and 30.2 (mean 24.1) and 0.77 and 0.98 (mean 0.87), respectively. Hemodynamics were related to the two anthropometric indexes by bivariate regression analyses. Cardiac output and stroke volume were positively correlated to body mass index (p = 0.05 and p = 0.005), but inversely to waist/hip ratio (p = 0.01 and p = 0.01). Mental stress augmented the hemodynamic patterns. Total peripheral resistance during stress correlated inversely to body mass index (p = 0.02), whereas high waist/hip ratio was associated with higher systemic vascular resistance p = 0.002). The delta CO/delta MAP ratio, i.e., relative contribution of cardiac output for the stress-induced increase in mean arterial pressure, showed a strong positive association with body mass index (p = 0.004), but was inversely related to the waist/hip ratio (p = 0.002). Serum insulin correlated significantly to the stress-induced change in total peripheral resistance (r = 0.54; p = 0.02), whereas the increase in cardiac output was inversely related to insulin (r = -0.59; p = 0.007). Thus, central obesity is associated with a specific hemodynamic pattern characterized by higher total peripheral resistance, lower cardiac output, and a vasoconstrictor response to psychosocial stress.
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Hypertrophic adaptation of the left ventricle and blood vessels is a prominent feature of established essential hypertension. Presence of left ventricular hypertrophy in hypertension increases, independently of other risk factors, the risk for a number of the most important cardiovascular hypertensive complications. Available evidence indicates that left ventricular hypertrophy develops in close parallel with the peripheral vascular changes. Structural involvement can be detected already in early phases of borderline hypertension. The pathophysiology of structural changes in hypertension appears to be dependent on a complex interplay between genetic, hemodynamic, and humoral-metabolic factors.
OBJECTIVE: The aim of the study was to investigate the haemodynamic effects of hormonal changes during the menstrual cycle in 11 hypertensive women aged between 29 and 38 years. DESIGN: In randomized order, the subjects were examined on days 2-7 (follicular phase) and on days 20-24 (luteal phase). All medication was withdrawn on average 5 weeks prior to the experiment. The results in the hypertensive group were compared with those of a control group consisting of 11 normotensive women aged between 21 and 46 years who had earlier taken part in an identical experiment. METHODS: A standardized mental stress test and a 24-h ambulatory blood pressure and heart rate recording were performed. RESULTS. Prestress resting heart rate was significantly higher in the hypertensive group and a significant difference was maintained throughout the entire stress experiment. Heart rate, systolic and diastolic blood pressure increased highly significantly in both groups during the exposure to mental stress, but no difference in heart rate or blood pressure reactivity between the normotensive and hypertensive groups was found in either phase. Heart rate reactivity did not differ during the two phases in the hypertensive group, in contrast to our previous findings in normotensives. During 24-h ambulatory recording both groups had slightly but significantly higher heart rate and systolic blood pressure in the luteal phase. In the hypertensives the diastolic blood pressure was also higher in this phase. Both groups had significantly higher serum oestradiol and progesterone levels in the luteal phase. CONCLUSIONS: The findings of the present study support the hypothesis that female sex hormones affect cardiovascular control in both normotensive and hypertensive women.
A male fat distribution pattern with abdominal obesity increases the risk for hypertension and cardiovascular disease, and is closely linked to a number of metabolic aberrations including insulin resistance. Recent observations suggest that changes in the peripheral vasculature may be of pathophysiological importance for the development of hypertension and its associated metabolic disturbances. We therefore investigated the hemodynamic correlates of abdominal obesity. A central fat distribution was found to be associated with a specific hemodynamic profile, characterized by elevated total peripheral resistance and lower cardiac output. In response to sympathoadrenal activation during mental stress, the normal cardiac output-dependent pressor response was reversed into a systemic vasoconstrictor response. There was a direct relationship between degree of abdominal obesity (expressed as waist-hip ratio) and fasting serum insulin. Furthermore, the stress-induced increase in total peripheral resistance correlated positively with fasting serum insulin concentration, whereas there was an inverse relation between serum insulin and cardiac output and heart rate. In a second study, the circulatory responses to stress during physiological hyperinsulinemia were investigated. During hyperglycemic hyperinsulinemia the central hemodynamic response to stress was changed into a systemic vasoconstrictor response. In the forearm the physiological vasodilation during stress was markedly attenuated, suggesting that insulin may have peripheral vascular effects. In conclusion, central obesity is associated with a specific hemodynamic pattern characterized by higher total peripheral resistance and lower cardiac output, and a vasoconstrictor response to psychosocial stress. This hemodynamic response pattern may be related to insulin metabolism.
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To study the effect of sex hormones on the hemostatic responses to stress, blood samples were collected before, during, and after 20 min of mental stress from 9 healthy, non-smoking female volunteers, examined in the follicular and luteal phase. Mental stress caused significant increases in heart rate, blood pressure, and plasma catecholamines. In addition, analysis of variance indicated significant changes of leukocyte count, hematocrit, fibrinogen, von Willebrand factor antigen, t-PA activity and antigen in response to the stress test. However, in contrast to a male group previously investigated, there were no significant changes in factor VII coagulant activity in either menstrual phase. Overall the responses were more pronounced in the luteal as compared to the follicular phase. The findings support the concept that both gender and physiological variations in female sex hormones may modulate hemostatic responses to psychosocial stress.
The effects of cholinergic blockade on haemodynamic reactivity to standardized mental stress has been studied in nine normotensive males during infusion of atropine (bolus dose 10 micrograms x kg-1 followed by a constant-rate infusion of 0.02 microgram x kg-1 x min-1) or placebo given in a randomized order on two different days. Partial cholinergic blockade increased resting heart rate by 25-30 beats per minute. The magnitude of the heart rate response to stress (reactivity) however was unaffected by the atropine infusion. Also, in four subjects who received a higher dose of atropine (approximately 1.8-1.9 mg), heart rate responses to stress were the same as during placebo infusion. Cholinergic blockade was associated with a small but prolonged increase in diastolic blood pressure. These findings suggest that parasympathetic withdrawal does not contribute to the tachycardia caused by mental arithmetic, and that the pattern of neurogenic activation may differ from that elicited during a classic defence-alarm reaction and by somatomotor activation.
To determine the importance of emotional stress for relative polycythaemia, we studied 11 subjects with the Type A and 11 subjects with the Type B behaviour patterns during short-term mental stress. All subjects were healthy, normotensive non-smoking young males aged 20-34 yr. without any medication. During rest there were no significant differences in heart rate, blood pressure, or plasma catecholamines between the two groups, but the A-group had significantly higher haemoglobin concentration (147 vs 140 g/l; p less than 0.005) and haematocrit (43.8 vs 42.1%: p = 0.05) than the B-group. In the whole group, there was a positive correlation between resting diastolic blood pressure and haemoglobin concentration (r = 0.53; p less than 0.05). In response to 10 min of mental arithmetic, haematocrit, haemoglobin and erythrocyte count rose approximately 2% (p less than 0.001 throughout). The stress-induced changes were not significantly different between the A- and B-groups. It is concluded that mild relative polycythaemia could be induced by acute emotional stress. In subjects with the Type A behaviour pattern a slight haemoconcentration is present already at rest, which further increases during stress.
1. The haemodynamic effects of hormonal changes during the menstrual cycle were examined in 11 normotensive women (age 20-46 years). The subjects were studied on days 2-8 (follicular phase) and days 18-26 (luteal phase) in a randomized order. A standardized mental stress test and a 24 h recording of ambulatory blood pressure and heart rate were performed. 2. Pre-stress resting levels of heart rate and blood pressure were similar during the two phases of the menstrual cycle. 3. During mental stress, the heart rate response was significantly greater during the luteal phase than during the follicular phase (14.7 versus 9.7 beats/min; P less than 0.05). 4. Blood pressure, plasma catecholamine concentrations and subjective stress experience increased significantly in response to stress, without any significant differences between the two phases. 5. During 24 h ambulatory monitoring, higher levels of systolic blood pressure and heart rate were observed in the luteal phase than in the follicular phase (P less than 0.005 and P less than 0.0001, respectively). 6. These data indicate that cyclic variations in female sex hormones not only affect systolic blood pressure and heart rate, but also alter the haemodynamic responses to psychosocial stress.
1. To evaluate the short-term reproducibility of heart rate, oscillometrically determined blood pressure, antecubital venous plasma catecholamine concentrations and subjective responses to strictly standardized mental arithmetic, we performed two identical tests 1 h apart in 14 young, healthy and normotensive male subjects (age 22-35 years). 2. Heart rate and blood pressure responses to the two stress tests were highly correlated, when expressed both as correlations between levels attained during stress (rs greater than 0.80 throughout) and as absolute reactivity measures (all rs greater than 0.75). Also, subjective stress responses were highly correlated, when considering both levels during stress and reactivity (r = 0.97 and r = 0.85, respectively). Stress levels of catecholamines were correlated, but the change scores (reactivity) were unrelated. 3. The measurement error SD for heart rate was 2.6 and 3.0 beats/min for reactivity and stress levels, respectively. The corresponding SD for blood pressure ranged between 2.7 and 4.4 mmHg. Subjective stress experience showed an SD of a similar magnitude. The responses of plasma catecholamine concentrations were subject to considerable variability. 4. It is concluded that haemodynamic and subjective stress responses and stress levels during the mental arithmetic stress test show acceptable reproducibility and high test-retest correlations. However, stress-induced changes in venous plasma catecholamine concentrations show low reproducibility.
Circulating epinephrine may facilitate neural release of norepinephrine both during and after periods of sympathoadrenal activation by stimulation of prejunctional beta-adrenergic receptors. The present study was undertaken to examine possible effects and aftereffects of epinephrine on the hemodynamic reactivity to mental stress. To this end, two strictly standardized mental stress tests were performed in 14 normotensive men during and 1 hour after double-blind infusion of epinephrine (50 ng x kg-1 x min-1) or placebo given in random order. During epinephrine infusion, the systolic pressor response to psychosocial stress was augmented (+17 versus +10 mm Hg during epinephrine and placebo, respectively; p = 0.02). This was associated with an attenuated post-stress recovery, with the result that the stress exposure induced a prolonged elevation of systolic blood pressure. Heart rate was elevated and diastolic blood pressure lowered during epinephrine infusion without any change in the reactivity to stress. One hour after the end of the epinephrine infusion resting heart rate was still maintained on a higher level independently of level of arousal, but heart rate and blood pressure responses to stress were unaffected. The findings are consistent with the hypothesis that high circulating epinephrine levels amplify pressor responses to mental stress but do not support the suggestion that short-term infusion of epinephrine causes prolonged augmentation of blood pressure responses to psychosocial stress.