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Biomedical subjects

M Pilhall

Publications and source records attributed to M Pilhall.

16 recordsLinked to original sources

Nutcracker oesophagus: a double-blind, placebo-controlled, cross-over study of the effects of lansoprazole.

BACKGROUND: Nutcracker oesophagus is characterized by high-amplitude oesophageal contractions. Recent data have shown a high prevalence of gastro-oesophageal acid reflux in patients with nutcracker oesophagus and, in open-label trials, patients seemed to benefit from acid suppression. Therefore, it has been suggested that non-cardiac chest pain in patients with nutcracker oesophagus may be related to reflux rather than to the motor abnormality itself. AIMS: To investigate the effect of intensive acid-suppressive treatment on chest pain in patients with nutcracker oesophagus. METHODS: Nineteen patients with nutcracker oesophagus received lansoprazole or placebo in a double-blind, randomized, cross-over study. RESULTS: Significant reductions in pain intensity (P < 0.006) and pain duration (P < 0.05) were registered during the study. The magnitude of symptom relief achieved with lansoprazole did not differ significantly from that achieved with placebo. The motility pattern did not change during the study. CONCLUSIONS: This study does not prove that acid-suppressive therapy is effective for pain relief in nutcracker oesophagus. As the amelioration of pain was not accompanied by any change in the nutcracker oesophagus pattern, it is unlikely that the high-amplitude oesophageal contractions are the cause of pain. Thus, the possible role of acid in the pathophysiology of pain in nutcracker oesophagus needs further study.

2-Pyridinylmethylsulfinylbenzimidazoles↗

Diagnosis of nutcracker esophagus, segmental or diffuse hypertensive patterns, and clinical characteristics.

Different criteria have been used for the diagnosis of nutcracker esophagus, but the clinical importance of this is largely unknown. To this end, 45 patients with hypertensive esophageal peristalsis were identified from 572 esophageal investigations, and thereafter explored with regard to diagnostic criteria and clinical background data. The numbers of patients classified as having nutcracker esophagus with different criteria were 25 (by Richter criteria), 39 (by Achem criteria), and 45 (by Gothenburg criteria). In comparison with patients with segmental hypertensive peristalsis, patients with diffuse hypertensive peristalsis were more often referred for chest pain (P < 0.05), less often for reflux symptoms (P < 0.05), and tended to have arterial hypertension less often (P < 0.08). In conclusion, the choice of criteria for the diagnosis of nutcracker hypertensive peristalsis has prominent effects on the number of patients receiving this diagnosis. Moreover, a diffuse nutcracker peristaltic pattern appears more strongly linked to chest pain.

Chest Pain↗

Gastroesophageal acid reflux in patients with nutcracker esophagus.

BACKGROUND: Hypertensive esophageal contraction, called nutcracker esophagus (NE), is the most common motility abnormality associated with cardiac-like chest pain. However, its significance for the development of symptoms has been a matter of controversy for decades, and recently it has been suggested that NE might represent a primarily acid-related esophageal disorder. The frequency of acid-related esophageal dysfunction is studied in an unselected group of patients with NE. METHODS: During the period March 1993 to June 1998, 572 consecutive patients underwent esophageal manometry and 24-h pH monitoring. RESULTS: A motility pattern consistent with NE was found in 45 subjects referred because of chest pain (n = 35), reflux dyspepsia only (n = 8) or epigastric pain (n = 2). Acid-related esophageal dysfunction was noted in 30 (70%) of the NE patients; abnormal acid exposure time (n = 21), esophagitis (n = 2) or positive symptom index (n = 7). In addition, an increased number of reflux episodes were found in another three subjects. NE was more prevalent in subjects referred for chest pain than in those referred for other symptoms (14.3% versus 4.5%; P < 0.0001) and, conversely, 78% of the patients with NE were referred because of chest pain. CONCLUSIONS: Various aspects of acid-related esophageal dysfunction occur frequently in patients with NE, suggesting that acid may play a role in the development of symptoms in NE. Nonetheless, given its association with chest pain, NE could be a marker of a subgroup of patients with acid reflux, distinct from other reflux patients.

Chest Pain↗

Effects of spinal cord stimulation and coronary artery bypass grafting on myocardial ischemia and heart rate variability: further results from the ESBY study.

In the present study, 24-hour ECG recordings were analyzed from the Electrical Stimulation versus Coronary Artery Bypass Surgery (ESBY) Study where spinal cord stimulation was compared to CABG (coronary artery bypass grafting) in selected patients with severe angina pectoris. During the monitoring period, the spinal cord stimulation was discontinued to evaluate possible long-term effects of this treatment. The number of ischemic episodes and the duration of ischemia decreased in the CABG group at the follow-up when compared to spinal cord stimulation (p<0.05). In spite of this, the number of anginal attacks decreased (p<0.0001) in both groups. The fact that the anginal symptoms decreased in the spinal cord stimulation group in spite of discontinued stimulation and lack of effects on ischemic ST changes could indicate a long-term primary analgesic effect of this treatment in addition to the well-documented acute anti-ischemic effect.

Angina Pectoris↗

Esophageal dysfunction in syndrome X.

Syndrome X is defined as anginal chest pain accompanied by objective signs of ischemia on exercise testing or myocardial scintigraphy, but with angiographically "normal" coronary arteries. The etiology of this enticing syndrome is still not known. Besides myocardial ischemia, esophageal dysfunction and visceral hypersensitivity may play a role in the development of pain. The purpose of this study was to study esophageal function and visceral sensitivity in patients with syndrome X. Twenty consecutive patients with the diagnosis of syndrome X were investigated with esophageal manometry and a 24-hour pH recording. Visceral esophageal sensitivity was explored by balloon distention of the distal esophagus, as well as by instillation of acid. Twelve patients (67% of the 18 evaluated) had some abnormality on 24-hour pH monitoring; 2 had abnormal global acid exposure time (pH <4) and 7 had symptoms coincidental with episodes of pH <4. Seven patients (35%) had esophageal dysmotility including 5 with the "nutcracker" esophagus. Esophageal hypersensitivity to acid (n = 9) or distention (n = 13) was seen in 14 of the 20 patients. Eleven patients received acid suppressive therapy that resulted in amelioration of chest pain in 8 (73%). Thus, results suggest that esophageal hypersensitivity rather than gross functional abnormality is an important factor for the development of chest pain in patients with syndrome X, and that acid in the context of a hypersensitive esophagus is the main culprit. Acid suppression may ameliorate pain in a substantial proportion of patients.

Adult↗

Esophageal visceral pain sensitivity: effects of TENS and correlation with manometric findings.

Increased esophageal visceral sensitivity has been suggested to be an important factor in the development of esophageal chest pain. Transcutaneous electrical nerve stimulation (TENS) has been found effective in the treatment of visceral heart pain in severe angina pectoris, but its effect on esophageal pain perception is not known. In this study, we used the method of graded intraesophageal balloon distension to study the effects of TENS on esophageal motility and pain sensitivity. In addition, we explored the relationship between manometric findings and esophageal susceptibility to pain. TENS reduced symptoms during balloon distension significantly and decreased peristaltic velocity. Increased visceral perception was positively correlated to the amplitude and duration of the esophageal peristalsis. This study suggests a correlation between increased peristaltic waves and visceral perception in the esophagus. TENS appears to reduce esophageal pain sensitivity and thus may be a useful treatment for noncardiac chest pain of esophageal origin.

Aged↗

Estrogen and progestagen modify the hemodynamic response to mental stress in young women.

OBJECTIVE: To evaluate separately the effects of estrogen and progestagen on the cardiovascular response to a standardized mental stress test. METHODS: Seven women were studied during the early follicular phase (day 1-4) of three different menstrual cycles after randomized oral administration of either 6 mg estradiol valerate or 15 mg norethisterone acetate or placebo. Heart rate and blood pressure were recorded at rest for 2 hours after administration and throughout the stress test. Forearm plethysmography was recorded at rest and during stress. RESULTS: Estrogen had no effect on heart rate or blood pressure at rest. After estrogen administration the increases in heart rate (delta 14 bpm/10 bpm; p < 0.01) and diastolic blood pressure (delta 14 mmHg/9 mmHg: p = 0.06) from baseline to stress were augmented compared to those observed after placebo administration. Heart rate, systolic and diastolic blood pressures reached higher levels during stress after estrogen administration compared to placebo (delta 5 bpm, and delta 7 mmHg and delta 5 mmHg respectively; p < 0.05). Estrogen administration also caused a prolongation of the diastolic blood pressure response to stress. Progestagen compared to placebo induced an increase in heart rate already at rest (delta 4 bpm; p < 0.01), and heart rate was maintained on a higher level throughout the stress test (p < 0.05). Blood pressure at rest and pressor responses to stress were not significantly changed after progestagen administration. CONCLUSIONS: The results indicate that estrogen is responsible for the enhanced cardiovascular responses to stress, whereas progestagen provokes a parallel upward shift of basal heart rate which is independent of level of activation.

Adult↗

Changes in the QRS segment during exercise: effects of acute beta-blockade with propranolol.

Changes in the QRS complex during exercise may provide information with respect to ischaemic heart disease. The intention with present investigation was to shed light on mechanisms behind QRS changes and to study the possibly confounding effects of beta-blockade on such alterations with exercise. Placebo or propranolol respectively was infused in randomized and double-blinded order in seven young healthy men before a maximum exercise test. Advanced computerized vectorcardiography and impedance cardiography was recorded continuously together with blood pressures and blood samples. The Y-lead magnitude increased significantly with propranolol infusion (P < 0.05), but it tended to decrease in the Z-lead (P < 0.07). While the serum potassium concentrations increased (P < 0.0005), the spatial QRS magnitude tended to decrease irrespective of treatment (P < 0.07). These changes correlated with changes in QR-duration (adj r2 > 0.58). With exercise, the mean spatial QRS magnitude decreased with similar amounts irrespective of treatment. However, propranolol made the magnitude decrease earlier (P < 0.01). No effect of treatment was detected on the decrease in QRS-duration. Immediately after exercise, the QRS complex continued to change as during exercise in the placebo investigations, but did not with propranolol (P < 0.05). These different patterns were most obvious in the first half of the QRS complex in the Y-lead. It is concluded that acute beta-blockade modifies QRS alterations both during and after exercise in healthy subjects. This indicates that such drugs may have confounding effects in evaluations of the diagnostic value of QRS alterations.

Adult↗

Changes in QRS segments during exercise in relation to scintigraphic myocardial perfusion defects: a multivariate analysis.

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.

Adult↗

Exercise-induced QRS changes in healthy men and women: a multivariate analysis on their relation to background data and exercise performance.

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.

Adult↗

Ischaemic heart disease and the changes in the QRS and ST segments during exercise: a pilot study with a novel vectorcardiographic system.

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.

Coronary Disease↗

Cardiovascular responses to stress in young hypertensive women.

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.

Adult↗

Effect of cholinergic blockade on heart rate, blood pressure and plasma catecholamine responses to mental stress in normal subjects.

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.

Adult↗

Haemodynamic responses to psychosocial stress during the menstrual cycle.

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.

Adult↗

Short-term reproducibility of a mental arithmetic stress test.

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.

Adult↗

Infusion of epinephrine augments pressor responses to mental stress.

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.

Adult↗