The ACCESS study.
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Biomedical subjects
Publications and source records attributed to M Fotherby.
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OBJECTIVES: To describe the findings in the first year of an integrated syncope clinic for older patients and to review the published literature on "integrated" syncope clinics investigating older people. DESIGN: Review of syncope clinic database and Medline search for relevant literature. SETTING: Outpatient syncope clinics in two district hospitals in the same city. PARTICIPANTS: Secondary referrals from the in- and outpatient population with recurrent unexplained presyncopal and syncopal symptoms. RESULTS: The results of testing in 76 patients over the age of 60 years were available for analysis. A diagnosis was achieved in 67 (88%) of the patients with 76% of the diagnoses being cardiovascular in origin. The prevalence rates of neurocardiogenic syncope (32%) and carotid sinus syndrome (17%), however, differed from previously reported rates. CONCLUSIONS: Evaluation of presyncopal and syncopal events in an "integrated syncope clinic" achieves a high diagnostic yield in older subjects.
Little is known about orthostatic blood pressure regulation in acute stroke. We determined postural haemodynamic responses in 40 patients with acute stroke (mild or moderate severity) and 40 non-stroke control in-patients, at two days ('Day 1') and one week ('Week 1') post-admission. Following a 10-minute supine rest and baseline readings, subjects sat up and blood pressure and heart rate were taken for 5 minutes. The procedure was repeated with subjects moving from supine to the standing posture. Haemodynamic changes from supine data were analysed. On standing up, the control group had a transient significant fall in mean arterial blood pressure on Day 1 but not Week 1. No significant changes were seen on either day when sitting up. In contrast to controls, the stroke group showed increases in mean arterial blood pressure on moving from supine to the sitting and standing positions on both days. Persistent postural hypotension defined as > or = 20 mmHg systolic fall occurred in < 10% of either of the study groups on both days. Sitting and standing heart rates in both groups were significantly faster than supine heart rate on both days. The orthostatic blood pressure elevation is consistent with sympathetic nervous system overactivity which has been reported in acute stroke. Upright positioning as part of early rehabilitation and mobilisation following mild-to-moderate stroke would, therefore, not predispose to detrimental postural reductions in blood pressure.
To determine early and delayed orthostatic BP responses in elderly hospitalized patients on prolonged standing, 85 patients, including normotensive and hypertensive persons, both treated and untreated, aged between 60 and 90 years, were studied. Following 10 min rest a series of nine supine BP measurements were undertaken, first with a mercury sphygmomanometer, immediately followed by an automatic oscillometric BP monitor (SpaceLabs 90207), then again by the sphygmomanometer. Patients then stood and the series of BP measurements was repeated, giving a total of nine standing BP determinations at 1 min intervals. Orthostatic BP measurements recorded by both devices were assessed at 1-3 min (early phase), 4-6 min (mid-phase), and 7-9 min (late phase). The orthostatic fall in SBP was greater during the late than early phase when measured by both the sphygmomanometer (-7.5+/-14.9 vs -2.6+/-10.3 mmHg; difference 4.9+/-8.7 mmHg, p<0.001, 95% CI: 3.0, 6.7 mmHg) and the automatic monitor (-3.5+/-16.9 vs 0.5+/-14.5 mmHg, difference 4.0+/-11.6 mmHg; p=0.002, CI: 1.5, 6.5 mmHg). Orthostatic changes in DBP were similar during early and late phases. More patients had systolic orthostatic hypotension (SBP fall > or =20 mmHg on standing) measured by the sphygmomanometer during the late than early phase (19 [22%] vs 6 [7%]; respectively, p=0.009), but not when measured by the monitor (10 [12%] vs 9 [11%], respectively). Many hospitalized elderly patients may exhibit systolic orthostatic hypotension as measured by sphygmomanometry only after prolonged (> or =7 min) standing.
The sweatspot test assesses the local sweat response to an intradermal injection of acetylcholine. It has been reported as a more sensitive indicator of autonomic dysfunction in important diabetic men than either pupillary or cardiovascular tests, and has been used to establish the presence of autonomic dysfunction in patients with idiopathic chronic constipation. However, the usefulness of this test as a simple and quick method of diagnosing autonomic dysfunction in an elderly population has not been established. This is important given the high prevalence of reduced autonomic function with ageing and hypertension. We compared the age-associated responses in the sweatspot test and its relation to cardiovascular autonomic function in elderly normotensive and hypertensive subjects. We studied eleven normotensive and 24 untreated hypertensive elderly subjects (mean age 75.7 years, range 63-85) and compared the results of the sweatspot test to a young control group (n = 11, mean age 32.0 years, range 25-41), and to a standard battery of cardiovascular autonomic function tests. The median sweatspot score was significantly lower in the elderly compared with young subjects (1.9 vs. 12.0, p < 0.0001) although there was no difference between elderly normotensive and hypertensive subjects (1.6 vs. 2.4, p = 0.8). No correlation was demonstrated between the median sweatspot score and the number of abnormal cardiovascular tests. The sweatspot test was grossly abnormal in all elderly subjects and was not correlated to changes in cardiovascular autonomic function. Its diagnostic use in the elderly is therefore of very limited value.
The effect of an acute oral caffeine load (250 mg capsule) and matching placebo on blood pressure and pulse rate were studied after 48 h caffeine abstention in 8 elderly, normotensive regular caffeine users. The caffeine loading phase was repeated after only 12 h abstention. Following 48 h abstention, supine systolic and diastolic blood pressure were higher for the 120 min study period after the acute caffeine load than placebo (12.1 mm Hg, 95% C.I. 4.3-19.9 mm Hg; P = 0.008 and 7.4 mm Hg, 3.6-11.2 mm Hg; P < 0.001 respectively). Similar differences were seen in standing blood pressure, though pulse rate was unchanged throughout. The pressor response to the acute caffeine load was significantly greater after a 48 h than a 12 hour caffeine abstention period, for supine and standing systolic and diastolic blood pressure. The changes in plasma caffeine levels after acute loading were similar after the 2 different abstention periods. Caffeine ingestion after 48 h abstention has an acute pressor effect in normotensive elderly subjects which is abolished if the abstention period is reduced to 12 h. Acute caffeine ingestion is unlikely to have a significant pressor effect in elderly normotensive subjects who are regular caffeine users as the normal period of caffeine abstention (i.e. overnight) is too short to abolish tolerance.
In young hypertensive patients, after a short period of abstention, caffeine ingestion has a significant pressor effect, although the acute cardiovascular responses have not been reported in elderly hypertensives. This study assessed the acute changes in BP, pulse rate, plasma renin activity (PRA) and arterialised plasma catecholamines after 250 mg of caffeine and matching placebo following 12 and 48 hours of caffeine abstention. After 48 hours caffeine abstention supine SBP was higher over the 120 minute study period following acute caffeine loading than following placebo (10 mmHg; 95% Cl 3-17 mmHg, P = 0.016) although the overall post-caffeine rise from baseline values was small (2 mmHg; -3 to 8 mmHg, P = 0.30). Similar differences were seen for supine DBP and standing SBP and DBP although pulse rate was unchanged throughout. After 12 hours abstention no acute pressor effect of caffeine was seen, in fact SBP fell over the study period (-5 mmHg; -10 to 0 mmHg, P = 0.05), and there was no difference between the caffeine and placebo phases. No change in plasma catecholamines or PRA values was found during any of the phases. These results suggest that in elderly hypertensives the pressor effect of caffeine (the equivalent of two to three cups of coffee) is small even after prolonged abstention. After the shorter abstention period, of the duration likely to be seen in clinical practice, no pressor response to caffeine was demonstrated. It is unlikely that acute caffeine ingestion has a significant effect on clinic BP measurements in elderly hypertensives who are regular caffeine consumers.