Nocturnal blood pressure predicts left ventricular mass index in normotensive elderly.

Blood pressure (BP) predictors of left ventricular mass index (LVMI) were studied in 40 healthy normotensive (71.4 +/- 4.4 years) and 31 hypertensive (73.5 +/- 4.8 years) elderly community-dwelling subjects using short-axis cardiac cine magnetic resonance imaging and 24-h ambulatory BP monitoring. Mean night-time BPs were calculated from the average of readings during sleep and mean daytime BPs were calculated from the remaining recordings. The hypertensive subjects were all receiving anti-hypertensive therapy with angiotensin-converting enzyme (ACE) inhibitors, calcium-channel blockers, beta-blockers or diuretics. Nocturnal systolic BP was a strong predictor of LVMI in both normotensive (beta = 0.38, p = 0.02) and treated hypertensive (beta = 0.39, p = 0.03) subjects. By contrast, daytime systolic BP was a weaker predictor of LVMI in the treated hypertensives (beta = 0.36, p = 0.04) and did not predict LVMI in the normal subjects (beta = 0.27, NS). Nocturnal BP may partly explain the increase in LVMI with ageing in subjects thought to be normotensive on the basis of daytime clinic BP recordings.

Effects of hormone replacement therapy on ambulatory blood pressure and vascular responses in normotensive women.

The effects of chronic oestrogen replacement therapy (ERT) (conjugated equine oestrogen 0.625 mg/day) and combined oestrogen and progestogen replacement therapy (HRT) (ERT plus continuous medroxyprogesterone acetate 5 mg/day) on 24-h ambulatory blood pressure recordings, forearm vascular resistance (FVR) and FVR responses to noradrenaline, angiotensin II, acetylcholine and nitroprusside were studied in 17 normotensive postmenopausal women in a 3-month randomized, double-blind, placebo-controlled crossover trial with 1 month of therapy in each treatment arm. During the last few days of each 1-month treatment period, the subjects underwent 24-h ambulatory blood pressure recordings and measurements of FVR responses. ERT and HRT reduced mean 24-h diastolic blood pressure by 4 and 5 mmHg, systolic blood pressure by 6 and 9 mmHg and mean 24-h heart rate by 5 and 3 beats/min, respectively for ERT and HRT (p < 0.05). Basal FVR was reduced by approximately 18% by ERT and HRT, but FVR responses to noradrenaline, angiotensin II, acetylcholine and nitroprusside were unaffected. ERT and HRT therapy for 1 month lowers blood pressure and basal FVR, but does not appear to influence FVR responses to acetylcholine, nitroprusside, noradrenaline and angiotensin II.

The effects of hormone replacement therapy on plasma lipids in type II diabetes.

OBJECTIVES: The effects of hormone replacement therapy on cardiovascular risk factors in postmenopausal women with non-insulin dependent diabetes mellitus (type II diabetes) is uncertain. METHODS: The effects of estrogen replacement therapy (ERT, conjugated equine estrogen0.625mg orally daily), combined estrogen and continuous progestogen therapy (HRT, 0.625 mg of conjugated equine estrogens plus medroxyprogesterone acetate 5 mg daily) or placebo was compared in 20 postmenopausal type II diabetic women and 20 normal postmenopausal women in a double blind, randomised, crossover study. Patients receiving insulin were excluded from the study and all lipid modifying drugs were ceased at least 4 weeks prior to randomisation. Other medication including oral hypoglycaemics was kept constant for the duration of the study. RESULTS: Women with type II diabetes were a similar age (58.7+/-1.3 years) to the non-diabetic women (59.6+/-1.6 years) but they had a significantly greater body mass index, a higher incidence of treated hypertension, higher fasting plasma glucose levels, higher triglycerides and lower HDL cholesterol levels than non-diabetic women. ERT reduced total cholesterol and LDL cholesterol by a similar extent (8.9-12.3%) in normal and type II diabetic women and increased HDL cholesterol to a similar extent in both groups (11.0 and 8.9% respectively). ERT did not significantly alter fasting triglyceride levels in either group. The addition of medroxyprogesterone acetate 5 mg daily abolished the increase in HDL cholesterol associated with ERT in both groups but did not significantly affect any of the other lipid measurements. ERT and HRT did not significantly alter fasting insulin levels nor alter fasting glucose levels in either non-diabetic women or women with type II diabetes. CONCLUSIONS: ERT and HRT have similar effects on lipids in women with type II diabetes and non-diabetic women after 1 month of therapy.

Effects of glibenclamide on blood pressure and cardiovascular responsiveness in non-insulin dependent diabetes mellitus.

OBJECTIVE: To compare the effects of chronic glibenclamide therapy and placebo on blood pressure and cardiovascular responsiveness in patients with non-insulin-dependent diabetes. DESIGN AND METHODS: Fourteen patients with non-insulin-dependent diabetes mellitus, seven of whom were receiving angiotensin converting enzyme inhibitor therapy, received glibenclamide or placebo for 1 month in a double-blind, randomized crossover study. At the end of each treatment period patients attended for studies of forearm vascular responsiveness to intra-brachial arterial infusions of angiotensin II, acetylcholine, sodium nitroprusside and noradrenaline, responses of blood pressure to intravenous infusions of noradrenaline and angiotensin II and 24 h ambulatory blood pressure monitoring. RESULTS: Administration of glibenclamide produced significantly better glycaemic control than placebo (fasting blood glucose level 8.5 +/- 2.4 versus 13.5 +/- 4.5 mmol/l, P < 0.001) and plasma insulin levels were significantly higher during glibenclamide treatment than they were with placebo (12.9 +/- 4.4 versus 9.2 +/- 4.1 mU/l, P < 0.05). Body weights at the ends of the glibenclamide treatment and placebo phases were similar (92.1 +/- 14.3 versus 91.1 +/- 14.3 kg, P = 0.085). Night-time systolic blood pressures were significantly higher during glibenclamide treatment than they were with placebo (128 +/- 17 versus 118 +/- 10 mmHg, P < 0.05) due to there being a smaller day-night difference in systolic blood pressure during glibenclamide treatment that appeared to occur mainly in patients receiving angiotensin converting enzyme inhibitors. Responses of diastolic blood pressure to intravenous infusion of angiotensin II and forearm vascular responses to intra-brachial arterial infusion of angiotensin II were significantly greater during glibenclamide treatment than they were with placebo (P < 0.05). However, the enhancement of forearm vascular responses during glibenclamide treatment appeared to be restricted to patients receiving angiotensin converting enzyme inhibitors. Responses of blood pressure to intravenous infusion of noradrenaline and forearm vascular responses to infusions of noradrenaline, acetylcholine and nitroprusside did not differ between glibenclamide treatment and placebo; neither did basal forearm vascular resistance. CONCLUSIONS: Glibenclamide therapy is associated with greater responses of blood pressure and forearm vascular responses to infusion of angiotensin and higher nocturnal blood pressures. This effect appears to be influenced by concomitant angiotensin converting enzyme inhibition.

Inflammatory polyneuropathy in the setting of diabetes mellitus.

The authors report a patient with type II diabetes mellitus and an inflammatory polyneuropathy. The association is discussed and the importance of diagnosing treatable neuropathies in the diabetic patient is emphasized.

Relationship between serum parathyroid hormone levels in the elderly and 24 h ambulatory blood pressures.

BACKGROUND: An association between serum parathyroid hormone (PTH) levels in normotensive elderly subjects and blood pressure values had been reported. OBJECTIVE: To examine the relationship between PTH levels and other biochemical markers of calcium metabolism in elderly subjects and 24 h ambulatory blood pressures. METHODS: We performed 24 h ambulatory blood pressure recordings for 123 independent elderly subjects aged 63-88 years using a SpaceLabs 90207 recorder. Mean night-time blood pressures were calculated from the average of readings during sleep; mean daytime blood pressures were calculated from the remaining recordings. Demographic data and details concerning the alcohol consumption and medication usage of the subjects were recorded. Serum PTH, 25-hydroxy-vitamin D, albumin, renin, aldosterone, noradrenaline, creatinine and calcium levels were measured. RESULTS: Fifty-five patients were being administered antihypertensive therapy. Serum PTH levels correlated to the nocturnal systolic blood pressure (SBP; beta = 0.29, P = 0.002), nocturnal diastolic blood pressure (DBP), daytime SBP and mean 24 h SBP on univariate and multivariate analysis. Aldosterone levels were related to nocturnal SBP in univariate analysis (beta = 0.21, P = 0.02) but the relationship was weakened when PTH levels were included in the analysis (beta = 0.16, P = 0.09). Nocturnal, daytime and mean 24 h blood pressures were not significantly related to serum calcium, 25-hydroxy-vitamin D, age, body mass index and alcohol consumption. Sex was a significant predictor of the DBP, men having higher levels than did women (daytime DBP beta = 0.29, P = 0.001). CONCLUSIONS: Serum PTH levels are related strongly to the blood pressure, particularly the nocturnal blood pressure in the elderly. It is not known whether PTH levels are a consequence or a cause of the elevation in blood pressure.

Nocturnal fall in blood pressure in the elderly is related to presence of hypertension and not age.

AIMS: To determine whether the reduced nocturnal fall in blood pressure (BP) reported in elderly hypertensives is due to ageing or to the presence of hypertension. METHODS: Twenty-four hour ambulatory BP recordings of 68 normotensive elderly were compared with those of 55 elderly treated hypertensives, aged 63-88 years. Mean night-time BPs were calculated from the average of readings during sleep and mean daytime BPs from the remaining recordings. The maximum day-night BP differences were calculated. Plasma renin, aldosterone and noradrenaline were measured. RESULTS: Normotensive subjects were aged 72.0 +/- 4.7 years and treated hypertensives 73.7 +/- 4.9 years (p = 0.049). Normotensives had lower systolic BP (SBP) than hypertensives (125 +/- 12 mmHg versus 135 +/- 14 mmHg, p < 0.01). The fall in SPB at night was greater in normotensives than in hypertensives (18 +/- 9 versus 14 +/- 9 mmHg, p < 0.02). Non-dipping occurred in 24% of all subjects, with 59% of these being hypertensives. The nocturnal fall in SBP was not related to age (beta = -0.04, p < 0.62) but was inversely related to a history of hypertension (chi (2) = 5.82, p = 0.02). Serum noradrenaline was significantly related to nocturnal SBP fall (beta = 0.28, p = 0.01). CONCLUSIONS: Elderly normotensives have a greater decline in nocturnal SBP than treated elderly hypertensives. The failure of SBP to fall at night appears to be more a feature of hypertension than of ageing. Early morning noradrenaline estimations are higher in patients with a greater nocturnal blood pressure fall.

Blood pressure changes in acute cerebral infarction and hemorrhage.

BACKGROUND AND PURPOSE: We sought to investigate the changes in blood pressure (BP) that occur after hospitalization of patients with different types of acute stroke. METHODS: Twenty-four-hour ambulatory BP monitoring was performed on days 1 and 7 after admission to the hospital in 72 patients with acute stroke (44 thromboembolic strokes, 18 lacunar infarcts, and 10 intracerebral hemorrhages) and in 22 control patients. Stroke was categorized clinically into the above stroke subtypes with radiological confirmation. The controls were patients admitted with a range of acute medical problems other than stroke who were not severely ill or in significant pain. Left ventricular hypertrophy was assessed with echocardiography. Multiple linear regression was used to determine the effect of stroke category on BP after adjustment for the effects of potential confounders. RESULTS: Patients with thromboembolic and lacunar strokes had significantly higher systolic BP (SBP) on day 1 than control subjects (mean, 8.6% and 13.2%, respectively). Diastolic BP (DBP) was also significantly higher for patients with thromboembolic and lacunar strokes on day 1 (mean, 11.7% and 14.6%, respectively). Patients with intracerebral hemorrhage had SBP 9.7% and DBP 6.3% higher than control subjects on day 1, but the results did not achieve statistical significance. By day 7 there was no significant difference in SBP or DBP between the stroke subgroups and control subjects. CONCLUSIONS: BP is elevated after stroke but resolves spontaneously after 7 days. This transient elevation in BP does not appear to result solely from the stress of hospitalization.

24 hour ambulatory blood pressure profiles in the acute phase of stroke.

1. Twenty-four hour ambulatory blood pressure monitoring (ABPM) was used to evaluate the blood pressure (BP) changes in acute stroke. 2. Stroke was categorized according to the probable underlying vascular mechanism into lacunar infarction (L), thrombotic infarction (T) and intracerebral haemorrhage (ICH). A total of 37 stroke patients were studied (T = 21, L = 9, ICH = 7). Control patients (n = 15) were acute medical admissions not severely ill or in significant pain. ABPM was performed on day 1 and day 7 following admission. 3. Day 1 mean +/- s.d. 24 h systolic BP (SBP) were L (159 +/- 15.8), ICH (151 +/- 33.4), T (147 +/- 15.2) and controls (134 +/- 17.8). Day 7 mean 24 h SBP were L (138 +/- 9.8), ICH (143 +/- 26.9), T (138 +/- 19) and controls (134 +/- 14.8). In each stroke group BP fell to levels similar to control on day 7, while control mean SBP remained unchanged between days 1 and 7. The highest day 1 BP and the greatest subsequent fall on day 7 occurred for lacunar infarction. Diastolic BP showed similar changes to SBP. 4. The acute stress of hospitalization does not appear to explain elevated BP in acute stroke. Lacunar infarction appears to be particularly associated with temporary BP elevation.