Changes in N-terminal pro-B-type natriuretic peptide and incidence of diabetes: The Multi-Ethnic Study of Atherosclerosis (MESA).

AIMS: This study looked at whether the inverse association of circulating N-terminal pro-B-type natriuretic peptide (NT-proBNP) with incident diabetes is modified by changes in NT-proBNP (ΔNT-proBNP) levels. METHODS: Plasma NT-proBNP was assayed at baseline and 3.2 years later (visit 3) in the Multi-Ethnic Study of Atherosclerosis (MESA). ΔNT-proBNP was calculated as NT-proBNP visit3-NT-proBNP baseline. A Poisson distribution was fitted to determine the incidence density of diabetes, adjusted for age, race, gender, educational attainment, antihypertensive medication, total intentional exercise and plasma IL-6 levels. In the primary analysis (n=3236 without diabetes up to visit 3, followed for a mean of 6.3 years), incidence density was regressed for the following categories of baseline NT-proBNP: (1)<54.4 pg/mL; (2) 54.4-85.9 pg/mL; and (3) 86-54.2 pg/mL. This was crossed with categories of ΔNT-proBNP as medians (ranges): (1) -6.2 (-131-11.7) pg/mL; (2) 19.8 (11.8-30.1) pg/mL; (3) 44.0 (30.2-67.9) pg/mL; and (4) 111.2 (68.0-3749.9) pg/mL. RESULTS: The incidence density of diabetes followed a U-shaped association across categories of ΔNT-proBNP within categories of baseline NT-proBNP after adjusting for other covariates (P=0.02). At each level of baseline NT-proBNP, the incidence density of diabetes was lowest for small-to-moderate increases in NT-proBNP. CONCLUSION: This analysis suggests that NT-proBNP has a biphasic association with diabetes in which the risk of incident diabetes decreases within a 'physiological range' of ΔNT-proBNP, and plateaus or increases as NT-proBNP concentrations increase, probably in response to pathophysiological conditions leading to high levels of NT-proBNP.

Baseline cardiovascular risk in the INSIGHT Strategic Timing of AntiRetroviral Treatment (START) trial.

OBJECTIVES: The Strategic Timing of AntiRetroviral Treatment (START) trial has recruited antiretroviral-naïve individuals with high CD4 cell counts from all regions of the world. We describe the distribution of cardiovascular disease (CVD) risk factors, overall and by geographical region, at study baseline. METHODS: The distribution of CVD risk factors was assessed and compared by geographical region among START participants who had a baseline electrocardiogram (n = 4019; North America, 11%; Europe/Australia/Israel, 36%; South America, 26%; Asia, 4%; Africa, 23%; median age 36 years; 26% female). RESULTS: About 58.3% (n = 2344) of the participants had at least one CVD risk factor and 18.9% (n = 761) had two or more. The most common CVD risk factors were current smoking (32%), hypertension (19.3%) and obesity (16.5%). There were significant differences in the prevalence of CVD risk factors among geographical regions. The prevalence of at least one risk factor across regions was as follows: North America, 70.0%; Europe/Australia/Israel, 65.1%; South America, 49.4%; Asia, 37.0%; Africa, 55.8% (P-value < 0.001). Significant regional differences were also observed when risk factors were used as part of the Framingham and Data Collection on Adverse events of Anti-HIV Drugs (D:A:D) risk scores or used to define a favourable risk profile. CONCLUSIONS: CVD risk factors are common among START participants, and their distribution varies by geographical region. Better understanding of how and why CVD risk factors develop in people with HIV infection and their geographical distributions could shed light on appropriate strategies for CVD prevention and may inform the interpretation of the results of START, as CVD is expected to be a major fraction of the primary endpoints observed.

Effect of carvedilol, lisinopril and their combination on vascular and cardiac health in patients with borderline blood pressure: the DETECT Study.

Antihypertensive therapy is aimed at improving vascular and cardiac health, as well as lowering blood pressure (BP). The benefit of such drugs in untreated patients with borderline BP has not been demonstrated. Subjects with BPs ≥130 mm Hg systolic or ≥85 mm Hg diastolic and at least one additional risk factor were randomly assigned to treatment with carvedilol, lisinopril, their combination or placebo. Cardiovascular health was assessed by a disease score (DS), which combines the following tests of cardiovascular function and structure: resting BP, large- and small-artery elasticity (SAE), BP response to exercise, retinal vasculature analysis, electrocardiogram, carotid intima-medial thickness, left ventricular mass, microalbuminuria and N-terminal pro B-type natriuretic peptide. DS was assessed at baseline, after 3 and 9 months of therapy and 1 month after discontinuation of therapy. All active treatment groups displayed a sustained reduction in BP during 9 months of treatment, with the greatest reduction in the cardvedilol+lisinopril group. DS and SAE improved in all the treatment groups but the changes were of borderline significance and exhibited no evidence for progressive improvement from 3 months (functional) to 9 months (structural). All changes were reversed within 1 month after discontinuation of therapy. We conclude that 9 months of treatment with carvedilol, lisinopril or their combination produce a sustained and well-tolerated functional improvement but not a structural improvement, perhaps because of a lack of the nitric oxide-enhancing effects of other agents that inhibit structural changes in the vasculature.

Aliskiren for geriatric lowering of systolic hypertension: a randomized controlled trial.

Efficacy and safety of the direct renin inhibitor aliskiren was compared with ramipril for treatment of essential systolic hypertension in elderly patients. A 36-week, randomized, double-blind, parallel-group, active-controlled, optional-titration study was performed in 901 patients (aliskiren, n=457; ramipril, n=444) > or =65 years of age with systolic blood pressure (SBP) > or =140 mm Hg. Aliskiren 150-300 mg per day or ramipril 5-10 mg per day for was administered for 12 weeks with optional add-on therapy of hydrochlorothiazide (12.5-25 mg per day) at week 12 and amlodipine (5-10 mg per day) at week 22. The primary end point was non-inferiority of aliskiren vs ramipril monotherapy for change from baseline in mean sitting SBP (msSBP) at week 12. Decreases from baseline msSBP and mean sitting diastolic BP with aliskiren monotherapy (-14.0 and -5.1 mm Hg, respectively) were non-inferior (P<0.001 for both values) and superior to ramipril monotherapy (-11.6, -3.6 mm Hg; P=0.02, P<0.01, respectively). More patients achieved BP control with aliskiren (42%) than ramipril (33%; P<0.01). At week 36, fewer patients receiving aliskiren-based therapy required add-on treatment with hydrochlorothiazide or amlodipine (P=0.01 and 0.048, respectively). Tolerability was similar, but more patients receiving ramipril reported cough (P<0.001). In elderly patients with systolic hypertension, aliskiren proved to be more effective and better overall anti-hypertensive therapy compared to ramipril.

Relationship between carotid artery stiffness index, BNP and high-sensitivity CRP.

Arterial stiffness is an independent predictor of cardiovascular morbidity and mortality. Brain natriuretic peptide (BNP) and high-sensitivity C-reactive protein (hs-CRP) are considered as novel biomarkers that are useful in the prediction of early cardiovascular risk. We studied the relationship between carotid artery stiffness index beta and the cardiovascular biomarkers BNP and hs-CRP in 55 consecutive subjects. Carotid artery stiffness was assessed using the stiffness index beta derived from brachial artery blood pressure measurement and carotid ultrasonography. Venous blood samples were obtained for BNP and hs-CRP. Pearson's correlation coefficient suggested a strong bivariate relationship between carotid stiffness index beta and age (r=0.56, P<0.0001), BNP (r=0.45, P<0.004) and hs-CRP (r=0.26, P=0.06), respectively. On multiple regression analysis, significant correlations were found between carotid stiffness index beta and age (P=0.004), BNP (P=0.027) and hs-CRP (P=0.029). These findings suggest that there is a relationship between intra-cardiac pressures (measured by BNP), vascular inflammation (measured by hs-CRP) and vascular stiffness. Cardiovascular biomarkers are thus associated with functional parameters of the vascular tree.

Relationship between C-reactive protein and arterial stiffness in an asymptomatic population.

Plasma concentration of high sensitive C-reactive protein (hsCRP) is used as a marker for inflammatory states and is directly correlated with the risk for coronary heart disease. Evidence concerning the role of inflammation in atheroma formation has been derived from several models of atherosclerosis. Inflammation should exert its adverse vascular effects by structural changes in the artery wall and consequently alterations in arterial elasticity, which could be detected already in asymptomatic early vascular disease. We hypothesized that CRP is related to large artery elasticity, but not to small artery elasticity in early vascular disease. Therefore, we examined the association between arterial stiffness of large and small arteries and inflammation in an asymptomatic population referred for primary prevention cardiovascular screening. Studies were performed in 391 subjects (age 21-82 years; 254 men, 137 women) who underwent screening at the Cardiovascular Disease Prevention Center. Large artery (C1) and small artery (C2) elasticity indices were obtained by the CVProfiler 2000 (HDI, Eagan, MN, USA). After overnight fasting, venous samples were taken for measurement of hsCRP, lipids, glucose. There was a significant inverse correlation between hsCRP (0.29 +/- 0.40 mg/dl) and C1 (16.7 +/- 5.8 ml/mmHg), r = -0.133, P = 0.01; there was no significant correlation between hsCRP and C2 (6.6 +/- 3.2 ml/mmHg). C2, but not hsCRP, was inversely correlated with age, abnormal lipids and glucose, whereas C1, but not hsCRP, was inversely correlated with age and systolic blood pressure (SBP). In multiple regression analysis, the relationship between hsCRP and C1 was not affected by age, body mass index, SBP, serum glucose or lipids. In conclusion, these findings support the hypothesis that hsCRP, a marker for acute and low-grade inflammation, is associated with large artery but not with small artery elasticity in asymptomatic individuals undergoing primary prevention cardiovascular screening.

Relationship between periventricular or deep white matter lesions and arterial elasticity indices in very old people.

OBJECTIVE: To examine the relationship between the presence of cerebral white matter lesions and large and small artery elasticity indices in a population of healthy, very old subjects. METHODS: We studied 24 subjects (14 women, 10 men) with a mean age of 84+/-5 years, who were free from overt neurological, cardiovascular or psychiatric illness. We measured blood pressure and heart rate in supine and standing positions. Elasticity indices of the large arteries (C1) and small arteries (C2) were derived from radial artery pulse waves. Each subject had multi-slice spin-echo cerebral magnetic resonance imaging. The severity of white matter lesions was graded as 0, 1 or 2. RESULTS: Cerebral white matter lesions on magnetic resonance imaging were common in very old apparently healthy subjects: grade 0 (n=4, C1=2.68+/-1.80 ml/mmHg and C2=0.045+/-0.017 ml/mmHg), grade 1 (n=7, C1=2.13+/-0.36 ml/mmHg and C2=0.040+/-0.016 ml/mmHg) and grade 2 (n=13, C1=1.12+/-0.36 ml/mmHg and C2=0.018+/-0.003 ml/mmHg). There was no significant association between elasticity indices and blood pressure. CONCLUSION: In very old, apparently healthy subjects, both large and small artery elasticity indices were inversely related to the severity of cerebral white matter lesions on magnetic resonance imaging.

A comparison between systolic and diastolic pulse contour analysis in the evaluation of arterial stiffness.

Several methodologically independent measures of arterial stiffness derived from either the systolic or diastolic segments of the arterial pulse have been proposed. The exact nature of the large and small artery elasticity indices (C1 and C2, respectively) derived from diastolic pulse contour analysis remains largely unexplored, although C2 has controversially been termed to be "oscillatory" and "reflective." We investigated the relation between C2 and, respectively, a prototype of arterial reflectivity (ie, the augmentation index, AIx) and a covariate of arterial reflectivity (body height). A validated transfer function is used to transform a tonometrically obtained radial pressure wave into an ascending aortic pressure wave, from which AIx is derived using systolic pulse contour analysis. Diastolic pulse contour analysis using a modified Windkessel model is used to derive C1 and C2. One hundred subjects, who were free from atherothrombotic disease and 19 to 77 years of age, with a wide pressure range (97 to 186/52 to 104 mm Hg) were studied. Mean values of C1, C2, AIx, and body height were, respectively, 13.8+/-4.3 mL/mm Hgx10, 5.9+/-3.1 mL/mm Hgx100, 128.5+/-24.9%, and 169+/-9 cm. Coefficients of variation were 32.8% for C1, 33.3% for C2, and 6.7% for AIx. C2 was significantly and inversely correlated to AIx (r=-0.707, P<0.001). Both AIx and C2 were correlated to body height (r=-0.487, P<0.001, and r=0.514, P<0.001). In conclusion, the results of this study provide the first clinical evidence that validates a probable biophysical equivalent of the C2 element of a third-order, 4-element modified Windkessel model. We suggest that C2 is, at least in part, a measure of arterial wave reflectance. However, although short-term reproducibility of AIx is excellent, C2 showed markedly increased variability with the devices used.

Interchangeability of carotid and femoral intima-media thickness in risk stratification.

BACKGROUND: Carotid intima-media thickness (c-IMT) is an intermediate phenotype not only for the local but also the global arteriosclerotic status, a concept which has been validated by its ability to act as a marker for future cardiovascular and cerebrovascular events. Whether the association between c-IMT and risk factors, distant atherosclerotic disease and prognosis are the sole prerogative of the carotid artery, or whether these findings can be extrapolated to other arterial sites is less well studied. In view of the concept of vascular heterogeneity, we measured the IMT in a muscular, lower extremity artery, the common femoral (f-IMT), and in elastic upper extremity artery, the common carotid, in apparently healthy individuals and explored the relationship with risk factors and the individuals 10-year cardiovascular (CV) risk, calculated using the Framingham systolic blood pressure equation. METHODS: A population of 156 apparently healthy normotensive Caucasian volunteers between 18 and 65 years was studied (mean age 43+/-13 years; 68 men, 88 women; mean arterial blood pressure 126 +/- 15/70 +/- 10 mmHg). The c-IMT and f-IMT were measured using a 10 MHz vascular linear array transducer at the far walls 1 to 2 centimetres proximal to the right common carotid and right common femoral artery bifurcations, respectively. Risk factors were assessed and the 10-year cardiovascular risk was calculated using the Framingham systolic blood pressure equation. RESULTS: The median c-IMT was 0.52 mm (interquartile range 0.45-0.62 mm) and f-INT was 0.52 mm (0.39-0.67). Both parameters were significantly correlated (r = 0.363; p < 0.01) and both were significantly correlated to the calculated 10-year CV risk (r = 0.579; p < 0.01 and r = 0.574; p < 0.01 for the carotid and c-IMT and f-IMT, respectively). Median risk was low: 2.11% (0.27-5.50). Although measures of agreement were higher for the f-IMT versus risk (0.47) than for the c-IMT versus risk (0.30), the former showed a significantly wider scatter with increasing age and with quartiles of CV risk. The c-IMT and f-IMT do not share determinant risk factors to the same extent and with only 20% of mutual variance explained, cannot be regarded as interchangeable. CONCLUSIONS: Although the c-IMT and f-IMT are significantly intercorrelated and correlate to the calculated 10-year CV risk, they are not interchangeable. While the f-IMT is less suited as a continuous variable for risk stratification in a low-risk population, our data suggest its possible use as a dichotomised risk marker.

Small and large artery elasticity indices in peripheral arterial occlusive disease (PAOD).

In peripheral arterial occlusive disease (PAOD), arterial compliance of the central arteries has been reported to be reduced. It is, however, not clear whether, in PAOD, decreased arterial compliance is also accompanied by similar changes in the peripheral arteries. Therefore the aim of the study was to determine the large (C1) and small (C2) artery elasticity indices in PAOD and their relations to its well-accepted characteristics (ankle-brachial index, ABI; pulse pressure, PP; absolute claudication distance, ACD). A total of 43 patients with PAOD (mean age 68 +/- 9 years; ABI of the limiting leg 0.65 +/- 0.14; SBP (systolic blood pressure) 149 +/- 20 mmHg, and ACD 488 +/- 187 m) were enrolled as well as 16 control subjects of comparable age (69 +/- 4 years) and blood pressure (SBP 147 +/- 27 mmHg). All subjects underwent non-invasive pulse wave analysis in order to determine arterial compliance of the aorta and major side branches (C1) and of the distal circulation (C2), using a modified Windkessel model. In PAOD, both C1 (1.41 +/- 0.56 ml/mmHg) and C2 (0.023 +/- 0.012 ml/mmHg) were comparable to values in an age and blood pressure-matched control group (C1, 1.25 +/- 0.66 ml/mmHg; C2, 0.027 +/- 0.008 ml/mmHg). C1 was significantly correlated with ACD (r = 0.36, p = 0.02), PP (r = -0.33, p < 0.02) and only borderline with ABI (r = 0.28, p = 0.07). C2 was correlated with PP (r = -0.38, p < 0.01), ABI (r = 0.36, p < 0.02) but not with ACD. Large (C1) and small (C2) artery elasticity indices in PAOD were decreased but comparable to values in an elderly group with isolated systolic hypertension. Moreover, C1 and C2 correlated with markers (ABI and PP) of severity of vascular disease.

Relationship between arterial elasticity indices and carotid artery intima-media thickness.

Functional and structural changes of the arterial wall appear to serve as early hallmarks of the hypertensive disease process. Structural vascular changes can be studied by the determination of the intima-media wall thickness (IMT) at the carotid artery. The elastic behavior of the proximal and distal parts of the arterial tree can be assessed from noninvasively recorded radial artery waveforms. The aim of the study was to compare large (proximal, C1) and small (distal, C2) artery elasticity indices in two age-matched study groups with high- and low-normal blood pressure (BP) and to assess the relation between elasticity indices and IMT. A total number of 22 subjects with high-normal BP (40 +/- 2 years; BP, 147 +/- 2.5/84 +/- 1.5 mm Hg) and 22 matched controls with low-normal BP (40 +/- 2 years; BP, 123 +/- 1.9/69 +/- 1.5 mm Hg) were enrolled. The IMT was echographically determined at the common carotid artery by the leading-edge technique. Large artery (C1) and small artery (C2) elasticity indices were calculated from a third-order, four-element model of the arterial circulation. In the group with high-normal BP large and small artery elasticity indices were significantly decreased versus controls with low-normal BP (C1: 1.63 +/- 0.08 v 1.99 +/- 0.09 mL/mm Hg, P < .01; C2: 0.059 +/- 0.005 v 0.076 +/- 0.007 mL/ mm Hg, P < .05) and IMT increased significantly (0.607 +/- 0.039 v 0.516 +/- 0.027 mm, P < .05). Moreover, there was an inverse relationship between IMT and small artery elasticity index (r = -0.60, P = .004). In subjects with a high-normal BP there is already a change in the IMT of the carotid artery versus normotension. The IMT is related to the small artery elasticity index (C2).

A non-invasive cardiovascular index for the quantification of arterial load.

OBJECTIVE: Our aim is to quantify steady and pulsatile components of arterial load in a concise and sensitive way by means of a new non-invasive cardiovascular index (NICI). METHODS AND RESULTS: NICI is based on non-invasively measured pressure (sphygmomanometer), stroke volume index and cardiac index (Doppler echocardiography and ECG) and yields a numerical value (in mm Hg). It expresses the difference between the actual arterial load and reference loading conditions as determined in a control group (29 M/35 F, age 34 +/- 13 yr.) of healthy subjects, with blood pressure 116/61 mm Hg (systolic/diastolic), stroke volume index (SVI) 34 +/- 18 ml.m-2 and cardiac index (CI) 2.1 +/- 0.5 l.min-1.m-2. NICI was calculated in the control group and in 23 borderline hypertensive subjects (10 M/13 F, age 65 +/- 12 yr.) with blood pressure 156/79 mm Hg, SVI 36 +/- 10 ml.m-2 and CI 2.4 +/- 0.6 l.min-1.m-2. NICI was higher in borderline hypertensives (33 +/- 51 vs. 0 +/- 34 mm Hg; P < 0.001) and was strongly correlated with total peripheral resistance index (r = 0.89; P < 0.001) and with the ratio of SVI and pulse pressure (r = -0.89; P < 0.001), expressing the combined effect of both known determinants of cardiac load. NICI was also correlated with effective arterial elastance index (r = 0.89; P < 0.001). CONCLUSIONS: NICI quantifies, within a logical biomechanical framework, the arterial load as seen by the ejecting ventricle. It combines steady and pulsatile components of arterial load and has a single control value of zero mm Hg.

Inverse relation between aldosterone and venous capacitance in chronically treated congestive heart failure.

The purpose of this study was to examine if there is a relation between the aldosterone escape phenomenon and venous capacitance of the upper and lower limbs in patients with long-term congestive heart failure (CHF) receiving chronic treatment with angiotensin-converting enzyme (ACE) inhibitors. The study group consisted of 16 subjects with ischemic CHF in New York Heart Association functional class II (age 59 +/-2 years, ejection fraction 24+/-4%), stabilized under a constant drug regimen comprising furosemide, captopril 50 mg 3 times daily, and digoxin for at least 3 months. Thirteen apparently healthy volunteers, aged 50+/-4 years acted as controls. Forearm and calf venous capacitances were measured simultaneously by venous occlusion plethysmography using mercury-in-silastic strain gauges. The equilibration technique was used to derive venous capacitance from the recorded pressure-volume curves. Active renin, angiotensin II, and aldosterone levels were determined on venous blood samples obtained in the supine position. Angiotensin II (p<0.05) and aldosterone (p<0.01) were statistically significantly higher in patients with CHF under long-term ACE inhibition than in controls (aldosterone escape phenomenon). In CHF, forearm venous capacitance was 2.19+/-0.18 ml/100 ml; calf venous capacitance was 2.83+/-0.27 ml/100 ml. Aldosterone significantly and inversely correlated with venous capacitance in both upper (r = -0.586; p = 0.017) and lower (r = -0.625; p = 0.01) limbs. No correlations were found between forearm or calf venous capacitance and renin or angiotensin II. In patients with heart failure chronically treated with diuretics and full ACE inhibition, venous capacitance is inversely correlated with aldosterone through the mechanism of aldosterone escape, creating the potential for further deterioration of the CHF process.

Inverse relationship between aldosterone and large artery compliance in chronically treated heart failure patients.

AIMS: The purpose of this study was to examine, in chronically treated heart failure patients vs control subjects, the influence of neurohumoral activation and aldosterone escape on arterial elastic behaviour, assessed by non-invasive mathematical lumped-parameter modelling of the compliance of the arterial system. METHODS AND RESULTS: Radial arterial pulse waves were recorded non-invasively for 30 s with an arterial tonometer sensor array in 13 chronic heart failure patients (mean age, 59 +/- 2.5 years) in New York Heart Association class II. The patients had been taking digoxin, furosemide, captopril and aspirin for more than 3 months. Thirteen healthy subjects (mean age, 50 +/- 4.0 years) acted as controls. Compliance of the proximal (aorta and major branches, C1) and distal parts (C2) of the circulation were derived from a third order four-element modified Windkessel model which can reproduce arterial pressure waveforms, including both exponential and oscillatory sections. Active renin, angiotensin II and aldosterone levels were determined on venous blood samples in the supine position and after 30 min active standing. There was decreased proximal (C1, 1.51 +/- 0.11 ml x mmHg(-1), P<0.01) and distal (C2, 0.050 +/- 0.011 ml x mmHg(-1)) arterial compliance in the chronic heart failure patients vs controls (C1, 1.71 +/- 0.16 ml x mmHg(-1); C2, 0.054 +/- 0.006 ml x mmHg(-1)). The chronic heart failure patients were characterized by an aldosterone escape phenomenon which was inversely correlated with the proximal arterial compliance in both supine (r= - 0.795, P=0.002) and standing (r= - 0.628, P=0.029) positions. CONCLUSIONS: In chronically treated heart failure patients with full angiotensin-converting enzyme-inhibition and diuretics, there is decreased compliance of the aorta and its major branches, which is inversely correlated with the aldosterone escape phenomenon.

Calcium antagonists, is there a real concern about safety?

Calcium antagonists are widely used in the treatment of arterial hypertension and, or in ischemic heart disease. During the last 3 years, controversial articles and editorials have been published concerning the potential risk of calcium antagonists in regard to mortality, cancer and haemorrhage. The information has been mainly derived from case-control studies. The major concern about such observational studies of treatment outcome is the large potential for systematic error to affect the results. However, overviews of controlled trials with calcium antagonists do not provide clear evidence of an effect of calcium antagonists on mortality, risk of cancer and risk of bleeding.

Long- and short-term blood pressure and RR-interval variability and psychosomatic distress in chronic fatigue syndrome.

1. Chronic low blood pressure has been associated with fatigue and low mood. However, in the chronic fatigue syndrome (CFS) the blood pressure (BP) and heart rate profile and their variabilities have not been characterized as yet. 2. We performed office and 24 h ambulatory BP recordings in 38 subjects (age, 34.8 +/- 8.0 years) who fulfilled the Holmes criteria for CFS and in 38 healthy control subjects (age 35.6 +/- 10.5 years), as well as short-term beat-to-beat BP and RR-interval recordings for 10 min in supine and standing position, and calculated spectral indices. 3. In CFS office (123 +/- 19/70 +/- 12 mmHg) as well as 24-h, day- and night-time blood pressure values (116 +/- 11.1/71 +/- 11.1, 121 +/- 9.2/77 +/- 8.0 and 110 +/- 10.5/65 +/- 9.2 mmHg respectively) were within reference limits. 4. Heart rate was consistently higher (P < 0.01) in CFS patients, based on both office (77 +/- 12 compared with 68 +/- 12 beats min-1) and 24 h ambulatory recordings (77 +/- 12 compared with 67 +/- 15 beats min-1). 5. In supine position, spectral indices of BP variability (total, low-frequency and high-frequency variances) were all significantly (P < 0.01) lower in CFS. In standing position the differences disappeared. Analysis of RR-interval variability could not detect major alterations in autonomic function in CFS.

Angina in the elderly.

Coronary artery disease (CAD) remains the most common cause of heart disease in the elderly, in whom it exhibits some unique features. It is more likely to be diffuse and severe and left main coronary artery stenosis and triple-vessel disease are more prevalent. Diagnosis is less dependent on the presence of chest pain since other symptoms may present as an anginal equivalent in such patients. The ECG of elderly patients often shows abnormalities that are not specific for myocardial ischaemia. In such patients, and in those who are unable to perform sufficient exercise to increase the heart rate to > or = 85% of predicted maximal heart rate for age and sex, radionuclide or pharmacological stress testing may be used. When the diagnosis of CAD remains questionable, coronary arteriography should be considered. Physical examination and basic laboratory screening should be used to identify conditions which exacerbate myocardial ischaemia and will, therefore, affect treatment. The initial approach to treatment should include risk factor modification and initiation of an anti-ischaemic pharmacological regimen. The usual anti-anginal medications are as efficacious in the elderly as in the young; however, attention must be paid to altered pharmacodynamics and pharmacokinetics. When symptoms are poorly controlled by medical therapy or when multivessel or left main coronary artery stenosis is identified, myocardial revascularization should be considered. In elderly patients with symptomatic angina or unstable angina symptoms, uncontrolled by medical therapy, percutaneous transluminal coronary angiography may be a reasonable alternative to surgical revascularization.