Atherosclerosis in rheumatoid arthritis versus diabetes: a comparative study.

OBJECTIVE: The extent to which atherosclerosis is accelerated in chronic inflammatory diseases is not established. We compared preclinical atherosclerosis in rheumatoid arthritis with diabetes mellitus, a known coronary heart disease equivalent. METHODS AND RESULTS: Endothelial function, arterial stiffness, carotid intima-media thickness, and analysis of atheromatous plaques were examined in 84 rheumatoid arthritis patients without cardiovascular disease versus healthy controls matched for age, sex, and traditional cardiovascular disease risk factors, as well as in 48 diabetes patients matched for age, sex, and disease duration with 48 rheumatoid arthritis patients. Rheumatoid arthritis duration associated with arterial stiffening, whereas disease activity associated with carotid plaque vulnerability. All markers of preclinical atherosclerosis were significantly worse in rheumatoid arthritis compared to controls, whereas they did not differ in comparison to diabetes despite a worse cardiovascular risk factor profile in diabetics. Both diseases were associated independently with increased intima-media thickness; rheumatoid arthritis, but not diabetes, was independently associated with endothelial dysfunction. CONCLUSIONS: Preclinical atherosclerosis appears to be of equal frequency and severity in rheumatoid arthritis and diabetes of similar duration with differential impact of traditional risk factors and systemic inflammation. Cardiovascular disease risk factors in rheumatoid arthritis may need to be targeted as aggressively as in diabetes.

Gender influence on metabolic syndrome's effects on arterial stiffness and pressure wave reflections in treated hypertensive subjects.

BACKGROUND: In hypertensive subjects, aortic stiffness, an independent predictor of cardiovascular (CV) risk, measured from pulse wave velocity (PWV), contributes to enhance augmentation index (AI), a marker of the timing and amplitude of wave reflections. Whether PWV and AI are correlated and reflect CV risk in hypertensive men and women with metabolic syndrome (MS) remains unknown. METHODS: In a cohort of 613 (364 males) treated hypertensive subjects with and without MS (41% MS) pulse wave analysis was used to determine aortic PWV and carotid AI. CV risk was estimated from standard Framingham equations. RESULTS: In females, but not in males, aortic PWV was higher in subjects with MS, when compared with those without MS (12.7+/-0.3m/s versus 11.1+/-0.4m/s, p<0.001). This result was independent of age and blood pressure. Only in females AI was independently related to the presence of MS; AI did not differ between subjects with or without MS, both males and females. AI did not correlate with PWV, except in males without MS. The overall CV risk was strongly associated to PWV independently of MS and gender, but AI was associated to CV risk only in males. CONCLUSION: In treated hypertensive subjects, the effect of MS on PWV and AI is modulated by gender. The dissociation between PWV and AI observed in women with MS was due to "blunted" wave reflections. This finding is associated with the fact that PWV, but not AI, was a constant marker of CV risk in subjects with MS, whether men and women.

Increased pulse pressure amplification in treated hypertensive subjects with metabolic syndrome.

BACKGROUND: Brachial pulse pressure (PP) is physiologically higher than central PP. This PP amplification, which protects the heart from increased afterload, is related to the progressive increase of arterial stiffness along the vascular tree and subsequent changes in pressure wave reflections. The PP amplification increases with high heart rate (HR), which is observed in subjects with metabolic syndrome (MS). The objective of this study was to investigate whether PP amplification is affected by MS and is related to cardiovascular (CV) risk. METHODS: In 613 subjects treated for hypertension (41% with MS) pulse wave analysis was used to investigate carotid blood pressure (BP), pressure wave reflections from carotid augmentation index (AI), and arterial stiffness from aortic pulse wave velocity (PWV). The CV risk was estimated from standard Framingham equations. RESULTS: Pulse pressure amplification, HR, and PWV, but not AI, were increased in subjects with MS compared to control subjects without MS with the same age, gender, and mean arterial pressure. The difference in PP amplification between the two groups disappeared after adjustment for both HR and PWV. The AI was the main predictor of PP amplification, representing 28% and 19% of its total variance in subjects without and with MS, respectively. The CV risk for coronary, but not for cerebral, mortality was related to PP amplification. CONCLUSIONS: Although PWV is increased in treated hypertensive subjects with MS, compared to control, PP amplification is increased due to the effect of increased HR and attenuated pressure wave reflections. The observed relation of increased PP amplification with organ-specific CV risk needs further investigation.

Arterial wave reflections are associated with left ventricular diastolic dysfunction in Adamantiades-Behçet's disease.

BACKGROUND: Adamantiades-Behçet's disease (ABD) is characterized by systemic vasculitis. We investigated whether aortic distensibility and arterial wave reflections are linked to left ventricular (LV) diastolic dysfunction in ABD. METHODS AND RESULTS: Eighty-two patients and 40 controls with similar atherosclerotic risk factors were examined by applanation tonometry of the radial artery (SphygmoCor) and echocardiography. Augmentation index (AI%) and arrival time (Deltat, ms) of reflected arterial waves as well as aortic distensibility (AoD) assessed by echocardiography were estimated. Doppler diastolic abnormalities were defined as proposed by the European Study Group on Diastolic Heart Failure by measurement of E/A ratio, isovolumic relaxation time, deceleration time, and flow propagation velocity. Patients had impaired central augmentation index (CAI), Deltat, and AoD compared with controls (P > .05). After adjusting for age, atherosclerotic risk factors, left ventricular mass, and medication the odds-ratio of AoD and CAI for left ventricular diastolic dysfunction was 0.664 (95%CI 0.449-0.982), P = .04, and 1.073 (95% CI 1.014-1.140), P = .001, respectively. The addition of CAI to the multivariable model including AoD significantly increased the power of the model for prediction of left ventricular diastolic dysfunction (-2 Log likelihood change = 18.8, P for change > .01). CONCLUSION: Augmentation index has a complementary value to aortic distensibility in the assessment of left ventricular diastolic dysfunction in ABD.

Pressure wave reflections, central blood pressure, and aortic stiffness in patients with Adamantiades-Behcet's disease: a cross-sectional case-control study underlining the role of chronic corticosteroid treatment.

BACKGROUND: Adamantiades-Behcet's disease (ABD) is a multisystemic inflammatory/autoimmune disease involving both microcirculation and macrocirculation. Aortic stiffness index and aortic augmentation index (AI) are indices for the estimation of arterial stiffness and pressure wave reflections, respectively. The effect of anti-inflammatory and immunosuppressive drugs used in ABD on these indices is unknown. METHODS: In this cross-sectional study we examined 74 subjects with ABD (aged 40.1 +/- 12.5 years, 24 men) and 24 control subjects by using the noninvasive technique of radial artery applanation tonometry and pulse wave analysis for assessment of aortic AI by application of transfer functions. Echocardiography was used for assessment of aortic stiffness index. Classic cardiovascular (CV) risk factors, left ventricular and endothelial function of the brachial artery, as well as intima-media thickness of carotid artery, were also assessed. RESULTS: Corticosteroids were the only drug having a negative and independent effect on aortic AI, but not on aortic stiffness. Patients taking corticosteroids had lower aortic AI and central systolic blood pressure (BP), but not aortic stiffness and peripheral systolic BP, when compared to those without corticosteroids (21+/-14% v 12+/-14%, P < .050). Medication, traditional CV risk factors, and functional or structural CV parameters were all comparable among the two groups. The AI was similar between the control group and patients with ABD taking corticosteroids. CONCLUSIONS: The AI, but not aortic stiffness, is lower in patients with ABD taking corticosteroids compared to patients not taking corticosteroids and similar to the control group. These results imply a role of inflammation or immunomodulatory mechanisms in the regulation of pressure wave reflections.

Circadian variation of arterial pressure wave reflections.

BACKGROUND: Various factors are implicated in the circadian pattern of cardiovascular vulnerability. The exact mechanisms involved in the peak incidence of cardiovascular events occurring during the early morning hours after awaking are not completely known. The purpose of our study was to investigate the circadian variation of timing and intensity of wave reflections in healthy individuals and to test the hypothesis that significant changes occur during the day. METHODS: Thirteen healthy non-smokers (seven women and six men, mean age 40.7 +/- 16.5 years) were examined. Aortic pulse wave analysis was performed to estimate surrogates of wave reflections intensity (augmentation index [AIx]) and timing. Twelve measurements separated by 1-h intervals were performed from 8 am to 7 pm each study day. RESULTS: Analysis of variance for repeated measures indicated significant changes during the 12-h period for heart rate corrected AIx (P = .033) and heart rate (P = .035). The AIx was maximal at 8 am within 1-h after awaking (17% +/- 3.6%); it was gradually diminished until 3 pm (9% +/- 4.1%) and again increased to a second (albeit lower) peak value during the late afternoon (7 pm). CONCLUSIONS: It is possible that the increased intensity of reflected waves occurring during the early morning in combination with the rising trend of blood pressure and heart rate at the same time results in an aggravated left ventricular afterload and an increase in myocardial oxygen demand. The morning-related enhancement of wave reflections may have potential implications for the increased risk for cardiovascular events during the early morning, which remains to be clarified.

Twenty-four-hour heart rate and blood pressure are additive markers of left ventricular mass in hypertensive subjects.

BACKGROUND: We investigated whether mean heart rate (HR(24)) and blood pressure (BP) parameters during 24-h ambulatory BP monitoring (ABP) are independent or additive markers of left ventricular (LV) mass in subjects with newly diagnosed, untreated hypertension. METHODS: A total of 250 patients (40% women, 60% men; mean age 59.6 +/- 11 years) with essential hypertension who were attending the outpatient Hypertension Unit were studied. All patients underwent 24-h ABP and HR monitoring as well as echocardiography for assessment of left ventricular (LV) dimensions and function. RESULTS: A decreasing HR24 or increasing ABP parameters (ie, systolic, diastolic, mean BP, and pulse pressure) were associated with increasing LV mass (P < .001) and wall thickness (P < .01). In multivariate analysis, after adjusting for age, gender, body surface area, body mass index, hematocrit, glucose, cholesterol, smoking, and each of the measured ABP parameters separately, decreasing HR24 was independently related to increasing LV mass in addition to ABP and body size parameters (P < .001). The addition of HR24 in different multivariate models for prediction of LV mass significantly increased the adjusted model r2 (range of r2 change: 0.039 to 0.064, P for change <.05). Decreasing HR24 or HR during daytime (6 am to 10 pm) was associated with a higher likelihood of LV hypertrophy in addition to ABP parameters (adjusted odds ratio 0.92 (CI 0.87 to 0.98), per 1 beat/min greater HR24 P = .002 and 0.93 (CI: 0.87 to 0.98), per 1 beat/min greater HR in the daytime P = .017). CONCLUSION: The 24-h HR and BP during ABP are independent and additive markers of increased LV mass in untreated hypertensive individuals.

Transmission of calibration errors (input) by generalized transfer functions to the aortic pressures (output) at different hemodynamic states.

BACKGROUND: Aortic pressure waveforms are calculated non-invasively by applying generalized transfer functions (GTF) to tonometric radial pressure waveforms. Input errors mainly during acquisition and calibration of tonometric pressures are "transferred" to aortic pressure calculation. The present study aimed to quantify the proportion of specific input errors which is "transferred" by the GTFs in a wide range of hemodynamic conditions and for different error combinations in brachial systolic (SBP) and diastolic (DBP) blood pressure measurements. METHODS: Aortic pulse wave analysis was performed in 103 subjects (52 normotensive and 51 untreated hypertensive) by the SphygmoCor System. Each pressure waveform was initially calibrated by sphygmomanometrical brachial pressures. Isolated, parallel and reverse errors in brachial SBP/DBP from -10 to +10 mmHg were simulated, by recalibration of the recorded radial pressure waveforms, inducing specific "errors" of GTF-input values. For every recalculated aortic SBP and DBP, the difference from the initial estimated value was considered to represent the "transferred error" to the aortic pressure estimation. RESULTS: Parallel errors by +/-5 mmHg in both SBP and DBP resulted to an identical change in GTF-derived aortic pressures, as expected. When an overestimation in SBP by 5 mmHg and an underestimation in DBP by -5 mmHg occurred (reverse errors), almost 56% of this error (approximately 2.8 mmHg) was transferred. An isolated error in brachial SBP by +/-5 mmHg was transmitted by 76% ( approximately 3.8 mmHg) to GTF-derived aortic SBP. In subjects with mean blood pressure>117 mmHg or with heart rates<74 bpm, a greater percent of the calibration error was transferred to GTF-derived blood pressures. CONCLUSIONS: Input errors in brachial pressure values result in a quantifiable effect on transfer function output (aortic pressures). The percent of the "error transfer" by the GTFs depends on heart rate and BP levels, which should be taken into account when applying GTFs at populations with different hemodynamic conditions.

Aortic elastic properties and left ventricular diastolic function in patients with Adamantiades-Behcet's disease.

OBJECTIVES: We investigated whether Adamantiades-Behcet's disease (ABD) is related to impaired aortic (Ao) elastic properties and left ventricular (LV) function. BACKGROUND: Adamantiades-Behcet's disease is an inflammatory disorder characterized by vasculitis leading to vascular complications and, rarely, myocarditis. METHODS: We studied 82 patients with ABD (age: 40 +/- 12 years) and 24 normal control subjects by echocardiography. Abdominal Ao diameter (mm/m(2)) and Ao elastic indexes--namely, Ao strain (%), distensibility (cm(2) x dyn(-1)x 10(-6)), stiffness index, and pressure strain modulus (Ep) (cm(2) x dyn(-1) x 10(-6))--were calculated from the echocardiographically derived thoracic Ao diameters (mm/m(2)), and the measurement of pulse pressure obtained by cuff sphygmomanometry. Isovolumic relaxation time (IVRT) (ms), deceleration time (DT) (ms), and flow propagation velocity (FPV) (cm/s) were measured by Doppler echocardiography to assess diastolic LV function. The duration of disease and presence of vascular complications were noted. RESULTS: Patients versus control subjects had increased Ao diameters (p < 0.01), lower mean Ao strain and distensibility (4 vs. 9 and 1.4 vs. 3.4, respectively, p < 0.01), higher mean aortic stiffness index and Ep (15.6 vs. 6 and 1.17 vs. 0.44, respectively, p < 0.01), and impaired IVRT and FPV (p < 0.01). Aortic function indexes were related to the duration of disease (p < 0.01) and increased DT (p < 0.01). Deceleration time >190 ms predicted vascular complications with 80% sensitivity and 71% specificity (odds ratio 6.52 [confidence interval: 2.23 to 19.03]). CONCLUSION: Aortic elastic properties and diastolic LV function are impaired in patients with ABD and are interrelated. The link between diastolic LV dysfunction and vascular complications suggests the presence of a common pathophysiologic pathway and provides a possible marker of risk for vascular disease.

Red wine acutely induces favorable effects on wave reflections and central pressures in coronary artery disease patients.

BACKGROUND: To investigate red wine's acute effects on aortic pressures and arterial stiffness in patients with coronary artery disease (CAD). METHODS: Fifteen patients with CAD were recruited in a double-blind, cross-over study, which was comprised of 2 study days. Each volunteer consumed either 250 mL of regular or 250 mL of dealcoholized red wine. Wave reflections, expressed as augmentation index (AIx), as well as central and peripheral blood pressures (BP) were assessed at fast and 30, 60, and 90 min postprandially. RESULTS: Both regular and dealcoholized red wine caused a significant decrease in AIx by 10.5% +/- 1.4% (P = .001) and 6.1% +/- 1.4% (P = .011), respectively, whereas no significant change was induced in mean BP and timing of wave reflections expressing pulse wave velocity. Peripheral systolic BPs remained unaltered in both beverages, whereas a significant decrease in peripheral and central diastolic BPs was observed after the dealcoholized red wine consumption (P = .03 and P = .035, respectively). Central systolic BP was decreased after the consumption of regular (-7.4 +/- 2.4 mm Hg, P = .05) and dealcoholized red wine (-5.4 +/- 2.7 mm Hg, P = .019). CONCLUSIONS: Both types of red wine provoked favorable acute effects on wave reflections and central systolic pressures, whereas no such effect was evident at the brachial artery. Therefore, these findings could be attributed mainly to red wine antioxidant substances, rendering it a possible means of at least acute attenuation of increased wave reflections, arterial stiffness, and central pressures in patients with coronary artery disease.

Acute effects of caffeine on blood pressure and wave reflections in healthy subjects: should we consider monitoring central blood pressure?

BACKGROUND: Data concerning blood pressure changes, acutely induced by caffeine consumption, are conflicting. Furthermore, limited data exist regarding central hemodynamic response to caffeine ingestion by healthy young subjects. We investigated the acute effect of coffee (80 mg of caffeine) and decaffeinated coffee on peripheral and central hemodynamics, as well as on wave reflections. SUBJECTS: For this purpose, 16 healthy volunteers (eight females and eight males, mean age 29+/-3.2 years) were investigated. METHODS: Repeated measurements were performed at baseline and 30, 60, 90 and 120 min after oral administration of each beverage in a double-blind crossover design. Aortic blood pressures, augmentation index (AI) and pressure (AP) and timing of reflected waves were evaluated by using applanation tonometry and pulse wave analysis. RESULTS: Regular coffee increased central systolic (SBP) and diastolic pressure (DBP) from 96.2+/-9.9 to 101.1+/-10.1 mmHg, p=0.011 and from 72.6+/-9.4 to 76.5+/-9.0 mmHg, p=0.027, respectively, but no change was observed following consumption of decaffeinated coffee. Peripheral systolic blood pressure did not change significantly after the administration of either coffee. Augmentation index increased significantly following regular coffee consumption. The change in AI was significantly higher following regular compared to decaffeinated coffee consumption as shown by analysis of variance (ANOVA) for repeated measures (p=0.001). CONCLUSIONS: These caffeine effects reveal an unfavourable effect on wave reflections and therefore on left ventricular (LV) pulsatile afterload. It also revealed a significant acute effect of caffeine consumption on central hemodynamics which is not observed at peripheral pressures.

Rapid effect of pravastatin on endothelial function and lipid peroxidation in unstable angina.

BACKGROUND: Oxidative stress contributes to endothelial dysfunction, an important step to the pathogenesis of atherosclerosis and coronary events. Latest studies revealed the existence of pleiotropic and especially antioxidant properties of statins. We sought to examine the effects of pravastatin on lipid peroxidation and endothelial function, independently from lipid-lowering, in patients with unstable angina (UA). METHODS: Thirty-seven patients (males), 64.46+/-9.09 years, suffering from UA enrolled in the study. Patients were not on statin medication before admission and they received after randomization either 40 mg pravastatin daily (group A, n = 20), or placebo (group B, n = 17). Malondialdehyde (MDA) concentration, an index of lipid peroxidation and plaque instability, flow-mediated dilatation (FMD) of the brachial artery and blood lipids were measured on the second day of hospitalization and 10 days later. RESULTS: MDA decreased significantly in both groups (A, p = 0.008; B, p = 0.003). FMD increased significantly in group A (p = 0.007), whereas in group B it did not change. Serum lipids remained unaltered in all three groups. CONCLUSIONS: Pravastatin administration improved FMD within 10 days and this favorable effect occurred before any significant reduction in blood lipids, revealing its pleiotropic effects during the early phase of an acute coronary syndrome. Circulating lipid peroxidation products in patients with UA decreased significantly during the same period independently of endothelial function and pravastatin therapy.

Arterial stiffness assessed by pulse wave analysis in essential hypertension: relation to 24-h blood pressure profile.

BACKGROUND: Arterial stiffness is a risk factor for cardiovascular morbidity and mortality and appears to be increased in arterial hypertension. The purpose of the present study was to relate systemic arterial stiffness assessed by pulse wave analysis to variables of 24-h ambulatory blood pressure monitoring (ABPM) in patients with essential hypertension. METHODS: Seventy-two subjects with untreated mild to moderate arterial hypertension underwent evaluation with 24-h ambulatory blood pressure monitoring. In the same subjects, applanation tonometry and pulse wave analysis was performed for evaluation of systemic arterial stiffness expressed as augmentation index and estimated aortic pulse wave velocity. RESULTS: Clinic systolic blood pressure, mean heart rate during 24-h blood pressure monitoring and height were independent predictors of augmentation index and estimated aortic pulse wave velocity. The 41 patients with blunted reduction in nighttime blood pressure (nondippers) showed higher mean systolic blood pressure (p=0.02), lower systolic and diastolic blood pressure variability (p<0.001), higher pulse pressure during 24-h monitoring (p=0.05) and higher estimated aortic pulse wave velocity (p=0.03), indicating stiffer arteries in this group. CONCLUSIONS: These results suggest that blood pressure change from day- to nighttime is an important determinant of arterial stiffness assessed by pulse wave analysis; this association could contribute to the higher cardiovascular risk in nondippers.

Association of blunted nocturnal blood pressure dip with intracerebral hemorrhage.

OBJECTIVES: Nondipping pattern of nocturnal blood pressure is associated with silent ischemic cerebrovascular lesions and lacunar infarctions. In this case-control study, we aimed to evaluate the association of diurnal blood pressure variation with the occurrence of intracerebral hemorrhage. METHODS: Ambulatory blood pressure monitoring was performed at 21-28 days after ictus in 78 first-ever unselective consecutive patients with intracerebral hemorrhage and in 80 age-adjusted and sex-adjusted controls who were referred to the hypertension center of our institution. The degree of nocturnal blood pressure dip was calculated as [(mean daytime values-mean night-time values)/mean daytime values]x100. Nondippers were defined as patients who exhibited a <10% nocturnal dip in systolic blood pressure. Logistic regression models were constructed to assess the association of nondipping status with intracerebral hemorrhage after adjusting for potential confounders (cardiovascular risk factors, office and ambulatory blood pressure levels). RESULTS: Prevalence of nondipping was significantly greater among cases than among controls (74.4% vs. 43.8%, P<0.001). Nondipping status was independently (P=0.033) associated with intracerebral hemorrhage (OR: 2.326, 95% CI: 1.068-5.050) in a multiple variable logistic regression model that adjusted for baseline characteristics, cardiovascular risk factors, office and ambulatory blood pressure variables. The magnitude of the nocturnal systolic blood pressure dipping was inversely related to the risk of intracerebral bleeding; the odds ratio for intracerebral hemorrhage associated with every 1% decrease in nocturnal systolic blood pressure dip was 1.143 (95% CI: 1.058-1.235, P=0.001). CONCLUSIONS: Given the previous reports that nondipping contributes to the risk of cerebral infarction, our results indicate that blunted nocturnal blood pressure dip may be also associated with the occurrence of intracerebral hemorrhage.

Red wine's antioxidants counteract acute endothelial dysfunction caused by cigarette smoking in healthy nonsmokers.

BACKGROUND: Long-term smoking is believed to cause endothelial dysfunction via increased oxidative stress, whereas short-term smoking impairs vasodilatation through an as yet undefined mechanism. However, red wine and its constituents have a powerful antioxidant effect both in long-term and acute consumption. The aim of the current study was to investigate whether red wine, with or without alcohol, influences endothelial dysfunction induced by acute cigarette smoking. METHODS: Sixteen healthy volunteers (8 males and 8 females) were recruited for a double-blind, crossover study, comprising 3 study days. Each subject smoked 1 cigarette, or smoked and drank 250 mL of red wine, or smoked and drank 250 mL of dealcoholized red wine. Flow-mediated dilatation (FMD) was measured after fasting and 15, 30, 60, and 90 minutes after each trial (smoke or smoke and drink either beverage). RESULTS: Acute smoking of 1 cigarette caused a reduction in FMD (P <.001), which was statistically significant 15, 30, and 60 minutes after the inhalation of smoke compared to baseline levels (P <.001, P <.001, P =.043, respectively). However, simultaneous ingestion of either red wine or dealcoholized red wine with smoking did not lead to a change in FMD. CONCLUSIONS: Acute smoking caused a significant impairment in endothelial function. Simultaneous consumption of red wine or dealcoholized red wine with smoking decreased smoke's harmful effect on endothelium.

Association between 24-h blood pressure monitoring variables and brain oedema in patients with hyperacute stroke.

OBJECTIVE: To assess the effects of blood pressure (BP) values on oedema formation following hyperacute stroke. DESIGN: Prospective observational study. SETTING AND PATIENTS: Acute stroke-unit in University hospital. A total of 240 consecutive first-ever ischaemic or haemorrhagic stroke patients were recruited within 3 h of ictus. METHODS Casual and 24-h BP values were measured. Known stroke risk factors and clinical findings on admission were documented. Patients were imaged with computed tomography (CT) scan within 24 h from stroke onset and 5 days later in order to determine the presence of brain oedema. Patients who received antihypertensive medication during the BP monitoring were excluded. RESULTS: The main outcome measure was brain oedema formation, which was present in 78 (32.5%) patients. The 24-h systolic (SBP), diastolic (DBP) and mean BP values, 24-h pulse pressure and heart rate values were significantly higher in patients with brain oedema than in the reference group (stroke patients without brain swelling). On multiple variable analysis, containing clinical, demographic and BP monitoring variables, 24-h SBP remained significantly (P = 0.019) associated with brain oedema. The odds ratio for oedema formation associated with each 10-mmHg increase in 24 h SBP was 1.25 (95% confidence intervals: 1.04-1.51). During the first 27 h after onset SBP course showed a spontaneous decline in the reference group, which was not documented in patients with brain oedema. CONCLUSION: Elevated 24-h SBP values in the acute stroke period are associated with subsequent brain oedema formation.

Myocardial adrenergic denervation in patients with primary (AL) amyloidosis.

Three patients, 2 women and 1 man, with primary (AL) amyloidosis without congestive heart failure are described; all 3 patients presented reduced I-123 metaiodobenzylguanidine (MIBG) myocardial uptake suggesting marked cardiac sympathetic denervation. This is the first time myocardial adrenergic denervation is described in patients with AL amyloidosis without evidence of congestive heart failure; the observed denervation could be implicated in the pathogenesis of cardiac conduction disturbances which are common in this disease.

Constituents of red wine other than alcohol improve endothelial function in patients with coronary artery disease.

BACKGROUND: Several studies suggest that red wine is beneficial in coronary artery disease (CAD). Although the long-term effect of moderate red wine consumption on endothelial function is currently under investigation, there is little knowledge about its effect on postprandial endothelial function and haemostatic factors. The aim of the present study was to investigate the postprandial effects of alcohol content and the antioxidants of red wine on endothelial function and fibrinogen levels in CAD patients. METHODS: Fifteen males with angiographically documented CAD were recruited for the study. All volunteers ingested 250 ml of either red wine or de-alcoholized red wine on two different days. Blood samples (for analysis of fibrinogen and blood lipids) were collected and flow-mediated dilatation (FMD) was determined before and 30, 60 and 90 min following consumption of each beverage RESULTS: FMD was higher following the consumption of de-alcoholized red wine [type of wine effect, P=0.05 repeated measures analysis of variance (ANOVA)]. Furthermore, the pattern of the response was different between the two beverages, as FMD increased following the ingestion of de-alcoholized red wine, but it decreased after consumption of regular red wine (type of wine by time interaction effect, P=0.006 repeated measures ANOVA). Fibrinogen concentrations were unaltered CONCLUSIONS: Acute ingestion of red wine without alcohol led to higher FMD than ingestion of regular red wine in CAD patients. The acute effect of red wine on endothelial function may be different than its long-term effect and it could be attributed to its constituents other than alcohol.

Cardiac hypertrophy in hypertension: relation to 24-h blood pressure profile and arterial stiffness.

BACKGROUND: In subjects with essential hypertension peripheral blood pressure profile contributes to the pathogenesis of left ventricular hypertrophy. It is not known if central arterial pressure is superior to peripheral blood pressure profile for predicting left ventricular hypertrophy. In the present study 24-h blood pressure profile and central hemodynamics were examined to evaluate mechanical loading factors as determinants of cardiac hypertrophy in mild to moderate untreated essential hypertension. METHODS: Forty-eight untreated subjects with mild to moderate essential hypertension were examined by echocardiography for evaluation of left ventricular mass, 24-h ambulatory blood pressure monitoring (ABPM), and applanation tonometry of the radial artery with pulse wave analysis for evaluation of central hemodynamics. RESULTS: Left ventricular mass showed a statistically significant correlation with age, clinic systolic blood pressure, mean heart rate and heart rate variability during 24-h ABPM, augmentation pressure and index and central systolic blood pressure. In a multiple regression analysis including clinic systolic blood pressure, central systolic pressure, mean systolic pressure and pulse pressure during ambulatory monitoring as well as age, independent predictors of left ventricular mass were only age (P=0.006) and central systolic blood pressure (P=0.04). In conclusion, pulse wave analysis is a valuable method in predicting cardiac hypertrophy in untreated mild to moderate essential hypertension. Central systolic blood pressure should be taken into account for planning therapeutic strategies for prevention of left ventricular hypertrophy in hypertensive patients.

Ascorbic acid does not improve endothelium-dependent flow-mediated dilatation of the brachial artery in patients with Raynaud's phenomenon secondary to systemic sclerosis.

Previous studies have shown that patients with Raynaud's phenomenon secondary to systemic sclerosis present abnormal endothelial function; the mechanisms responsible for the endothelial dysfunction are unknown but increased vascular oxidative stress could be a possible cause. The hypothesis that a potent water-soluble antioxidant can reverse endothelial dysfunction in these patients was tested in the present study. We examined 11 female patients with Raynaud's phenomenon secondary to systemic sclerosis and ten healthy control women by ultrasound imaging of the brachial artery to assess flow-mediated (endothelium-dependent) and nitrate-induced (endothelium-independent) vasodilatation. Flow-mediated dilatation and nitrate-induced dilatation were significantly reduced in patients with Raynaud's phenomenon, indicating abnormal endothelial and smooth muscle cell function. Patients with Raynaud's phenomenon entered a double-blind, randomized, crossover placebo-controlled trial and received orally 2 g of ascorbic acid or placebo; vascular studies were repeated two hours after ascorbic acid or placebo administration. Flow-mediated dilatation did not improve after ascorbic acid (1.6 +/- 2.2% to 2.2 +/- 2.5%, ns) or placebo administration (1.2 +/- 1.9% to 1.7 +/- 1.4%, ns); also nitrate-induced dilatation was similar after ascorbic acid or placebo (16 +/- 7.4% vs 17 +/- 8%, ns), suggesting no effect of ascorbic acid on endothelial and vascular smooth muscle function. In conclusion, ascorbic acid does not reverse endothelial vasomotor dysfunction in the brachial circulation of patients with Raynaud's phenomenon secondary to systemic sclerosis. The use of different antioxidants or different dosing of ascorbic acid may be required to show a beneficial effect on endothelial vasodilator function.