Endothelial Function In Healthy Subjects Research Articles

Relationship between heart rate variability and endothelial function in healthy subjects

In various diseased states reduced cardiac vagal activity is accompanied by impaired endothelial function. Evidence from animal studies indicates interaction between the two systems, but such data from human studies is limited. The aim of this study was to test the hypothesis that cardiac vagal activity and endothelial function are related in healthy individuals. 46 young males were studied. From 10 minute long ECG recordings mean RR-interval and time and frequency domain vagal heart rate variability indices (RMSSD; pNN50 and HF, respectively) were determined. Heart rate variability indices were used to define cardiac vagal activity. Endothelial function was assessed by measuring brachial artery flow mediated dilation. Hyperemic, diastolic shear rate was used to normalize flow mediated dilation. All three vagal heart rate variability indices correlated significantly and positively with flow mediated dilation across subjects, with r values within the range of 0.43-0.52, p<0.01 for all relations. After adjusting for potential confounders, vagal heart rate variability indices remained significantly associated with normalized flow mediated dilation. RR-interval was related to most heart rate variability indices, but was not related to flow mediated dilation. Our data demonstrate that vagal heart rate variability indices are related to flow mediated dilation across healthy male subjects. The results cannot serve as evidence of a causal relationship, but are of interest and render for further investigation into underlying mechanisms.

Sympathetic regulation of vascular function in health and disease

The sympathetic nervous system (SNS) is known to play a pivotal role in short- and long-term regulation of different functions of the cardiovascular system. In the past decades increasing evidence demonstrated that sympathetic neural control is involved not only in the vasomotor control of small resistance arteries but also in modulation of large artery function. Sympathetic activity and vascular function, both of which are key factors in the development and prognosis of cardiovascular events and disease, are linked at several levels. Evidence from experimental studies indicates that the SNS is critically influenced, at the central and also at the peripheral level, by the most relevant factors regulating vascular function, such as nitric oxide (NO), reactive oxygen species (ROS), endothelin (ET), the renin-angiotensin system. Additionally, there is indirect evidence of a reciprocal relationship between endothelial function and activity of the SNS. A number of cardiovascular risk factors and diseases are characterized both by increased sympathetic outflow and decreased endothelial function. In healthy subjects, muscle sympathetic nerve activity (MSNA) appears to be related to surrogate markers of endothelial function, and an acute increase in sympathetic activity has been associated with a decrease in endothelial function in healthy subjects. However, direct evidence of a cause-effect relationship from human studies is scanty. In humans large artery stiffness has been associated with increased sympathetic discharge, both in healthy subjects and in renal transplant recipients. Peripheral sympathetic discharge is also able to modulate wave reflection. On the other hand, large artery stiffness can interfere with autonomic regulation by impairing carotid baroreflex sensitivity.

Inhibition of endothelial microparticles-mediated oxidative stress by berberine and its relation with endothelial function in humans

BackgroundCirculating endothelial microparticles (EMPs) lead to impaired endothelial vasodilation accompanied by increased oxidative stress. The authors previously demonstrated that berberine protects endothelial function which is associated with decreased circulating EMPs,...

Effect of shift work on endothelial function in young cardiology trainees

Long-term shift work (SW) is associated with an increase in cardiovascular disease (CVD). Previous studies have shown that prolonged SW is associated with endothelial dysfunction, suggesting that this abnormality may contribute to the SW-related increase in cardiovascular risk. The immediate effect of SW on endothelial function in healthy subjects, however, is unknown. We studied endothelial function and endothelium-independent function in 20 healthy specialty trainees in cardiology at our Institute, without any cardiovascular risk factor (27.3 ± 1.9 years, nine males), at two different times: (1) after a working night (WN), and (2) after a restful night (RN). The two test sessions were performed in a random sequence. Endothelial function was assessed by measuring brachial artery dilation during post-ischaemic forearm hyperaemia (flow-mediated dilation, FMD). Endothelium-independent function in response to 25 µg of sublingual glyceryl trinitrate (nitrate-mediated dilation, NMD) was also assessed. FMD was 8.02 ± 1.4% and 8.56 ± 1.7% after WN and RN, respectively (p = 0.025), whereas NMD was 10.5 ± 2.1% and 10.4 ± 2.0% after WN and RN, respectively (p = 0.48). The difference in FMD between WN and RN was not influenced by the numbers of hours slept during WN (<4 vs >4 hours) and by the duration of involvement of specialty trainees in nocturnal work (<12 vs >12 months). Our study shows that in healthy medical residents, without any cardiovascular risk factor, FMD is slightly impaired after WN compared to RN. Disruption of physiological circadian neuro-humoral rhythm is likely to be responsible for this adverse vascular effect.

Dose-response effects of omega-3 fatty acids on triglycerides, inflammation, and endothelial function in healthy persons with moderate hypertriglyceridemia

Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been shown to reduce cardiovascular mortality at a dose of ≈1 g/d. Studies using higher doses have shown evidence of reduced inflammation and improved endothelial function. Few studies have compared these doses. The objective of this study was to compare the effects of a nutritional dose of EPA+DHA (0.85 g/d) with those of a pharmaceutical dose (3.4 g/d) on serum triglycerides, inflammatory markers, and endothelial function in healthy subjects with moderately elevated triglycerides. This was a placebo-controlled, double-blind, randomized, 3-period crossover trial (8 wk of treatment, 6 wk of washout) that compared the effects of 0.85 and 3.4 g EPA+DHA/d in 23 men and 3 postmenopausal women with moderate hypertriglyceridemia (150-500 mg/dL). The higher dose of EPA+DHA lowered triglycerides by 27% compared with placebo (mean ± SEM: 173 ± 17.5 compared with 237 ± 17.5 mg/dL; P = 0.002), whereas no effect of the lower dose was observed on lipids. No effects on cholesterol (total, LDL, and HDL), endothelial function [as assessed by flow-mediated dilation, peripheral arterial tonometry/EndoPAT (Itamar Medical Ltd, Caesarea, Israel), or Doppler measures of hyperemia], inflammatory markers (interleukin-1β, interleukin-6, tumor necrosis factor-α, and high-sensitivity C-reactive protein), or the expression of inflammatory cytokine genes in isolated lymphocytes were observed. The higher dose (3.4 g/d) of EPA+DHA significantly lowered triglycerides, but neither dose improved endothelial function or inflammatory status over 8 wk in healthy adults with moderate hypertriglyceridemia. The trial was registered at clinicaltrials.gov as NCT00504309.

Noninvasive Visualization of Coronary Artery Endothelial Function in Healthy Subjects and in Patients With Coronary Artery Disease

The goal was to test 2 hypotheses: first, that coronary endothelial function can be measured noninvasively and abnormal function detected using clinical 3.0-T magnetic resonance imaging (MRI); and second, that the extent of local coronary artery disease (CAD), in a given patient, is related to the degree of local abnormal coronary endothelial function. Abnormal endothelial function mediates the initiation and progression of atherosclerosis and predicts cardiovascular events. However, direct measures of coronary endothelial function have required invasive assessment. The MRI was performed in 20 healthy adults and 17 patients with CAD. Cross-sectional coronary area and blood flow were quantified before and during isometric handgrip exercise, an endothelial-dependent stressor. In 10 severe, single-vessel CAD patients, paired endothelial function was measured in the artery with severe stenosis and the contralateral artery with minimal disease. In healthy adults, coronary arteries dilated and flow increased with stress. In CAD patients, coronary artery area and blood flow decreased with stress (both p ≤ 0.02). In the paired study, coronary artery area and blood flow failed to increase during exercise in the mildly diseased vessel, but both area (p = 0.01) and blood flow (p = 0.02) decreased significantly in the severely diseased, contralateral artery. Endothelial-dependent coronary artery dilation and increased blood flow in healthy subjects, and their absence in CAD patients, can now be directly visualized and quantified noninvasively. Local coronary endothelial function differs between severely and mildly diseased arteries in a given CAD patient. This novel, safe method may offer new insights regarding the importance of local coronary endothelial function and improved risk stratification in patients at risk for and with known CAD.

Coffee and endothelial function: a battle between caffeine and antioxidants?

Although coffee is largely consumed by adults in Western countries, controversy exists about its impact on the cardiovascular system. We recently demonstrated that caffeinated and decaffeinated espresso coffee have different acute effects on endothelial function in healthy subjects, measured using flow-mediated dilation (FMD) of the brachial artery. In this study, we measured the anti-oxidant capacity of two coffee substances in terms of free stable radical 2,2-diphenyl-1-picryl-hydrazyl 50% inhibition (I(50) DPPH). The caffeinated coffee had a slightly higher anti-oxidant capacity than decaffeinated espresso coffee (I(50) DPPH: 1.13±0.02 vs 1.30±0.03 μl; P<0.001). We suggest that the unfavourable effects observed after caffeinated coffee ingestion are due to caffeine and that the antioxidant activity is responsible for the increased FMD observed after decaffeinated coffee ingestion. Further clinical and epidemiological studies are needed to understand the chronic effects of coffee consumption on health.

Observations of time-based measures of flow-mediated dilation of forearm conduit arteries: implications for the accurate assessment of endothelial function

Endothelium-dependent flow-mediated dilation (FMD) is measured as the increase in diameter of a conduit artery in response to reactive hyperemia, assessed either at a fixed time point [usually 60-s post-cuff deflation (FMD(60))] or as the maximal dilation during a 5-min continuous, ECG-gated, measurement (FMD(max-cont)). Preliminary evidence suggests that the time between reactive hyperemia and peak dilation (time to FMD(max)) may provide an additional index of endothelial health. We measured FMD(max-cont), FMD(60), and time to FMD(max) in 30 young healthy volunteers, 22 healthy middle-aged adults, 16 smokers, 23 patients with hypertension, 40 patients with coronary artery disease, and 22 patients with heart failure. As previously reported, FMD(max-cont) was similar in healthy cohorts and was significantly blunted in smokers and all patient groups, whereas FMD(60) was significantly blunted only in heart failure patients. There was a wide within-group variability between measures of time to FMD(max) with no significant difference between normal and patient groups. Intra-arterial infusion of the nitric oxide synthase inhibitor N(omega)-monomethyl-l-arginine in eight healthy subjects resulted in a blunting of FMD(max-cont) (P < 0.001) and FMD(60) (P = 0.02) but not time to FMD(max). Both FMD(max-cont) and FMD(60) demonstrated good repeatability in 30 young healthy volunteers studied on two separate occasions (P < 0.01 for both), whereas time to FMD(max) varied widely between visits (P = not significant). In conclusion, although time to FMD(max) does not appear to be a useful adjunctive measure of endothelial health, the use of continuous diameter measurements provides important data in the study of endothelial function in healthy subjects and patients with cardiovascular disease.

The diagnostic value of endothelial function as a potential sensor of fatigue in health

Many epidemiological research studies have shown that vital exhaustion and psychosocial factors are associated with the occurrence of cerebrocardiovascular disease (CCVD). Fatigue is thought to induce endothelial dysfunction and may be linked to the occurrence of CCVD; however, no studies have investigated this potential link. We studied to determine the effect of fatigue on endothelial function in healthy subjects with no traditional CCVD risk factors or potential confounding factors to be controlled. Peripheral arterial tonometry (PAT) was used to evaluate endothelial function. The influence of the following parameters on endothelial function was analyzed in 74 office workers without traditional CCVD risk factors at health check-ups: endothelial function before and after work, subjective fatigue, lifestyle factors such as sleeping time, and psychosocial factors such as depression and social support. Twenty-five subjects (33.8%) had low endothelial function; reactive hyperemia (RH)-PAT index <1.67, even though no abnormalities were reported in the health check-ups. There was no significant difference in endothelial function before versus after labor. Of note, endothelial function was associated with the individual's level of subjective fatigue (t = 2.98, P = 0.008) and showed a daily fluctuation, sometimes to a pathological degree (<1.67). We showed that, even in healthy people, endothelial function fluctuates diurnally, with an interaction between the individual's cognitive fatigue and the environment, sometimes to a pathological degree. Based on these findings, we suggest that endothelial function is an objective assessment tool of fatigue in healthy individuals.

Acute effects of coffee on endothelial function in healthy subjects

Coffee is the most widely consumed beverage in the world, but its effect on the cardiovascular system has not been fully understood. Coffee contains caffeine and antioxidants, which may influence endothelial function, both of which have not yet been investigated. The objective of this study was to investigate the acute effects of coffee on endothelial function measured by brachial artery flow-mediated dilation (FMD). A total of 20 (10 males and 10 females) healthy non-obese subjects underwent a double-blind, crossover study. Subjects ingested one cup of caffeinated (CC) and one cup of decaffeinated (DC) Italian espresso coffee in random order at 5- to 7-day intervals. Following CC ingestion, FMD decreased progressively and significantly (mean+/-s.e.m.: 0 min, 7.7+/-0.6; 30 min, 6.3+/-0.7; 60 min, 6.0+/-0.8%; ANOVA (analysis of variance), P<0.05), but it did not significantly increase after DC ingestion (0 min, 6.9+/-0.6; 30 min, 8.1+/-0.9; 60 min, 8.5+/-0.9%; P=0.115). Similarly, CC significantly increased both systolic and diastolic blood pressure; this effect was not observed after DC ingestion. Blood glucose concentrations remained unchanged after ingestion of both CC and DC, but insulin (0 min, 15.8+/-0.9; 60 min, 15.0+/-0.8 muU/ml; P<0.05) and C-peptide (0 min, 1.25+/-0.09; 60 min, 1.18+/-0.09 ng/ml; P<0.01) blood concentrations decreased significantly only after CC ingestion. CC acutely induced unfavorable cardiovascular effects, especially on endothelial function. In the fasting state, insulin secretion is also likely reduced after CC ingestion. Future studies will determine whether CC has detrimental clinically relevant effects, especially in unhealthy subjects.

Dose-dependent effects of decaffeinated coffee on endothelial function in healthy subjects

Coffee is known to contain antioxidant substances whose effects may be blunted because of caffeine that may unfavorably affect the cardiovascular system. This study was designed to investigate the acute dose-dependent effects of decaffeinated coffee (DC) on endothelial function measured by the brachial artery flow-mediated dilation (FMD). A total of 15 (8 men and 7 women) healthy nonobese subjects underwent a single-blind, crossover study. Subjects ingested one and two cups of decaffeinated Italian espresso coffee in random order at 5- to 7-day intervals. In the hour following the ingestion of two cups of DC, FMD increased (mean+/-s.e.m.): 0 min, 7.4+/-0.7%; 30 min, 8.0+/-0.6%; 60 min, 10.8+/-0.8%; P<0.001) as compared to consumption of one cup of DC (0 min, 6.9+/-0.7%; 30 min, 8.4+/-1.2%; 60 min, 8.5+/-1.1%; 3 x 2 repeated-measures analysis of variance: P=0.037 for time x treatment effect). Blood pressure did not differ between groups, and basal heart rate was lower in the two-cup group at baseline and 60 min. The present study demonstrated a significant acute favorable dose-dependent effect of decaffeinated espresso coffee on endothelial function. Further studies are needed to investigate the effects of chronic use of DC especially with respect to caffeinated coffee and in subjects with cardiovascular diseases.

Berberine-induced decline in circulating CD31+/CD42− microparticles is associated with improvement of endothelial function in humans

Elevated circulating endothelial microparticles (EMPs) are associated with endothelial dysfunction. This study is to investigate whether berberine-induced fall in circulating EMPs facilitates improvement of endothelial function in healthy subjects. Fourteen healthy subjects received 1-month berberine therapy (1.2 g/d) and 11 healthy subjects served as control. Circulating EMPs were measured by flow cytometric analysis before and after therapy. Brachial artery endothelium-dependent and -independent function was assessed by flow-mediated vasodilation (FMD) and sublinqual nitroglyceride-mediated vasodilation (NMD). In vitro, human umbilical vein endothelial cells (HUVECs) were stimulated by EMPs (106/ml) with or without the presence of berberine (10 μM). Intracellular endothelial nitric oxide synthase (eNOS) protein expression was detected by flow cytometry. After berberine therapy, circulating CD31+/CD42− microparticles were reduced, which was in parallel with the improvement of flow-mediated vasodilation while nitroglyceride-mediated vasodilation kept unchanged. A robust relationship was found between drop of circulating CD31+/CD42− microparticles and increased flow-mediated vasodilation. The EMPs in vitro led to diminished eNOS protein expression in HUVECs and this EMP-mediated detrimental effect was markedly inhibited by berberine. Berberine-induced decline in circulating CD31+/CD42− microparticles contributes to upregulation of endothelial function in healthy subjects. Deceasing EMPs may be a novel therapeutic target for the improvement of endothelial dysfunction in humans.

Postprandial Improvement of Endothelial Function by Red Wine and Olive Oil Antioxidants: A Synergistic Effect of Components of the Mediterranean Diet

Objective: Consumption of olive oil may cause postprandial impairment of endothelial function, while acute ingestion of red wine seems to improve it. The purpose of the present study was to investigate the combined postprandial effects of two essential components of the Mediterranean diet, red wine and olive oil, on endothelial function.Methods: Fifteen healthy subjects were enrolled in the study, which was comprised of 4 study days. Subjects were asked to consume a standard meal at each study day containing 50gr of olive oil and 250 ml of wine. Two types of wine (red and white; rich and poor in antioxidants respectively) and two types of olive oil (green and refined; rich and poor in antioxidants respectively) were used in a 2*2 design. Endothelium dependent, flow mediated dilatation (FMD) was measured with a B-Mode ultrasound device at fast and 1, 2 and 3 hours postprandially.Results: Combined consumption of red wine and green olive oil (both rich in antioxidants) improved FMD postprandially (p = 0.002, ANOVA for repeated measures), which remained significant 1 hour (p = 0.002) and 2 hours (0.037) following the meal compared to fasting levels. No other combination of wine and olive oil caused any significant alteration on FMD.Conclusion: Acute consumption of both red wine and green olive oil, rich in antioxidants, led to an improvement in the postprandial endothelial function in healthy subjects. These findings provide an additional favorable effect of components of the Mediterranean diet and of their antioxidant substances on endothelial function, at the postprandial state.

The relation of arterial stiffness to endothelial function in healthy subjects

Local wall stiffness affects endothelial responsiveness but how global measures affect responsiveness is unanswered. We assessed this by comparing reactive hyperaemic responses of brachial diameter (RHRBD) with central (heart-to-brachial artery pulse wave velocity (PWV); large (C1)) and peripheral (C2) arterial stiffness. Twelve healthy subjects were investigated. RHRBD was induced via an upper- or forearm occluding cuff. Arterial diameter changes were measured using echo ultrasound. Arterial stiffness and RHRBD were compared using a Pearson correlation coefficient (r) and Bland–Altman analysis of Z-scores (indicated as 95% confidence intervals (CI) and expressed in units of standard deviation (SD) from the mean). Weak relations were found between upper-arm RHRBD responses and C2 (r = 0.56, P = 0.06; 95% CI ± 1.84 SDs) and C1 (r = 0.55, P = 0.06; 95% CI ± 1.86 SDs). An inverse relation was found between upper-arm RHRBD responses and PWV (r = −0.55, P = 0.06), but Bland–Altman plots revealed no agreement between these parameters (P > 0.05; 95% CI ± 3.46 SDs). Forearm RHRBD were not related to PWV, C1 or C2 (P > 0.05; 95% CI > 2 SDs). The weak relation between upper-arm endothelial responses and C2 and C1 seems to suggest that C2, and also C1, is not a good and reliable method for assessments of endothelial health. Furthermore, if anything, upper-arm mediated RHRBD responses are more affected by arterial stiffness than forearm responses.

Analyse spectrale par transformée de Fourier du flux sanguin cutané dans la sclérodermie systémique

ObjectivesEndothelial dysfunction is an early event and a critical step in the pathogenesis of systemic sclerosis. Accurate and sensitive tests are needed to correctly assess the degree of microvascular endothelial dysfunction. Spectral analysis of skin blood flow contains a characteristic low frequency reported to be associated with endothelial function in healthy subjects. We hypothesized that the relative amplitude of the oscillation recorded for this low frequency spectrum (0.008 to 0.021 Hz) would be less pronounced in patients with systemic sclerosis than in healthy subjects and in patients with primary Raynaud's phenomenon. Patients and methodTwenty-one patients with systemic sclerosis, twenty patients with primary Raynaud phenomenon and eleven healthy subjects were enrolled. Skin perfusion was recorded at rest for 30 minutes using laser Doppler flowmetry on the pad of the left third left. Fourier transform spectral analysis was applied to obtain the mean amplitude of the cutaneous blood perfusion signal of the total spectrum from 0.008 to 1.6 Hz and the mean amplitude of each characteristic frequency in the laser Doppler flowmeter blood flow oscillations. ResultsThe relative amplitudes of each characteristic frequency in the laser Doppler flowmeter blood flow oscillations were not statistically different in the three groups, particularly for frequency spectrum from 0.008 Hz to 0.021 Hz. ConclusionFourier transform spectral analysis of baseline cutaneous blood flow does not provide significant information. Further studies are required, perhaps using wavelet spectral analysis or stimulated conditions.

Effect of coffee on endothelial function in healthy subjects: the role of caffeine

Coffee is one of the most widely used pharmacologically active beverages. The present study was designed to evaluate the acute effect of coffee ingestion on endothelial function in healthy individuals, and the potential role of caffeine. We studied 17 healthy young adults (28.9+/-3.0 years old; nine men), who were regular non-heavy coffee drinkers. The endothelial performance was estimated by endothelium-dependent FMD (flow-mediated dilatation) of the brachial artery before and 30, 60, 90 and 120 min after ingestion of a cup of caffeinated coffee (80 mg of caffeine) or the corresponding decaffeinated beverage (< 2 mg of caffeine) in two separate sessions, following a randomized single-blind cross-over design. There was no difference in baseline FMD values between the two sessions [7.78 compared with 7.07% after caffeinated and decaffeinated coffee respectively; P = NS (not significant)]. Caffeinated coffee led to a decline of FMD (7.78, 2.86, 2.12, 4.44 and 4.57% at baseline, 30, 60, 90 and 120 min respectively; P < 0.001). This adverse effect was focused at 30 (P = 0.004) and 60 min (P < 0.001). No significant effect on FMD was found with the decaffeinated coffee session (7.07, 6.24, 5.21, 7.41 and 5.20%; P = NS). The composite effect of the type of coffee consumed over time on FMD was significantly different (P = 0.021). In conclusion, coffee exerts an acute unfavourable effect on the endothelial function in healthy adults, lasting for at least 1 h after intake. This effect might be attributed to caffeine, given that decaffeinated coffee was not associated with any change in the endothelial performance.

Interleukin-6 gene -573G>C promoter polymorphism is associated with plasma fibrinogen level and hypertension in Hong Kong Chinese

Inflammation is an important mechanism in cardiovascular disease. Interleukin-6 (IL-6) is the major regulator of acute phase protein synthesis1 and plays important roles in the pathogenesis of cardiovascular disorders. Elevated IL-6 levels are associated with the development and severity of coronary disease as well as the transition to plaque instability and subsequent poor outcome in atherosclerotic processes. Several single nucleotide polymorphisms (SNPs) in the IL-6 gene promoter have been reported, of which the -174G>C has been shown to influence the basal level of circulating IL-6 in vivo and endothelial function in healthy subjects. We sought to study IL-6 gene promoter polymorphisms in the Hong Kong Chinese and determined their association with hypertension and plasma fibrinogen levels. SNPs in the IL-6 gene promoter was identified by direct sequencing of a 945-bp segment of the 5′-flanking region of IL-6 gene in which most known SNPs are located in 40 Hong Kong Chinese subjects [20 subjects with a history of ischemic heart disease (IHD) or stroke, and 20 normal controls]. Large-scale screenings of the identified SNPs were performed in 111 essential hypertensives and 118 sex and age-matched normotensive controls, using the Sequenom genotyping platform. Plasma levels of acute phase proteins were determined. A major SNP: -573C>G (rs1800796) polymorphism was found in our population (-573G allele frequency 0.24). The genotypes of -573C>G polymorphism were in Hardy-Weinberg equilibrium (p=0.92). The -174G>C and -598G>A polymorphisms, which are present in Caucasians, were almost 100% homozygous in our population. Subjects with -573G allele (CG+GG genotypes) had a higher blood level of fibrinogen than with CC (3.12±0.05 vs. 2.92±0.06, p=0.018). The -573G allele was also found to be associated with hypertension (P=0.047). In conclusion, our results raise the possibility that IL-6 gene might play a role in the pathogenesis of hypertension.

52 The increase of dietary antioxidant intake improves endothelial function in healthy subjects

52 The increase of dietary antioxidant intake improves endothelial function in healthy subjects

Acute inflammatory state during influenza infection and endothelial function

Chronic inflammatory stimulus seems to contribute to atherosclerotic process. Several studies have established a relationship between infective agents as Chlamydia pneumoniae, herpes virus and cytomegalovirus and atherosclerotic lesions. Aim of this study was to investigate the effects of influenza infective state on endothelial function of healthy young subjects, expressed as brachial flow-mediated vasodilation (FMV) and soluble form of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1). In 10 male subjects (mean age 35 ± 14 years) exhibiting influenza symptoms for 3 days, we determined total cholesterol, high-density lipoproteins (HDL), low-density lipoproteins (LDL), triglycerides, sVCAM-1, sICAM-1 and brachial FMV. All subjects had an antibody pattern characteristic of influenza A or B virus infection. After 3 months brachial FMV was significantly increased (8.6 ± 2.3% versus 11.5 ± 3.2%; p < 0.001), while HDL (46 ± 10 mg/dL versus 49 ± 9 mg/dL; p < 0.05), sICAM-1 and sVCAM-1 were reduced (respectively: 488 ± 105 ng/mL versus 340 ± 127 ng/mL; p < 0.001, 1710 ± 80 ng/mL versus 1216 ± 63 ng/mL; p < 0.001). Univariate analysis showed a positive correlation between changes in CRP and sICAM-1 levels ( r = 0.95, p < 0.001), a negative one between changes in sICAM-1 and brachial FMV ( r = −0.65, p < 0.05) and between CRP and brachial FMV ( r = −0.64, p < 0.05). This small study suggested that inflammatory state determined by viral agents may transitorily alter endothelial function in healthy subjects.

Impact of physical training and detraining on endothelium-dependent vasodilation in patients with recent acute myocardial infarction

Background There is evidence that aerobic exercise improves endothelial function in healthy subjects as well as in patients with chronic heart failure. However, it is unknown whether this effect occurs in patients with recent myocardial infarction (AMI). Methods Fifty-two patients with a recent first uncomplicated AMI underwent endothelial function evaluation before and after 3 months of moderate aerobic exercise training. We measured brachial artery vasomotor reactivity using flow-mediated dilation (FMD), a cold pressor (CP) test, and sublingual nitroglycerin. Patients were randomized into 2 groups: 28 patients (G1) underwent training, while 24 patients (G2) served as controls. Brachial artery vasomotor reactivity was reassessed after 1 month of detraining (DT). Results At baseline the FMD was 1.66% ± 4.11% in G1 and 2.04% ± 3.4% in G2 ( P = NS) and vasoconstriction was evident after a CP test. The diameter reduction was −4.1% ± 3.89% in G1 and −4.39% ± 5.67% in G2 ( P = NS). At follow-up the FMD had increased to 9.39% ± 4.87% in G1 ( P < .01) and to 4.4% ± 3.9% in G2 ( P < .01 vs G1). Vasoconstriction during a CP test was observed only in G2. Endothelium-independent vasodilation was unchanged in both groups. Effort tolerance increased by 32% in G1 patients ( P < .01 versus G2) and was correlated with FMD change ( R = 0.51, P < .01). After detraining the FMD was significantly reduced in G1 ( P < .01) and a further vasoconstriction was evident after CP testing. Conclusions Exercise training improves endothelium-dependent vasodilation in post-AMI patients. This improvement is associated with a significant increase in exercise tolerance. These benefits disappeared after detraining.