Early Marker Of Cardiovascular Disease Research Articles

Race, Psychosocial Factors, and Aortic Pulse Wave Velocity: The Health, Aging, and Body Composition Study

Increasingly, researchers have begun to explore pathways through which psychosocial factors might influence cardiovascular disease, with some emphasis on early markers. The current study examined the cross-sectional association between psychosocial factors and aortic pulse wave velocity (an early marker of cardiovascular disease) in a biracial cohort of older adults. We were particularly interested in determining whether the association between psychosocial factors and aortic pulse wave velocity differed for older blacks compared with whites. Participants were 2,488 (40% black and 52% female) older adults from the Health, Aging, and Body Composition Study. Carotid-femoral aortic pulse wave velocity was assessed using standard methodologies. Depressive symptoms, anxiety symptoms, negative life events, and inadequate emotional support were assessed, and a summary psychosocial risk index was created. In multivariable linear regression models, psychosocial risk was not associated with aortic pulse wave velocity (Estimate [Est] = .00, p = .83), but there was a significant Race × Psychosocial risk interaction (Est = .07, p = .01), after adjusting for age, race, sex, and education. Further analyses revealed that this association was driven by the inadequate emotional support component of psychosocial risk (Race × Inadequate emotional support, p = .005). In race-stratified analyses, inadequate emotional support was associated with higher levels of arterial stiffness in older blacks (Est = .05, p = .04) but not whites (Est = -.04, p = .13). This association persisted after adjusting for demographics, cardiovascular risk factors, and social network characteristics. Findings suggest that older blacks may be particularly vulnerable to the effects of inadequate emotional support on vascular health. Interventions aimed at increasing social support among this population might be beneficial in reducing cardiovascular disease risk.

Following the Arterial Switch Operation, Obese Children have Risk Factors for Early Cardiovascular Disease

Children who have undergone the arterial switch operation (ASO) are at risk for premature coronary artery disease due to coronary re-implantation. Obesity may also pose cardiovascular risk. The purpose of this study was to evaluate comorbidities and markers of early cardiovascular disease in obese ASO patients. Obese [body mass index (BMI) >or= 95th %] and normal weight (NW, BMI < 85th %) ASO patients, and NW controls without heart disease were enrolled, and underwent prospective vascular, echocardiographic, laboratory, exercise, and ambulatory blood pressure (BP) testing. Results were compared between groups. BP load was defined as proportion of recordings >or= 95th %. Thirty patients [13.2 years (11.2-16.8), 57% male] were evaluated: 10 obese ASO, 10 NW ASO, and 10 NW controls. Obese ASO patients, in comparison to NW ASO and controls, had higher systolic BP% [96% (90-99) vs. 67% (30-91) P= 0.07 (trend) and 34% (21-43) P= 0.005], night-time diastolic BP load [18% (14-24) vs. 0% (0-0) P= 0.01 and 0% (0-0) P= 0.01], left ventricular mass index [51.7 g/m(2.7) (46.6-53.3) vs. 40.7 g/m(2.7) (29.2-41.6) P < 0.01 and 28.9 g/m(2.7) (27.3-33.7) P < 0.01], and lower brachial artery reactivity [8.7% (6.2-11.9) vs. 14.6% (10.8-23.0) P= 0.03, and 16.7% (12.8-17.8) P= 0.05]. There was a trend toward increased carotid intima-media thickness, and significantly higher triglyceride and lower high-density lipoprotein levels in obese ASO patients. Following the ASO, obese patients have associated comorbidities, and markers of early cardiovascular disease. These may pose additional risk for future cardiovascular events in this unique population who underwent coronary artery re-implantation in infancy.

Erectile Dysfunction and Men's Health: Developing a Comorbidity Risk Calculator

The association between erectile dysfunction (ED) and cardiovascular risk factors is well established and ED can be considered an early marker for cardiovascular disease. Aim. To generate a calculator to predict the risk of diabetes, hypertension, hyperlipidemia or angina in men with ED, based on an analysis of data from the Men's Attitudes to Life Events and Sexuality (MALES) 2004 study. A logistic regression model using the variables overall health, ED severity, having/not having a sexual partner, and waist size. The MALES was a multinational, population-based study conducted in 2001, in which the prevalence of ED and comorbid medical conditions was assessed in 27,839 men aged 20-75 years. In 2004, the cohort of men with ED (N = 1843) were recontacted and 919 (50%) agreed to participate in the MALES 2004 longitudinal study. Multistep analysis of data from 808 patients was performed, with 289 variables evaluated. Only those variables significantly correlated with outcome and those making clinical sense were retained. A logistic regression model was applied to 90% of the sample; results were validated in the remaining 10% with sensitivity and specificity testing. Of the 2004 cohort, 20.7% had been diagnosed with diabetes, 44.3% with hypertension, 42.5% with hyperlipidemia, and 25.7% with angina. The following modifiable factors affected the risk of comorbidities, and were therefore included in the risk calculator: health status, waist size, ED severity, and having or not having a sexual partner. Using these variables in the model resulted in a sensitivity of 86.2% and specificity of 54.5%. The primary limitation of the calculator is that it is not a prediction calculator. Erectile dysfunction is a key factor in calculating the probability of major risks to men's health, such as diabetes, hypertension, hyperlipidemia, and angina.

Factors Associated with Paraoxonase Genotypes and Activity in a Diverse, Young, Healthy Population: The Coronary Artery Risk Development in Young Adults (CARDIA) Study

Paraoxonase may mitigate oxidative damage and thus lower risk of macrovascular disease. DNA samples from 2252 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study were genotyped for the L55M and Q192R polymorphisms of the PON1 (paraoxonase 1) gene, and paraoxonase activity was measured in serum. The 192R (67.4% vs 29.7%) and 55L (80.0% vs 63.8%) alleles were more common in blacks vs whites. The Q192R locus was the strongest correlate of paraoxonase activity (100.4 nmol/mL/min greater in the 192RR than the 192QQ genotype). After adjustment for the Q192R locus, the L55M locus (12.7 nmol/mL/min difference between 55LL and 55MM) and race (6.6 nmol/mL/min difference between blacks and whites) were correlated with paraoxonase activity (P < or =0.0001), as were concentrations of HDL cholesterol (23.9 nmol/mL/min difference between highest and lowest quintiles), triglycerides (12.6 nmol/mL/min difference between highest and lowest quintiles), LDL cholesterol (8.2 nmol/mL/min difference between highest and lowest quintiles), smoking status (6.3 nmol/mL/min difference between current smokers of > or =15 cigarettes/day and never smokers), and glucose concentrations at the highest quintile (6.5 nmol/mL/min difference between highest and lowest quintiles in nondiabetic participants). There was no cross-sectional or longitudinal association between paraoxonase enzyme activity and coronary artery calcification (CAC), an early marker of cardiovascular disease, or its progression over 5 years. Paraoxonase may not play an important role during the early pathogenesis of cardiovascular disease. However, associations with lipids and glucose suggest that paraoxonase may modify or react to macrovascular disease pathogenesis.

Visceral fat is associated with cardiovascular risk in women with polycystic ovary syndrome

Women with polycystic ovary syndrome (PCOS) have been reported to have subclinical cardiovascular disease (CVD) and increased abdominal fat. The aim of this study was to evaluate the relationship between visceral fat (VF) and early markers of CVD in PCOS women. Two hundred overweight PCOS women [(mean +/- SD) age 24.6 +/- 3.2 years, body mass index (BMI) 28.5 +/- 2.8 kg/m2] and 100 healthy age- and BMI-matched volunteer controls entered this cross-sectional study. In all subjects, the amount of VF was measured by ultrasonography. Anthropometric measurements [BMI and waist circumference (WC)], complete hormonal and metabolic pattern, carotid intima-media thickness (IMT), brachial arterial flow-mediated dilation (FMD) and inflammatory biomarkers [C-reactive protein (CRP), fibrinogen, white blood cells count and plasminogen activated inhibitor-1] were also obtained from all subjects. A stepwise linear regression model was used in PCOS patients to verify if IMT or FMD as dependent variables are affected by other independent variables. VF amount was significantly (P < 0.001) higher in PCOS subjects than in healthy controls [31.4 +/- 7.3 versus 28.0 +/- 6.1 (mean+/-SD) mm, respectively] and directly related to insulin resistance: HOMA (r = 0.918, P < 0.001) and AUC(INS) (r = 0.879, P < 0.001), and to WC (r = 0.658; P < 0.001). In PCOS, the two linear regression analyses showed that IMT is positively affected by VF and CRP, whereas FMD is positively affected by IMT and negatively by VF and CRP. VF amount is associated with subclinical CVD in PCOS patients.

Noninvasive measures of cardiovascular changes in diabetes mellitus

Advances in noninvasive medical technology have led to more aggressive pursuit of cardiovascular disease detection in patients with diabetes mellitus. Studies measuring carotid intima-media thickness, arterial stiffness and coronary artery calcification have documented early markers of cardiovascular disease. Such markers have gained popularity for research and clinical use. This paper reviews recent studies using noninvasive technology for detection and monitoring of cardiovascular disease as it pertains to diabetes patients. Studies published in the review period have utilized noninvasive techniques to monitor subclinical cardiovascular disease in diabetes patients, including carotid intima-media thickness to evaluate carotid atherosclerosis, pulse wave velocity and pulse wave analysis to measure arterial stiffness, electron beam computed tomography to evaluate coronary artery calcification, and magnetic resonance imaging to study cardiovascular plaque. These techniques have shown promising results and will have useful application for diabetes patients in the future. Noninvasive testing is being redefined to include new techniques for detection and monitoring of cardiovascular changes. In the appropriate clinical setting, these tests offer novel approaches to monitoring - each with its own benefits and caveats. Further refinement of techniques will lead to increased applicability and improved ability for early detection of subclinical cardiovascular disease.

Sleep-Disordered Breathing and C-Reactive Protein: A Commentary

C-REACTIVE PROTEIN (CRP) HAS BEEN EXTENSIVELY STUDIED IN THE LAST DECADE BECAUSE OF ITS POSSIBLE ROLE AS AN EARLY MARKER OF CARDIOVASCULAR disease. More recently, sleep disordered breathing (SDB) has been investigated as a possible cause of increase in CRP. To date, no definite conclusion has been reached on the importance of SDB in low-grade systemic inflammation. The article by Punjabi and Beamer published in the January issue1 reported a strong association between CRP levels and sleep disordered breathing in 69 men, even after adjusting for several measures of obesity. Unfortunately, this study did not shed new light on this issue. Adiposity and CRP are so strongly related that complete adjustment may not be achieved by statistical methods. It is also troubling that adjustments were made for the 3 adiposity measures (body mass index, waist circumference, and body fat percentage): while they showed strong correlations between them, introducing the 3 variables in the same model created a multi-collinearity effect, rendering it difficult or impossible to distinguish their individual influences on CRP and thus devaluating their effect. Furthermore, the mean BMI of the sample was so high that it is likely that the majority of the subjects were overweight or obese. Therefore, adjusting for a condition that is present in nearly all the participants has little or no impact on the outcome. The same can be said about sleep duration. Although the authors did not provide the total sleep time, this variable was introduced in the multivariate regression models. A recent study has shown that even partial sleep deprivation in healthy subjects provokes an increase in CRP levels.2 This is another reason why the authors found that the adjusted models have only small attenuation in the association between AHI and CRP. Even with adjustment for known risk factors, residual confounding was likely to occur because no correction for intra-individual variability was done in major risk factors that have reversible effects on CRP, such as tobacco smoke exposure or alcohol intake. More recently, new factors have been found to have a profound impact on CRP levels.3,4 There is not yet a lot of evidence showing that treating SDB reduces the CRP levels. Two intervention studies, one using nC-PAP and the other using surgical interview, reported a significant decrease of CRP levels after intervention.5 There was no information about the magnitude of weight changes in these patients. Two long-term intervention studies with CPAP6,7 found no significant change in CRP levels, these last being associated only with BMI. A recent systematic review of 33 studies on weight loss intervention pointed out that for each 1 kilogram loss the mean change in CPR level was −0.13 mg/L.8 The interaction between CRP, SDB, and adiposity is complex. Using samples composed mostly of overweight or obese individuals cannot isolate the adiposity effect on the relationship between CRP and SDB, even with sophisticated statistical analyses, because weight excess is implicitly part of the sample definition.

The Visual Scoring of Sleep in Adults

The 1968 Rechtschaffen and Kales (R & K) sleep scoring manual was published 15 years after REM sleep was discovered. Advances in the ensuing 28 years warranted a re-look at visual scoring of sleep stages. This paper describes the work of the AASM Visual Scoring Task Force, including methodology, a literature review and the rationale behind the new rules. Reliability studies of R & K scoring were reviewed; reliability was low for stage one and moderate for slow wave sleep. Evidence indicated that K complexes and slow waves are expressed maximal frontally, spindles centrally and alpha rhythm over the occipital region. Three derivations of EEG, two of electro-oculography, and one of chin EMG were recommended. Scoring by 30-second epochs was retained. New terminology for sleep stages was proposed. Attenuation of alpha rhythm was determined to be the most valid electrophysiological marker of sleep onset. Alternative measures were proposed for non-alpha generating subjects. K complexes associated with arousals were determined to be insufficient alone to define the new stage N2. No evidence was found to justify dividing slow wave sleep into two stages. No reasons were found to alter the current slow wave amplitude criteria at any age. The phenomena of REM sleep were defined. The rules for defining onset and termination of REM sleep periods were simplified. Movement time was eliminated and major body movements defined. Studies are needed to test the reliability of the new rules. Future advances in technology may require modification of these rules with time.

P-858: Acarbose in polycystic ovary syndrome reduces arterial blood pressure, p-selectin and improve the lipid profile

Polycystic ovary syndrome (PCOS) is associated with increased prevalence of cardiovascular disease (CVD). Endothelial dysfunction has been identified as an early marker of CVD and has been shown to predict future coronary artery disease, before atherosclerotic changes appear in arteries. Measurement of endothelial function might identify at-risk individuals early and be a useful means of assessing response to treatment aimed at reducing long-term morbidity and/or mortality from CVD. Acarbose, an α-Glucosidase inhibitor, promotes a reduction of insulin secretion on PCOS patients.

Early markers of cardiovascular disease

Vascular endothelium function plays a pivotal role in cardiovascular pre-clinical markers. Nitric oxide secreted by the vascular endothelium has a vasodilatory effect that reduces blood pressure which, in turn, prevents increases of left ventricular mass and intima-media thickness and improves left ventricular relaxation. Modern ultrasound technique allows noninvasive assessment of endothelial function and permits identification of functional alteration prior to manifestation of anatomical changes in the cardiovascular system. However, effort is needed to improve the reliability and reproducibility of ultrasound derived measure of endothelial function. This article provides an overview of challenges of clinical determination of endothelium-dependent arterial dilatation. In addition, we highlight the necessity of targeting the pediatric population in studies aimed at preventing and treating cardiovascular disease.

Microalbuminuria as an Early Marker for Cardiovascular Disease

Excretion of albumin in the urine is highly variable, ranging from nondetectable quantities to milligrams of albumin and even grams of albumin. Microalbuminuria is defined as low levels of urinary albumin excretion of 30 to 300 mg/d. Microalbuminuria is highly prevalent; in hypertensive and diabetic populations, its prevalence varies from 10 to 40%. It is interesting that microalbuminuria also is found frequently in seemingly healthy individuals (5 to 7%). The variable excretion of albumin in the urine is related to the risk for the individual to develop cardiovascular (CV) disease: Absence or very low levels of albuminuria is associated with low CV risk, whereas the CV risk increases markedly with increasing amount of albumin in the urine (even within the now considered normal range). The predictive power of urinary albumin levels for CV risk is independent of other CV risk factors and not only is present in individual with diabetes and/or hypertension but also in healthy individuals. Treatments that lower albuminuria are associated with CV protection, as demonstrated in randomized, controlled trials of patients with diabetes as well as in patients with hypertension. There is preliminary evidence that albuminuria lowering is CV protective in healthy individuals with an elevated albumin excretion rate. Differences between individuals in their level of albumin excretion are already observed at a very early age (just after birth). In fact, the interindividual variability seems to be relatively constant in the first 5 decades of life, indicating that microalbuminuria is not necessarily a consequence of vascular damage at later age. Higher levels of urinary albumin seem to reflect the ordinary interindividual variability in (renal and systemic) endothelial function. Experimental data show that between strains and even within strains, rats at young age show a remarkable difference in individual endothelial function, and this is strongly related to the susceptibility of that rat to organ damage. In conclusion, albuminuria seems to be a sensitive marker very early in life for the susceptibility of an individual to CV disease. It therefore may be an ideal target for early primary prevention using CV-protective therapy regimens.

Postprandial lipid metabolism

Atherogenic effects of postprandial lipoproteins are supported by many studies comparing patients with advanced clinical signs or early markers of cardiovascular disease with subjects without vascular disease. Postprandial lipoprotein abnormalities are more frequent in individuals with type 2 diabetes and other states of insulin resistance, which could be a major factor accounting for the higher rate of cardiovascular diseases observed in these conditions. In patients with type 2 diabetes multiple abnormalities of lipoproteins of both endogenous and exogenous origin are observed also in the presence of good blood glucose control and normal fasting triglyceridaemia, and a direct role of insulin resistance in the development of postprandial dyslipidaemia has been demonstrated. Clinical and experimental studies have demonstrated that a high fat consumption is associated with impaired insulin sensitivity and may worsen postprandial hypertriglyceridemia in individuals with type 2 diabetes and/or hyperlipidaemia. In addition to the amount of fat also the physical structure of the food in which fat is present is able to influence postprandial lipaemia. Data on the effects of dietary fatty acid (FA) modifications in humans are scarce. These studies have provided some evidence that dietary polyunsaturated FA, particularly those of the n-3 class, induce an attenuated postprandial lipaemic response as compared to saturated FA (SFA) and monounsaturated FA (MUFA); however, the data are often conflicting and their interpretation is, generally, controversial. Very little is known in patients with type 2 diabetes, in whom both insulin sensitivity and postprandial lipaemia are particularly relevant. In a medium term (3 weeks) study in type 2 diabetic patients, a MUFA rich diet did not modify insulin sensitivity as compared to the SFA rich diet. The MUFA diet induced a higher early peak of chylomicrons and a significantly lower postprandial response o f small VLDL after a standard test meal, rich in saturated fat. In conclusion, postprandial lipoprotein abnormalities are a frequent feature of type 2 diabetes and of other conditions clustering with insulin resistance. The total amount of fat, more than the specific type of fatty acid, seems to influence postprandial lipoproteins. Data are needed on long term interventions as well as on the interactions between dietary fat and other food components or physical structure. Keywords: postprandial lipoproteins; metabolism of dietary fat

Getting Serious About Pediatric Chronic Kidney Disease

Getting Serious About Pediatric Chronic Kidney Disease

Hypertension: Definitions and Guidelines

Hypertension: Definitions and Guidelines

Induction of Proinflammatory Cytokines and C-Reactive Protein in Human Macrophage Cell Line U937 Exposed to Air Pollution Particulates

Exposure to particulate matter air pollution causes inflammatory responses and is associated with the progression of atherosclerosis and increased cardiovascular mortality. Macrophages play a key role in atherogenesis by releasing proinflammatory cytokines and forming foam cells in subendothelial lesions. The present study quantified the inflammatory response in a human macrophage cell line (U937) after exposure to an ambient particulate sample from urban dust (UDP) and a diesel exhaust particulate (DEP). The effect of native UDP and DEP was compared with their corresponding organic extracts (OE-UDP/OE-DEP) and stripped particles (sUDP/sDEP) to clarify their respective roles. Exposure to OE-UDP, OE-DEP, UDP, DEP, and 2,3,7,8-tetrachlorodibenzo-p-dioxin led to a greater increase of interleukin (IL)-8, tumor necrosis factor-α, and cyclooxygenase-2 mRNA expression than did the stripped particles, whereas sUDP, sDEP, UDP, and DEP led to a greater production of C-reactive protein and IL-6 mRNA. The particles and the organic extract-induced expression of cyclooxygenase-2 and cytochrome P450 (CYP)1a1 was significantly suppressed by co-treatment with an aryl hydrocarbon receptor (AhR) antagonist, indicating that these effects are mainly mediated by the organic components, which can activate the AhR and CYP1a1. In contrast, the induction of C-reactive protein and IL-6 seems to be a particle-related effect that is AhR independent. The inflammatory response induced by particulate matter was associated with a subsequent increase of cholesterol accumulation, a hallmark of foam cells. Together, these data illustrate the interaction between particulate matter and the inflammatory response as well as the formation of cholesterol-accumulating foam cells, which are early markers of cardiovascular disease.

Vascular Dysfunction and Metabolic Parameters in Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is associated with insulin resistance (IR) and the metabolic syndrome; however, the cardiovascular (CV) manifestations of PCOS remain unclear. The objective of this study was to examine the relationships between IR, metabolic parameters, androgens, and markers of early CV disease in PCOS. We conducted an observational study examining noninvasive markers of early CV disease in women with PCOS including structural [carotid intimal media thickness (IMT)] and functional measures (arterial function with pulse wave velocity and endothelial function with brachial arterial flow-mediated vasodilation). Metabolic parameters included insulin and glucose during an oral glucose tolerance test and lipid and androgen levels. Participants were recruited from the general community. Eighty overweight women with PCOS who were nonsmokers and not on oral contraceptives or other medications known to affect IR participated in the study. Stepwise regression analysis showed that after adjustment for age and body mass index, IMT was significantly correlated with blood pressure (BP) load (P = 0.03) and inversely with dehydroepiandrosterone sulfate (DHEAS) (P = 0.01). After correction for androgen status, IMT was correlated with fasting glucose and area under curve (AUC) insulin. Flow-mediated vasodilation was inversely related to lipids (P = 0.02), whereas pulse wave velocity was related to BP (P < 0.001), AUC insulin (P = 0.04), and AUC glucose (P = 0.035). In overweight women with PCOS, insulin resistance and BP interacted negatively with arterial structural and functional measures. DHEAS correlated inversely with arterial structure, suggesting possible cardioprotective effects of endogenous DHEAS in women with PCOS. Additional research is needed to clarify these findings.

The underlying pathophysiology and causes of erectile dysfunction

Physical organic causes are now thought to account for most cases of erectile dysfunction (ED), although there is often a psychogenic contribution to the condition. Atherosclerotic disease is estimated to account for 40% of ED in men over 50 years, and vascular disease, including diabetes, is a common cause of ED. ED may be considered an early marker for cardiovascular disease. Ageing is a strong risk factor, and both psychological conditions such as anxiety and depression and neurological conditions such as Parkinson's disease are also common risk factors. Pelvic surgery, with which there is a risk of nerve damage, may also result in ED. Other causes include endocrine disorders, and interactions from prescribed drugs such as antihypertensives, antidepressants, antipsychotics, hormone treatments, and histamine H2 antagonists such as cimetidine. Anatomical features and anatomical conditions such as Peyronie's disease are a less common cause of ED.

Risk factor criteria.

The concept of the risk factor for chronic diseases, such as cardiovascular disorders, is derived from the application of epidemiological methods initially developed for infectious and nutritional deficiency diseases to chronic conditions to identify the factor(s) linked to the development of the chronic disease. Typically in infectious or nutritional deficiency conditions, a single causative agent or primary cause is identified. Thus, the cause of tuberculosis is the tubercle bacillus, and the cause of pellagra is niacin deficiency. However, for cardiovascular diseases, in which causes are usually complex and multifactorial, new concepts were required. For example, individuals with hypertension have a far greater risk for cardiovascular disease than those without hypertension, but many individuals with hypertension never have clinical sequelae, and many individuals with diagnosed cardiovascular diseases have no hypertension. One can also argue that many individuals who are exposed to the tubercle bacillus do not develop clinical tuberculosis, but the converse is not true; no one has tuberculosis without the tubercle bacillus. This provides a clear distinction between multifactorial diseases, such as coronary disease where the risk factor concept is paramount, and other health conditions. The initial application of the risk factor concept was well developed long before the term was coined. Early in the previous century, insurance companies noted that individuals with high blood pressure were at higher risk for premature mortality1 and therefore would be accepted for life insurance only on payment of an additional premium. Insurance companies also recognized the related risk factor of obesity, and imposed higher premiums on overweight clients. In this context, risk factors are used as predictors of disease and mortality. Surprisingly, insurance companies failed to recognize the enormous contribution of smoking to cardiovascular risk until later. Although the underlying concept had been widely discussed and applied, the term “risk factor” was …

Disfunção Endotelial no Diabetes do Tipo 2

A principal etiologia para a mortalidade e grande morbidade dos diabéticos é a ateroesclerose. A hipótese para a lesão inicial da ateroesclerose é a disfunção endotelial, pelo reconhecimento de que o endotélio tem um papel fundamental na manutenção das características de fluidez do sangue, tônus vascular e sua permeabilidade, sendo o óxido nítrico derivado do endotélio (e-NO) o principal protetor contra a moléstia ateroesclerótica por inibir as diversas vias envolvidas na aterogênese. A disfunção endotelial identificada como um marcador precoce de moléstia cardiovascular poderá prever coronariopatia no futuro, mesmo antes que alterações ateroescleróticas evidentes apareçam nas artérias. Assim, medidas da função endotelial poderiam identificar indivíduos com risco para moléstia cardiovascular, como determinar a vaso-dilatação endotélio-dependente pelo fluxo após isquemia induzida, que requer a produção de e-NO. Além disso, pode-se também avaliar a reatividade vascular da microcirculação bem como dosar os marcadores bioquímicos da função endotelial. Finalmente, pode-se fazer a mensuração da espessura da camada médio-intimal de grandes artérias, como as carótidas, um marcador indireto da função do endotélio. A disfunção endotelial tem sido documentada no diabetes (DM), em indivíduos com resistência à insulina ou com alto risco para desenvolver DM do tipo 2, nos quais a hiperglicemia está associada a um aumento do estresse oxidativo, levando a um incremento na formação de radicais oxigênio tais como o superóxido, que reage com o e-NO, levando à sua degradação. No DM do tipo 1 o estado diabético predispõe para a alteração endotelial mas não é suficiente para causá-lo, outros agentes tendo provavelmente um papel. No tipo 2 estão presentes os efeitos do envelhecimento, hipertensão arterial e outros fatores e, em contraste à disfunção no tipo 1, esta pode ser observada anos antes da manifestação da vasculopatia, associada com a resistência à insulina.

Endothelial function in the post-prandial state.

In recent years the endothelium has emerged as an important protective barrier against the development of atherosclerosis. Endothelial dysfunction, often characterised by impaired endothelium-dependent vasodilation, is generally considered to be an early marker of cardiovascular disease. Recently, it has been noted that the post-prandial state is associated with impaired endothelium-dependent vasodilation. Since man lives in a post-prandial state most of the day, prolonged exposure to dietary factors which impair endothelial function or delayed post-prandial recovery of the endothelium could negatively affect the cardiovascular risk profile. This review will focus on post-prandial endothelial function characterised by endothelium-dependent changes in vasomotion.