RESUMO
Arrhythmogenic effects of alcohol may be intermediated by its effects over heart rate variability (HRV). Most studies about the effects of alcohol over HRV were observational and did not explore the temporal influence of alcohol ingestion over autonomic modulation. The aim of this study was to verify if an acute ingestion of alcohol has a time-dependent influence over time-domain indices of HRV. The effect of the ingestion of 60 g of ethanol or placebo over autonomic modulation was compared in healthy men (35 per group), with 18-25 years of age, before and during 17 h after ingestion. Alcohol promoted a fall in the standard deviation of all normal R-R intervals, root mean square of successive differences, and percentage of pairs of adjacent R-R intervals differing by more than 50 ms and in two indices of the three-dimensional return map, by a period up to 10 h after the ingestion of alcohol, accompanied by an increase in heart rate. The indices returned to values similar of the control group 10 h after ingestion. The effects over HRV indices were attenuated by adjustment for heart rate. The ingestion of alcohol induces a broad cardiovascular adaptation secondary to vagal withdrawal and sympathetic activation that may be responsible for arrhythmogenic effects of alcohol ingestion.
Assuntos
Sistema Nervoso Autônomo/efeitos dos fármacos , Etanol/farmacologia , Frequência Cardíaca/efeitos dos fármacos , Adolescente , Adulto , Sistema Nervoso Autônomo/fisiologia , Eletrocardiografia/métodos , Frequência Cardíaca/fisiologia , Humanos , Masculino , Dinâmica não Linear , Fatores de TempoRESUMO
Cardiovascular diseases are among the worldwide leading causes of shorter life expectancy and loss of quality of life. Thus, any influence of diet or life habits on the cardiovascular system may have important implications for public health. Most world populations consume alcoholic beverages. Since alcohol may have both protective and harmful effects on cardiovascular health, the identification of biochemical mechanisms that could explain such paradoxical effects is warranted. The vascular endothelium is the target of important mediating pathways of differential ethanol concentrations, such as oxidative stress, lipoproteins, and insulin resistance. Alcohol-induced endothelial damage or protection may be related to the synthesis or action of several markers, such as nitric oxide, cortisol, endothelin-1, adhesion molecules, tumor necrosis factor alpha, interleukin-6, C-reactive protein, and haemostatic factors. The expression of these markers is consistent with the J-shaped curve between alcohol consumption and cardiovascular health. However, there is genetic and phenotypic heterogeneity in alcohol response, and despite the apparent beneficial biochemical effects of low doses of ethanol, there is not enough clinical and epidemiological evidence to allow the recommendation to consume alcoholic beverages for abstemious individuals. Considering the potential for addiction of alcoholic beverage consumption and other negative consequences of alcohol, it would be worthwhile to identify substances able to mimic the beneficial effects of low doses of ethanol without its adverse effects.
Assuntos
Consumo de Bebidas Alcoólicas/efeitos adversos , Consumo de Bebidas Alcoólicas/psicologia , Doenças Cardiovasculares/prevenção & controle , Doenças Cardiovasculares/fisiopatologia , Endotélio Vascular/fisiopatologia , Consumo de Bebidas Alcoólicas/fisiopatologia , Bebidas Alcoólicas/efeitos adversos , Biomarcadores , HDL-Colesterol , Doença da Artéria Coronariana , Etanol/efeitos adversos , Etanol/uso terapêutico , Humanos , Resistência à Insulina , Óxido Nítrico , Estresse Oxidativo , Fatores de RiscoRESUMO
Previous investigations have shown a biphasic effect of alcohol on blood pressure (BP). However, there are no studies on possible simultaneous influences in endothelial function. This study aims to evaluate the early and late effects of alcohol ingestion on vascular and endothelial function parameters in healthy young men. The diameter of brachial artery (DBA), endothelium-dependent flow-mediated dilatation, endothelium-independent nitroglycerin-mediated dilatation, systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate were measured 30 min before intake, 4 h after intervention (when there is a reported hypotensive effect of alcohol), and after 13 h (subsequent increase in BP). The study group consisted of 100 males aged 18-25 years who were evaluated by brachial artery ultrasound. Subjects were randomized to drink either an alcoholic (60 g of ethanol) or a similar nonalcoholic beverage. Alcohol induced a biphasic effect on SBP and DBP, with a 4-h decrease followed by an increase after 13 h. After 4 h, the alcohol-drinking group presented a DBA increase that was significant at baseline and after hyperemia but not after nitroglycerin administration. There were no DBA differences between the intervention and control groups 13 h after drinking. This study replicates the initial reports of alcohol-induced biphasic alteration in BP. Our results showed that despite the late increase in BP, there were no accompanying changes in endothelial function.
Assuntos
Pressão Sanguínea/efeitos dos fármacos , Endotélio Vascular/efeitos dos fármacos , Endotélio Vascular/fisiologia , Etanol/administração & dosagem , Adolescente , Adulto , Consumo de Bebidas Alcoólicas , Artéria Braquial/anatomia & histologia , Diástole , Coração/efeitos dos fármacos , Humanos , Cinética , Masculino , Nitroglicerina , Sístole , Vasodilatação/efeitos dos fármacosRESUMO
Although obesity is associated with increased cardiovascular risk, the mechanism has not been fully explained. Since thrombosis is a critical component of cardiovascular disease, we examined the relationship between obesity and hemostatic factors. We studied 3230 subjects (55% females, mean age 54 years) without a history of cardiovascular disease in cycle 5 of the Framingham Offspring Study. Obesity was assessed by body mass index and waist-to-hip ratio. Fasting blood samples were obtained for fibrinogen, plasminogen activator inhibitor (PAI-1) antigen, tissue plasminogen activator (tPA) antigen, factor VII antigen, von Willebrand factor (VWF), and plasma viscosity. Body mass index was directly associated with fibrinogen, factor VII, PAI-1 and tPA antigen in both men and women (p>0.001) and with VWF and viscosity in women. Similar associations were present between waist-to-hip ratio and the hemostatic factors. With minor exceptions for VWF and viscosity, all associations persisted after controlling for age, smoking, total and HDL cholesterol, triglycerides, glucose level, blood pressure, and use of antihypertensive medication. The association between increased body mass index and waist-to-hip ratio and prothrombotic factors and impaired fibrinolysis suggests that obesity is a risk factor whose effect is mediated in part by a prothrombotic state.
Assuntos
Obesidade/sangue , Trombofilia/etiologia , Adulto , Biomarcadores/sangue , Índice de Massa Corporal , Fator VII/análise , Saúde da Família , Feminino , Fibrinogênio/análise , Hemostasia , Humanos , Masculino , Pessoa de Meia-Idade , Obesidade/fisiopatologia , Inibidor 1 de Ativador de Plasminogênio/sangue , Fatores de Risco , Trombofilia/sangue , Ativador de Plasminogênio Tecidual/sangue , Relação Cintura-QuadrilRESUMO
OBJECTIVE: Despite being recognized as a cause of hypertension at higher doses, consumption of lesser amounts of alcohol appears to protect against cardiovascular disease and acutely reduces blood pressure. We tested the hypothesis that two glasses of red wine, taken together with the noon meal, would cause postprandial reduction in blood pressure in hypertensive individuals. METHOD: Thirteen (8 female) middle-aged, centrally obese, hypertensive and otherwise healthy participants received, in an open randomized crossover experiment, red wine (250 ml to approximately 23 g of ethanol) and a placebo equivalent, together with a standardized lunch. Blood pressure was measured with 24-hour ambulatory monitoring. RESULTS: Wine with the meal produced a mean (SD) reduction of 5.3 (7.66) mmHg in postprandial blood pressure (p = .03), which persisted for most of the remaining daytime interval. The maximal blood pressure reduction was 8.5 (11.84) mmHg, occurring 3 hours after intervention (p = .02). In addition, nocturnal dipping in systolic blood pressure was lessened during the wine intervention period (5.3 [10.19] vs 11.1 [8.08] mmHg; p = .03). CONCLUSIONS: Ingestion of 250 ml of red wine, together with the noon meal, resulted in reduction of the postprandial blood pressure of centrally obese, hypertensive subjects. The effect lasted throughout most of the remaining daytime interval and appeared to modify the usual blood pressure variation pattern.
Assuntos
Pressão Sanguínea/fisiologia , Hipertensão , Obesidade , Período Pós-Prandial/fisiologia , Vinho , Adulto , Idoso , Pressão Sanguínea/efeitos dos fármacos , Estudos Cross-Over , Feminino , Humanos , Hipertensão/tratamento farmacológico , Hipertensão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Obesidade/tratamento farmacológico , Obesidade/fisiopatologia , Período Pós-Prandial/efeitos dos fármacosRESUMO
OBJECTIVES: In the present study, we evaluated sinus and atrioventricular (AV) node electrophysiology of endurance athletes and untrained individuals before and after autonomic pharmacologic blockade. BACKGROUND: Endurance athletes present a higher prevalence of sinus bradycardia and AV conduction abnormalities, as compared with untrained individuals. Previous data from our laboratory suggest that nonautonomic factors may be responsible for the longer AV node refractory period found in well-trained athletes. METHODS: Six aerobically trained male athletes and six healthy male individuals with similar ages and normal rest electrocardiograms were studied. Maximal oxygen uptake (O(2)max) was measured by cardiopulmonary testing. The sinus cycle length (SCL), AV conduction intervals, sinus node recovery time (SNRT), Wenckebach cycle (WC) and anterograde effective refractory period (ERP) of the AV node were evaluated by invasive electrophysiologic studies at baseline, after intravenous atropine (0.04 mg/kg) and after addition of intravenous propranolol (0.2 mg/kg). RESULTS: Athletes had a significantly higher O(2)max as compared with untrained individuals. The SCL was longer in athletes at baseline, after atropine and after the addition of propranolol for double-autonomic blockade. The mean maximal SNRT/SCL was longer in athletes after atropine and after propranolol. The WC and anterograde ERP of the AV node were longer in athletes at baseline, after atropine and after propranolol. CONCLUSIONS: Under double-pharmacologic blockade, we demonstrated that sinus automaticity and AV node conduction changes of endurance athletes are related to intrinsic physiology and not to autonomic influences.