RESUMO
The endothelium is the common target of all cardiovascular risk factors, and functional impairment of the vascular endothelium in response to injury occurs long before the development of visible atherosclerosis. The endothelial cell behaves as a receptor-effector structure which senses different physical or chemical stimuli that occur inside the vessel and, therefore, modifies the vessel shape or releases the necessary products to counteract the effect of the stimulus and maintain homeostasis. The endothelium is capable of producing a large variety of different molecules which act as agonists and antagonists, therefore balancing their effects in opposite directions. When endothelial cells lose their ability to maintain this delicate balance, the conditions are given for the endothelium to be invaded by lipids and leukocytes (monocytes and T lymphocytes). The inflammatory response is incited and fatty streaks appear, the first step in the formation of the atheromatous plaque. If the situation persists, fatty streaks progress and the resultant plaques are exposed to rupture and set the conditions for thrombogenesis and vascular occlusion. Oxidant products are produced as a consequence of normal aerobic metabolism. These molecules are highly reactive with other biological molecules and are referred as reactive oxygen species (ROS). Under normal physiological conditions, ROS production is balanced by an efficient system of antioxidants, molecules that are capable of neutralizing them and thereby preventing oxidant damage. In pathological states, ROS may be present in relative excess. This shift of balance in favor of oxidation, termed 'oxidative stress', may have detrimental effects on cellular and tissue function, and cardiovascular risk factors generate oxidative stress. Both type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetic patients have mostly been described under enhanced oxidative stress, and both conditions are known to be powerful and independent risk factors for coronary heart disease, stroke, and peripheral arterial disease. Hyperglycemia causes glycosylation of proteins and phospholipids, thus increasing intracellular oxidative stress. Nonenzymatic reactive products, glucose-derived Schiff base, and Amadori products form chemically reversible early glycosylation products which subsequently rearrange to form more stable products, some of them long-lived proteins (collagen) which continue undergoing complex series of chemical rearrangements to form advanced glycosylation end products (AGEs). Once formed, AGEs are stable and virtually irreversible. AGEs generate ROS with consequent increased vessel oxidative damage and atherogenesis. The impressive correlation between coronary artery disease and alterations in glucose metabolism has raised the hypothesis that atherosclerosis and diabetes may share common antecedents. Large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosclerosis being a complication of diabetes, both conditions may share genetic and environmental antecedents, a 'common soil'.
Assuntos
Angiopatias Diabéticas/fisiopatologia , Endotélio Vascular/fisiologia , Glucose/metabolismo , Óxido Nítrico/fisiologia , Antioxidantes/metabolismo , Aterosclerose/fisiopatologia , Citoesqueleto/fisiologia , Diabetes Mellitus Tipo 1/fisiopatologia , Diabetes Mellitus Tipo 2/fisiopatologia , Endotélio Vascular/fisiopatologia , Humanos , Isquemia Miocárdica/fisiopatologia , Sistema Renina-Angiotensina/fisiologiaRESUMO
The endothelium is a thin monocellular layer that covers all the inner surface of the blood vessels, separating the circulating blood from the tissues. It is not an inactive organ, quite the opposite. It works as a receptor-efector organ and responds to each physical or chemical stimulus with the release of the correct substance with which it may maintain vasomotor balance and vascular-tissue homeostasis. It has the property of producing, independently, both agonistic and antagonistic substances that help to keep homeostasis and its function is not only autocrine, but also paracrine and endocrine. In this way it modulates the vascular smooth muscle cells producing relaxation or contraction, and therefore vasodilatation or vasoconstriction. The endothelium regulating homeostasis by controlling the production of prothrombotic and antithrombotic components, and fibrynolitics and antifibrynolitics. Also intervenes in cell proliferation and migration, in leukocyte adhesion and activation and in immunological and inflammatory processes. Cardiovascular risk factors cause oxidative stress that alters the endothelial cells capacity and leads to the so called endothelial "dysfunction" reducing its capacity to maintain homeostasis and leads to the development of pathological inflammatory processes and vascular disease. There are different techniques to evaluate the endothelium functional capacity, that depend on the amount of NO produced and the vasodilatation effect. The percentage of vasodilatation with respect to the basal value represents the endothelial functional capacity. Taking into account that shear stress is one of the most important stimulants for the synthesis and release of NO, the non-invasive technique most often used is the transient flow-modulate "endothelium-dependent" post-ischemic vasodilatation, performed on conductance arteries such as the brachial, radial or femoral arteries. This vasodilatation is compared with the vasodilatation produced by drugs that are NO donors, such as nitroglycerine, called "endothelium independent". The vasodilatation is quantified by measuring the arterial diameter with high resolution ultrasonography. Laser-Doppler techniques are now starting to be used that also consider tissue perfusion. There is so much proof about endothelial dysfunction that it is reasonable to believe that there is diagnostic and prognostic value in its evaluation for the late outcome. There is no doubt that endothelial dysfunction contributes to the initiation and progression of atherosclerotic disease and could be considered an independent vascular risk factor. Although prolonged randomized clinical trials are needed for unequivocal evidence, the data already obtained allows the methods of evaluation of endothelial dysfunction to be considered useful in clinical practice and have overcome the experimental step, being non-invasive increases its value making it use full for follow-up of the progression of the disease and the effects of different treatments.
Assuntos
Doenças Cardiovasculares/epidemiologia , Endotélio Vascular/fisiopatologia , Aterosclerose/epidemiologia , Humanos , Óxido Nítrico/fisiologia , Sistema Renina-Angiotensina , VasodilataçãoRESUMO
La vasodilatación y el aumento de flujo posisquemia de la arteria humeral, evaluados por eco-Doppler, son provocados por la liberación de sustancias vasodilatadoras del endotelio arterial, principalmente óxido nítrico, y expresan su estado funcional. La arteria humeral es considerada "subrogante" de las arterias coronarias y su respuesta es similar a la del resto de la circulación, permitiendo conocer el estado funcional del endotelio de la circulación coronaria y general. En el presente estudio se observó una marcada disminución de la vasodilatación posisquémica en sujetos asintomáticos, sin evidencia clínica de enfermedad cardiovascular y portadores de factores de riesgo, especialmente en los fumadores, hipercolesterolémicos e hipertensos. Por otra parte, se comprobó un deterioro de la función endotelial inversamente proporcional a la edad de los sujetos, independiente del sexo o los factores de riesgo. La prueba de vasodilatación posisquémica es incruenta, reproducible, al alcance de cualquier centro médico, y permite estratificar riesgos y evaluar terapéuticas en todas las edades
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Ecocardiografia Doppler , Endotélio Vascular , Vasodilatação , Aterosclerose , Hipercolesterolemia , Hipertensão , Fatores de Risco , FumarRESUMO
La vasodilatación y el aumento de flujo posisquemia de la arteria humeral, evaluados por eco-Doppler, son provocados por la liberación de sustancias vasodilatadoras del endotelio arterial, principalmente óxido nítrico, y expresan su estado funcional. La arteria humeral es considerada "subrogante" de las arterias coronarias y su respuesta es similar a la del resto de la circulación, permitiendo conocer el estado funcional del endotelio de la circulación coronaria y general. En el presente estudio se observó una marcada disminución de la vasodilatación posisquémica en sujetos asintomáticos, sin evidencia clínica de enfermedad cardiovascular y portadores de factores de riesgo, especialmente en los fumadores, hipercolesterolémicos e hipertensos. Por otra parte, se comprobó un deterioro de la función endotelial inversamente proporcional a la edad de los sujetos, independiente del sexo o los factores de riesgo. La prueba de vasodilatación posisquémica es incruenta, reproducible, al alcance de cualquier centro médico, y permite estratificar riesgos y evaluar terapéuticas en todas las edades (AU)
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Endotélio Vascular , Ecocardiografia Doppler , Vasodilatação , Fatores de Risco , Aterosclerose , Hipercolesterolemia , Tabagismo , HipertensãoRESUMO
En la cardiopatía isquémica la valoración de la función ventricular de reposo es un índice de alto valor predictivo. Numerosos estudios demostraron el rol de la cirugía de by pass coronario en pacientes con fracción de eyección <0.35. Tambien es sabido que estos pacientes con mal ventrículo tienen mayor mortalidad quirúrgica. Se han desarrollado métodos sensitivos para valorar la "viabilidad miocárdica" y poder seleccionar cuáles individuos tendrán mejor sobrevida al ser sometidos a técnicas de revascularización. Para esto se describe un algoritmo diagnóstico y terapéutico. Sin embargo, es preciso profundizar acerca de la biologia del miocardio atontado (M.A) y del miocardio hibernado (M.H), para obtener una buena relación costo-beneficio en la utilización de dichos procedimientos.
Assuntos
Humanos , Doença das Coronárias , Revascularização MiocárdicaRESUMO
En la cardiopatía isquémica la valoración de la función ventricular de reposo es un índice de alto valor predictivo. Numerosos estudios demostraron el rol de la cirugía de by pass coronario en pacientes con fracción de eyección <0.35. Tambien es sabido que estos pacientes con mal ventrículo tienen mayor mortalidad quirúrgica. Se han desarrollado métodos sensitivos para valorar la "viabilidad miocárdica" y poder seleccionar cuáles individuos tendrán mejor sobrevida al ser sometidos a técnicas de revascularización. Para esto se describe un algoritmo diagnóstico y terapéutico. Sin embargo, es preciso profundizar acerca de la biologia del miocardio atontado (M.A) y del miocardio hibernado (M.H), para obtener una buena relación costo-beneficio en la utilización de dichos procedimientos. (AU)