Farmacología de someprazol / Pharmacology of esomeprazol

Esomeprazol es un enantiómero del omeprazol (S-omeprazol). Es más potente que omeprazol para inhibir la secreción gástrica y produce un aumento más rápido del pH, manteniéndolo durante más tiempo por encima de 4. Esto permite que pueda ser utilizado a demanda para tratar a enfermos con enfermedad por reflujo gastroesofágico. Actúa bloqueando la ATPasa-H+/Na+ de la membrana de las células parietales gástricas. Se absorbe rápidamente en intestino delgado y en hígado se transforma por acción de las isoformas del citocromo P450 CYP2C19 y, en menor grado CYP34A, que actúan de forma distinta a como lo hacen con omeprazol lo que da lugar a una biodisponibilidad de esomeprazol mayor y una mayor área bajo la curva de la concentración plasmática. Es bien tolerado y disponible por vía intravenosa para administrar en inyección en 3 minutos o en infusión (AU)

Esomeprazole is an enantiomer of omeprazole (S-omeprazole). The gastric secretion suppression is better for esomeprazole in comparison with omeprazole; esomeprazole increases the pH faster, maintaining it above 4 during more time. Thus, it can be used on demand in patients with gastroesophagic reflux disease. The esomeprazole action pattern includes the blockade of H+/Na+ ATPase in the gastric parietal cell membrane. It is absorbed rapidly in the small bowel and transformed in the liver by the action of P450 CYP2C19 cytochrome isoenzymes and, in lesser extent, by P450 CYP34A cytochrome isoenzymes, as they perform in a different way with esomeprazole. This feature increases the esomeprazole bioavailability and the area under the plasmatic concentration curve. Esomeprazole is well tolerated and it can be administrated by intravenous injection or infusion (AU)

Seguridad cardiovascular de los inhibidores de la ciclooxigenasa 2 / Cardiovascular safety of ciclooxigenase 2 inhibitors

Los inhibidores de la ciclooxigenasa 2 (celecoxib y rofecoxib) son fármacos antiinflamatorios no esteroideos potentes y con un excelente perfil de seguridad cardiovascular. Sin embargo, en un artículo reciente se sugiere que estos fármacos podrían presentar un incremento del riesgo de complicaciones cardiovasculares tromboembólicas. En el presente artículo analizamos los datos disponibles hasta la fecha sobre la seguridad cardiovascular de los inhibidores de la ciclooxigenasa 2 (AU)

Moxonidina: un nuevo simpaticolítico de acción central

Moxonidina y rilmenidina representan a una familia de fármacos simpaticolíticos de reciente aparición con propiedades antihipertensivas que actúan estimulando los receptores imidazolínicos I-1 localizados en el bulbo. La eficacia antihipertensiva de estos fármacos ha sido confirmada en estudios clínicos y experimentales con efectos favorables sobre la hipertrofia ventricular izquierda y la distensibilidad arterial. El efecto adverso más significativo es la bradicardia, por lo que debe evitarse en pacientes con menos de 50 latidos/minuto. Se puede combinar con otros fármacos excepto con aquellos que inducen bradicardia (AU)

[New concepts on atrial fibrillation]. / Nuevos conceptos sobre la fibrilación auricular.

Atrial Fibrillation (AF) is the most common sustained arrhythmia in humans. AF has a self-perpetuating nature. Perpetuation has been attributed to shortening of atrial action potential duration (APD) and APD adaptation to rate, the so called atrial electrical remodeling. There is evidence that alterations in gene expression of proteins involved in the Ca handling may be, at least partly, responsible for AF-induced electrical remodeling. This review focus on the possible cellular mechanisms involved in atrial remodeling, followed by a brief description of new therapeutic approaches that target the development of the arrhythmogenic substrate, rather than simply attacking the final electrophysiologic environment.

[Pharmacology of nitrates]. / Pharmacologie des dérivés nitrés.

Nitrates (nitroglycerin, isosorbide dinitrate and isosorbide 5-mononitrate) are drugs used in the treatment of angina pectoris and in the prevention of myocardial ischaemia. By providing nitric oxide (NO), which, in turn, increases the level of cGMP and decreases (Ca)i, they induce effects of vasodilatation and anti-platelet aggregation. In patients suffering from endothelial dysfunction, they therefore act like exogenous NO providers. At low doses, they act as venous vasodilators by decreasing the tension (preload) and volume of the ventricle, as well as myocardial oxygen requirements (MVO2). The reduction of ventricular tension and volume also indirectly increases subendocardial blood flow. In the coronary vessels, they produce epicardial vasodilatation (all the more marked the smaller the calibre of the vessels), increase collateral blood flow and, through stenoses, induce reduction of coronary tone and the excess pressure due to vasospasm. At higher doses, the vasodilator effect is exerted on arteries and, although it reduces peripheral vascular resistance (afterload) and blood pressure, it can also produce reflex tachycardia which annihilates the reduction of MVO2. Finally, nitrates exert anti-platelet aggregation effects. All these properties account for the beneficial effects of nitrates in acute or chronic coronary ischaemic syndromes, in patients suffering from left ventricular dysfunction, during the acute phase of myocardial infarction and in post-myocardial infarction ventricular remodelling. There are many pharmaceutical formulations allowing administration of nitrates via a variety of routes. However, the efficacy of repeated nitrate administration is limited by the appearance of tolerance, which can be prevented by observing short periods without nitrates (8-24 hours). The use of sustained-release formulations, with a single daily dose, ensures a maximum anti-ischaemic effect, reduces the risk of tolerance and facilitates the patient's compliance with treatment, which makes it the treatment of choice in angina patients.

[Neurohormonal factors in heart failure (and III)]. / Factores neurohormonales en la insuficiencia cardíaca (y III).

Heart failure is a physiopathological condition, with an increasing incidence and prevalence, involving the action of a series of mechanisms known as "compensators", which are phylogenetically ready to normalize minute volume and blood pressure. These mechanisms include the activation of a series of neurohormonal systems: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin arginine, endothelin, which are basically vasoconstrictors, with the counterpoint of other vasodilator systems, such as the endothelial relaxation factor, certain prostaglandins and the bradykinin-kallikrein system, which modulate global response. The authors review the physiopathology of each of these system, as well as their significance in the diagnosis and prognostic evaluation of heart failure. We analyze the possible deleterious effects of neurohormonal activation, anatomically and at cardiovascular function level, and try to determine if they are capable of explaining the evolution and progression of heart failure, in a truly vicious circle, up until the irreversible heart failure phase. We review the current importance of the inhibition of the aldosterone renin-angiotensin system in the prophylaxis and treatment of heart failure. Furthermore, we describe the present-day value of the inhibition of the sympathetic nervous system in some forms of heart failure. We also analyze the different pharmacological treatments for heart failure: diuretics, inotropic agents, vasodilators (in their different pharmacological types), paying particular attention to their action on neurohormonal systems and their implications in the prognosis and evolution of heart failure.

[Neurohormonal factors in heart failure. II]. / Factores neurohormonales en la insuficiencia cardíaca (II).

Heart failure is a physiopathological condition, with an increasing incidence and prevalence, involving the action of a series of mechanisms known as "compensators", which are phylogenetically ready to normalize minute volume and blood pressure. These mechanisms include the activation of a series of neurohormonal systems: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin arginine, endothelin, which are basically vasoconstrictors, with the counterpoint of other vasodilator systems, such as the endothelial relaxation factor, certain prostaglandins and the bradykinin-kallikrein system, which modulate global response. The authors review the physiopathology of each of these systems, as well as their significance in the diagnosis and prognostic evaluation of heart failure. We analyze the possible deleterious effects of neurohormonal activation, anatomically and at the cardiovascular function level, and try to determine if they are capable of explaining the evolution and progression of heart failure, in a truly vicious circle, up until the irreversible heart failure phase. We review the current importance of the inhibition of the aldosterone renin-angiotensin system in the prophylaxis and treatment of heart failure. Furthermore, we describe the present-day value of the inhibition of the sympathetic nervous system in some forms of heart failure. We also analyze the different pharmacological treatments for heart failure: diuretics, inotropic agents, vasodilators (in their different pharmacological types), paying particular attention to their action on neurohormonal systems and their implications in the prognosis and evolution of heart failure.

[Neurohormonal factors in heart failure. I]. / Factores neurohormonales en la insuficienica cardíaca (I).

Heart failure is a physiopathological condition, with an increasing incidence and prevalence, involving the action of a series of mechanisms known as 'compensators', which are phylogenetically ready to normalize minute volume and blood pressure. These mechanisms include the activation of a series of neurohormonal systems: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin arginine, endothelin, which are basically vasoconstrictors, with the counterpoint of other vasodilator systems, such as the endothelial relaxation factor, certain prostaglandins and the bradykinin-kallikrein system, which modulate global response. The authors review the physiopathology of each of these systems, as well as their significance in the diagnosis and prognostic evaluation of heart failure. We analyze the possible deleterious effects of neurohormonal activation, anatomically and at the cardiovascular function level, and try to determine if they are capable of explaining the evolution and progression of heart failure, in a truly vicious circle, up until the irreversible heart failure phase. We review the current importance of the inhibition of the aldosterone renin-angiotensin system in the prophylaxis and treatment of heart failure. Furthermore, we describe the present-day value of the inhibition of the sympathetic nervous system in some forms of heart failure. We also analyze the different pharmacological treatment for heart failure: diuretics, inotropic agents, vasodilators (in their different pharmacological types), paying particular attention to their action on neurohormonal systems and their implications in the prognosis and evolution of heart failure.

[Drug treatment of angina pectoris. Study Group on Angina Pectoris of the Ischemic Cardiopathy and Coronary Units Section of the Spanish Society of Cardiology]. / Tratamiento médico de la angina de pecho. Grupo de Estudio de Angina de Pecho de la Sección de Cardiopatía Isquémica y Unidades Coronarias de la Sociedad Española de Cardiología.

Medical treatment in angina pectoris is supported by: 1) slowing in coronary artery disease progression; 2) control of the angina episodes and the enhanced of the functional status, and, 3) prognosis improvement. The authors describe in this review, inside the own experience and the large body of evidence, the general measures and pharmacological treatment of both stable and unstable angina. There are included some therapeutic options in associated clinical conditions.