心力衰竭的药物和器械治疗课件，幻灯，PPT.ppt

* Beta-blockers act principally to inhibit the adverse effects of the sympathetic nervous system in patients with HF, and these effects far outweigh their well-known negative inotropic effects. Whereas cardiac adrenergic drive initially supports the performance of the failing heart, long-term activation of the sympathetic nervous system exerts deleterious effects that can be antagonized by the use of betablockers. Sympathetic activation can increase ventricular volumes and pressure by causing peripheral vasoconstriction and by impairing sodium excretion by the kidneys. Norepinephrine can also induce cardiac hypertrophy but restrict the ability of the coronary arteries to supply blood to the thickened ventricular wall, leading to myocardial ischemia. Activation of the sympathetic nervous system can also provoke arrhythmias by increasing the automaticity of cardiac cells, increasing triggered activity in the heart, and promoting the development of hypokalemia. Norepinephrine can also increase heart rate and potentiate the activity and actions of other neurohormonal systems. Finally, by stimulating growth and oxidative stress in terminally differentiated cells, norepinephrine can trigger programmed cell death or apoptosis. These deleterious effects are mediated through actions on alpha-1-, beta-1-, and beta-2-adrenergic receptors. * Angiotensin converting enzyme inhibitors are the best studied class of agents in HF, with multiple mechanisms of benefit for both HF, coronary disease, and other atherosclerotic vascular disease, as well as diabetic nephropathy. for initiation rather than maintenance of therapy. Which approach should be followed? In the controlled clinical trials of ACEIs, low or intermediate doses were commonly prescribed if higher doses could not be tolerated. In controlled trials with newer agents for HF, intermediate doses rather than high doses of ACEIs were generally used as background therapy. Higher doses of an ACEI were better than low doses in re