心力衰竭的诊断和治疗解释.ppt

对HF认识的逐渐演变也导致了不同时期心衰治疗原则及药物的变化 OPTIME-HF试验已经证明米力农可提高心衰患者的远期死亡率，临床限制使用。 Let’s compare our heart to this donkey, and our body to the wagon that this donkey has to pull every day. A healthy heart is like an energetic donkey, which without fatigue, pulls the wagon full of weights. Conversely, a diseased heart will have difficulty meeting metabolic demands (or pulling the wagon). Angiotensin II is the central molecule of the RAS, with a multitude of actions. Both the antihypertensive and the protective effects of RAS modulators are related to their influence on angiotensin II actions. ACE inhibitors block the conversion of angiotensin I to angiotensin II and also have other substrates including bradykinin, substance P, neurotensin, enkephalin, LHRH, N-acetyl-Ser-Asp-Lys-Pro. The effects on kinins is suggested to be responsible for the cough associated with ACE inhibitors. ACE inhibitors do not block the conversion of Ang I to Ang II by alternative enzymes prominent in heart tissue, such as chymase. Ang II receptor blockers such as valsartan block the action of Ang II directly at its receptor, regardless of synthesis pathway. In heart failure, angiotensin II activity may play a pathological role. The deleterious effects of angiotensin II are mediated via the AT1 receptor subtype. There is also accumulating evidence that many of the more beneficial actions of angiotensin II are mediated via the AT2 receptor. Therefore selective blockade of the effect of angiotensin II at the AT1 receptor level (whilst leaving the AT2 receptor free for angiotensin II stimulation) may be expected to offer advantages over non specific blockade of the renin angiotensin system (e.g. by ACE inhibitors). As can be seen, metoprolol and bisoprolol block only one of the damaging pathways, propranolol two of them, whereas carvedilol blocks all three pathways leading from sympathetic activation to cardiotoxicity. Comprehensive adrenergic blockade provided by carvedilol is likely to provide gre