Of all the risk factors to cardiovascular disease (CVD), age is the most powerful: CVD incidence and prevalence rise progressively at all ages beyond young adulthood. This reflects the central role of time, and hence duration, in the atherogenic process. It also reflects age-related changes in physiology - notably alterations in body mass and composition favoring increased adiposity and in sex hormone secretion (combining adverse effects of androgens on lipoprotein lipid levels in males, lowering HDL, and of the decline in estrogens in postmenopausal females, raising LDL). The interactions among the passage of time, these physiological changes and perhaps aging per se, and pathological forces such as cigarette smoking, hypertension, and genetically determined dyslipoproteinemia conspire to accelerate the rate of atherogenesis. Thus clinical atherosclerosis and its complications rise exponentially with increasing age in the population at large. However, the relationship between dyslipoproteinemia and CVD risk in the individual patient actually declines with advancing age. This apparent paradox reflects confounding introduced by the advent of disease processes that cause wasting and inflammation such as cancer, infection, diabetes, trauma, and even CVD that actually lower lipid levels, frequently to the level of hypocholesterolemia. Thus, while with age the population-attributable risk of hypercholesterolemia (and/or low HDL) rises, the cholesterol-attributable risk in the individual falls. As a result the prescription of lipid-lowering therapy in elderly patients requires exquisite individualization: patients most likely to benefit are those with existing CVD (i.e., in secondary prevention) who nevertheless enjoy robust health and are highly motivated to comply with demanding regimens of diet and exercise plus drugs where needed to reach target LDL levels (less than 100 mg/dl). At the other extreme are those least likely to benefit: patients who are frail and failing from CVD or other wasting diseases of old age that present a more immediate threat to survival.

译文

在心血管疾病 (CVD) 的所有危险因素中,年龄是最强大的: CVD的发病率和患病率在成年后的所有年龄段都逐渐上升。这反映了时间以及持续时间在动脉粥样硬化过程中的核心作用。它还反映了与年龄相关的生理变化-特别是体重和组成的变化,有利于肥胖和性激素分泌增加 (结合雄激素对男性脂蛋白脂质水平的不利影响,降低HDL和雌激素的下降) 绝经后女性,提高LDL)。时间的流逝,这些生理变化以及可能的衰老本身以及诸如吸烟,高血压和遗传决定的血脂异常等病理力量之间的相互作用共同加速了动脉粥样硬化的发生速度。因此,随着人口年龄的增长,临床动脉粥样硬化及其并发症呈指数增长。然而,个体患者的血脂蛋白血症与CVD风险之间的关系实际上随着年龄的增长而下降。这种明显的悖论反映了由引起消瘦和炎症的疾病过程的出现所引起的混淆,例如癌症,感染,糖尿病,创伤甚至CVD,这些疾病实际上降低了脂质水平,通常降低到了低胆固醇血症的水平。因此,随着年龄的增长,高胆固醇血症 (和/或低HDL) 的人群归因风险上升,个体的胆固醇归因风险下降。因此,老年患者的降脂治疗处方需要精巧的个体化: 最有可能受益的患者是患有CVD的患者 (即,在二级预防中),尽管如此,他们仍然享有健康,并且在需要达到目标LDL水平 (低于100 mg/dl) 的情况下高度积极地遵守饮食和运动加药物的要求。另一个极端是那些最不可能受益的人: 虚弱且因CVD或其他老年消耗性疾病而失败的患者,这些患者对生存构成了更直接的威胁。

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