Person Ameen F, Patterson Cam
Division of Cardiology and Carolina Cardiovascular Biology Center, The University of North Carolina at Chapel Hill, 8200 Medical Biomolecular Research Building, Chapel Hill, NC 27599, USA.
Curr Treat Options Cardiovasc Med. 2008 Aug;10(4):294-303. doi: 10.1007/s11936-008-0050-9.
Although cardiovascular disease is commonly recognized as a disease of the elderly, young patients are also at risk for coronary atherosclerosis, which has a devastating impact on their more active lifestyle. In identifying patients at risk for a cardiovascular event, global risk models often fail to assess family history, an important risk factor in patients with premature coronary artery disease (P-CAD). P-CAD refers to the accelerated development of coronary atherosclerosis before age 55 in men and 65 in women, which may be the result of acquired or primary causes. Acquired P-CAD is associated with an underlying medical condition or influencing factor, such as systemic lupus erythematosus or cocaine use, that directly contributes to the rapid progression of coronary atherosclerosis. It is important to evaluate young patients for acquired P-CAD because in many instances treatment may be tailored to the underlying medical condition. Most cases of P-CAD, however, are the result of primary causes involving more complex interactions among genetic, metabolic, and environmental risk factors. Patients with primary P-CAD usually have a family history of coronary disease, suggesting a strong genetic component. With the use of genome-wide association analysis, several chromosome loci have been identified as being linked to the development of coronary atherosclerosis and risk factors. The chromosome 9p21.3 locus, which is the most replicated to date, has provided some insight into the pathologic mechanism of coronary disease. The confirmation and replication of these associations through further study will lead to earlier detection of P-CAD in at-risk patients and a better understanding of the underlying pathologic mechanisms, thereby influencing the development of preventive therapies.
尽管心血管疾病通常被认为是一种老年疾病，但年轻患者也有患冠状动脉粥样硬化的风险，这对他们更积极的生活方式有着毁灭性的影响。在识别有心血管事件风险的患者时，全球风险模型往往未能评估家族史，而家族史是早发性冠状动脉疾病（P-CAD）患者的一个重要风险因素。P-CAD是指男性在55岁之前、女性在65岁之前冠状动脉粥样硬化的加速发展，这可能是后天或原发性原因导致的。后天性P-CAD与一种潜在的疾病状况或影响因素有关，如系统性红斑狼疮或使用可卡因，这些因素直接导致冠状动脉粥样硬化的快速进展。评估年轻患者是否患有后天性P-CAD很重要，因为在许多情况下，治疗可以根据潜在的疾病状况进行调整。然而，大多数P-CAD病例是由原发性原因导致的，这些原因涉及遗传、代谢和环境风险因素之间更复杂的相互作用。原发性P-CAD患者通常有冠心病家族史，这表明有很强的遗传成分。通过全基因组关联分析，已经确定了几个染色体位点与冠状动脉粥样硬化的发展和风险因素有关。9号染色体p21.3位点是迄今为止重复验证最多的，它为冠心病的病理机制提供了一些见解。通过进一步研究对这些关联进行确认和重复验证，将有助于在高危患者中更早地检测出P-CAD，并更好地理解潜在的病理机制，从而影响预防性治疗的发展。
