Libby Peter, Nahrendorf Matthias, Swirski Filip K
Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts.
J Am Coll Cardiol. 2016 Mar 8;67(9):1091-1103. doi: 10.1016/j.jacc.2015.12.048.
Physicians have traditionally viewed ischemic heart disease in a cardiocentric manner: plaques grow in arteries until they block blood flow, causing acute coronary and other ischemic syndromes. Recent research provides new insight into the integrative biology of inflammation as it contributes to ischemic cardiovascular disease. These results have revealed hitherto unsuspected inflammatory signaling networks at work in these disorders that link the brain, autonomic nervous system, bone marrow, and spleen to the atherosclerotic plaque and to the infarcting myocardium. A burgeoning clinical published data indicates that such inflammatory networks-far from a mere laboratory curiosity-operate in our patients and can influence aspects of ischemic cardiovascular disease that determine decisively clinical outcomes. These new findings enlarge the circle of the traditional "cardiovascular continuum" beyond the heart and vessels to include the nervous system, the spleen, and the bone marrow.
传统上，医生一直以心脏为中心看待缺血性心脏病：动脉中形成斑块，直至阻塞血流，引发急性冠状动脉综合征和其他缺血性综合征。最近的研究为炎症在缺血性心血管疾病中的综合生物学作用提供了新的见解。这些结果揭示了在这些疾病中发挥作用的此前未被怀疑的炎症信号网络，该网络将大脑、自主神经系统、骨髓和脾脏与动脉粥样硬化斑块及梗死心肌联系起来。大量已发表的临床数据表明，这类炎症网络并非仅仅是实验室里的新奇事物，而是在我们的患者体内发挥作用，并且能够影响缺血性心血管疾病中对临床结局起决定性作用的各个方面。这些新发现将传统“心血管连续体”的范围从心脏和血管扩展到包括神经系统、脾脏和骨髓。
