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CHRONIC THERAPEUTICALLY REFRACTORY ANGINA PECTORIS

机译:慢性难治性心绞痛

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摘要

In contrast to the tremendous increase in practical opportunities and theoretical knowledge in the western world, resulting in a doubling of our average life expectancy, the number of diseases has not been reduced during the last 150 years. This apparent contradiction, secondary to changes in environmental influences and sociocultural developments such as smoking habits, sedentary lifestyles, fast food meals, stressful jobs, etc, have led to the introduction of newer definitions for illnesses. From this perspective, the illness pattern has changed during the last century and a half from infectious diseases to more culturally influenced diseases, such as coronary artery disease (CAD). However, to date, following thorough research, no evidence is available that these cultural influences are the sole initiators in the process of atherosclerotic plaque formation. Albeit that plaque formation is the result of a variety of processes culminating in CAD, the search for the initial trigger is ongoing. During the last few years, more and more evidence has become available that an inflammatory response plays a key role in atherosclerotic plaque formation leading to CAD. These mediators of inflammation interact with nervous signalling transduction pathways arising from the environment of the atherosclerotic plaque. The inflammatory substances released during myocardial ischaemia are relevant to progression of the atherosclerotic process in the narrowed coronary arteries. In contrast, the recruited nervous and neurohumoral pathways during cardiac ischaemic challenges are thought to be involved in maintaining the integrity of the myocytes. Subsequently, myocardial ischaemia, angina pectoris signalling pathways, and neurohumoral and inflammatory responses are considered to be key players in atherosclerotic heart disease. This article discusses newer insights into the pathophysiology of chronic (refractory) angina pectoris, resulting from stable atherosclerotic CAD, and suggests some potential additional treatments.
机译:与西方世界实践机会和理论知识的大量增加(导致我们的平均预期寿命增加一倍)相比,过去150年来疾病的数量并未减少。这种明显的矛盾是继环境影响和社会文化发展变化(如吸烟习惯,久坐的生活方式,快餐餐,压力大的工作等)之后产生的,从而引入了新的疾病定义。从这个角度来看,在过去的一个半世纪中,疾病模式已经从传染性疾病转变为受文化影响较大的疾病,例如冠状动脉疾病(CAD)。然而,迄今为止,经过深入研究,尚无证据表明这些文化影响是动脉粥样硬化斑块形成过程中的唯一引发因素。尽管斑块的形成是CAD过程中各种过程的结果,但仍在寻找初始触发因素。在过去的几年中,越来越多的证据表明炎症反应在导致CAD的动脉粥样硬化斑块形成中起着关键作用。这些炎症介质与动脉粥样硬化斑块环境引起的神经信号转导途径相互作用。心肌缺血期间释放的炎性物质与狭窄冠状动脉中动脉粥样硬化过程的进展有关。相反,在心脏缺血性发作期间募集的神经和神经体液途径被认为与维持心肌细胞的完整性有关。随后,心肌缺血,心绞痛心绞痛信号通路以及神经体液和炎性反应被认为是动脉粥样硬化性心脏病的关键因素。本文讨论了由稳定的动脉粥样硬化CAD引起的对慢性(难治性)心绞痛的病理生理学的新见解,并提出了一些潜在的其他治疗方法。

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