Chronic therapeutically refractory angina pectoris.

Correspondence to: Dr Mike J L DeJongste, Department of Cardiology, Thoraxcenter, University Hospital of Groningen, PO Box 30,001, 9700 RB Groningen, The Netherlands; m.j.l.de.jongste@ thorax.azg.nl _________________________ I n 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.