Angina pectoris : neurophysiological mechanisms with special references to adenosine and Syndrome X

Angina pectoris is the major symptom of ischemic heart disease (IHD). It is a visceral pain and the clinical presentation is complex. Its character is not well defined and this is reflected in a lack of specific pain-mediating neural structures. The organisation of the cardiac nervous system involves complex interactions between intrinsic cardiac neurones, mediastinal ganglia, the spinal cord and big brain areas. Adenosine is the only substance that fulfils criteria for a pain messenger between the ischemic cardiomyocyte and the nervous system. Clinical conditions such as silent myocardial ischemia and Syndrome X are manifestations of alterations in the cardiac nociceptive system.

Aims of the study: 1. To study the phenomenology of angina pectoris in coronary care patients; 2. To study the role of endogenous opioids in adenosine-provoked angina pectoris-like pain; 3. To study the analgesic effects of low dose adenosine; 4. To study neuropathic pain mechanisms in Syndrome X patients; 5. To study exercise and skeletal muscle performance in Syndrome X patients; 6. To study the effects of physical training in Syndrome X patients.

Conclusions: 1. Qualities and intensity of chest pain did not differentiate between patients with and without acute myocardial infarction (AMI). The extension of pain on the chest-related body area and the presence of one (as opposed to more than one) pain had diagnostic power; 2. [beta]-endorphin but not met-enkephalin counteracted the experience of adenosine-provoked chest pain; 3. Adenosine can have analgesic effects exerted at membrane-bound adenosine receptors both during provoked myocardial ischemia and during regional muscular ischemia; 4. The chest pain in Syndrome X patients fulfils criteria for being a sympathetic maintained pain: (1) typical chest pain is induced by epinephrine infusion without signs of myocardial ischemia; (2) hypersensitivity is present at tissue manipulation and (3) adrenergic stimulation provokes a hyperreactive response; 5. Exercise capacity is markedly decreased due to deconditioning in Syndrome X while skeletal muscle fibre type composition and energy charge at rest are normal; 6. Endurance exercise training improves exercise capacity with a 100% shift of the pain response to the exercise curve. Hyperalgesia remains unaffected.