Angina — further questions
Predictable, effort-related, chest pain is called stable angina. The consensus view is that ‘diseased’ (or atherosclerotic) arteries, partly occluded with cholesterol-rich plaques, require raised blood pressure, so more effort is required from the heart. If the coronary arteries supplying the heart muscle are healthy, blood pressure would rise, and in time ventricular hypertrophy would be evident. But if they are themselves partially occluded, part of the heart muscle becomes inadequately oxygenated when under this increased work load; this ischaemia causes pain — in the myocardium (and referred areas such as: neck, jaw, shoulder, or arm).
There are two main coronary arteries, but they branch and fuse, and there is considerable variation between individuals. Occlusion can occur in one, or more limbs, and can, in time, cause the vascular network to adapt. When 130 patients with chest pain syndromes were examined for physical evidence of coronary artery disease 93 patients showed positive, but 37 showed no sign of disease . I understand that ischaemia in a small part of the heart can be as painful as in a large part. So it is possible that the physical tests for occlusion were not sufficiently discriminating. But it is also stressed that not every chest pain shows the effort-induced aetiology of stable angina. A very similar pain can be caused by emotional stress, where the transient cardiac ischaemia presumably results from adrenaline stimulating β1 receptors, which results in increased cardiac effort (and oxygen-demand) by increasing heart rate, conduction velocity, and stroke volume. According to one source , in about 2% of people with angina, the closure of the artery (or arteriole) is due to “coronary artery spasm”. According to another source  this aetiologiy is 5 times more common in women than men.
One question that nags me is as follows: Does the pain experienced during exercise coincide with (and thus 'flag') further damage occurring to the coronary vessels? There seem to be two ways in which this might be the case.
- The pain (ex hypothesi) indicates ischaemia, which in turn can cause cell-death (when the cells are unprepared). Dead cells may lead to scar tissue and possible foci for plaque build-up.
- Ischaemia can cause cells to generate superoxide radicals, which can modify lipids (including cholesterol), or can react with nitric oxide to form peroxynitrite. Peroxynitrite can nitrate protein tyrosines. The presence of antibodies against nitrotyrosine in patients with atherosclerosis, myocardial ischemia, have confirmed the occurrence of such nitration. 
This question is important, because the patient will want to know whether to exercise as much as possible, or to avoid (as much as possible) the pain of over-exertion.
 Cohn et al., (1971) Circulation; 44:196-202
 Bugiardini, et al. (2005) JAMA.; 293:477-84; https://doi.org/10.1371/journal.pmed.0040012.
 Beckman and Koppenol (1996) Am J Physiol. 1996;271:C1424-37.