Chronic coronary disease

Coronary disease is primarily caused by atherosclerosis.

Less common, non-atherosclerotic causes include vasospasm, endothelial and microvascular dysfunction, spontaneous thrombosis or embolism, coronary artery dissection, extrinsic compression, systemic vasculitis/arteritis, and damage from radiation.[1][2][21][22] These aetiologies are more common in younger patients, women, and those without traditional risk factors for coronary disease.[21][22]

At present there is limited evidence to guide diagnostic and therapeutic strategies for coronary disease aetiologies other than atherosclerosis, but there are statements of expert consensus. Epicardial vasospasm and coronary microvascular dysfunction (also known as microvascular angina) are increasingly grouped as INOCA (ischaemia with non-obstructive coronary arteries).[23][24][25][26][27][28] Spontaneous coronary artery dissection (SCAD) is usually considered separately.[29]

Atherosclerosis is the development of lipid-rich plaques in the arterial wall. Plaque development is the result of an inflammatory process that can involve not only lipids but also altered smooth muscle cells, matrix proteins, calcification, necrosis, and haemorrhage. Plaques do not occur uniformly through the arterial tree and tend to occur at bends, branch points, and other areas of turbulent flow.[30]

A traditional model suggests two means of plaque progression. Large thick-walled plaques are thought to slowly obstruct the lumen of coronary arteries, thereby causing decreased perfusion and chronic intermittent exertional symptoms when they reach 70% to 80% stenosis. Thin-walled 'vulnerable plaques' may not cause meaningful obstruction until the wall is disrupted, at which point acute haematoma and thrombus formation cause sudden myocardial infarction (MI) by occluding the arterial lumen locally or embolising distally into the coronary circulation. This model explains two clinically important phenomena: 1) MI may occur in patients at anatomical sites without baseline flow limitation; 2) therapies that reduce chronic intermittent angina (improve flow) may be different from those that reduce mortality from coronary disease (stabilise plaque, prevent thrombosis).

The actual process is more varied and complex. In many cases arteries can expand outwards, meaning that plaque size may not correlate with luminal stenosis, which in turn may not correlate with functional flow limitation.[31][32] Additionally, plaque development is not linear; plaques may move repeatedly through development, regression, and erosion/rupture.[31]

The Canadian Cardiovascular Society grades angina by the extent of limitation of physical activity.[3]

Grade I: Ordinary physical activity (walking, climbing stairs) does not cause angina. Angina occurs with strenuous or rapid or prolonged exertion at work or recreation.

Grade II: Slight limitation of ordinary activity. Angina may occur with moderate exertion, such as walking or climbing stairs rapidly, walking uphill, walking or climbing stairs after meals, in cold or wind, under emotional stress, or during the few hours after awakening, or walking more than two blocks on level ground, or climbing more than one flight of ordinary stairs at a normal pace and in normal conditions.

Grade III: Marked limitation of ordinary physical activity. Angina occurs with mild exertion, such as walking one or two blocks on level ground and climbing one flight of stairs in normal conditions and at normal pace.

Grade IV: Inability to carry on any physical activity without discomfort, anginal syndrome may be present at rest.

Pathophysiology

Classification