Atherosclerosis is a pathological process where lesions (plaque) form in the coronary vessels and impede blood flow and oxygen delivery. Ischemia occurs when there is an inability of oxygen delivery (blood flow) to meet cardiac muscle oxygen demands, resulting in pain, pressure and weakness in the chest, and exercise intolerance. Angina Pectoralis describes transient vessel occlusion lasting less than 10 minutes. When the occlusion lasts longer, there is irreversible tissue death (myocardial infarction or heart attack) leading to impaired cardiac function.
The normal blood vessel is characterized by a lack of inflammation, a balanced level of circulating lipids, and a reactive endothelium and smooth muscle. Atherosclerosis is the result of local endothelial dysfunction, lipid accumulation, and inflammatory responses. This results in the formation of a fatty streak within the vessel, which over time, becomes enclosed in a fibrous cap. This fibrous cap reduces the size of the coronary vessel, impeding blood flow, and in certain instances can detach and move further downstream completely blocking blood flow.
Damage to cardiac muscle results in reduced function and may limit exercise capacity and in severe cases may limit resting function or lead to death. The amount of damage is dependent on the size of the occlusion (area at risk), the location of the occlusion, and the duration of the occlusion.
Pharmacological interventions are used to reduce symptoms (e.g., nitro for angina), reduce blood pressure (ACE inhibitors) and reduce cardiac work (e.g., β-blocker to reduce heart rate). Appropriate exercise intensity alterations must be made with these drug-exercise interactions in mind. For example, heart rate will be reduced at any workload when using a β-blocker and thus the use of heart rate alone as an intensity variable is not recommended or consideration of the reduced heart rate response for a given exercise intensity must be determined.