MSN, RN
The human body is a miracle in itself! As most of us learned in nursing school, the body will compensate to protect and heal the body to maintain homeostasis. However, sometimes the healing protective mechanism of the body can lead to further complications.
For example, on the outside of the body, if a person has a cut or a laceration to the skin – the body stops the bleeding and repairs the injured area with a plaque buildup or what we call a scab. On the inside of the body, if the inner layer/endothelium lining of a coronary artery (the vessels that supply oxygen and nutrition to the heart) is damaged, the body recognizes the damaged area and repairs it with plaque.
Unfortunately, the repair of an artery inside the body leads to plaque buildup (atherosclerosis) and hardening of that artery (arteriosclerosis). It can become a vicious cycle since high levels of low-density lipoprotein (LDL) can adhere and then infiltrate the damaged intima layer of the vessel and then the body has to repair the site again.
As the body continues to repair the coronary artery, the plaque buildup or scab leads to severe stenosis (narrowing of the artery) and partial obstructions.
Anything that can damage the inner lining of the coronary artery can lead to plaque buildup/atherosclerosis. The initial injury or assault to the endothelium lining can be caused by: high cholesterol and triglycerides levels, smoking, diabetes, and/or hypertension.
A family history of coronary artery disease (CAD) and age can also play a part in the dysfunction of the smooth lining and/or make a person more inclined to have high levels of LDH lipids.
Atherosclerosis of the coronary arteries does not usually cause any symptoms until it becomes severe and affects the supply of oxygen and nutrition to the heart muscle.
Symptoms of ischemia (lack of oxygen to the heart muscle) can include:
As nurses learned in anatomy class, there are two main coronary arteries that branch off the aorta (the left and the right main coronary arteries). These two main arteries branch off to smaller coronary arteries and supply the entire heart muscle with nutrition and oxygenated blood.
If a patient has CAD, the amount of oxygen and nutrition that these arteries supply is compromised since the patient has chronic narrowing of the arteries from plaque buildup. The plaque buildup in itself can complicate the narrowing more since it can crack and promote the development of a blood clot/thrombus or it can rupture and break off causing an embolism (a piece of plaque that travels in the blood then obstructs a smaller blood vessel).
In either case, it is the sudden occlusion of a coronary artery from the thrombus or embolism that causes a myocardial infarction or death to a portion of the heart muscle from the lack of oxygen.
The most common type of myocardial infarction (MI) is considered Type 1. It is caused by CAD and it is the leading cause of death in the United States.
Type 1 MIs are caused by the rupturing or cracking of the plaque and the sudden occlusion of the artery by the formation of a thrombus/blood clot. Type 1 MIs include non-ST segment elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI). An NSTEMI is a partial occlusion or a distal coronary artery occlusion by an embolism while a STEMI is usually more severe and caused by a total occlusion.
A type 2 MI is transient ischemia usually characterized by chest pain or ECG changes. Type 2 MIs do not cause permanent damage or death to the heart muscle. This type of MI is related to demand ischemia or otherwise described as a mismatch of supply and demand (the amount of oxygen the heart muscle needs compared to the amount of oxygen available).
This type of infarction is self-limiting and after the underlying cause of the ischemia is corrected, it is resolved. Common causes of MI type 2 include severe anemia, atrial fibrillation with rapid ventricular rate (RVR), bradycardia, respiratory failure, shock, hypertension (HTN), or a sudden spasm of a coronary artery.
A Type 3 MI is the sudden death of a patient from a coronary cause prior to any diagnostic changes that can be evaluated by elevated troponins or ECG changes. It takes about 6 hours post MI for the troponin level to rise, so if the patient has a sudden death from a heart attack, it is commonly only diagnosed on an autopsy after a patient expires.
The last two types of myocardial infarction are related to surgery. Type 4 MI is associated with percutaneous coronary interventions – within 48 hours of a procedure or from an in-stent stenosis/occlusion. Type 5 MI is myocardial infarction that occurs within 48 hours of a coronary artery bypass grafting (CABG).
There are multiple ways to lower the risk factors associated with CAD:
There are multiple ways a doctor can diagnose CAD:
Coronary artery disease is the most common type of heart disease and even though it can be extremely dangerous, there is an extensive amount of care and prevention that can be done to offer effective treatment.
It is important for individuals to be aware of the proper ways to manage CAD in order to achieve the most positive and efficient outcomes.
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