Coronary artery disease is essentially what happens when the coronary arteries (the arteries supplying the heart) get blocked for some reason. I recommend reviewing the anatomy of the heart and the blood supply if you're not familiar. I wrote about it on a previous post, but if you can find diagrams somewhere that's even better.
First, some definitions. Arteriosclerosis is a condition in which the arteries become thick and stiff, causing them to have a narrow lumen and thus decreased blood flow. One common type of arteriosclerosis is atherosclerosis, which is caused by the formation of fatty plaques called atheromas. There are a whole bunch of risk factors for atherosclerosis. Some of these aren't controllable, like genetics, age and gender (males are more likely to suffer than females), whereas others are a bit more controllable, like smoking, having a sedentary lifestyle or having uncontrolled diabetes.
There are four main steps for the progression of atherosclerosis. First, the endothelial layer of the blood vessel is damaged. This is usually really tiny damage- maybe just a few cells torn off by high-pressure blood flowing through. Nevertheless, it still provides a surface for some fatty streaks to adhere, which develops into a fibrous plaque. Plaques slow down the blood flowing through, so that further complications like further plaque formation or thrombus (clot) formation are more likely to occur.
Artery blockage is obviously pretty bad, because it means that areas of the body are being deprived of blood. When the coronary arteries are blocked, as in coronary artery disease, this can lead to angina (chest pain) or myocardial infarction (heart attack). Treatment tends to try and get at the root cause by addressing lifestyle factors- for example, losing weight and quitting smoking. Antihyperlipidemic agents (i.e. drugs that get rid of too many lipids) may also be used.
Coronary artery disease has a range of manifestations. Some people are asymptomatic until they suddenly drop dead. Others may have a range of warning signs, from angina and dysrhythmias (i.e. problems with the heart rhythm) to myocardial infarction. Let's look at angina first.
Angina
Angina
Angina pectoris, often simply known as angina, is sudden chest pain due to myocardial ischaemia (i.e. not enough blood flow to the heart muscle). It tends to be felt in the chest and down the left arm. There are two main types of angina: typical (exertional) angina and variant (Prinzmetal's) angina. As you can probably guess from the names, typical angina tends to be brought on by exertion (but not always, as you'll see later) and is caused by obstruction of the coronary arteries by atherosclerosis or whatever, whereas variant angina tends to occur at rest and is caused by vasospasm (constriction of the arteries).
Typical (exertional) angina can be further broken down into stable and unstable typical angina. Stable angina follows the classic pattern of chest pain during exercise which is relieved during rest, whereas unstable angina is more prolonged and can occur during rest. Unstable angina can be differentiated from variant angina by the cause: while both occur at rest, unstable angina is due to a blockage in the arteries whereas variant angina is due to vasospasm.
There are several different treatments for angina. Short-term, rest and organic nitrates might be helpful, especially for stable angina. Antianginal drugs such as slower-acting nitrates, β-blockers, calcium channel blockers and anti-platelet drugs (e.g. small doses of aspirin) might be helpful as well. An important point to note is that β-blockers should be avoided in patients with variant (Prinzmetal's) angina, as these may increase the risk of vasospasm. Instead, calcium channel blockers are the drug of choice. Longer term, the underlying cause of angina, whether that be atherosclerosis or something else, should be treated.
Here's a mnemonic for remembering some of the guidelines for treatment and things to look out for with regards to stable angina, courtesy of the American Heart Association:
There are several different treatments for angina. Short-term, rest and organic nitrates might be helpful, especially for stable angina. Antianginal drugs such as slower-acting nitrates, β-blockers, calcium channel blockers and anti-platelet drugs (e.g. small doses of aspirin) might be helpful as well. An important point to note is that β-blockers should be avoided in patients with variant (Prinzmetal's) angina, as these may increase the risk of vasospasm. Instead, calcium channel blockers are the drug of choice. Longer term, the underlying cause of angina, whether that be atherosclerosis or something else, should be treated.
Here's a mnemonic for remembering some of the guidelines for treatment and things to look out for with regards to stable angina, courtesy of the American Heart Association:
- A is for Aspirin and Anti-anginals
- B is for Beta-blocker and Blood pressure
- C is for Cholesterol and Cigarettes
- D is for Diet and Diabetes
- E is for Education and Exercise
Myocardial Infarction
Myocardial infarction, a.k.a. a heart attack, is pretty much angina gone extreme. While angina is chest pain due to reduced blood flow to a certain area, myocardial infarction is necrosis of the heart muscle due to a complete lack of blood flow to an area. Scar tissue later forms in place of the necrotic area, further affecting heart function. Myocardial infarction is caused by complete occlusion of the artery, and can be caused by atherosclerosis (just like angina except now you've got a plaque that's completely shutting off blood flow). It is usually transmural, meaning that it affects the entire thickness of the heart wall, and most commonly affects the left ventricle, which doubly sucks because that's the ventricle pumping blood to most parts of the body.
Myocardial infarction manifests as pain, except this pain is more severe and prolonged than angina. It also does not respond to rest or nitrates. In addition to pain, the patient may also be pale, sweating, short of breath and/or have a low-grade fever.
When someone has a myocardial infarction, obviously the most important thing is to stabilise the patient: time is muscle! After that, other tests can be done to definitively determine whether or not the patient was experiencing a myocardial infarction. Blood tests can be used to detect levels of cardiac enzymes released when heart cells die. The most specific markers are Troponin I and CK-MB (a form of creatine kinase only found in the heart), but there are other less specific markers such as myoglobin (the earliest marker) and AST (aspartic transaminase). Coronary angiography can be used to figure out which vessels are blocked and echocardiogram can be used to find other structural abnormalities.
A whole lot of drugs are employed in order to try and treat an acute myocardial infarction. These include nitrates, beta blockers and antiplatelets, just like for angina. Other drugs include thrombolytics (clot-busters), anticoagulants, ACE (angiotensin-converting enzyme) inhibitors and medications for pain relief. More invasive therapies can also be applied: Percutaneous Coronary Intervention (PCI) includes angiography, angioplasty (inflating a small balloon into the artery to make it expand) and stenting. Coronary artery bypass grafting (CABG), which takes a vessel from another part of the body and uses it to bypass the blockage, may also be used.
Phew! This guy's lectures are long...
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