Angina comes from the latin angere, which means to strangle, and pectoris comes from
pectus, meaning chest—so angina pectoris loosely translates to “strangling of the
chest”, which actually makes a lot of sense, because angina pectoris is caused by reduced
blood flow which causes ischemia to the heart muscle, or lack of oxygen to the heart, almost
like the heart’s being strangled which causes terrible chest pain.
Stable angina or chronic angina is the most common type of angina and it usually happens
when the patient has greater than or equal to 70% stenosis, meaning 70% of the artery
is blocked by plaque buildup.
This small opening that blood flows through might be enough to supply the heart during
rest, but if the body demands more blood and oxygen, like during exercise or stressful
situations, the heart has to work harder, and therefore needs more blood and oxygen
itself.
It’s during these time of exertion or emotional stress that people with stable angina have
chest pain, since the blood flow isn’t meeting the metabolic demands of the heart muscle,
or myocardium.
But the pain usually goes away with rest.
In the majority of cases, the underlying cause of stable angina is atherosclerosis of one
or more the coronary arteries—arteries supplying blood to the heart muscles.
Other heart conditions that might lead to stable angina are ones that cause a thickened
heart muscle wall, which would require more oxygen.
This increase in muscle size can be due to hypertrophic cardiomyopathy from a genetic
cause, or as a result from the heart having to pump against higher pressures, as is the
case in aortic stenosis, which is a narrowing of the aortic valve, or hypertension.
These larger, thicker heart muscles require more oxygen, and if the patients can’t meet
increasing demands, they feel pain in the form of angina.
Whatever the case, the heart needs blood, and if we look at the heart wall, there’s
three layers—the outermost layer, the epicardium, then the myocardium in the middle, and the
endocardium inside the heart.
The coronary arteries start up in the epicardium, and then dive down and supply all the heart
tissue.
If blood flow’s reduced or the myocardium is thicker, blood has a harder time reaching
this deeper layer just under the endocardium, called the subendocardium.
Therefore the classic finding with angina is subendocardial ischemia, meaning less oxygen
is reaching the region just under the endocardium.
This ischemia is thought to trigger release of adenosine, bradykinin, and other molecules
that stimulate nerve fibers in the myocardium that result in the sensation of pain.
That chest pain is usually described as feeling like pressure or squeezing and it can radiate
to the left arm, jaw, shoulders, and back, and sometimes is accompanied by shortness
of breath and diaphoresis or sweating.
Usually the pain and symptoms last less than 20 minutes and subside after the exertion
or stress is taken away, and therefore the heart muscle isn’t demanding as much blood.
Now, unlike stable angina which describes when patients have pain only during periods
of exertion or stress, but not during rest, there is also unstable angina which is when
patients have pain during exercise or stress as well as during rest—it never really goes
away.
Unstable angina is usually caused by rupture of atherosclerotic plaque with thrombosis,
meaning a blood clot forms on top of a mound of plaque.
Although the occlusion might not block the entire vessel, there is now even less room
left for blood to flow by, and the heart tissue is starting to feel starved for oxygen even
while pumping at a normal rate.
Unstable angina, for the same reason as stable angina, involves subendocardial ischemia and
it should be treated as an emergency, because patients are at a high risk of progressing
to myocardial infarction, or heart attack.
The key distinction is that unstable angina means that the heart tissue is alive but ischemic
or starving for oxygen, whereas myocardial infarction means that the areas of heart tissue
have already begun to necrose or die.
Now a third type of angina is vasospastic angina, also known as prinzmetal angina, and
patients may or may not also have atherosclerosis.
Ischemia, and resulting chest pain is due to coronary artery vasospasms, meaning the
smooth muscles around the arteries constrict extremely tightly and reduce blood flow enough
to cause ischemia.
Episodes of vasospastic angina don’t correlate with exertion and can happen anytime, including
at rest.
The underlying mechanism causing vasospasms isn’t well understood, but likely involves
vasoconstrictors like platelet thromboxane A2.
Unlike both stable and unstable angina, in this case the coronary artery’s constricted
so severely that all layers of the heart wall being supplied are affected, therefore it’s
referred to as transmural ischemia.
Alright, so if we line these three up side-to-side, there’s some important clinical similarities
and differences.
First, it’s super important to remember that in each case, the injury to cardiomyocytes
isn’t permanent, meaning it’s reversible and the cardiomyocytes don’t die (which
is how this differs from myocardial infarction).
On an electrocardiogram, or ECG, both stable and unstable angina show an ST-segment depression
since ischemia’s limited to the subendocardium.
In contrast, vasospastic angina shows ST-segment elevation due to transmural ischemia.
Rest tends to relieve stable angina, whereas unstable angina and vasospastic angina can
occur anytime, including at rest.
In terms of medications, all three can be treated with Nitroglycerin which is a vasodilator
that increases blood vessel diameter to allow more blood flow.
In addition, vasospastic angina also responds to calcium channel blockers.