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.
