Chapter 20: Major risk factors for coronary artery
Age is the most imp risk factor (cannot control) -45 for males; 55 for women – why? Higher
estrogen levels, which affect HDL levels. Risk factor for CAD is not LDL, its HDL. HDL visits fatty
streaks, sucks LDL out, takes it to the liver to be metabolized. 55 in women b/c that is the age
of menopause; not taking estrogens and that is the age when estrogens go down; HDL levels go
down and risk goes up. Family history of premature artery dz, cig smoking, HP, HDL<35,
diabetes, LDL (cholesterol is not a risk factor, LDL is) b/c all therapeutic decisions are based on
LDL levels, not cholesterol levels. HDL is a negative risk factor: if your HDL is greater than 60,
you can subtract one from your major risk factor - ie 58 y/o, but HDL is above 60, can subtract
the age risk factor and will have no risk factors.
VII. Ischemic Heart Disease:
4 types: Angina, Myocardial Infarct, Sudden Cardiac Death Syndrome, Chronic Ischemic Heart
Sudden cardiac death syndrome = death within the last hr – what will you see at autopsy? Will
NOT see a coronary thrombus, will see severe coronary artery atherosclerosis. So, usually these
pts do not have a thrombus, but do have severe coronary artery dz, leading to ischemia, PVC’s,
ventricular fibrillation (die of ventricular arrhythmia just like in MI); die so fast that there are no
changes in the heart (ie pallor/Coagulation necrosis); see severe coronary artery dz and dx
sudden cardiac death. Very high risk in smokers.
Chronic ischemia heart dz –It’s a lot of our parents, uncles and aunts who have coronary artery
dz with little infarcts, or had a small heart attack, basically talking about subendocardial
infarctions. What happens is that the muscle gets replaced by fibrous tissue and eventually the
poor LV is all fibrous tissue, with no muscle therefore the ejection fraction is very low. Its 0.2
instead of the normal 0.66 and they die from heart failure. Fibrous tissue does not have
contractility; this dz is the 2 MC indication for a heart transplant.
Angina (MC type of heart dz)
3 types – exertional, prinzmetal, unstable (resting) angina
1. Exertional – chest pain on exertion, goes away within 5-10 minutes of resting; ST depression
on EKG (1-2 mm depression) – therefore a candidate for coronary angiogram to see what’s
2. Prinzmetal’s – seen in women, occurs in morning; due to vasospasm of the coronary
arteries, NOT atherosclerosis. In some people, TxA2 is implicated for the vasospasm. ST
depression means subendocardial ischemia. Coronary arteries penetrate the outside of the
heart and go in, so the subendocardial tissue get screwed b/c its furtherest from the blood
supply. Therefore, with coronary artery atherosclerosis, and decreased blood flow, who gets
screwed? Subendocardium and it reacts to it with pain and ST depression. With vasospasm of
coronary artery, get transmural ischemia – therefore there is ischemia throughout the entire thickness of the muscle – this produces ST elevation. So, Prinzmetal’s angina has ST elevation
b/c transmural ischemia.
3. Unstable – aka pre-infarction angina – get angina on resting. Classic hx: initially had stable
angina, now pt just get it when they are sitting. This means that they will need angioplasty and
put into the hospital. Do not put on treadmill, they will die. What veins do they use? Saphenous
vein – over 10 years will become arterialized (it will look exactly like an artery). If you take a
vein, and put arterial pressures into it, it will change its histology and look exactly like an artery.
They have a high tendency for fibrosing off after 10 years b/c they are veins.
Internal mammary is an artery, therefore won’t have the same problem b/c it is used to those
pressures. They will remain patent, but cannot do four vessel bypass with one internal
mammary artery. So, they use the saphenous vein, which has the tendency to undergo fibrosis
over time b/c they are arterialized under pressure. They can also use the internal mammary.
Thrombus composed of group of platelet cells bound together with fibrin. TPA doesn’t have a
problem with this b/c it just breaks the fibrin bonds to destroy the clot. It has a much bigger
problem with the breakdown of a venous clot b/c those have more fibrin. The
thromboses/clots in the heart do not have that much fibrin. Another factor to deal with is
reperfusion injury – O2’d blood goes into injured tissue, superoxide free radicals form, Ca form,
and a few of the injured myocardial cells will die. Once those die, it will still improve longevity.
Complications of MI:
a) LAD coronary artery is MC vessel thrombosed, and supplies entire anterior part of your
heart and the anterior 2/3’s of the interventricular septum. So, there will be paleness, with the
ant 2/3’s knocked off. Where are most of the conduction bundles? Anterior 2/3’s. So, if you
have complete heart block that requires ectopic pacemaker, what is the most likely vessel
thrombosed? LAD. When you have LAD occlusion, you have classical signs – pain radiating the
jaw, pain down the left arm, substernal chest pain.
b) RCA = 2 MC thrombosed artery – which supplies the entire posterior part of the heart and
the posterior 1/3 of the ventricular septum and the entire right ventricle. So, it supplies the
post heart, post 1/3 of the septum and the entire right ventricle. The mitral valve has two
valves with papillary muscles – posteromedial papillary muscle and posteromedio papillary
muscle. So, what supplies the posterior? RCA. Also have the SA node and AV node. The SA
node has an equal distribution between left and right. However, the AV node has a 95% supply
from the branches of the RCA – this brings up interesting complications. Example: pt with
mitral regurg murmur, which is related to posteromedial papillary muscle dysfunction, or may
break – what is the problem? Thrombosis of the RCA b/c the RCA supplies that papillary muscle.
So, mitral regurg murmur that occurs during MI would be due to RCA. If you knock off the AV
node, this is sinus bradycardia, and atypical chest pain. The RCA is dangerous b/c sometimes
pt will get epigastric pain, which is an atypical pain. This simulates GERD; ie pt sent home with
pepto bismol, and ends up dying