CHAPTER 7: CARDIOVASCULAR THE HEART
B. 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 2nd MC indication for a heart transplant.
C. 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 going on.
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.
D. Acute MI
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.
1. 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 = 2nd 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 at home (b/c of missed dx). They should have been sent to hospital.
Therefore, elderly pt with epigastric pain could be GERD or coronary artery thrombosis of the RCA.
2. Gross/microscopic features
Need to know when the heart is softest and has a chance for rupturing – this is between 3-7 days.
When do you see gross manifestation of being a pale infarct? 24 hrs – begin seeing paleness.
Coagulation necrosis in 4-6 hrs.
Example: LAD thrombosis b/c see pale anterior 2/3 of heart. Rupture – pericardium filled with blood (hemopericardium) – most are interior, and therefore is from the LAD thrombosis – how does this manifest itself? Day 3 or day 4 complain of chest pain, have muffled heart sounds, neck vein distension, and know they have ruptured.
Example: rupture of post medial papillary muscle – and it was infracted, therefore the RCA is the cause
of the rupture – so, what would the murmur be? Mitral regurg –On day 3 pt goes into heart failure, have a pansystolic murmur, increases on expiration, and S3 and S4 heart sound. It wasn’t there a day before – meaning the posterior medial papillary muscle was dysfunctional b/c it was infracted or it ruptured. So, it’s something that wasn’t there before and suddenly arise between days 3-7. Will go into heart failure b/c massive volume overload and go right back to the lungs.
Example: rupture of ant wall
Example: rupture of papillary muscle, and the posteromedial one is MC Example: Coag necrosis
Example: interventricular septum ruptures, therefore a left to right shunt and a step up. Most interventricular ruptures are LAD thromboses.
Example: mural thrombus (mural = wall) – in this case, mural is a thrombus, on the wall. They are almost always LAD thrombi b/c need a place to stick. With anterior MI, always give aspirin and put pt on warfarin/heparin – why do they do that? To prevent mural thrombus from forming. So, when you have an anterior prob, they will anticoagulate you. Mural thrombi are mixed clots – they are not a pure venous like clot or a platelet like clot, they are mixed. Here’s how it works: you have a transmural infarction and therefore injury to endothelial cells of the heart, therefore platelets will stick – so platelets are the first things that stick and then b/c the muscle is not contracting that well (b/c infracted muscle does not contract), there is stasis, and so on top of the platelets is a venous like clot, which Coagulation factor 5,8, and RBC’s, so its mixed (platelets with fibrin and venous clot from stasis). With aspirin, you not only preventing a coronary thrombus with
decreasing platelet aggregation, but also preventing a mural thrombus from initially forming b/c it inhibits the platelets from aggregating. Also, by putting on warfarin and heparin, you prevent the other part of the clot from forming. Don’t want these b/c it can embolize and therefore are very dangerous.
3. Fibrinous pericarditis – can occur 2 times in a person with MI: 1) 1st week – get a friction rub, chest pain (relieved when leaning forward and worse when leaning back - a 3 component friction
rub). That’s due to transmural infarction and increased vessel permeability. And 2) hx of transmural infarct, comes in 6 weeks later with fever, muscle aches and pains, and a 3 component friction rub in the chest = Dresslers’s syndrome , which is an autoimmune pericarditis. When had infarct, damage of the pericardial surface led to autoAb’s against pericardial tissue. This took 6 weeks to build up, and they start attacking the pericardium leading to systemic symptoms related to immunologic rxn = Dresslers’s. Therefore, 2 types are 1st week, not autoimmune, and 6 weeks, autoimmune. Basically treat with NSAIDS.
4. Later complications – ventricular aneurysm
Example: pt 3 weeks out of MI – chest bulges – what under there? Massive pectoralis major – ie systolic bulge of pericardium is ventricular aneurysm. Blood is collecting in the aneurysm and making the chest bulge out. This is a late manifestation – know it’s a vent aneurysm; the MC complication is NOT rupture, this aneurysm is lined by scar tissue and therefore will not rupture.
MCC death in a vent aneurysm = heart failure. Most of heart has scar tissue, which leads to decreased ejection fraction, therefore, die of HEART FAILURE not rupture.
Example:Acute MI – wasn’t – it is fibrous tissue, which is whiter and more patchy. Fibrous tissue (scar) can be anywhere from 3 weeks to 10 years
Must look at EF (ejection fraction) before leaving hospital; if you don’t have a good EF, probably will die. If you have a low EF, you had a big infarct, with a lot of muscle that was destroyed.
Therefore, EF is the biggest prognostic factor. If its close to 0.66, that’s good. But if your 0.4, ie its very bad.
5. How do we dx MI? CK-MB is dx of choice
Not an EKG b/c it has only an 80% sensitivity showing a new q wave, ST elevation. They have great specificity: Troponin I; CK-MB is an isoenzyme of creatinine kinase – have CK-MM, MB, and BB.
CK – MB is primarily in cardiac muscle. Therefore, when you infarct the muscle, you will see a primary increase in cardiac muscle, and when the muscle is infracted, will see an increase in that enzyme. Starts to go up at 6 hrs. Peaks in 24 hrs, and gone in 3 days b/c if CK MB is present after 3 days defines REinfarction. So, the reappearance of CK-MB = REinfarction.
Troponin I elevates a few hrs earlier than CK MB – its goes up at about 4 hrs, and peaks in about 24 hrs, too. It lasts 7 days, which is good. However, cannot dx reinfarction. So, after day 3 Troponin will still be there and therefore, you cannot dx reinfarction. CK-MB replaces LDH isoenzymes.
LDH isoenzyme: Normally, LDH2 is higher than LDH1. However, LDH1 is in cardiac muscle.
So, when you have an infarct, you release LDH1, and 1 becomes higher than 2 – which is called the flip. When you infarct through the muscle, 1 will be higher than 2, and that is the flip. This occurs in about 18 hours and peaks in about 3 days and last for a week. Most of the time, we use LDH enzymes if the pt came in 2-3 days after symptoms and CK-MB will have been gone by then. Then, look at LDH isoenzymes, and recognize that there is a flip and realize that there was an MI few days ago. This will be replaced by Troponin 1 b/c its elevated during this time period.
VIII. Valvular Heart Disease
A. Mitral Valve Prolapse – MC mitral valve lesion – more common in women; too much valve