patho sheet # 9 - Hala Alansari

Myocardial Infarction (MI):
- Infarct if not treated, might extend or spread, in all directions.

- Has many causes, one of them is thrombus in the lung ,the most important cause is background of atherosclerosis ( 75-90% obstruction), and on top of them might be one or more of the complication,

 So, one of the most important is thrombosis.
- Thrombus if left ,might propagate in one way or another.

- Then usually there’s a reflex called proximal vasospasm ; coronary artery contract proximal to that particular area and so on.
The conclusion: if the infarct is left untreated, it’s likely to extend in all direction.

Transmural infarction:
It almost always affects the left ventricle, it usually involves part of the left ventricle somewhere near the apex and/or the interventricular septum, and has specific distance ( maximum approximately 1 inch from the apex).
 The chance that the right ventricle is affected alone (isolated right ventricle) is less than 3% .

 Right coronary dominant (RCD) :
Happens when the left posterior descending branch of the coronary artery branches from the right coronary artery, this is called “ right dominant”.
- more or equal to 90% of people are right dominant artery.

 In those people, the type of infarction and coronary artery affected are alike, mostly LAD (left anterior descending branch) , 40-50% are affected. In this case, the anterior part of the left ventricle might be affected,and the anterior interventricular septum, near the apex.

- When the right coronary artery is affected, which happens in about 30% of the cases, the posterior part of the left ventricle, posterior aspect of the interventricular septum, and maybe the right ventricle, will be affected.
- In left circumflex , 15-20 % or less (because it has channels and on it’s own is small), the lateral left part of the left ventricle might be affected. ( so every artery affects its distribution areas).

 Diagnosis or clinical aspect:
Generally speaking,there’s 3 major categories:
1. Clinical:
The patient may have:
a) tachycardia,
b) hypertension,
c) pain,
d) dyspnea that means that the left ventricle is starting to fail, therefore the pulmonary congestion and edema,and so he gasps for air because of the congestion and the edema.

2) ECG change:
ECG changes are important, but not 100% of myocardial infarcts will manifest these changes.
Sometimes in 2-3% of the cases, ECG changes are not clear enough, but mostly about 98% of the cases ECG changes are present.
That’s why someone may do ECG test and it shows that he’s normal and that there’s nothing wrong with him, and the next day he maye have MI and may also be complicated.
 So, most of the times ECG shows changes, but in rare cases (2-3%) it won’t show any changes.

 Another thing that discomfort or pain is common from the clinical signs and symptoms, but sometimes 20-30% or even less, don’t feel any pain and continue their activities without knowing that they have MI.
This happens mostly with patients with diabetes and hypertension and especially the elderly people.
Q. if the MI doesn’t show on the ECG, how can we make the diagnosis??
Answer: using the other measures we discussed, clinically and in the lab,because sometimes ECG doesn’t show changes,there’s no enough changes. Some clinical symptoms maybe : hypotension,pain, dyspnea.so they repeat the ECG, but also may or may not find changes.
 The most complication associated with the MI is arrhythmia,and anything related to the conduction, and in 2/3 or less of the cases, acute heart failure may happen, accompanied with hypotension and maybe syncope. (these numbers differ somehow from what we have in Jordan).

 Another thing is thrombus formation, it may produce a number of emboli that may reach the brain and cause stroke in addition to the MI.

 Little number of the patients have shock on the spot ( around 10-12% ).

 Also rupture of the papillary muscle happens in small percentage, about 5-7%, especially in case of softness of the heart.


3) Enzymes and proteins:
Number of enzymes and chemical substances might leave into the circulation because of the necrosis of the myocardium. Eg. SGPT, SGOT, serum glutamic transaminases..etc.
There’s so many enzymes and chemical substances that might leak into the circulation, but the greater number of them are not highly dependable, and not highly specific.
The best and highly specific, highly sensitive, are 2 :
i. Creatine phosphokinase (CPK) (or creatin kinase , CK) :

 appears in the fisrt 2-4 hours, and may keep up in the first 18-24 hours,and it drops in about 3 days.
 It’s sensitive, but not much, because it might reflect injury to the skeletal muscles other than the myocardium. Eg. If someone injured his leg, and skeletal muscle injury happened, CPK might rise.
 So it might not be very specific for myocardium, but it’s rather sensitive.

 There are several isoenzymes for CPK, most important of which are 5 isoenzymes.
Most important isoenzyme is CPK-MB ( MB= Muscle and Brain). This isoenzyme might be more sensitive and more specific than the general CPK. We can calculate CK index=(CPK-MB)/(total CPK) , if the result is higher than normal, there’s myocardial infarction, if the next day the number is even higher, there might be another infarction, if the number decreases , then the patient is healing.
ii. Troponin:

 Troponin leaks only when there is myocardial infarction (MI) . it’s an protein enzyme that leaks whenever there is damage to myocardium.

 The best types to use is troponin I and troponin T.

- Most hospitals have it nowadays. It rises in about 2-4 hours, then it stays for 1 week, and then it will drop.

 Advantages of troponin  it stays elevated for 1 week up to 10 days.
 Drawback of troponin because if there’s another myocardial infarction (after 3-4 days), we wouldn’t know  it doesn’t show, because of the long duration that troponin stays elevated in the circulation,so it would be already high.

 That’s why sometime in the hospital they do both tests for the enzymes, and they refer to the ECG and clinical symptoms.

 Troponin is the best, because it stays elevated starting from 2-4 hours and up to 7-10 days,and it’s specific.

 There’s other enzymes other than troponin,but the majority of them are not either sensitive or specific for MI.


• Note: These numbers below were made in countries other than Jordan.

 15-20% of the patients die before arriving to the hospital or on their first day in the hospital.
 35% of the patients die in the first year ( including the previous 20%).
 1/3 of the patients ( including the ones who die in the ambulance, in the first day at the hospital,and in the first year) die.
 20% of patients admitted to hospital, check out with no further complications at all. (because they might have had small MI, or there was fast management,etc)

 5-10% of what’s left of these patients of acute MI , might die year after year, due to complication. This varies according to the country and other things.


 Other complication:
Includes pericarditis, in 2-3 days, it can be heard by stethoscope, and it’s called “ pericardial rub” ,( due to friction between the visceral and costal pleura.)
 There are many types of pericarditis:
• Serous.
• Fibrinous.
• Serofibrinous.
• Sanguineous.
These types can cause pericardial rub, because it causes “Constrictive Pericarditis”.

 In the museum in the faculty of medicine, you can see heart samples , some of which have aneurysm (like a balloon, near the apex ). With thinning of the myocardium, looks like it’s fibrosed  called “aneurysm”, although the thickest myocardium is at or near the apex.
 In the past, they were afraid that it may cause rupture, but it rarely rupture in the heart, (which is different from the atherosclerotic in abdomen), because there’s fibrosis, and number of aneurysm is low.

 Infarcts rupture in the first 2 weeks.

 papillary muscle rupture also in that period (the first 2 weeks) ,and other complications includes :

1) thrombosis, due to :
a) the surface area is rather rough because of necrosis.
b) Asynchronous contraction , it doesn’t go in harmony with the rest of the heart. therefore, It lags behind, there’s relative stasis, and therefore it promotes thrombosis. Then from thrombosis  emboli anywhere, eg in brain ,kidney..
2) Infective endocarditis.
 Chronic Ischemia of the heart.
Usually, in older age group, the heart is hypertrophic, has hypertension or concentric of the heart, or later, heart failure.
 Associated with this, is “chronic ischemic heart disease”, might be a sign of angina attack, so every now and then he feels discomfort in that area.
 in autopsy, we find small area of infarction with fibrosis

 Microinfarcts, we see it in microscopy, and sometimes even in macroscopy.
The end result is heart failure, due to repetition of chronis ischemis heart disease,and then sudden death may happen.

NOW, some notes while showing some of the labs slides:
MI:
 Subendocardial infarctions  20-30% of the inner aspect of myocardium, specially the left ventricle (LV) is involved.
 transmural infarction  >50% of the myocardium is involved.

Diseases of the heart valves:
One of the most important causes is pharyngitis, repeated pharyngitis in child hood, with certain microorganisms, especially in case of humid weather , overcrowdedness, poverty, lack of hygiene in childhood. All these factors might promote rheumatic fever, due to pahryngitis, inflammation of the focis in the upper respiratory tract by certain microorganisms.
It varies from one area to another, one ethnic group with another, from the poverty area compared to the richer area,and so on.
There’s always variations, but in general, it starts in childhood but can also happen in middle age and even old age.
Attack of Rheumatic fever usually comes following acute pharyngitis, especially in childhood, between the age of 5-15 years are the most incidence in the whole wolrd.
2-4 weeks following acute pharyngitis with beta hemolytic streptococci type A , which is the major causative agent. But there’s many people who have frequent pharangytis, and don’t develop rheumatic fever, on the other hand, many people have less frequent pharyngitis but develop rheumatic fever. There’s several concepts , one of them says that some people are more susceptible than others, another reason may be that some beta hemolyticus group A are rheumatogenic, and some are not.
But the general rule that Rheumatic fever coincidence with poverty, over crowdedness, repeated attacks of upper respiratory tract infections and pharyngitis by this particular microorganism, and number of promoting factors.
Then, 2-3 weeks later, immunological response developes for disinfection.
This response make antibodies that react with body antigens, connective tissue antigens, especially in the heart , certain joints, or in loins , or maybe be in kidneys and other connective tissues.
 That’s why rheumatic fever is also considered as one of the connective tissue disease, because it will cross react the antibodies raised against beta hemolyticus group A, with body connective tissue, specially heart and other joints.
So, repeated attacks causes number of diseases ( rheumatic fevers), and there’s many clinical sign and symptoms, e.g. Fever( might reach 40, high grade fever), pain in lower limbs, manifestations in skin, and in hearts . These signs and symptoms were called “John’s major clinical sign and symptoms”.
Mostly happens in large joints, and are called “ migratory poly arithritis” or “ fever associated migrating poly arthritis”, mostly in knee joint, then large joints for example shoulder joint, then right shoulder joint, then left hip joint etc..
It’s irregular, asymmetrical, unlike rheumatoid arithritis which affect small joint of both hands, or small joints of the jaw.
Opposite to rheumatoid arthritis is migratory poly arthritis, which affects large joints in asymmetrical , irregular manner, so the name “ migrating” .
 it causes 5 major manifestations:

1- Fever: high grade fever that might reach 40 degrees.
2- Migratory Polyarthritis,
3- Manifestations on skin: it causes rashes in a lot of cases, and it has a unique distribution called “swimming suite” appearance, it’s like the female swimming suit. Its distribution is on front and back, without upper and lower limb, covered with rash.
4- subcutaneous nodules: they are small soft bodies especially near joints, eg elbow, we find some nodularity,
5- and then it may affect the brain with what’s called “ chorea” ( which means purposeless involuntary movements, especially in the face, lips, and so on, and tremors), and then in the heart ( leaving residues on the heart).

chorea has several types, most known are :
 Huntington's Chorea
 Sydenham chorea : this is the one we’re talking about here.
And there’s a britihsh British saying:
“ rheumatic fever licks the joint, but bites the heart”, especially knee joint.
 so the joints after that within 1-2 weeks, with aspirin 2 pills up to 6 times a day, the joint will be much better, the heart a little bit better. But one time after another it will leave certain residues on the heart. Acute attack after another..etc

Acute attack :
Acute inflammation, that might affect the 3 layers of the heart ,(endocardium, myocardium, pericardium).
 It causes a special type of pericarditis, the English calls it ” bread and butter” pericarditis.
 The 2 layers of the pericardium ( visceral and parietal layers) may be affected by acute inflammation, usually serofibrinous  fibrin threads.
Just like when u take 2 slices of toast, spread butter over them just like a sandwich, and then open it, you’ll find grayish/yellow color, granular, irregular. That’s exactly like the bread and butter pericarditis when it make serofibrinous appearance, when you remove parietal and visceral pericardium from each others. And that happens in the rheumatic fever pericarditis.






 Acute myocarditis:
Causes acute inflammation, but modified with certain appearances. ( that we won’t discuss)
Conclusion: acute rheumatic myocarditis is important because it may be the cause of death of the patient. Although it’s rare, but it’s one of that responsible of mortality.

 Endocarditis:
Acute inflammation, specially on the valves.

 The rule is , endocarditis mostly affect the valves .

 65% is the mitral valve , 20% mitral + aortic valves.
 The two other valves only very very rarely affected.
 Acute inflammation causes erosions, ulcerations. E.g. on closure lines of the mitral valve instead of opposing one another,we find that the line of closure is irregular with erosions ,ulceration, and reaction of acute inflammation.
One after another , on top of these, it develops vegetations, small wart-like irregular elevations, made up of certain substances, these are called “ aschoff bodies” .
• Morphology of aschoff bodies:

- consist of central fibrinoid necrosis, surrounded by modified macrophages,and round cells (lymphocytes).macrophages are Modified macrophages (tissue histocytes), they have many names, one of which is “caterpillar cells”,because it has serrated nucleus, or also called “anichkov’s” cells. ( we must know the name “aschoff bodies”).

- The classical lesion for rheumatic carditis is aschoff’s bodies. In acute rheumatic fever, aschoff’s bodies are not well formed, but in repeated attacks, and with chronicity their number becomes bigger. sometimes it can’t be seen because they’re healed in acute phases, where there’s no well defined aschoff nodules. ,or healed with fibrous tissue around it and may have some inflammatory cells and rarely find anichkov’s cell or caterpillar cell,etc.. , or not completely formed( early, in acute cases).
- Acuteness is importants ,but the most important is that repeated attacks will distort the mitral valve, so that it’s fibrosed and it is stenosed because of fibrosis ( narrower than usual, called “mitral stenosis” : cannot pass enough blood from left atrium to left ventricle). In the same time, because it’s fibrosed, it’s regergital; can’t hold the blood in systole.
So it’s stenosed, and don’t close well enough to hold the blood through the systole (so part of the blood coming to left ventricle will go back into the left atrium), and therefore , there’s a great burden on the heart that it will end with heart failure.

Infective endocarditis:
Another type of the heart valves diseases.
- It used to be called Acute endocarditis., Subacute endocarditis, according to the course it does.
Nowadays, it’s called infective endocarditis, because sometimes there may be overlap between acute and subacute endocarditis, and it’s not only caused by bacteria, but also fungus and viruses may cause it.
- Acute endocarditis can affect normal heart. There’s a trigger for that, which is mostly surgery or procedure, and sometimes minor injury ,or iatrogenic,eg. Extraction of a tooth with no coverage of broad spectrum antibiotics, can cause it.

- Acute endocarditis is caused by staphylococcus auries, with an incidence of up to 30% of all infective endocarditis,

- it attack the diseased and the healthy hearts

- it attack specially the endocardium, and specially the valves( mostly the mitral, but can attack any other valve, unlike the rheumatic heart disease ,only the mitral valve)

- it runs a high grade fever, within a few days to few weeks maximum, it might kill the patient, because it results in:

a) Erosion of the valve and the perivalvular tissue.
b) Production of very large vegetations that are very friable, and might send emboli that may stop in brain, kidney, anywhere.
 Clinical signs and symptoms:
Changeable Murmurs: according to vegetations itself, vegetations grow bigger or smaller according to the fragmentations of the vegetations themselves .so they are very irregular.
- Subacute bacterial endocarditis: lower grade fever, associated usually with heart disease, and usually doesn’t affect healthy heart.
Caused by streptococcus veredans, it might cause low grade fever for long periods.
- Might kill the patient by changes like the acute, but much less frequently than the acute.

 Other than bacteria are viruses, but more important is :

candida ( fungi):

- incidence is low, much lower than that caused by bacteria.
- They cause much larger vegetations than those in both acute and subacute bacterial endocarditis, and also much more friable, and that’s why we find them everywhere.


Done by: Hala Al-Ansari.
Last lecture for Dr. Faisal, Tuesday 14.12.2010

 GOOD LUCK 