ISCHEMIC HEART DISEASE (cont’d)



Thursday, January 4, 2001 Scribe: Justin Reid

Pathology 1PM Proof: Justin Reid

Dr. Graham

ISCHEMIC HEART DISEASE (cont’d)

I. Reperfusion effects

A. If injured tissue is reperfused within an hour to several hours there maybe no death of tissue

B. Tissue: dead, stunned (semi alive), and alive

1. Reperfusion can save stunned but not dead tissue

C. Contraction bands—irreversibly injured myocytes

1. Histologically appear to be alive but sarcomeres are non-functional

2. Mark of reperfusion injury

D. Many times there is obvious dead tissue—Remember—>Red is Dead

1. Hypereosinophilic and wavy b/c other fibers around this dead tissue is contracting while it isn’t—not the same as contraction bands (good picture in the book!)

D. Hemorrhage will occur with reperfusion to injured tissue

E. Injured tissue adjacent to alive tissue will appear wavy due to its lack of contraction

F. Cardiac enzymes will appear worse with reperfusion because of additional damage to myocytes by O radicals

G. Stunned (reversibly injured) myocytes may take a while to recover and therefore there functional recovery should be monitored

II. Cardiac Enzymes

A. Released by the myocardium as the tissue dies

B. Creatine Kinase (CK) dimers M/B

1. CK-MB fraction is specific for cardiac muscle

2. Pro: peaks in 18 hr

3. Con: gone in 2-3 days

C. Troponin I and T (TnI;TnT)—associated with sarcomeres of cardiac and skeletal muscle but selectivity to cardiac muscle can be achieved through antibodies

1. Pro: peaks in 18 hr

2. Pro: lasts 7 to 10 days

D. Most people are moving toward TnI b/c of its lasting power

SLIDE: 3-6 day heart; hypertrophy of left ventricle (LV); ant. transmural yellowing; old subendocardial scarring

SLIDE: ant. MI; yellowing with some hemorrhaging probably 3-5 days old; transmural in the septum

SLIDE: viable myocardium with cellular granulation tissue (appear as early as 3 days); macrophages, neutrophils

SLIDE: mononuclear cells cleaning the place up

III. Complications of MI

A. Early complications are very rare

B. Lethal complications are cardiac rupture syndromes

SLIDE: LV with a transmural infarction of left circumflex with complete rupture of the wall

SLIDE: large rent (?) in the free wall of the LV

1. Free wall rupture-- lead to hemopericardium (which acutely can occlude intake and therefore output)

2. Interventricular septum rupture—lead to increased load on the right ventricle

SLIDE: transmural rupture into the free wall of the ventricle

SLIDE: heart bathed in cloud of blood--hemopericardium

SLIDE: heart ruptured through the right ventricle (RV)

3. Ruptures can lead to papillary muscle damage with acute mitral insufficiency, which can lead to acute hemodynamic changes on the left side

C. Ventricular aneurysm

1. Thinned scar and therefore it doesn’t work and just takes up space

2. Late complication

3. Rarely ruptures

SLIDE: old (white) heart with a very thin wall distinct of an aneurysm

SLIDE: LV aneurysm, which isn’t contributing anything to cardiac output but is a source of emboli and is taking up space

SLIDE: LV with huge laminated mural thrombus; removal can prolong life

SLIDE: Huge ballooning aneurysm looks like another chamber

D. Early pericarditis can occur in a transmural infarction as well as an autoimmune pericarditis which can cause friction rubs and pain a couple of weeks after an MI therefore producing a different pain syndrome

E. Mural thrombus—source of emboli and results from aneurysms or any injured surface

F. Infarct extension

1. Hypotension

2. Additional ischemic extension of the infarction

3. Attempts are made to prevent these secondary symptoms

G. Papillary muscle dysfunction and therefore valvular dysfunction

IV. Mortality

A. Make hospital: only 7-13% die

B. Don’t make hospital: 40% die

C. 30% of people who have an MI die within year one

D. 3-4% of people die each year thereafter

Side notes: After you have gotten through the first few weeks after an MI, what happens?

You will scar down—you eat up the bad dead stuff, the macrophages leave, the vessels hang around while you continue to scar, and vessels lessen in number until there gone when the scarring is complete. Some MIs take longer to scar than others depending on the size of the MI. After approximately a month, the scarring is finished and whether the MI was 3 months ago or 10 years ago we wouldn’t be able to tell b/c a scar is a scar. Thin scars can result in dilatations (aneurysms). Scars with many cells containing macrophages are symbolic of a new scar. Trichrome is used to stain collagen green, which is the component of scars.

V. Chronic Ischemic HD

A. Diffuse dysfunction from long term subacute disease or postinfarction decompensation

B. Chronic CAD of varying degrees

C. Patchy or old transmural fibrosis

D. Myocardial hypertrophy b/c as myocardium is lost other myocardium needs to make up for the loss

E. Diffuse subendocardial vacuolization--long-term low-grade injury that may be reversible in the subendocardial cells

VI. Sudden Cardiac Death---death occurring within one hour of a cardiac event

A. 300,000 to 400,000 deaths/year in the US

B. Arrhythmias

C. Causes:

1. Critical stenosis i.e. occlusion of a coronary vessel >75% (80-90% of cases)

a. Acute plaque disruption, which is not occlusive but subocclusive

D. Younger patients--other non-ischemic causes

VII. Systemic hypertension

A. Causes:

1. Idiopathic in 90-95% of cases

2. Increased vascular resistance

3. 60, mitral valve prolapse, high left ventricular pressure, and complications are usually related to poor movement of the valves

I. Mitral Stenosis

1. #1 cause is chronic Rheumatic HD

2. 75% of cases the mitral valve alone is involved in rheumatic HD

3. 25%(the rest) involves both aortic and mitral valve stenosis

4. **The left ventricle does not become hypertrophic with isolated mitral valve stenosis.**

5. **What is significant and becomes gigantic is the right atrium**

6. Also associated is secondary pulmonary hypertension b/c of massive backup of blood into the lungs

7. SLIDE: slitlike appearance—fishmouth mitral valve—buzzword for mitral stenosis assoc. with chronic rheumatic HD

J. Mitral valve prolapse

1. #1 valvular HD in industrialized countries-3%; Females>males

2. Developmental abnormality

3. Notable for a mid-systolic click b/c of a big ballooning mitral valve leaflet that in the middle of systole goes SNAP! and it clicks and you can hear it through your stethoscope +/- murmur Mitral insufficiency

4. Dilated ring with some myxoid changes

5. Atrial mural thrombi assoc. with jetflows of blood in abnormal fashion causing scarring resulting in thrombi (classic one is in the left atrium)

SLIDE: mitral valve with big ballooning leaflets that snap up when they close

SLIDE: picture from the atrium shown into the ballooning leaflet

6. Complications: ~3% RARE

a. Infective endocarditis

b. Mitral insufficiency

c. Arrhythmia with sudden death seen but RARE

If you have questions concerning the scribe e-mail me at medsjjr@ttuhsc.edu and I’ll try my best to resolve the issue.

Just imagine: a year and a half ago we were stepping up to the plate now we’ve just finished rounding third and we’re headed for home, although I’m recovering from tripping over third base.

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