Define Ischemic Heart Disease.
Imbalance (generally shortage) between supply & demand of oxygen, nutrients, and waste removal of heart tissue.
Why is ischemia worse than hypoxia?
Ischemia involves a lack of nutrient delivery & metabolite removal in addition to interrupted oxygen supply.
Give four possible causes of heart ischemia.
1. Fixed obstruction
2. Acute plaque change
What is the consequence of a >90% obstruction of coronary flow?
>90% results in resting ischemia, as opposed to exertional only (>70%)
What vessels are most susceptible to fixed atherosclerotic obstruction?
LAD (left anterior descending) > LCX (left circumflex) > RCA (right coronary)
What factors contribute to the risk of acute plaque changes?
Intrinsic: eg Foam cells, lipid, inflammation, cap integrity.
Extrinsic: eg Adrenergic stimulation
What are the typical outcomes of total and partial coronary thromboses?
Total = Acute transmural MI and/or sudden cardiac death.
Partial = Unstable angina, subendocardial infarction, embolization. Sudden death still possible.
Recall where lipids deposit in an atherosclerotic plaque.
Where does the calcification occur?
Lipid deposition in the intima.
Calcification also occurs in intima (as opposed to media)
What factors contribute to inappropriate coronary vasoconstriction?
How would this present clinically?
Adrenergics, platelet & mast cell contents, endothelial dysfunction.
Severe, but transient angina.
Distinguish between the outcomes typical of immature/vulnerable plaques and mature/stable ones.
Immature/vulnerable may undergo acute changes >> thrombus or embolization >> acute MI.
Stable results in severe fixed obstruction >> chronic ischemic heart disease.
What are the four clinical syndromes of heart ischemia?
Chronic ischemic heart disease
Sudden cardiac death
Recall the 3 types of Angina pectoralis.
Which can occur at rest? Which is most dangerous?
Stable - Elicited by exertion or emotional response.
Prinzmetal - Due to artery spasm, can occur at rest.
Unstable - Progressively worsening plaque, will eventually occur at rest and often precedes acute MI.
What is the difference between angina pectoralis and myocardial infarction?
In angina pectoralis, pain is elicited from reversible ischemia of heart tissue. In myocardial infarction, ischemia is severe enough to cause irreversible damage (necrosis).
Distinguish between transmural and subendocardial infarctions.
Transmural - Usually results from complete vessel obstruction; full thickness necrosis confined to one vessel's territory.
Subendocardial - Milder obstruction; necrosis limited to inner 1/3 of myocardium but may extend laterally.
Why is the inner 1/3 of the myocardium most susceptible to necrosis in myocardial infarctions?
Why is the subendocardium affected, and not the whole endocardium?
Perfusion pressure there is lower, and subendocardial resistance is higher.
Innermost layers of endocardium receive oxygen from the blood in the ventricle.
What occurs almost immediately upon infarction?
After how long is the ischemic damage irreversible?
Ceasing of contraction of the infarcted area.
20-40min until the ischemia results in necrosis.
An infarction results in the death of the left lateral wall of the left ventricle. What vessel was occluded?
What ischemic outcome results from global hypotension?
What would cause multiple intramural infarctions?
Left lateral wall supplied by Left circumflex branch.
Global hypotension can cause infarction of the entire circumferential subendocardium. (pressure inadequate to reach subendocardium)
Hypertension or multiple emboli from an upstream thrombus can cause multiple intramural infarctions.
Describe the changes in gross morphology of an infarcted heart.
<12hrs: Subtle. Tetrazolium stain reveals pale areas.
12-24hrs: Dark red-blue mottling from clotting blood.
1-14days: Yellow-tan area with peripheral hyperemia.
>14days: Grey-white scar.
What does a tetrazolium stain detect?
Tetrazolium stains dehydrogensase enzymes red. This can reveal dead tissue as pale.
Describe the changes in histology of an infarcted heart.
4-12hrs: Wavy fibers.
12hrs-7days: Coagulative necrosis (loss of nuclei, eosinophilia), neutrophil infiltration.
7-14days: Granulation tissue present.
>14days: Dense fibrous scar. (blue trichrome stain)
How does reperfusion injury occur?
Reperfusion of infarcted tissues results in damage from leukocyte ROS, platelet/complement activation, and microvascular injury.
How does a typical MI patient present?
With severe chest pain ("crushing", may radiate to L arm or neck). Weak pulse, diaphoresis, dyspnea.
(Labs: Elevated cardiac enzymes, CRP)
How many MIs are silent?
What patient population is especially prone to these?
Heart transplant patients (since the heart isn't innervated)
Describe 3-4 possible complications that result form MIs.
Contractile dysfunction (severe >> cardiogenic shock)
Arrhythmias (>> sudden death)
Distinguish between the consequences of myocardial ruptures at the following sites:
Free wall: Hemopericardium/tamponade.
Ventricular septum: L>R shunt.
Papillary muscle: Mitral regurgitation.
How does fibrinohemorrhagic pericarditis present?
Friction rub (can be auscultated).
What is a mural thromboembolism?
A thrombus that forms in the unmoving area around the infarction, which may embolize to circulation (L/R).
What factors influence the prognosis of acute MI?
How large the infarct is, where it is, how much tissue is involved, how extensive the necrosis is (how much time has passed). How much funciton remains?
What are some causes of chronic ischemic heart disease?
Describe these hearts.
Cardiac decompensation secondary to infarction, or severe coronary obstruction.
Enlarged, usually with LV hypertrophy & dilation.
What is Sudden Cardiac Death? Why does it usually occur?
Unexpected death from cardiac causes; usually due to arrhythmias & related to heart ischemia.
What arrhythmias are potentially fatal?
Asystole and Ventricular Fibrillation (V-Fib)
When is contraction band necrosis seen?
In reperfusion injury of infarcted tissue (due to calcium return; not seen without reperfusion!)