Path-ischemia Flashcards
Risk factors for atherosclerosis and IHD
Family hx Age Men>women Hypercholesterolemia Diet Smoking DM Lack of exercise Obesity Stress
Clinical syndromes of IHD
- Acute coronary syndromes:
a. Angina pectoris (stable, prinzmetal, or unstable)
b. MI
c. Sudden cardiac death - Chronic IHD, resulting in HF
Substernal or precordial chest pain from transient myocardial ischemia lasting from 15 seconds to 15 minutes
Angina pectoris
Angina pectoris is most common in ____. Pain is described as ____
- Middle aged and older males (women are usually affected after menopause)
- Constricting, squeezing, choking, or knife-like. May radiate, or may be diffuse. Not related to breathing
What is the most common variant of angina?
Stable angina
Angina with exercise, excitement, or other sudden increase in cardiac load with subsequent in trade in demand for blood flow.
Stable angina
True or false:
Myocardial ischemia is usually irreversible
False
Only irreversible if there is myocyte necrosis. Otherwise it is reversible
\_\_\_\_ angina is usually associated with >70% chronic stable stenosis of a coronary a. It is (usually/not usually) associated with plaque disruption. And (is/is not) relieved with rest or a vasodilator.
Stable
Not usually
Is
Within a year of dx, how many people with stable angina will develop unstable angina or MI?
20%
Episodic angina at rest due to intense coronary a. vasospasm. Unrelated to exercise, heart rate, or BP
Variant (Prinzmetal) Angina
Variant (Prinzmetal) Angina typically responds to ___
Nitroglycerin (vasodilator)
Ca channel blockers
Things that can cause vasospasms
Primary Raynaud disease
A lot of vasoactive mediators
Elevated TSH
Autoantibodies and T cells in scleroderma
Extreme psycho stress and release of catecholamines
Occurs with progressively lower levels of physical activity or at rest
Increases in frequency over time
Often of prolonged duration
Unstable (Crescendo) Angina
Aka Preinfarction Angina
Unstable (Crescendo) Angina is usually caused by ___
Disruption of plaque and superimposed partial thrombosis and possibly embolization or vasospasm or both
Sequence of events in coronary a. occlusion
- Sudden change in atheromatous plaque
- Collagen exposed, causing platelet adhesion and aggregation to form thrombus
- Vasospasm
- Tissue factor activates coag pathway, increasing size of thrombus
- Thrombus evolves to occlude lumen
- Occlusion causes ischemia, dysfunction, and potentially myocyte death
Vasospasm is initiated by ___
Mediators from platelets
Prolonged ischemia for greater than ___ causes damages to microvasculature
1 hour
Reperfusion injury probably results from ___.
Free radical damage to the microvascular circulation
Potential complications of MI
DARTH VADER Death Arrhythmia Rupture Tamponade HF Valve disease Aneurysm of ventricle Dressler's syndrome Embolism Recurrence/Regurgitation
Progressive congestive heart failure as a result of long term ischemic damage to myocardium.
Chronic ischemic heart disease
Aka ischemic cardiomyopathy
Chronic ischemic heart disease often results in ___
Cardiomegaly
LV hypertrophy
Ventricular dilation
Some degree of obstructive coronary a. atherosclerosis
In ___ of sudden cardiac death cases you will see coronary artery atherosclerosis with critical (>___%) stenosis involving one or more of the three major coronary vessels
80-90%
75%
True or false: most cases of sudden cardiac death are associated with acute MI
False
Sudden cardiac death is thought to result from ___
Ischemia-induced myocardial irritability that initiates dangerous arrhythmias
___% of sudden cardiac death are of non-atherosclerotic causes
10-20
___ is the most common cause of death in adults in the USA
MI
Some causes of MI
Vasospasm
Emboli from left atrium
Disorders of coronary arteries
___ is an ST elevation infarct
___ is a non-ST elevation infarct
Transmural infarct
Subendocardial infarct
True or false: most MIs are subendocardial infarcts
False. Most are transmural
Infarct in which ischemic necrosis involves the full thickness of the ventricular wall vs. 1/3 to 1/2 of the wall
Transmural
Subendocardial
A subendocardial infarct may result from ___
A thrombus lysed before necrosis that extends across the wall or from prolonged severe hypotension (global).
Frequencies of involvement of the three main coronary arteries?
LAD > RCA > Left circumflex
Corresponding sites of infarcts for LAD
Anterior wall of LV near apex
Anterior portion of ventricular septum
And Apex circumferentially
Corresponding sites of infarcts for RCA
Inferior/posterior wall of LV
Posterior portion of ventricular septum
Inferior/posterior RV free wall
Corresponding sites of infarcts for left circumflex a.
Lateral wall of LV except at the apex
Necrosis is usually complete within ___ after the onset of the severe ischemia
6 hours
Location, size; and morphologic features of an infarct depend on:
- Location, severity, and rate of development of obstruction
- Size of vascular bed
- Duration
- Metabolic/oxygen needs
- Extent of collateral vessels
- Vasospasm
- Rate, rhythm, and blood oxygenation
Morphologic changes in infarction:
1/2-4 hours
Gross: none
Micro: none, maybe wavy fibers at border
Morphologic changes in infarction:
4-12 hours
Gross: dark mottling
Micro: early coag necrosis, edema, hemorrhage
Morphologic changes in infarction:
12-24 hours
Gross: dark mottling
Micro: coag necrosis, wavy fibers, edema fluid, neutrophils
Morphologic changes in infarction:
1-3 days
Gross: dark mottling with yellow-tan infarct center
Micro: coag necrosis, loss of nuclei and striations, neutrophils
Morphologic changes in infarction:
3-7 days
Gross: hyperemic border, central yellow-tan softening
Micro: disintegration if dead myofibers, dying neutrophils, early phagocytosis of dead cells by macrophages at infarct border
Morphologic changes in infarction:
7-10 days
Gross: max yellow-tan and soft with depressed red-tan infarct margins
Micro: phagocytosis of dead cells, granulation tissues at margins
Morphologic changes in infarction:
10-14 days
Gross: red-gray depressed borders
Micro: granulation with new vessels and collagen
Morphologic changes in infarction:
2-8 weeks
Gross: gray-white scar
Micro: increased collagen decreased cellularity and fewer capillaries
Morphologic changes in infarction:
>8 weeks
Gross: scarring complete
Micro: dense collagenous scar (blue on trichrome stain)
Lab diagnosis of MI:
CPK/CK
- CK-MB in heart (rises within 2-4 hrs peaks at 24 hours
- sensitive but not specific
- elevated in other stuff too
Lab diagnosis of MI:
Troponin
- T and I are specific for cardiac muscle
- early phase: release of free cytosolic troponin, detectable in 2-4 hours
- late phase: levels peak at 48 hrs, but persist for 10-14 days
