04.21 - Ischemic HD 1 (Nichols) Flashcards
Ischemic Cardiac myocytes die after about
20 minutes
___ often triggers the acute coronary syndromes
Thrombosis associated with a disrupted plaque
2/3 of ruptured plaques are ___ stenotic or less before rupture
50% (so they would be asymptomatic)
3 Components of Coag Necrosis
(1) Loss of Normal Cytoplasmic Striations; (2) Cytoplasmic Hypereosinophilia; (3) Nuclear changes
4 features that are “more” in Reperfusion MI
Contraction Band Necrosis, Macrophages, Interstitial Fibrosis, Patchy
90% of Transmural MI’s are associated with
Occlusive thrombosis superimposed on athersclerotic plaque with an acute change (disruption of plaque)
Acute Coronary Syndrome is applied to
Any of the 3 catastrophic manifestations of IHD: Unstable Angina, Acute MI, and SCD
Additional benefit of statins in CAD and IHD
Reduce plaque inflammation and increase stability
Are myocytes with Myocytolysis viable?
Yes, can be (but less effective)
Asystole from MI is usually preceded by
V Tach, then V Fib
By 12-24 hours, infarct can be grossly ID’d how?
Red-blue discoloration caused by stagnated, trapped blood
Cardiac Rupture is more common in
Females, Older patients, Hx of HTN, first MI, Anterior Wall
Clinically significant coronary plaques tend to occur
first few cm’s of LAD and LCX, and entire legnth of RCA
Colors of Acute, Subacute, and Old MI
Light brown, tain; Yellow; White
Critical Stenosis
70% of lumen
Cut off for gross appearance of MI (no stain)
12 hours
Dead myocytes in classic MI show what type of necrosis?
Coagulative
Death of myocytes in transmural MI starts
in the Subendocardial Zone, spreads to Subepicardial Zone
Earliest finding of Classic MI
Thin Wavy Myocytes (30minutes)
ECG evidence of Ischemia includes
ST-segment elevation and T-Wave Inversion
Explanantion for why incidence of MI is highest between 6am-12pm
Adrenergic stimulation with waking
Extensive Nuclear Dust is a feature of infarcts of what age
3-6 days old
Fissure frequently occur at
junction of fibrous cap and adjacent normal plaque-free arterial segment
Fixed obstructions that occlude less than __ of a coronary vessel lumen tend to be asymptomatic
70%
How does Myocardial Ischemia contribute to arrhythmias
Electrical Instability
How early can thin wavy myocytes appear as evidence of MI
30 minutes
How long before dead cardiac muscle shows macroscopic manifestations of death?
12 hours
How long does death of myocytes take in Transmural MI
3 hours
How long does it take for dead myocytes to show microscopic evidence of death?
4 hours
How much of ventricular thickenss has to be affected to classfiy as transmural
50%
I, aVL, V5-V6
Lateral: Left Circumflex
IHD is usually synomous with
CAD, unless otherwise specified
II, III, aVF localize MI to where?
Inferior: Right Coronary
In more than 90% of cases, IHD is a consequence of
Reduced Coronary Blood Flow secondary to obstructive atherosclerotic vascular disease
In most patients, unstable angina, infarction, and often SCD occur b/c of
Abrupt plaque change followed by thrombosis
Leading cause of mortality in US and developed nations
Ischemic HD
Most common cause of death in elderly women?
IHD (menopause, and decline in estrogen, exacerbates CAD)
Myocyte death leads to what type of necrosis
Coagulative
Myocytolysis
Cytoplasmic clearing of contractile proteins; Seen in Thin Subendocardial layer of cardiac myocytes after infarct
Occlusion of what coronary artery is most often responsible for MI
LAD (40-50%)
Organizing thrombi produce potent activators of
SM proliferation
Pain of Stable Angina
Crushing or squeezing, often radiating down left arm
SCD in setting of myocardial ischemia is most often due to
V Fib caused by Myocardial Irritability (80-90% of cases)
Severe ischemia lasting at least ___ causes irreversible damage
20-40 mintues
Subendocardial Infarction vs Transmural
More likely to be patchy, have episodic extension, becoming more common
Sudden Cardiac Death most commonly results from
a lethal arrhythmia without myocyte necrosis
T/F: HF from MI is often sudden
False, rarely sudden
T/F: Left and Right ventricular infarcts occur at comparable frequency
False, isolated right 1-3%
T/F: Once an MI is healed, it is impossible to distinguish its age
True can be 8 weeks or 10 years old
T/F: Plaque ruptures are often predicatble
FALSE
T/F: Prinzmetal angina always occurs at atherosclerotic plaques
FALSE
T/F: significant atherosclerosis and thrombosis of penetrating coronaries is also relatively common
FALSE
T/F: Women have higher risk of MI during reproductive years?
False, protective effect
The PDA usually arises from which other artery
RCA (90%), or LCX
The vast majority of MI’s are caused by
Acute Coronary Thrombosis
Typcial ECG findings in Subendocardial Infarctions
Typically do not have ST elevation or Q waves
Typical ECG findings in Transmural Infarctions
STEMI, negative Q wave, loss of R wave amplitude
V1-V4 localize MI to where?
Anterior: LAD
Vacuolated (cleared) cytoplasm =
Myocytolysis
What causes destabilization of atherosclerotic plaque
Macrophage Metalloproteinase Secretion
What causes Myocyte Vacuolization
Sublethal ischemia
What color is a Subacute MI
Yellow
What color is an Acute MI
Light brown to tan
What color is an old MI
White
What determines dominant vessel of heart
The one, either RCA or LCX, that gives of the PDA
What does Coagulation necrosis look like histologically
Hypereosinophilia, Loss of Striations, Nuclear Chanes
What is becoming more common than Transmural MI
Subendocardial Infarction
What is Prinzmetal Angina
Caused by vessel spasm
What is stable angina
Occuring predictably at certain levels of exertion
What is the widow maker lesion
Occlusions in Left Main
What is unstable angina
Occurs with progressively less exertion or even at rest
What leads localize to LAD MI
V1-V4
What leads localize to Left Circumflex (Lateral) MI?
I, AVL, V5-V6
What leads localize to Right Coronary (Inferior) MI?
II, III, aVF
What percent stenosis causes Unstable Angina
90%
What serves as nidus for thrombus generation in most instances of MI
Disruption of pre-existing athersclerotic plaque
What type of myocytes may be visible as early as half hour after infarct?
Dead thin wavy
What types of plaques are more likely to rupture
Large atheromatous cores, or have thin overlying fibrous caps
When are features of Coag Necrosis visible microscopicaly
4-12 hours
When are infarcts ringed by hyperemic granulation tissue
10-14 days
When can MI’s be visualized grossly with vital stain
3 hours (LDH stain)
When do Fibroblasts first enter in Classic MI
Day 4
When do Lymphocytes first enter in Classic MI
day 2
When do Macrophages first enter in classic MI
day 3
When do neutrophils in acute MI begin contributing their breakdown debris
After a few days
When does Acute Neutrophilic Response to Acute MI reach maximum
Around 2 days
When does neovascularization occur in Classic MI?
Day 4, same as fibroblasts
When is acute inflammation most prominent following MI
1-3 days after
When is Cardiac Rupture most common following MI
5th day
When is granulation tissue replacement most prominent
1-2 weeks after
When is Neutrophilic Infilatration visible following Classic MI
6-12 hours
When is wave of macrophages most prominent following MI
5-10 days after
Where is the fibrous cap the thinnest
Junction of fibrous cap and adjacent normal plaque-free arterial segment
Which are more affect by MI: blacks or whites?
Equal
