Pathology of Heart Disease II and III Flashcards
****How long ago did this MI occur? why?
3-4 weeks ago - because there is extensive collagen with few remaining fibers
*****What has occurred here?
Apical Left Ventricular Aneurysm
What findings are you likely to see at at the GROSS and LIGHT MICROSCOPY level at the following time points following a heart attack?
- 10-14 days
- 2 months
10-14 days
Gross: Red-Grey
LM: New vessels and collagen deposition
2 months
Gross: Scar
LM: DENSE COLLAGENOUS SCAR
**cor pulmonale
Right Side Ventricular enlargement due to primary lung dysfunction
What is the Appearance of a Heart in someone that has Chronic Ischemic Heart Disease?
**LEFT Ventricular HYPERTROPHY and DILATION -often you can see scarred areas of pervious healed infarcts
*****WHAT IS THIS????
MURAL THROMBOSIS
**Collateral Circulation
• why could this be important in ischemic heart disease?
• ischemic heart disease is caused by poor fluid flow through vessels. If this occurs slow enough collateral circulation may form allowing for tissue perfusion despite complete occlusion of Coronary Arteries.
***When did this Myocardial Infarction probably occur?
3-7 days ago - gross appearance of necrosis with hyperemic area surrounding it
**Thrombus
•what often causes this in IHD?
IHD - most often caused by Atherosclerosis, therefore most thrombi likely form due to EXPOSED NECROTIC TISSUE or SUBENDOTHELIAL collagen from a plaque
****What changes can you see in the heart as a result of the thrombus?
• Ischemic changes are seen (before coag. necrosis). You can see DARKENING of the myocytes as they become a deeper red color
*****What is seen in this histology (move from left to right) ?
• Reversibility of Injury?
- endocardium - may not be dead, still fairly pink
- Myocardium (left) - Definitely dead - Vacuolar changes and Absence of nucleus conferms this
- Myocardium (right) - still fairly well perfused but we can see Spead out and Swollen Cells
Prinzmetal Angina
• cause
• angina type
STABLE angina caused by vessel spasm
What is this?
Chronic Cor Pulmonale - Right Ventricle is Dilated and Hypertrophied with HUGE trabeculae
****When did this MI occur? why?
1-3 weeks ago because you can see macrophages and fibroblasts
****Was the appearance of the heart here most likely caused by an acute event or chronic?
• how do you know?
• Collateral Circulation development implies that this happened over an extended period of time
****What is seen here?
• Boxcar nucleus in top left corner of picture - indicative of hypertension (specifically pulmonary HTN in this pt)
What does ACUTE CORONARY SYNDROME refer to?
any of the three catastrophic manifestions of IHD
- UNSTABLE ANGINA
- ACUTE MI
- SCD (sudden cardiac death)
****What is wrong with the appearance of this left ventricle? why has this happened?
• Left Atrium - Dilated due to HUGE HYPERTROPHIED ventricle (probably the result of HTN)
****When did this MI most likely occur?
• 1-2 days before death
• You can see contraction bands and neutrophils
• most nuclei are gone
• acute inflammation is kicking in
*****When did this MI occur?
• what intervention likely took place to stop it?
• histological features?
- Day 1 after MI
- Contraction Bands and Lack of Nuclei indicates Necrosis
• Contraction bands may have been caused by placement of a stent when the patient was hospitalized (or pt. may have naturally cleared clot)
****When did this myocardial infarction occur? why?
2-3 days ago
- Extensive acute inflammatory infiltrate
- Myocardial fibers are necrotic with no nuclei
What findings are you likely to see at at the GROSS and LIGHT MICROSCOPY level at the following time points following a heart attack?
- 12 - 24 hours
- 3 - 7 days
- 7 - 10 days
12 - 24 hours
Gross: Dark Mottling
LM: Neurtophilic Infiltrate; Marginal contraction with BAND necrosis
3 - 7 days
Gross: Yellow tan Soft
LM: Macrophages
7 - 10 days
Gross: Yellow tan Soft
LM: Granulation Tissue
What is Ischemic Heart Disease?
• Most common cause?
- consequence of reduced coronary blood flow
- 90% of cases of Ischemic Heart Disease are due to ATHEROSCLEROTIC VASCULAR DISEASE
***What is the darker colored material in this artery?
Calcium
• Note: this plaque looks pretty stable with lipid core being completely surrounded by fibrous tissue
When did this MI probably occur? why?
Months ago - lots of Scar Tissue
• In what part of Coronary Arteries is Atherosclerosis most commonly seen? why?
- Most commonly seen at the proximal end of the coronary vessels
- This is the area where flow is the MOST TURBULENT
****What is the youngest this infarct can be?
**3 months at the youngest because of how extensive the collagen deposition is.
What two early interventions are very effective at minimizing damage caused by clogged coronary arteries?
• Risks associated?
- Thrombolysis (alteplas) - may shoot microemboli to brain
- Angioplasty - may cause reperfusion injury
What are two causes of sudden cardiac death?
- **HUGE MI or
- ARRYTHMIA (even w/o myocyte necrosis)**
**Ischemia
Lack of Blood Flow to Tissue
What gross changes in the heart would you see in a hypertensive patient?
• Ventricular Hypertrophy from Pressure Overload because myocytes must adapt to push against increased afterload
How long does it take myocardium to lose function in ischemic injury?
• What are some cellular changes that have occured?
Time:
• No perfusion for 1 minute leads to LOSS OF FUNCTION
Damage:
• Tissue damage at this point is likely reversible
• involves: myofibrillar relaxation, glycogen depletion, mitochondrial swelling
(note: glycogen depleted b/c of ineffecient glycolysis used for energy instead of ox-phos)
**Angina Pectoris Stable vs. Unstable
• Differentiate in Terms of Symptoms and Occlusion.
Stable Angina
• 70% of More occlusion
• chest pain on exertion
Unstable Angina
• 90% of More occlusion
• Occurs with less exertion or even while resting
*****What is seen here?
**Boxcar nuclei in the myocardium of a Hypertensive Patient (note: this can be due to pulmonary hypertension too)
What chemical markers are used for Myocardial Infarction?
• Times when they are the most useful?
Myoglobin - Peaks 1st ~4hrs and rapidly declines
• NOT SPECIFIC could be raised after excercise
CK-MB - Peaks ~10hrs and declines much more slowly
• More Specific
Troponin I - Peaks at around 1 day
• Very Specific - slow to rise but stays up for a long time
*****What is seen here?
• Myocardium of a Normal Adult
Contraction Bands
• what are they associated with?
• where are they typically seen?
• CAUSE?
Association:
• REPERFUSION, perioperative ischemia (during surgery), Sudden Cardiac Death
Where:
• Typically at margin of infarct in MI
CAUSE: ****
• HYPERCONTRACTION due to massive calcium influx
**Mural Thrombus, que es?
Thrombus that forms on the wall of an organ (typically wall of atria or ventricles if they are not contracting properly and blood is becoming stagnant) - e.g. fibriallation
T or F: ischemia even if not peristent may causes improper heart contraction and cause electrical instability.
TRUE - you may get rid of the thrombus but the heart still won’t work right
***what has occured here?
Recent Infarct with stretching and thinning of myocardial wall
What are the steps in athlerosclerotic plaque formation?
- Endothelial Cell injury attracts Luekocytes
- Macrophages come in with T-cell (secrete IFN-gammma)
- MATRIX is produced over the athlerosclerotic LIPID CORE
- METALLOPROTEINASES (secreted by macrophages) Destabilize Plaques
- Plaque Rupture and THROMBOSIS
***Would you suspect that this patient has chest pain?
• At Rest or on Exertion?
YES, this is ~90% occlusion so they probably have unstable angina and have pain even while at rest
How can someone survive with a COMPLETE occlusion of their Left Antierior Descending (LAD) coranary artery?
• If this occlusion happened slow enough it is possible that collaterals developed between it and another coronary artery
****What has occured here?
• Fibrinous Pericarditis
****When did this person’s MI occur?
• what is likely the gross appearance?
Wavy Fibers = 1.5-4 hours
BUT we see some neurtophils (12-24 hr marker) and dissappearance of nuclei so it may actually be a bit older
***NO Changes in the gross appearance have occurred yet (these start at >12 hours)
What cuases Chronic Ischemic Heart Disease with Congestive Heart Failure?
- Progressive Cardiac Decompensation after an acute Myocardial Infarction
- Small ischemic insults eventually causing failure
When are you at the greatest risk of developing an aneurysm as a result of MI?
• mural infarcts may leave behind thinned/weakened scar tissue that may become an aneurysm
****What has happened here?
• Myocardial Infarction - graying out of endocardium indicates that no blood is getting there = coagulative necrosis
****When did this injury likely occur? why?
1-3 weeks ago because you can see new blood vessel formation and debris from dead myocytes
**Critical Stenosis
- Classified as having 70% occlusion of the vessel lumen if - these people typically have stable angina
- Greater than 90% occlusion people probably have unstable angina
What are some complications of infarction?
- Ventricular Muscle Rupture
- Papillary Muscle Rupture
- Aneurysm Formation
- Mural Thrombus
- Arrhythmia
- Pericarditis
- CHR
At what point does irreversible myocardial damage occur?
• Severe ischemia lasting longer than ~20-40 minutes causes myocyte death and coagulative necrosis
**Contraction Band
Caused by Reperfusion injury - result of EXCESS CALCIUM release in the cells
What marker is most useful in measuring a re-infarct?
CK-MB, because Troponin will stay elevated but another spike in CK may indicate a patient has had a second infarction
****When did this MI likely occur? why?
1-3 weeks ago because we see MACROPHAGES, Vessel formation, and debris from dead myocytes
****What has occurred here?
Anterior wall Myocardial Rupture
Someone occlusions of coronary vessels spontaneously resolve. How does this happen?
• Occlusions may clear by lysis or relaxation of spasm
When is myocardial rupture most likely to occur? where?
Most likely 3-7 days post-infarction - being FEMALE and OVER 60 are some risk factors for this happening
*Most often occurs in anterior ventricular wall
*Results in Hemopericardium
****NOTE: this is not associated with aneurysm which occurs months after MI
**Cardiac Tamponade
*During the first 3-7 days when the heart is most suscepitble, it may rupture and leak a TON of blood into the pericardium leading to compression of the heart and inability to beat (the latter process = TAMPONADE)
**Arrhythmia
Can result from MI
What is Cor Pulmonale?
• Right Ventricular Hypertrophy and Dilation due to Primary Disorders of the lung parenchyma or pulmonary vasculature
T or F: myocytes actually die in myocardial infarction.
True
Who are you most likely to see a myocardial infarction in?
• MOST COMMON CAUSE?
- Males WHITE OR BLACK between 40 and 60
- After Menopause they are common in women too
- MOST myocardial infarctions are from ACUTE CORONARY THROMBOSIS
****What is this called?
• when is likely to occur in association with an MI?
Hemopericardium - 3-7 days after an MI if the wall ruptures
What are the other causes of Ischemic Heart Disease (aside from 90% of cases caused by athlerosclerosis)?
• Give Examples of Each of these Processes
- Increased Demand - with increased HR or Hypertension
- Diminished Blood Volume - seen in HYPOTENSION and shock (e.g. gunshot wound)
- Diminished Oxygenation - due to pneumonia or CHF
- Diminished O2 carrying capicity - Anemia or Lead Poisoning
**Aneurysm
****What has occurred here?
Papillary Muscle Rupture
****When did this MI likely occur? why?
Months ago - EXTENSIVE collagen deposition has occurred, myocytes have NO nuclei
**Congestive Heart Failure
****What is seen here?
- SEVERE athlerosclerosis of Aorta
- Atheromatous Plaques have undergone ULCERATION
- Ulceration has resulted in Overyling mural thrombus
What is your most probable site of injury in occlusion of:
• Left Anterior Descending Coronary Artery
• Right Coronary Artery
• Left Circumflex Coronary Artery
LAD:
- Antertior APEX of Left Ventricle
- ANTERIOR 2/3 of intraventicular Septum
RCA:
- Posterior Left Ventricle
- Posterior 1/3 of Intraventricular Septum
LC:
• Lateral Left Ventricle
When risks are associated with a ruptured myocardium?
• Hemopericardium which can lead to Tamponade
What do arrhythmias put patients at a high risk of?
Arrhythmia puts you at a risk of MURAL THROMBOSIS
What are some causes of chronic cor pulmonale?
Emphysema, COPD, Alpha-1-antitrypsin
**Myocardial Infarct
Death of tissue in myocardium typically 20-40 minutes after arterial occlusion in the coronaries
**Atherosclerotic Vascular Disease
• what Heart problems (beside heart attack) does this often lead to?
• Often leads to ischemic heart disease
****What process has occurred here?
Athlerosclerotic Plaque Rupture - causes by exposure of the atherlosclerotic lipid core/collagen to clotting factors
What happens in to the following during Angina?
• Blood Supply
• Sensation
• Myocytes
Ischemia is occuring, which is painful BUT does NOT cause MYOCYTES to die.
What often causes acute cor pulmonale? What changes will the heart shwo?
Caused by EMBOLISM typically leads to right ventricular DILATION (not hypertrophy)
What is a transmural infarct?
• What piece of tissue in that area remains perfused?
- Transmural infarct = full thickness of the myocardium
- Typically the Subendothelial area remains perfused because of exposure to blood within the heart
What is the underlying process that causes most of ischemic heart disease?
- Athlerosclerosis causes MOST IHD
- Underlying cause of Athlerosclerosis = INFLAMMATION
What microscopic appearance would you expect to see in the heart tissue of a hypertensive patient?
- Increased Transverse Diameter
- Nuclear enlargment with hyperchromasia = BOXCAR NUCLEI - this appearance comes from increased DNA production needed for cellular hypertrophy
• intracellular fibrosis
What findings are you likely to see at at the GROSS, LIGHT MICROSCOPY, and EM level at the following time points following a heart attack?
- 0 - 1.5 hours
- 1.4 - 4 hours
- 4 - 12 hours
0 - 1.5 hours
Gross - nothing
LM - nada
EM - Relaxation of Myofibrils; Glycogen Loss; Mitochondrial swelling
1.5 - 4 hours
Gross - none
LM - maybe Wavy Fibers
EM - Sarcolemmal Disruption; mitochondrial amorphous densities
4 - 12 hours
Gross - none
LM - Edemia and Hemorrhage, coagulative necrosis
EM - not important at this point
**Reperfusion Injury
Caused by blood rushing back into tissue leading to PMN infiltration and ROS from O2, characterized by contraction lines
**Hypertension
Causes increased afterload and boxcar nuclei that are hyperchomic due to increased DNA production to allow for ventricular hypertrophy (a compensatory mechanism to try to maintain SV)
****What has occurred here?
Ventricular Septal Rupture
***What is shown here?
Coronary Atherosclerosis complicated by Hemorrhage into the atheromatous Plaque
• This is more like an ulceration where an exposed area has been carved out by the metalloproteinases and you get bleeding of the plaque?
**Thromboembolism
• Thombus that gets displaced and most likely will infarct another organ or area
What sequence of events leads to thrombus formation after plaque rupture?
- Atheromatous plaque is suddenly disrupted by intraplaque hemorrhage or mechanical forces => necrotic plaque tissue and collagen is exposed
- Platelets adhere (via vWF Gp1b and Gp1a/11a) and release TXA2, ADP, and Serotonin => more aggregation and vasospasm
- Tissue Factor initiates Coag. cascade
- within MINUTES complete occlusion can occur
When are you most likely to get the following after a Myocardial Infarction?
- Pericardial Friction Rub
- Aneurysm
- Mural Thrombus
- Autoimmune Pericarditis (Dressler syndrome)
- Rupture of ventricular Wall/IV septum/Papillary m.
- Arrythmia
- Mural Thrombus - 1.5 - 4 hrs.
- Arrythmia - within 12 hours
- Pericardial Friction Rub - 2-3 days
- Rupture of ventricular Wall/IV septum/Papillary - 3-6 days
- Autoimmune Pericarditis (Dressler syndrome) - 1-8wks
• Aneurysm - months
