Cardiovascular Path 2 Flashcards
What are 4 features that make a fibrous plaque unstable?
- thin fibrous wall
- lots of inflammatory cells in the plaque
- more lipid than fibrous tissue
- spasm of the coronary artery on top of narrowing
What are the three types of angina pectoris?
- stable
- prinzmetal (variant)
- unstable (crescendo)
Which type of angina is associated with increased demand (physical activity, emotional excitement, stress, etc)
Stable (typical) angina
How do patients with stable angina relieve their pain?
Rest and vasodilators
What type of angina can occur at rest?
Prinzmetal (variant) and unstable (crescendo)
Which angina occurs at rest and awakens the patient from sleep?
Prinzmetal (variant)
What angina is associated with a ST elevation on ECG, indicative of ___________
Prinzmetal;
Transmural ischemia
_______ angina occurs due to coronary artery spasm producing a transient squeezing chest pain
Variant/prinzmetal
What is the mechanism of unstable angina?
Disruption of the plaque with superimposed thrombosis and possibly vasospasm
Patient has chest pain that has been getting worse and occurring more frequently with doing less and less effort and lasts a long time. What kind of angina is this?
Unstable
Which angina is the pre infarction angina?
Unstable
What is the major issue in variant/prinzmetal angina?
Coronary spasm; not necessarily due to coronary artery narrowing
What are the 4 major predisposing factors to MI?
- hypercholesterolemia
- smoking
- HTN
- Diabetes mellitus
Irreversible cell injury in MI occurs after ________
20 mins (coagulative necrosis)
What kind of MI is associated with cocaine abuse?
Transmural infarction (STEMI)
Which layer of the heart is the one that is the most susceptible to hypoxia?
Subendocardium because it is the farthest from the blood supply
In cases of global hypoxia such as shock, what layer of the ventricular wall is affected?
Only the subendocardium = (NSTEMI)
STEMI is associated with acute plaque changes and ________ thrombosis
Acute plaque changes and super imposed completely occlusive thrombosis
Describe the infarction you see in an NSTEMI?
Subendocardial infarction that is limited to the inner 1/3 of the ventricular wall
NSTEMI is associated with _________ or prolonged hypertension/hypotension
Diffuse stenosis coronary atherosclerosis or prolonged HYPOTENSION
What are the three different types of infarcts you can see in non transmural infarcts?
- regional subendocardial: transient/partial obstruction
- circumferential subendocardial infarct : global hypotension
- microinfarcts: small intramural vessel occlusions
4 major sequence of events of MI
Coagulative necrosis → inflammation → granulation tissue → collagen rich scar tissue
How long after an MI would you need to see gross changes to the heart indicative of an MI?
At least 4 hours (dark mottling on gross and early coagulation necrosis on histology)
When is the mycarodium (ventricles) the most vulnerable to rupture after an MI?
3-10 days after an MI because all the myocardium in the area is dead and there is no replacement of fibrous tissue
At what time frame is a patient most susceptible to developing cardiac tamponade after an MI?
3-10 days which is when the ventricles are the most susceptible to rupture
Maximum softening (no myocytes/no collagen) occurs _________ days after an MI
7-10
How long does it take for scarring to be complete after an MI
2 months
When can you see wavy fibers on cardiac myocytes histology after an MI?
4 hours;
reperfusion following an MI is achieved by:
- thromboylysis by using enzymes like streptokinase or tissue plasminogen activator
- angioplasty
High extracellular calcium and impaired calcium cycling leads to myocyte __________ leading to cytoskeletal damage
Hypercontracture;
Calcium causes the tropomyosin to move and so the myosin can bind to the actin and then cause contraction. However because in an MI, there is no more ATP left, that actin/myosin bond cannot be released → hypercontraction
Name 4 mechanisms of reperfusion injury following an MI
- mitochondrial dysfunction → apoptosis
- cytoskeletal damage due to myocyte hypercontraction
- free radical damage
- leukocyte aggregation and platelet activation
What is a classical sign of reperfusion injury on histology?
Contraction band necrosis; due to the high calcium levels from the restored blood flow that enters the ischemic myocytes. What you see is the actin myosin interaction in the absence of ATP → sarcomeres stuck in agonal tetanic state
Following an MI, the ______ of the myocyte falls to near 0 VERY QUICKLY while the _____ of the myocyte falls after 20 mins and not as precipitously
Fucntion; viability
What is the effect of reperfusion after an MI on the viability and fucntion of the myocyte?
Viability: does not go any Lower (also does not make it go higher)
Function: increases function
What features of chest pain see in an MI makes it different from that seen in angina?
- the pain is persistent and longer than 30 mins (unlike angina)
- pain is not relieved by vasodilators or rest
Define angina pectoris
- intermittent chest pain or discomfort due to transient, reversible myocardial ischemia but not quite infarction
Describe the pulse seen in someone suffering from an MI?
Rapid, weak pulse
What kind of patients can undergo an painless MI (silent MI)
- diabetics
- patients who have undergo an cardiac transplant
Th most common cause of sudden cardiac death is _______
Arrhythmias
Factors that can cause arrhythmia following an MI
- myocardial irritability and conduction disturbances
- electrolyte imbalance
- hypoxia
Ventricular aneurysm is a complication of _________ infarcts after ______ days post MI
Transmural; after 2 weeks - months (true ventricular aneurysm)
Acute fibrinous/fibrinohemorrhagic pericarditis is a likely compilation _________ days after an MI
2-3 days
Acute fibrinous/fibrinohemorrhagic pericarditis is due to ________________ in transmural infarcts
Direct irritation of pericardium; 2-3 days after MI
What is the pathogenesis of autoimmune pericarditis aka _____________ and when is the highest risk of developing it post MI
Dressler’s Syndrome
Autoantibodies that target damaged pericardial antigens
10-14 days following an MI
Complication for what kind of pericarditis occurs 10-14 days post MI?
Autoimmune/ Dressler’s Syndrome
T wave depression may be seen in _______ infarct causing MI
Subendocardial
What is the most specific marker for cardiac injury?
Troponin I and T; not usually detectable in circulation but rises in 3-12 hours and peaks at 48 hours and persists for 5-14 days
________ levels post cardiac injury peaks after 48 hours
Troponin I and T
________ marker of cardiac injury is useful in detecting reinfarction
CK-MB (CK MB is the most specific creatine kinase isoenzymes for the heart)
Which cardiac injury marker cannot be used after 3 days post MI?
CK - MB:
Rises: 3-12 hours
Peaks: 24 hours
Disappears: 72 hours
_______ rises in 24 hours and peaks at 3-6 days and returns to normal levels after 8-12 days
LDH
When do the levels of Tropinin I and T rise, peak, and disappear
Rise: 3-12 hours
Peaks 48 hours
Persists for 5-14 days
What is the first biomarker to rise after an MI?
Myoglobin (1-4 hours) but it is non specific to the heart
When do the levels of CK MB rise, peak and disappear?
Rise: 3-12 hours
Peak: 24 hours
Disappear: 72 hours
When do the levels of LDH rise, peak and disappear following cardiac injury?
Rises: 24 hours
Peaks: 3-6 days
Returns to baseline: 8-12 days
Diffuse subendocardial vacuolization aka ___________ is a histological finding in what cardiac disease?
Myocytolysis; seen in chronic ischemic heart disease
