L19- CVS Pathology II Flashcards
list the 4 consequences of IHD
- angina pectoris (AP)
- MI
- chronic IHD w/ CHF
- sudden cardiac death (SCD)
define AP and name its 3 types
angina pectoris: intermittent chest pain / discomfort due to transient / reversible (<30 mins) myocardial ischemia (severe with radiation of pain, but not quite an infarction)
- Stable, typical
- Prinzmental, variant
- Unstable, crescendo
alternate names for:
(1) stable AP
(2) variant AP
(3) unstable AP
1- typical
2- prinzmetal
3- crescendo
how does age, gender, and race relate to incidences of MIs
Age: at any age, but incidences inc w/ age
Gender: M:F
- (45-54 y/o) 5:1
- (55-80 y/o) 2:1
- (>80 y/o) 1:1
Race: equal among black and white people
list the 4 major contributing factors for MI
- hypercholesterolemia
- smoking (vasoconstriction, atherosclerosis, microvascular disease, high [CO])
- HTN
- DM (exaggerates atherosclerosis + microangiopathy affecting small BVs/capillaries)
90% of MIs are a result of (1), usually involves (2)
the other 10% are a result of (3), (4), (5)
1- acute thrombosis (–> coronary artery occlusion)
2- disruption of pre-existing plaque
3- vasospasm (isolated, intense, prolonged w/ or w/o coronary atherosclerosis)
4- emboli (via L sided mural thrombus)
5- unexplained (disease of small intramural coronary vessels or hematological abnormalities)
describe the biochemical events in the heart during MI, indicate timing
i) stop aerobic metabolism –> dec ATP, inc lactic acid (accumulates in myocytes), seconds
ii) ATP at 50% normal levels, 10 mins
iii) ATP at 10%, 40 mins
describe the changes in heart function during MI, indicate timing
loss of contractility, <2 mins
describe the (cellular) morphological events in the heart during MI, indicate timing
- reversible injury (cell swelling), <20 mins
- irreversible injury (coagulative necrosis), 20-50 mins
- microvascular injury, >1 hr
list the 3 morphological types of MIs
i) transmural
ii) subendocardial
iii) microscopic
(1) type of MI involves the full thickness of the ventricular wall in the disruption of (2), termed (3). It is usually associated with (4) and (5). It can also occur in (6) abuse.
1- transmural
2- single coronary artery (regional)
3- STEMI
4- acute plaque changes
5- superimposed / completely occlusive thrombosis
6- cocaine (inc catecholamines => severe vasospasm)
(1) type of MI is limited to affecting the inner 1/3 (or at most inner 1/2) of ventricular wall, termed (2). It is associated with (3) or (4). It may occur due to (5) type of obstruction.
(less serious than transmural)
1- subendocardial
2- NSTEMI
3- diffuse stenosing coronary atherosclerosis
4- prolonged hypotension
5- transient/partial arterial obstruction (regional)
describe the essential sequence of events in MI (4)
1) coagulative necrosis
2) inflammation, then resorption of necrotic myocardium
3) granulation tissue forms
4) granulation tissue organizes into collagen rich scar tissue
Describe heart histology / events post-MI at the following days:
- day 1
- day 3
- days 7-10
- step 1 after day 10 (day 11-14 –> 2-8 wks)
- step 2 after day 10 (2 mos+)
1- coagulative necrosis + wavy fibers
2- dense PMN leukocyte infiltration
3- removal of necrotic myocytes by phagocytosis
4- granulation tissue: loose collagen, abundant capillaries
5- healed MI, necrotic tissue replaced with dense collagenous scar + residual cardiac muscle hypertrophy
The initial goal during a MI is to initiate (1) either through (2) or (3). Although it is important and useful, (4) is a potentially dangerous outcome.
1- reperfusion
2- thrombolysis via enzymes: streptokinase, tissue plasminogen activator (<30-40 min onset)
3- angioplasty, CABG
4- reperfusion injury
describe the 4 (cellular) factors that lead to Reperfusion Injury (in terms of MI)
i) mitochondrial dysfunction => apoptosis (promotion)
ii) high extracellular [Ca] / impaired Ca cycling –> myocyte hypercontracture –> cytoskeletal damage (=> dark constriction band necrosis)
iii) free radical production after reperfusion => myocardial damage
iv) leukocyte aggregation + platelet activation –> microvasculature injury / occlusion (no reflow phenomenon)
describe the 2 morphologies of reperfusion injury post-MI
1) hemorrhage: vascular injury, leakiness
2) contraction band necrosis: hypercontracted sarcomeres show hyper-eosinophilic transverse bands via high extracellular [Ca] due to leaky plasma membrane + low ATP leaves actin-myosin interactions stuck
list the clinical features (presentation) of a MI
- CHEST PAIN: retrosternal, crushing, with radiation to neck, jaw, epigastrium, shoulder, L arm; persistent for >30 mins; no relief from vasodilators or rest
- dyspnea
- rapid weak pulse
- diaphoresis, n/v
25% of MI cases are (1), where they are discovered through (2). This is more common in (3) patients, usually with (4).
1- silent MIs (neuropathy)
2- EKG changes + lab tests
3- elderly
4- DM, HTN
list the 5 categories of post-MI complications
- ischemic
- arrhythmic
- embolic
- mechanical
- inflammatory
list the ischemic complications post-MI (hint- 3)
- extension of infarction
- reinfarction
- angina
_____ is the most common cause of SCD
(sudden cardiac death)
arrhythmias
list the factors that can produce an arrhythmia post-MI (hint- 3)
- myocardial irritability + conduction disturbances
- electrolyte imbalance
- hypoxia
(ventricular fibrillation, due to ischemia to nerve supply)
Post-MI, a (1) can form as a possible complication due to wall abnormalities and endocardial damage. (1) commonly form in (2) of the heart, and leads to (3). They most common result of (3) is (4), but the following may also occur: (5).
1- mural thrombus 2- LV 3- systemic emboli 4- stroke 5- limb ischemia, renal infarction, mesenteric ischemia
list the 4 mechanical complications post-MI
- contractile dysfunction
- papillary muscle dysfunction
- myocardial rupture
- ventricular aneurysm
Contractile dysfunction post-MI depends on (1) and can cause (2) type issues. If severe enough, (3) is a dangerous progression. (4) is the other more long-term progression.
1- size, site, thickness of infarct
2- variable range of ventricular failure
3- cardiogenic shock (10-15% of cases)
4- progressive HF (chronic IHD)
Papillary muscle dysfunction occurs secondary to (1), (2), (3). The major consequences are either (4) or (5).
1/2/3- rupture, ischemia, fibrosis (b/c its apart of ventricle wall)
4- mitral valve incompetence
5- tricuspid valve incompetence
Myocardial rupture can occur (1) days after MI because the following, (2), will cause a weakened myocardium. Rupture includes (3) and (4), which are very major concerns.
1- 3-10 days
2- necrosis, neutrophilic infiltration, myocardial tissue lysis
3- ventricular free wall rupture (=> cardiac tamponade)
4- ventricular septum rupture
Ventricular aneurysms are late complications of (1) type MIs. Aneurysms have (2) walls that will bulge during (diastole/systole). (4) are other complication that may occur. Rupture of the wall is unlikely due to (5).
1- large transmural infarcts 2- scar tissue walls 3- systole 4- mural thrombus, arrhthymias, HF 5- tough fibrotic wall
The main inflammatory complication post-MI is (1).
- it can occur in the (2) type, occurring (3) days post-MI because of (4)
- it can also be the (5) type, occurring (6) days post-MI because of (7)
1- pericarditis
2- acute fibrinous / fibrinohemorrhagic
3- 2-3 days
4- direct irritation of pericardium from transmural infarcts
5- autoimmune / Dresslers’ syndrome
6- 10-14 days
7- auto-antibodies target damaged pericardial Ags
list / describe the diagnostic approach or sequence to MIs
1) EKG (to suspect MI)
2) markers of cardiac injury (to confirm MI)
3) echocardiogram (observe MI complications)
4) Others: lipid profile, blood glucose
describe EKG presentation for the 2 evident types of MIs
Transmural (STEMI): **ST segment elevation, Q wave delayed appearance after 6 hrs of onset (possible T wave inversion)
Subendocardial (NSTEMI): no specific changes, **no ST segment elevation, possible T wave depression
list the 4 cardiac markers used for MIs
(in order of appearance)
1) myoglobin
2) troponins
3) creatinine kinase (CK-MB)
4) lactate dehydrogenase (LDH)
Myoglobin is the (1st/2nd/last) biomarker for MIs that rises during (2) time.
1- first
2- 1-4 hrs
- highly sensitive, but not heart specific
- rarely used in practice
Troponins include (1) and (2) as markers for MIs. They are useful because of (3). They rise during (4) period, peak at (5), and persist for (6).
1/2- TnI, TnT 3- highly sensitive, specific markers for the heart, not normally detectable in circulation 4- 3-12 hrs 5- 48 hrs 6- 5-14 days
The creatinine kinase isoenzyme measured for MIs is (1) because of (2). It rises during (3) period, peak at (4), and disappear at (5), therefore it is useful for (6).
1- CK-MB 2- most specific for heart vs CK-MM (muscle), CK-BB (brain) 3- 3-12 hrs 4- 24 hrs 5- 72 hrs 6- detecting reinfarctions
_______ is the cardiac marker used to detect reinfarctions
CK-MB (disappears by 72 hrs)
(1) is the last cardiac marker to appear, rising during (2) period, peaking at (3), and returning to baseline at (4)
1- LDH (lactate dehydrogenase)
2- 24 hrs
3- 3-6 days
4- 8-12 days
how are echocardiograms used in relation to MIs
- helps detect MI complications
- evaluated ventricular function, wall motion abnormalities
- identifies pericardial effusions, valve regurgitation, cardiac tamponade
list the interventions for MI
- primary prevention
- thrombolysis
- defibrillator
- angioplasty
- CABG
(1)% of MI patients suffer from SCD before hospitalization
If reaching the hospital alive, (2)% have an uncomplicated course, (3)% have a complicated course (not necessarily fatal)
1- 25%
2- 10-20%
3- 80-90%
list the complicated course events experienced during MI (indicate % chance)
- arrhthymias, 75-95% (SCD before hospital)
- LVF w/ pulmonary edema (60%)
- cardiogenic shock (10%)
- myocardium rupture (4-8%)
describe how chest pain can be affected or changed in angina pectoris (in comparison to MI)
- worsens with exertion, relief with rest (not seen in MI)
- relief with vasodilators (not seen in MI)
- pain lasts <30 mins
why is the incidence of MIs in females lower in younger people in comparison to men
- estrogen has some cardiac protective factor
- post-menopause female incidence approaches male incidence of MI
Typical / Stable angina presentation:
(1) pain type
(2) when it occurs
(3) what makes it worse/better
(4) EKG
(5) cause
1- crushing, squeezing, transient substernal pain with radiation lasting 15s-15mins
2- physical exertion, emotional excitement / stress
3- rest, vasodilators
4- normal
5- reduction in coronary artery perfusion (fixed stenosis - no myocardial necrosis)
Prinzmetal / Variant angina presentation:
(1) pain type
(2) when it occurs
(3) what makes it worse/better
(4) EKG
(5) cause
1- squeezing, transient substernal pain lasting <30mins
2- rest, sleep
3- vasodilators
4- ST segment elevation
5- coronary artery spasm (in normal or atherosclerotic vessels)
Unstable / Crescendo angina presentation:
(1) pain type
(2) when it occurs
(3) what makes it worse/better
(4) EKG
(5) cause
1- progressive pain with increasing frequency, long duration
2- initially physical exertion, progresses to occur at rest
3- vasodilators
4- normal
5- disruption of existing plaque with superimposed thrombus (possible vasospasm)
discuss the relationship of incidence of MI and pre-existing plaque with stenosis
MI will more likely occur in patient with pre-existing plaques and less stenosis of coronary vessels because patients with those issues are more likely to have collateral coronary blood flow, therefore will have less deadly MIs
when are post-MI patients most susceptible to complications
3-10 days post MI, infarct increases in softness, maximizing at day 10 –> ventricular wall / myocardium is most likely to rupture in this period => various post-MI complications
describe the gross and histological appearance of chronic IHD
Gross: enlarged, heavy heart due to dilation, hypertrophy with gray/white scars from previous MI and patchy fibrous mural endocardium thickening
Histo: myocardial hypertrophy, diffuse subendothelial vacuolization (Myocytolysis), scars from previous infarcts
most common cause of SCD in adults is (1) and in children are (2)
(sudden cardiac death: w/o Sxs or w/in 24 hrs of Sx onset)
1- CAD
2- various congenital defects, secondary infections, etc.
the ultimate mechanism of death in SCD is (1)
it has either a (2) or (3) appearance / morphology
1- lethal arrhythmias
2- (80-90%) critical stenosis of one or more coronary arteries with acute plaque disruption
3- (10-20%) non atherosclerotic origin
