Ischemic Heart Disease Flashcards
(44 cards)
1
Q
name the ischemic heart disease (IHD) syndromes
A
- angina pectoris (chest pain)
- stable angina
- unstable angina
- prinzmetal angina
- acute MI
- chronic IHD with CHF
- sudden cardiac death (SCD)
2
Q
describe the etiology of IHD
A
- etiology:
- atherosclerosis - 90% of cases
- other causes of ischemia:
- anemia → hypoxemia
- lowered systemic blood pressure → shock
- increased cardiac demand → hypertrophy exercise
- vasculitis
- aortic dissection
3
Q
describe the pathogenesis of IHD
A
- complex dynamic interaction between the following factors:
- coronary artery obstruction (fixed)
- acute plaque changes
- coronary intraluminal thrombosis
- vasoconstriction
4
Q
>90% of patients with IHD have atherosclerotic lesions that cause ___ of one or more coronary arteries
progressive plaque growth → ____
A
>90% of patients with IHD have atherosclerotic lesions that cause stable fixed narrowing of one or more coronary arteries
progressive plaque growth → critical stenosis
5
Q
lesions causing >___% reduction of vascular cross-sectional areas define significant coronary artery obstruction
A
lesions causing >75% reduction of vascular cross-sectional areas define significant coronary artery obstruction
6
Q
describe an unstable/vulnerable plaque
A
unstable/vulnerable plaque is characterized by:
- causes moderate stenosis (50-75%)
- has thinner fibrous cap
- has a core rich in lipid, macrophages and T-cells
- less evidence of smooth muscle proliferation
- markedly eccentric (not uniform around the vessel circumference)
7
Q
describe what occurs after plaque erosion/ulceration/rupture
A
- plaque erosion, ulceration, rupture → exposure of thrombogenic lipid and subendothelial collagen → platelet aggregation and thrombin generation → thrombus formation
- if the vessel is completely occluded → MI
- incomplete obstruction →
- unstable angina or arrhythmias → SCD
- embolization to distal branches → micro infarcts
8
Q
vasoconstriction is stimulated by…. (4 things)
A
vasoconstriction is stimulated by:
- locally released platelet contents → thromboxane A2
- impaired secretion of NO relative to contracting factors (endothelin)
- increased adrenergic activity
- smoking
9
Q
summarize the differences between stable, prinzmetal and unstable angina
A
10
Q
list the 4 major contributing factors for an MI
A
- hypercholesterolemia
- smoking
- HT
- DM
11
Q
describe the pathogenesis of an MI
A
- 90% of cases due to acute thrombosis that leads to coronary artery occlusion
- disruption of a pre-existing plaque
- remaining 10% due to:
- vasospasm: isolated, intense and relatively prolonged with or without coronary atherosclerosis
- emboli: from the left-sided mural thrombus
12
Q
describe the myocardial response and features during an MI
A
13
Q
describe transmural infarctions
A
- transmural infarctions:
- involve the full thickness of ventricular wall in the distribution of a single coronary artery (regional) also called STEMI (ST-elevation MI)
- usually associated with acute plaque changes and superimposed, completely occlusive thrombosis
- can also occur with cocaine abuse
14
Q
describe a subendocardial infarction
A
- limited to the inner 1/3 or at most 1/2 of the ventricular wall, aka NSTEMI (non-ST elevation MI)
- associated with diffuse stenosing coronary atherosclerosis or with prolonged hypotension (global/circumferential infarctions)
- may occur due to transient/partial arterial obstruction (regional)
- less serious than transmural infarction
15
Q
describe the essential sequence of events in an MI
A
16
Q
describe what is seen in the image
A
17
Q
A
18
Q
describe what is seen in the image
A
19
Q
describe what is seen in the image
A
20
Q
describe what is seen in the image
A
21
Q
describe what is seen in the image
A
22
Q
describe reperfusion for an MI
A
reperfusion is the goal of therapy to salvage maximal amount of ischemic cells
- achieved by:
- thrombolysis using enzymes e.g. streptokinase or tissue plasminogen activator
- angioplasty or CABG
- although it is useful, reperfusion or ischemic tissue can cause rebound myocardial damage → reperfusion injury
23
Q
describe reperfusion injury
A
- mitochondrial dysfunction → promote apoptosis
- high extracellular Ca2+ and impaired Ca2+ cycling → myocyte hypercontracture → cytoskeletal damage
- free radicals are produced within minutes of reperfusion → myocardial damage
- leukocytes aggregation and platelet activation → microvasculature injury and occlusion → “no reflow” phenomenon
24
Q
describe the morphology of reperfusion injury
A
- hemorrhage:
- due to vascular injury and leakiness
- contraction band necrosis:
- intense hyper-eosinophilic transverse bands (hypercontracted sarcomeres)
- induced by high amount of extracellular Ca2+ in restored blood flow which easily crosses the leaky plasma membrane of ischemic myocytes
- actin-myosin interaction in the absence of ATP → the sarcomeres are stuck in this agonal tetanic state
25
describe what is seen in the image
26
describe clinical features of an MI
* chest pain
* retrosternal pain, crushing in nature
* may radiate to the neck, jaw, epigastrium, shoulder or left arm
* the pain is persistent \>30 min (unlike angina)
* not significantly relieved by vasodilators (nitroglycerine) or rest
* dyspnea
* rapid weak pulse
* diaphoresis, nausea, vomiting
27
name the factors that can cause arrhythmias following an MI
* myocardial irritability and conduction disturbances
* electrolyte imbalance
* hypoxia
28
\_\_\_\_ are the most common cause of SCD
**arrhythmias** are the most common cause of SCD
29
following an MI, there may be wall motion abnormalities due to endocardial damage which can lead to \_\_\_\_
following an MI, there may be wall motion abnormalities due to endocardial damage which can lead to **mural thrombus → systemic emboli**
30
describe how an MI can cause contractile dysfunction
* depending on size, site, thickness of the infarction, it can cause variable range of ventricular failure
* if severe → **cardiogenic shock**
* progressive heart failure (chronic IHD)
31
describe myocardial rupture as a complication of MI
* occurs between 3-10 days when necrosis, neutrophilic infiltration and myocardial tissue lysis → weakened myocardium
* it includes:
* ventricular free wall rupture → tamponade
* ventricular septum rupture → ASD
32
describe ventricular aneurysm as a complication of MI
occurs ~2 months after MI
* late complication of large transmural infarcts
* scar tissue wall of an aneurysm bulges during systole
* mural thrombus, arrhythmias and HF can occur
* unlikely to rupture due to tough fibrotic wall
33
describe acute fibrinous/fibrinohemorrhagic pericarditis as a complication of an MI
* acute fibrinous/fibrinohemorrhagic
* due to direct irritation of the pericardium in transmural infarcts
* usually in day 2 or 3 post MI
34
describe Dresslers' syndrome as a complication of an MI
* Dresslers' syndrome
* occurs 10-14 days post MI
* autoantibodies that target damaged pericardial antigens
35
describe using EKG as a diagnostic factor in MI
* transmural infarct
* ST-segment elevation
* Q wave: delayed appearance after 6 hrs of onset
* subendocardial infarct
* no specific changes
* no ST-segment elevation
* may show T wave depression
36
describe the use of myoglobin as a marker of cardiac injury
* first biomarker to rise (1-4 hrs)
* highly sensitive but not specific for the heart
* rarely used in practice
37
describe the use of troponins (I and I) as a marker of cardiac injury
* most sensitive and specific marker
* normally not detectable in circulation
* rises in 3-12 hrs, peaks at 48 hours and persists for 5-14 days
38
describe the use of CK-MB as a marker of cardiac injury
* a dimer composed by M & B subunits; MM, MB, BB
* CK-MB: most specific for the heart among the CKs
* rises in 3-12 hrs, peaks at 24 hrs and disappears by 72 hrs
* **useful for detection of reinfarction**
39
describe the use of LDH as a marker of cardiac injury
* rises in 24 hrs, peaks at 3-6 days and returns to baseline within 8-12 days
40
describe the use of echocardiogram in diagnosing an MI
* useful in detecting complications of MI
* evaluate ventricular function and wall-motion abnormalities
* can identify pericardial effusion, valve regurgitation and cardiac tamponade
41
describe interventions after an MI
* primary prevention
* thrombolysis
* defibrillation
* angioplasty
* coronary bypass graft (CABG)
42
describe the pathogenesis of chronic ischemic heart disease
* pathogenesis:
* insidious onset of CHF in pts who have past episodes of MI or anginal attacks
* cardiac decompensation owing to exhaustion of the compensatory hypertrophy of non-infarcted viable myocardium or severe coronary obstructive disease leading to diffuse myocardial dysfunction
* arrhythmia, intercurrent MI are more common and fatal
43
describe gross and histological morphology seen in CIHD
* gross:
* enlarged and heavy heart due to hypertrophy and dilation
* discrete gray white scars of healed previous infarcts
* patchy fibrous thickening of mural endocardium
* histo:
* myocardial hypertrophy
* diffuse subendocardial vacuolization - **myocytolysis**
* scars of previously healed infarcts
44
describe sudden cardiac death in adults vs. younger people
* in adults: CAD is the most common cause
* younger victims:
* congenital coronary artery abnormalities
* aortic valve stenosis
* mitral valve prolapse
* myocarditis
* conduction system defects
* pulm. HT
* cardiomyopathy
* sarcoidosis
