Ischemic Heart Disease Flashcards
name the ischemic heart disease (IHD) syndromes
- angina pectoris (chest pain)
- stable angina
- unstable angina
- prinzmetal angina
- acute MI
- chronic IHD with CHF
- sudden cardiac death (SCD)
describe the etiology of IHD
- etiology:
- atherosclerosis - 90% of cases
- other causes of ischemia:
- anemia → hypoxemia
- lowered systemic blood pressure → shock
- increased cardiac demand → hypertrophy exercise
- vasculitis
- aortic dissection
describe the pathogenesis of IHD
- complex dynamic interaction between the following factors:
- coronary artery obstruction (fixed)
- acute plaque changes
- coronary intraluminal thrombosis
- vasoconstriction
>90% of patients with IHD have atherosclerotic lesions that cause ___ of one or more coronary arteries
progressive plaque growth → ____
>90% of patients with IHD have atherosclerotic lesions that cause stable fixed narrowing of one or more coronary arteries
progressive plaque growth → critical stenosis
lesions causing >___% reduction of vascular cross-sectional areas define significant coronary artery obstruction
lesions causing >75% reduction of vascular cross-sectional areas define significant coronary artery obstruction
describe an unstable/vulnerable plaque
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)
describe what occurs after plaque erosion/ulceration/rupture
- 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
vasoconstriction is stimulated by…. (4 things)
vasoconstriction is stimulated by:
- locally released platelet contents → thromboxane A2
- impaired secretion of NO relative to contracting factors (endothelin)
- increased adrenergic activity
- smoking
summarize the differences between stable, prinzmetal and unstable angina
list the 4 major contributing factors for an MI
- hypercholesterolemia
- smoking
- HT
- DM
describe the pathogenesis of an MI
- 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
describe the myocardial response and features during an MI
describe transmural infarctions
- 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
describe a subendocardial infarction
- 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
describe the essential sequence of events in an MI
describe what is seen in the image
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describe reperfusion for an MI
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
describe reperfusion injury
- 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
describe the morphology of reperfusion injury
- 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
describe what is seen in the image
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
name the factors that can cause arrhythmias following an MI
- myocardial irritability and conduction disturbances
- electrolyte imbalance
- hypoxia
____ are the most common cause of SCD
arrhythmias are the most common cause of SCD
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
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)
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
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
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
describe Dresslers’ syndrome as a complication of an MI
- Dresslers’ syndrome
- occurs 10-14 days post MI
- autoantibodies that target damaged pericardial antigens
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
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
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
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
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
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
describe interventions after an MI
- primary prevention
- thrombolysis
- defibrillation
- angioplasty
- coronary bypass graft (CABG)
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
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
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
