093014 ischemic heart disease Flashcards
ischemic heart disease
imbalance btwn supply and demand for oxygen and nutrients and removal of metabolites
IHD caused by atherosclerotic narrowing-coronary blood flow is reduced by how much
greater than 90%
causes of decreased blood flow
fixed atherosclerotic narrowing
acute plaque change (can rupture, embolize)
thrombosis overlying ruptured plaque
vasospasm
fixed obstruction
narrowing of greater than 70% causes symptomatic ischemia with exercise
greater than 90% stenosis causes ischemia at rest
often multiple arteries affected (most commonly-first several cm of LAD, left circumflex, entire length of right coronary artery
effects are modified by collaterals
acute plaque change
unpredictable and abrupt conversion of stable plaque to an unstable atherothrombotic lesion that results in myocardial ischemia (rupture, fissures, ulcerations…or hemorrhage into atheroma)
results in acute coronary syndromes (acute MI, unstable angina, sudden cardiac death)
what are the influences contributing to acute plaque change?
intrinsic and extrinsic factors
what are intrinsic factors contributing to acute plaque change
large areas of foam cells or lipid thin fibrous cap most dangerous lesions are the moderately stenotic (50-75%), lipid rich atheromas-soft core abundant inflammation few smooth muscle cells
mechanical stress
what extrinsic factors contribute to acute plaque change
adrenergic stimulation (upon awakening, emotional)
coronary thrombosis
partial or total thrombosis superimposed on a partially stenotic plaque
critical to pathogenesis of acute coronary syndromes
if total occlusion–get acute transmural MI or can get sudden death
if incomplete occlusion/mural thrombus–you’re more likely to have unstable angina, acute subendocardial infarction, or sudden death and can have emboli
unstable angina
usually as a result of rupture of plaque with thrombosis. incomplete occlusion of artery
four basic syndromes of ischemic heart disease
angina pectoris
myocardial infarction
chronic ischemic heart disease
sudden cardiac death
angina pectoris
paroxysmal and recurrent attacks of chest pain caused by transient myocardial ischemia-15 seconds to 15 minutes (no cellular necrosis)
three patterns: stable, prinzmetal, unstable
stable angina
produced by physical activity or emotional excitmenet, attributed to chronic stenosis
Prinzmetal angina
due to coronary artery spasm at rest
unstable angina
occurs with progressively increasing frequency and progressively less effort, often at rest and of prolonged duration (induced by disruption of plaque with superimposed partial thrombosis. often a prodrome of acute MI)
myocardial infarction
death of cardiac muscle due to ischemia
risk factors for MI
increasing age and predisposition to atherosclerosis (HTN, smoking, diabetes, increased cholesterol and/or lipids)
pathogenesis of MI in 90% is
acute plaque change resulting in thrombosis and occlusion of coronary artery
in 10% of cases, due to vasospasm, emboli or unexplained
myocardial response to ischemia
60 seconds of ischemia–loss of contractility
loss of blood supply causes reversible damage in early stages
in 20-40 minutes–IRREVERSIBLE damage (coagulative necrosis)
early thrombolytic therapy (3-4 hours)–reperfusion and limit the size of infarct
arrthymias (induced by myocardial irrititability secondary to ischemia–ventricular fibrillation)-can lead to sudden death
MI frequencies in three main coronary arteries
LAD-most common (40-50%)
RCA-second most common (30-40%)
LCA-least common (15-20%)
MI gross morphology
under 12 hrs: not apparent (tetrazolium stain–pale areas post 2-3 hrs)
12-24 hrs: dark red blue mottling (b/c of stagnant blood)
1-14 days:
early–sharply defined yellow tan area
late–still yellow tan centrally but with hyperemic peripheral zone due to granulation tissue
greater than 2 weeks:
gray-white scar begins to form
MI histology
4-12 hrs: wavy fibers
12 hrs-7 days: coagulative necrosis becomes well established and ongoing (initially pyknotic nuclei, hyper-eosinophilic myocytes. followed by neutrophils, loss of nuclei and striations. by day 7, macrophages at border)
7-14 days: granulation tissue well established. collagen begins to deposit
greater than 14 days: progressively more collagen deposition. eventually DENSE FIBROUS SCAR.
reperfusion injury for acute MI usually occurs after
thrombolysis, baloon angioplasty, or bypass grafts
reperfusion prevents necrosis if it occurs within how long?
20 minutes
necrotic cells have contraction bands because
influx of calcium (calcium is released from SR)
reperfusion injury may result from
oxygen free radicals released from leukocytes
microvascular injury causing hemorrhage and endothelial swelling that occludes capillaries-no flow
platelet and complement activation
chest pain in an MI is NOT relieved by
nitroglycerin or rest
what findings would you see with MI?
chest pain
rapid weak pulse
diaphoresis
dyspnea due to pulmonary edema
10-15% of pts-no symptoms
ECG
lab-cardiac enzymes, CRP
complications of MI
contractile dysfunction
cardiogenic shock (damage to 40% or more of left ventricle)
arrhythmia early in course (sudden death)
myocardial rupture (3-7 days)–free wall, ventricular septum, papillary muscle
pericarditis (2-3 days)
mural thrombus and thromboembolism (due to pooled blood)
ventricular aneurysm (late)
papillary muscle dysfxn (secondary to scarring or fibrosis)
progressive heart failure (late)
chronic ischemic heart disease
elderly pts with progressive heart failure due to ischemic myocardial damage (post infarction cardiac decompensation. or severe coronary artery disease without infarction but with myocardial dysfxn.)
morphology of chronic ischemic heart disease
enlarged heavy heart with left ventricular hypertrophy and dilation. dilation is due to blood staying behind in heart due to heart failure.
coronary atherosclerosis, scars
sudden cardiac death
unexpected death from cardiac causes. death due to lethal arrhythmia.
most often due to ischemic heart disease (80-90% of sudden cardiac death)
non-atherosclerotic causes are hypertrophy, cardiac conduction system abnormalities, mitral valve prolapse, congenital abnormalities, myocarditis, cardiomyopathy, pulmonary HTN
morphology of sudden cardiac death
typically coronary atherosclerosis with acute plaque change. typically has had MI before or has pathology associated with non-atherosclerotic causes.
