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Ischemic Heart Disease Histology
Terms in this set (41)
What are the four main kinds of ischemic cardiac syndromes?
1. Angina pectoris: stable (typical), Unstable (crescendo), variant (prinzmetal/spasm); 2. MI; 3. Chronic IHD with CHF; 4. Sudden Cardiac death
Atherosclerotic ischemic heart disease mostly occurs in the (proximal/distal) arteries.
! Also mostly
. Fixed narrowing of coronary aa, acute plaque changes, thrombosis, vasospasm
___ supplies 40% of LV myocardium
Occlusion to left main coronary artery would knock out ___% of LV myocardial blood supply.
Most patients have a (R/L) dominant coronary artery.
Right. SA and AV nodes are derived from RCA
<___% obstruction of arteries in ischemic heart disease is generally asymptomatic.
70-75 percent (unless anemic or significant hypertrophy--then smaller degree of obstruction can be bad!). Above 70-75% results in stable angina (Demand met at rest, symptoms develop with exertion); >90% obstruction=unstable angina; Complete obstruction=MI
Critical stenosis refers to ___ obstruction.
70-75 percent obstruction
Why do plaques rupture?
Macrophages releasing metallo-proteinases contribute to destabilization and rupture of an atherosclerotic lesion. The released enzymes digest collagen in the fibrous cap. More likely if greater than 40% core, thin fibrous cap, many macrophages, few smooth muscle cells in fibrous cap ("vulnerable plaque")
Describe the pathogenesis of coronary thrombosis
Plaque rupture exposes blood to thrombogenic core and damaged endothelium; Increase in thromboxane A and other platelet contents; Platelets are activated; Tissue thromboplastin released; clot is formed
Chronic stable angina. What would you expect pathologically?
Fixed lesions with at least one having >70-75% obstruction
Chronic unstable angina. What would you expect pathologically?
>90% obstruction; Plaque erosion or rupture, mural thrombi (Arterial), possibly microemboli
Myocardial infarction. What would you expect pathologically?
Plaque rupture followed by thrombosis with complete occlusion
Full thickness infarction of ventricular wall; associated with CA thrombosis; ST elevations on EKG (STEMIs)
Limited to inner one third of ventricular wall. In setting of severe CAD, transient decreases in O2 delivery or increases in O2 demand can cause SE infarction. Can also occur when a thrombus lyses before transmural infarction occurs (N-STEMI)
Permanent occlusion of LAD. Transmural or subendocardial MI?
Transmural (includes full thickness)
Global hypotension. Would I result in transmural or subendocardial MI?
Subendocardial MI (circumferential)
Transient obstruction. Would I result in transmural or subendocardial MI?
Subendocardial MI (partial obstruction--regional subendocardial infarct)
What are some early biochemical findings in MI?
Early on, significant drop in ATP. INCREASE of lactate.
How long after onset of MI is the damage potentially reversible?
What is the timecourse of ischemic myocardium?
Minutes: cell swelling, mitochondrial swelling, glycogen depletion; 20-40 min: irreversibility, EM defects in sarcolemmal membranes; Myocytes die in a wavefront from
subendocardium to subepicardium
in about 6 hrs; effectiveness of thrombolytic agents
The most susceptible region to ischemia is the (subendocardium/subepicardium)
What are the determining factors in development of an MI?
Location, severity and rate of occlusion; Size of vascular bed (eg. LCA); Duration of survival; Metabolic demands; Collateral vessels; Spasm; HR, rhythm, BP
Describe the gross pathology of an MI over time.
Nothing in 1st 12 hours; Special dyes (Tetrazolium) after 2-3 hours; Pallor or red blood hue 12-24 hours; Yellow with red-tan border 3-10 days; Yellow area rimmed by granulation tissue appearing hyperemic; White scar after a few weeks
What is the special dye that can help visualize pathology of an MI earlier on?
Tetrazolium salt (TTC). Viable myocardium=red; Infarced=yellow; Scar=white
Neutrophils peak at what time after an MI?
48 hours after MI
At what time is there MAXIMAL softening of myocardium with a high likelihood of cardiac rupture.
Vacuolar degeneration or colliquative myocytolysis; Appears as a nucleus in an empty sarcolemmal tube; Seen in LV subendocardium and at perimeter of MIs; Thought to be still viable; Unlike fibers in coagulative necrosis, stain for creatinine kinase and lactic dehydrogenase
Myocardial reperfusion: where is it most likely to occur?
Reduction is greatest in subepicardial region!
T/F: Reperfusion after temporary occlusion can significantly restore both function and viability.
True but can experience reperfusion INJURY too.
What are some reperfusion-associated changes?
Necrotic myocardium: contraction bands and hemorrhage; Ischemic myocardium: reperfusion-induced arrhythmias, myocardial stunning (both reversible), microvascular obstruction, lethal myocardial perfusion injury (both irreversible)
Contraction Band Necrosis
Accelerated necrosis of irreversibly injured myocytes (dead to begin with); Hypercontraction with massive influx of calcium;
Appear after as little as 2 minutes of reperfusion
; Margins of infarcts between dead and viable zones;
more numerous in infarcts after reperfusion
; Myocardium of sudden death cases; Perioperative ischemia during cardiac surgery
What are some reversible changes of reperfusion injury?
Arrhythmias; Myocardial stunning: reperfused myocytes are viable but temporarily have biochem changes and are unable to contract, may be stunned for hours to days, no light microscopic changes, temporary assist devices may be indicated
What are some irreversible changes of reperfusion injury?
Lethal injury to cells which might have survived otherwise: Microvascular obstruction; Cell Death: generation of ROS, intracellular calcium overload, mitochondrial transition pore opening, and hypercontracture
Reperfusion is more likely to save what layer of the myocardium?
The outer layer!
What are some complications of MI?
Tachyarrhythmias, AV block with bradycardia, shock, CHF, rupture, thromboembolism, ventricular aneurysm, pericarditis (Acute fibrinous pericarditis with transmural infarct OR Post-MI syndrome--Dressler, autoimmune)
Chronic ischemic heart disease
May have been asymptomatic and present with HF or long history of angina/prior MIs; Varying degrees of coronary atherosclerosis, usually severe; Hypertrophy with dilatation of LV, subendocardial vacuolization, replacement fibrosis (healed MIs)
Sudden Cardiac Death
80-90% have severe IHD; >75% stenosis in more than one vessel, often >90% stenosis in one vessel; Acute plaque changes and thrombosis in 1-20% and old MI in 40%; 80-90% of successfully resuscitated patients do not have EKG or enzymatic evidence of acute MI;
Most patients die of fatal arrhythmias
Most patients who experience sudden cardiac death is most often:
(maybe ventricular fibrillation)
How does cocaine affect the heart?
Sympathomimetic-->vascoconstriction, tachycardia, increased oxygen demand. 24 fold increase in MIs, unrelated to amount, route or frequency of use; Enhances platelet aggregation and thrombus formation; Arrhythmias
Limits long-term success of cardiac transplants; Marked progressive diffuse intimal thickening of coronary arteries with luminal narrowing; Denervation heart does not allow the patient to note anginal warning symptoms!
Changes found in graft arteriopathy can also be found from what other exposure?
Radiation to the heart looks very similar!
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