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Pathology
Lecture 28 Ischemic Heart Disease
1) Know the risk factors for atherosclerosis and myocardial infarction. Risk factors
for both include: advanced age, sex with males>females (↑postmenopausal women),
cigarette smoking, hyperlipidemia especially hypercholesterolemia (dietary or
genetic), hypertension, diabetes mellitus, and genetics (i.e. a positive family history or
familial hypercholesterolemia). Other risk factors may include lack of exercise,
stressful lifestyle with "Type a" personality, and obesity.
2) Describe the sequence of events in the formation of an occlusive coronary
thrombus and the myocardial response.
a) Sudden change in the morphology of atheromatous plaque, i.e. disruption
manifest as intraplaque hemorrhage, erosion or ulceration, or rupture/fissure.
b) Exposed to subendothelial collagen and necrotic plaque contents, platelets
undergo adhesion, aggregation, activation, and release of potent aggregators
including thromboxane A2, serotonin, and platelet factors 3 and 4.
c) Vasospasm is stimulated by platelet aggregation and the release of mediators.
d) Other mediators activate the extrinsic pathway of quite elation adding to the bulk
of the thrombus.
e) Within minutes, the thrombus evolves to completely occluded the lumen of the
coronary vessel.
Myocardial response: cessation of aerobic glycolysis and initiation of anaerobic
glycolysis leading to inadequate energy production. Myocardial necrosis begins
around 30 minutes after coronary occlusion, and therefore, reperfusion should occur
within the first 20 minutes if possible to reverse any damage.
3) List the gross and microscopic appearances of acute, organizing and healed
myocardial infarcts.
Type of MI
Acute MI
Gross
1/2-4 hr – none.
4-12 hr – occasionally dark mottling.
12-24 hr – dark mottling.
Organizing
MI
1-3 days – mottling with yellow-tan
infarct center.
3-7 days – hyperemic border; Central
yellow-tan softening.
Healed MI
7-10 days – maximally yellow-tan
and soft, with depressed red-tan
margins.
10-14 days – red-gray depressed
infarct borders.
2-8wk – gray-white scar, progressive
from border towards core of infarct.
>2 mo - scarring complete.
Microscopic
Usually none; variable waviness of border fibers
Beginning coagulation necrosis; edema; hemorrhage
Ongoing coagulation necrosis; pyknosis of nuclei;
myocyte hypereosinophilia; marginal contraction
band necrosis; beginning neutrophilic infiltrate.
Coagulation necrosis, with loss of nuclei and
striations; interstitial infiltrate of neutrophils.
Beginning disintegration of dead myofibers, with
dying neutrophils; early phagocytosis of dead cells
by macrophages at infarct border.
Well-developed phagocytosis of dead cells; early
formation of fibrovascular granulation tissue at
margins.
Well-established granulation tissue with new blood
vessels and collagen deposition.
Increased collagen deposition, with decreased
cellularity.
Dense collagenous scar.
4) List and give the pertinent details of the consequences and the complications of
myocardial infarcts.
a) Contractile Dysfunction (Cardiogenic Shock) – some degree of left ventricular
failure with hypotension, which may progress to pulmonary edema. 10-15% of
patients, generally large infarct (40%), with a 70% mortality rate accounting for
2/3 of in-hospital deaths.
b) Arrhythmias - conduction disturbances including sinus bradycardia, heart block
(asystole), tachycardia, ventricular premature contractions or ventricular
tachycardia, and ventricular fibrillation.
c) Myocardial Rupture - weakening from necrotic and inflamed myocardium results
in rupture of the ventricular free wall (most common), intraventricular septum
(left to right shunt produced), and papillary muscle rupture (least common)
usually the posteriormedial muscle resulting in acute mitral valve regurgitation.
Generally occurs in first week with 1-5% incidence.
d) Ventricular Aneurysms or Mural Thrombi – resulting from stasis of blood in the
area of hypo-contractibility. Systemic embolization of Meryl thrombus can
results in obstruction of arteries in the brain, kidneys, bowel, etc.
5) Describe the concept of chronic ischemic heart disease. Chronic Ischemic Heart
Disease (CIHD) describes patients who develop progressive heart failure as a
consequence of ischemic myocardial damage. In most instances, there's been a prior
MI and sometimes previous coronary arterial bypass graft surgery or other
interventions. Usually presents as insidious onset of CHF.
6) Define and give the pathophysiology of sudden cardiac death. Sudden cardiac
death implies that death at that time was unexpected and that it occurred within one
hour of the onset of symptoms (if symptoms exist). Most are caused by CAD and are
the result of fatal dysrrhythmias. The majority of successfully resuscitated patients
do not show subsequent clinical evidence of acute MI.
Pathophysiology: critical coronary atherosclerosis involving two or three of the major
epicardial arteries. Acute MI in less than 1/3.