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Path split 12b (Ischemic Heart Disease [IHD]- Valvular Heart Disease)-MA
Terms in this set (85)
leading cause of death in men and women worldwide
Ischemic Heart Disease (IHD)
which is worse, ischemia or hypoxia? why?
ischemia- lacking metabolites as well as oxygen
another name for IHD
coronary artery disease (CAD)
when does IHD usually present?
later in life- slow progression
IHD presents with which syndromes?
Chronic IHD w/ Heart failure
sudden cardiac death
what is the effect of tachycardia on an ischemic heart?
aggravate due to increasing oxygen demand and decreasing supply (relative time in diastole)
True or false? MI occurs in a large number of those with IHD
the risk of MI (not IHD) is associated with _____
modified leukotriene B4 metabolism
what amount of obstruction is required to cause ischemia precipitated by exercise?
Obstruction of ____ % of the lumen can lead to inadequat coronary blood flow at rest
what is one of the heart's protective measures against Ischemia?
fomation of collateral vessels over time
where in the coronary vessels do plaques tend to predominate?
first several cm of LAD and LCX and along the entire length of the RCA
what are the 3 acute coronary syndromes?
caused by plaque rupture complicated by partially occlusive thrombosis and vasoconstriction
transcient myocardial ischemia that falls short of inducing myocyte necrosis
ischemic event not perceived by the patient
what two things typically relieve angina pectoris?
rest (decrease demand)
nitroglycerine (increase supply/perfusion)
uncommon form of episodic myocardial ischemia that is caused by coronary artery spasm. how do you treat?
vasodilators such as nitroglycerine and calcium channel blocker
chest pain at rest
aka preinfarction angina
why are men more likely to have an MI?
Estrogens are protective against atherosclerosis by lowering lipids
what is the mechanism of coronary arterial occulusion?
Plaque alteration (hemorrhage, rupture, etc.)
platelets aggregate and release granules
vasospasm results from granules
tissue factors activate coagulation increasing thrombus size
complete vessel occlusion
atypical causes of MI (10%): (3)
Vasospasm (cocaine or platelets)
Emboli (left atrium or right [paradoxical])
Ischemia w/o atherosclerosis (vasculitis, sickle cell, etc.)
how long does it take for ischemia to cause loss of contractility of the heart
what are some ultrastructural changes that happen within a few minutes of ischemia to the heart? (3)
cell and mitochondrial swelling
how long must the heart be severely ischemic before irreversible damage is done
longer than 20-30 minutes
at what time is ATP reduced to 50% of normal in an ischemic event? 10% of normal?
how long does it take to induce microvascular injury in an ischemic heart?
over 1 hour
key feature that marks early phases of mycote necrosis
disruption of the integrity of the sarcolemmal membrane intracellular macromolecules leak out of cells into cardiac interstitium
where is ischemia of the heart most pronounced? i.e. where does injury occur first?
how long after onset of severe (acute) myocardial ischemia is necrosis complete? chronic?
about 12 hours because of development of collateral branches
what artery supplies most of the apex, the anterior wall of the left ventricle, and the anterior 2/3rds of the ventricular septum
in a right dominant heart, what does the right circumflex supply?
entire ventricular free wall, posterobasal wall of the left ventricle, and the posterior 1/3rd of the ventricular septum. Left circumflex only supplies lateral wall of left ventricle
what type of ischemic necrosis involves the full or nearly full thickness of the ventricular wall? what can cause this?
combination of chronic coronary atherosclerosis, acute plaque change, and superimposed thrombosis
what type of ischemic necrosis is limited to the inner 1/3-1/2 of the ventricular wall? what can cause this?
plaque disruption followed by a coronary thrombus that becomes lysed before myocardial necrosis extends across the full thickness of the wall
what are transmural infarcts also known as? (think EKG)
ST elevation myocardial infarcts (STEMI)
what are subendocardial infarcts also known as? (think EKG)
non ST Myocardial elevation infarcts (NSTEMI)
at what point does and MI cause irreversible cell injury?
over 30 mins
at what time do you see no gross features post MI, yet still have irreversible damage?
at what time might you occasionally see dark mottling post MI?
at what time will you definitely see dark mottling post MI?
at what time do you see mottling with yellow-tan infarct center post MI?
at what time do you see hyperemic border and a central yellow-tan softening post MI?
at what time do you see maximally yellow-tan and soft with depressed red-tan margins post MI?
at what time do you see red-gray depressed infarct borders post MI?
at what time do you see gray-white scar, progressive form border toward core of infarct post MI?
at what point is the scarring complete post MI?
how often is the LAD involved in MI? where does it effect?
40-50% involve anterior wall of left ventricle near apex; the anterior portion of ventricular septum, and the apex circumferentially
how often is the Right coronary involved in MI? where does it effect?
30-40% involve inferior/posterior wall of the left ventricular septum; and the inferior/posterior right ventricular free wall in some cases
how often is the left circumflex involved in MI? where does it effect?
15-20% lateral wall of left ventricle except apex
what is phenyltetrazolium chloride? how does it work?
stain for viewing necrosis
turns area where dehyrdogenases are present (noninfarcted) brick-red and infarcted areas look pale and unstained
sublethal ischemic change that may be seen in the margins of infarcts: so called vacuolar degeneration
what is the pattern by which infarcts heal?
outside (periphery) inward
true or false? once a lesion has completely healed, it is impossible to determine its age
no difference between 2 months and 10 years
what is the phenomenon of "extension"?
infarcts may expand beyond their original borders over a period of days to weeks via repetitive necrosis
complications of reperfusion
myocardial hemorrhage with contraction bands
prolonged ischemic dysfunction (myocardial stunning)
If you suspect irreversible cell damage upon reperfusion, what are you looking for on a microscopic exam?
contraction bands- intensely eosinophilic intracellular stripes exposed of closely packed sacromeres
what is hibernation?
when the myocardium is subjected to chronic, sublethal ischemia it may enter into a state of lowered metabolism and function
True or false? repetitive, short-lived transient severe ischemia may damage the myocardium prior to an infarction?
false- actually protect
phenomenon known as "preconditioning"
how do most patients present with MI?
rapid, weak pulse, and profuse sweating (diaphoresis) as well as dyspnea from pulmonary congestion from weakened heart
who is likely to have a silent MI?
elderly patients and those with DM (neuropathy)
what are of the few blood markers of MI? (4)
which are most specific?
troponin I and T**
MB fraction of creatine kinase (CK-MB)
lactate dehydrogenase and others
If you check the blood of a patient 1 hour after an MI, what shouldn't you see?
Troponins I and T. levels rise 3-12 hours post MI and peak at 24hours
where are the different dimers of creatine kinase found? which do we care most about?
MM - cardiac and skeletal muscle
BB- brain, lung
*MB- cardiac muscle (little in skeletal)
starts after 3 to 12 hours, peak in 24 hours
Unchanged levels of CK-MB and troponin over a period of 2 days essentially excludes ____
diagnosis of MI
how do you treat an MI and why? buckle up.
aspirin and heparin (prevent further thrombosis)
oxygen (minimize ischemia)
nitrates ( induce vasodilation and reverse bronchospasm)
beta-adrenergic inhibitors (beta-blockers, to diminsh cardiac demand and decrease risk of arrythmias)
ACE inhibitors (limit ventricular dilation)
maneuvers to open up blocked vessels, including administration of fibrinolytic agents, coconary angioplasty with or without stenting, CABG
which gender is associated with a poor MI prognosis
contractile dysfunction (left ventricle)
Arrhythmia (conduction fiber death)
pericarditis (Dressler syndrome)
Right ventricular infarction
Papillary muscle dysfunction
Progressive late heart failure
which myocardial rupture is the most common with hemopericardium and cardiac temponade
rupture of the ventricular free wall
which myocardial rupture is the second most common and results in acute VSD and left-to- right shunting?
rupture of the ventricular septum
which myocardial rupture is the least common and results in acute onset of severe mitral regurgitation?
rupture of the papillary muscle
most common site for post infarction free-wall rupture
anterolateral wall at the midventricular level
what is a localized hematoma communicating with the ventricular cavity?
what two things foster a mural thrombus?
local abnormality in contractility (causing stasis)
endocardial damage (creating a thrombogenic surface)
what factors affect postinfarct complications? what is the best case scenario?
infarct size- smaller= better
location- posterior/ inferior has better prognosis
thickness (subendocardial or transmural)- sub=better prognosis
what happens to the noninfarcted tissue of the heart? what is this called?
undergo hypertrophy and dilation ventricular remodeling
Why do ACE inhibitors mitigate the effects of ventricular remodeling?
when the ventricles hypertrophy ventricular dilation and increased oxygen demand can overwhelm the heart. ACE inhibitors lessen dilation
what two factors affect the long term prognosis post MI?
quality of what is left of the left ventricle
amount of coronary vascular obstructions
microscopic findings of chronic IHD include: (3)
Sudden cardiac death is usually a consequence of ___. what triggers this?
lethal arrhythmia ex: V fib/ asystole
acute myocardial ischemia
what is one of the usual first clinical manifestations of IHD?
sudden cardiac death
There are several electrical abnormalities of the heart that can cause sudden cardiac death, what are 3 that we are familiar with/ mean something to us?
long QT syndrome* prototypical "channelopathy" defect in ion channel genes- KCNQ1 most common
short QT syndrome
right sided hypertensive heart disease that is caused by pulmonary hypertension
what are the two minimal criteria for hypertensive heart disease?
1) left ventricular hypertrophy in absence of other cardiovascular pathology
2) history or pathologic evidence of hypertension in other organs
"It should be remembered, however, that _______ hypertension most commonly occurs as a complication of left-sided heart diseases of various etiologies
when would you see a marked dilation of the right ventricle without hypertrophy?
acute cor pulmonale
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