• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/228

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

228 Cards in this Set

  • Front
  • Back
what is the #1 cause of death worldwide?
heart disease

(40% of deaths in the US)
(1.5x all cancers combined)
normal heart morphology
250-300gm in women
300-350gm in men

RV thickness = 0.3-0.5cm
LV thickness = 1.3-1.5cm
**usually measured 1-2cm below the tricuspid or mitral valve**
where do the coronary arteries arise?
just distal to the aortic valve
how can coronary arteries be dominant?
the coronary artery that supplies the posterior descending branch is considered dominant

80% of patients are right dominant
what are the three major epicardial coronary arteries?
1) left anterior descending (LAD) artery
2) left circumflex (LCX) artery
3) right coronary artery (RCA)
when does most blood flow through the coronary arteries occur?
during ventricular diastole
what parts of the heart are supplied by the left anterior descending artery?
most of the apex
anterior left ventricle
anterior 2/3 of septum
what parts of the heart are supplied by the left circumflex artery?
lateral wall of left ventricle
posterior 1/3 of septum (20% of pts)
what parts of the heart are supplied by the right coronary artery?
right ventricle
posterior 1/3 of septum (80% of pts)
posterobasal left ventricle

**occlusion of the right coronary artery can damage the left ventricle**
aging heart
- can have reduction in size of LV cavity
- calcification of the mitral annulus and/or aortic valve (aortic valve calcification often causes stenosis)
- fibrous thickening of valves (can mimic prolapsed mitral valve)
- fewer myocytes (more fibrous tissue) compared to a younger person
- amyloid of aging
- lipofuscin granules
lipofuscin
wear/tear pigment found in aging hearts (sign of oxidative injury)

a lot is found in atrophic hearts (brown atrophy)
congestive heart failure
heart is unable to pump at the rate that is necessary for the requirements of metabolizing tissue, or can do so only from an elevated filling pressure

mortality is 50% in 5 years
what is the leading discharge diagnosis in hospitalized patients older than 65?
congestive heart failure

causes 1 million hospitalizations per year (pts are living longer, so there are more hospitalizations)
what are the causes of CHF?
1) most cases are deterioration of systolic dysfunction (contractile problems)
2) fewer cases have diastolic dysfunction (left ventricular hypertrophy)
3) iatrogenic causes (fluid overload can throw old ppl into heart failure)
cardiac hypertrophy
increase in mass and size of heart often accompanied by the deposition of fibrous tissue (heart is 2-4x heavier than normal)

often precedes onset of CHF, as heart responds to increased mechanical work or to trophic signals

more mass causes increased metabolic requirements and increased wall tension (both result in more O2 consumption)

heart rate and contractility inc. O2 consumption (often present in hypertrophic states)
patterns of cardiac hypertrophy
pressure overload
- concentric LV hypertrophy
- caused by HTN and aortic stenosis
- cavity is normal to reduced in size

volume overload
- caused by mitral/aortic valve regurg/insufficiency
- hypertrophy & dilation with increased ventricular diameter
- thickness doesn't correlate with pathology (pt could be compensated or decompensated)
how does the weight of the heart change in patients with hypertrophy?
the weight increases to 2-3x normal in HTN, ischemic heart disease, aortic stenosis, mitral insufficiency, and dilated cardiomyopathy

the weight increases to 3-4x normal in aortic insufficiency and hypertrophic cardiomyopathy
molecular changes in cardiac hypertrophy
with prolonged overload, re-expression of protein synthesis is similar to that in fetal heart development (ANP & BNP tries to dec blood volume)

alterations in handling of Ca may cause impaired contraction/relaxation

apoptosis of myocytes
what is the end result of cardiac hypertrophy?
hypertrophy is the balance between adaptation and potentially deleterious alterations

eventually the compensatory changes become an added cardiac burden

degree of structural abnormality does not necessarily correlate with level of dysfunction
causes of left heart failure
ischemic heart disease
hypertension (most common)
aortic and mitral valve disease
nonischemic myocardial disease
what is the most common cause of left heart failure?
hypertension
what causes the clinical presentations of left heart failure?
congestion of pulmonary circulation

stasis of blood in left-sided chambers

hypoperfusion of tissues
what is seen in the heart in left heart failure?
LV hypertrophy, often dilation (volume overload)

secondary enlargement of left atrium; if there is resultant a-fib, pt can get stasis and thrombus with substantial risk of stroke

microscopic: hypertrophy and fibrosis
what is seen in the lung in pts with left heart failure?
congestion and edema (frothy and pink)

with time, get siderophages (heart failure cells)

cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, rales
what is seen in the kidney in pts with left heart failure?
decreased CO activates RAAS and causes retention of salt and water with subsequent expansion of blood volume

salt retention is counteracted by ANP released via atrial dilation (decreases blood volume)

if perfusion deficit is severe, pre-renal azotemia can occur
what are heart failure cells?
aka siderophages

hemosiderin-containing macrophages in the alveoli (most common in left heart failure and chronic lung congestion)

a) in left heart failure, the left ventricle can not keep pace with the incoming blood from the pulmonary veins
b) resulting backup causes increased pressure on the alveolar capillaries, and red blood cells leak out
c) alveolar macrophages ingest the red blood cells, and become engorged with brownish hemosiderin
what is pre-renal azotemia?
abnormally high levels of nitrogen-containing compounds

BUN and creatinine are elevated, but BUN is elevated out of proportion to creatinine (in renal azotemia, the increase is proportional)

occurs following hemorrhage, shock, volume depletion, congestive heart failure, and narrowing of the renal artery
effects of left-sided congestive heart failure on the brain
in advanced CHF, pt can get cerebral hypoxia and hypoxic encephalopathy

causes loss of attention span and restlessness
what is the most common cause of right heart failure?
left heart failure (caused by back-up)
what are the two causes of right heart failure?
1) left heart failure (most common)
2) pure right failure with severe pulmonary hypertension (cor pulmonale)
what is seen in pts with pure right heart failure (cor pulmonale)?
- right sided hypertrophy and dilation
- septum may bulge into left side, causing some LV dysfunction
- minimal pulmonary congestion
- engorgement of systemic and portal venous systems
what is the main difference between the two causes of right heart failure?
in right heart failure caused by left heart failure, there is substantial pulmonary congestion

in pure right heart failure (caused by pulmonary HTN) there is minimal pulmonary congestion
what is seen in the liver/portal system in pts with right heart failure?
increased size and weight (congestive hepatomegaly)

chronic passive congestion
- congested red center of lobule
- paler periphery
- "nutmeg liver"

central hypoxia can cause centrilobular necrosis (if prolonged and severe, cardiac sclerosis/cirrhosis occurs from loss of hepatocytes)

pressure backs up through portal venous system causing congestive splenomegaly and sinusoidal dilation as well as ascites
what is seen in the kidney of pts with right heart failure?
more renal congestion than is seen in left heart failure

fluid retention, edema, azotemia
what is seen in the CNS of pts with right heart failure?
in advanced CHF, can get cerebral hypoxia and hypoxic encephalopathy

causes loss of attention span and restlessness
what happens in the body cavities of pts with right heart failure?
pleural and pericardial effusions (especially common are rt-sided pleural effusions)

ascites
what is seen in the subQ tissue of pts with rt heart failure?
dependent edema
- pedal and pretibial in ambulatory pts
- back and sacral areas in ambulatory pts

***pitting edema***
congenital heart disease
most arise from faulty embryogenesis during wks 3-8

the most severe are incompatible with intrauterine survival, but range from severe problems at birth to no clinical problems until late adulthood

seen in 1% of live births (more in premies and stillborns)
pathogenesis of congenital heart disease
main known causes are sporadic genetic abnormalities

recognizable genetic or environmental influences in about 10%
- genetic: trisomies (esp. 21), turner syndrome
- environment: rubella

most are multifactorial
genetics of congenital heart disease
heart is one of the first organs to form and develop

different defects in a family may have a common genetic defect b/c of common developmental pathways

- errors in mesenchymal tissue migration
- extracellular matrix abnormalities
- situs and looping defects determining laterality
how many congenital heart defects are caused by errors of mesenchymal tissue migration?
15% of CHD are anomalies in outflow tract(s)

can be failure of fusion or failure of septation

may be due to abnormal development of neural crest-derived cells
a region of what chromosome has a large role in the development of the conotruncus?
chromosome 22

deletions in this region are present in 15-50% of the congenital heart defects
- these deletions are also associated with other types of abnormalities
extracellular matrix abnormalities that cause congenital heart disease
endocardial cushion defects

AV septal defect in Down's syndrome (trisomy 21)
what is the most common genetic cause of congenital heart disease?
down's syndrome (trisomy 21)
what are the three major categories of congenital heart diseases?
1) left-to-right shunts
2) right-to-left shunts
3) obstructions
what is a shunt?
abnormal communication between chambers or blood vessels

direction of flow depends on pressure differentials
right to left shunts
shunted blood bypasses the lung and is not oxygenated

Sx: cyanosis, clubbing, polycythemia, paradoxical emboli
left to right shunts
increase in pulmonary flow causes low resistance, low pressure right-sided structures to be exposed to higher pressures

pulmonary HTN, then right ventricular hypertrophy, and subsequently right CHF

when right pressure rises enough, the shunt switches direction

once significant irreversible pulmonary HTN, cardiac disease is considered irreparable
obstruction
abnormal narrowing of chambers, valves, or vessels

- valve stenosis
- atresias
- coarctation
what are the different left-to-right shunts?
atrial septal defects (ASDs)
patent foramen ovale (PFO)
ventricular septal defect (VSD)
patent ductus arteriosus (PDA)
atrioventricular septal defect (AVSD)
atrial septal defects
L to R shunt
pulmonary blood flow is 2-4x normal (tolerated very well)

irreversible pulmonary HTN occurs in <10% of pts

usually asymptomatic from a functional point of view (may cause a murmur) until adulthood or late adulthood (symptoms are rare younger than 30yo)

three types:
1) secundum (90%)
2) primum (5%)
3) sinus venosus (5%)

Tx: surgery (low mortality)
- post-op survival is "normal"
secundum atrial septal defect
90% of ASDs

deficient or fenestrated (swiss cheese) fossa ovale, near the mid septum

most are isolated abnormalities, but if there is another defect the other is usually more dominant
primum atrial septal defect
5% of ASDs

adjacent to AV valves

usually associated with cleft anterior mitral leaflet (partial AVSD)
sinus venosus
ASD near the entrance of the superior vena cava

commonly associated with anomalous connection of right pulmonary veins to superior vena cava or right atrium
patent foramen ovale
L to R shunt (present in 20% of ppl)

important in fetal life to allow oxygenated blood from the placenta to bypass the non-oxygenated lungs

if it remains open, a R to L shunt can form if there is a significant rise in RV pressure; this shunt can either be sustained and permanent or temporary (caused by cough or bowel movement)
what are the three physiological fetal shunts? where are they?
1. Ductus arteriosus
… protects lungs against circulatory overload
… allows the right ventricle to strengthen
… hi pulmonary vascular resistance, low pulmonary blood flow
… carries mostly med oxygen saturated blood

2. Ductus venosus
… fetal blood vessel connecting the umbilical vein to the IVC
… blood flow regulated via sphincter
… carries mostly hi oxygenated blood

3. Foramen ovale
… shunts highly oxygenated blood from right atrium to left atrium
ventricular septal defect
incomplete closure of ventricular septum (most common congenital heart abnormality)

frequently associated with other abnormalities

depending on size, range from severe problems at birth to spontaneous closure (mostly seen in small muscular septal defects)

most are single holes, but can occasionally appear as "swiss cheese"
what is the most common congenital heart abnormality?
ventricular septal defect
how are ventricular septal defects classified?
size and location

90% involve membranous septum

remainder are below pulmonary valve (infundibular VSD) or in muscular septum

**small muscular VSDs are most likely to spontaneously close; others remain patent**
clinical features of VSDs
50% of small muscular defects close spontaneously and remainder are well tolerated for yrs

large membranous or infundibular VSDs remain patent, with significant L-R flow
- pts can have RV hypertrophy and pulmonary HTN from birth; even if they don't it will develop with time in any large VSD
- large ones have murmur and heart failure from birth (want to fix before pulmonary disease becomes irreversible)
patent ductus arteriosus
persistence after birth of communication btwn pulmonary (pulmonary artery) and arterial systems (aorta); forms a L-R shunt

isolated in 90% of cases

Sx: continuous, harsh murmur, but functionally asymptomatic during childhood

since it is a L-R shunt, more blood flow goes through pulmonary arteries and lungs and the shunt eventually switches to R-L

should be closed ASAP if isolated, but if necessary for life can be maintained with PgE
atrioventricular septal defect (AVSD)
L-R shunt caused by abnormal development of the AV canal
- superior and inferior endocardial cushions fail to fuse
- incomplete closure of AV septum
- inadequate formation of AV valves
what is a partial atrioventricular septal defect?
primum atrial septal defect combined with a cleft anterior mitral leaflet from MI
what is a complete atrioventricular septal defect?
large, combined AVSD with a large, common AV valve

essentially a hole in the center of the heart through which all four chambers can communicate

>1/3 are caused by Down syndrome

correctable
what are the congenital right-to-left shunts?
tetralogy of fallot (TOF)
transposition of the great arteries (TGA)
truncus arteriosus (TA)
tricuspid atresia (triA)
total anomalous pulmonary venous connection/return (TAPVC)
what are the four cardiovascular features of tetralogy of fallot?
1) ventricular septal defect
2) obstruction of right ventricular outflow tract (subpulmonary stenosis)
3) aorta overrides VSD (overriding aorta)
4) right ventricular hypertrophy
what is the most common form of cyanotic congenital heart disease?
tetralogy of fallot
tetralogy of fallot
R-L shunt that results from the anterosuperior displacement of the infundibular septum

pt can survive into adulthood, even if untreated (though Tx is necessary)

with increasing subpulmonary stenosis, get smaller, thin-walled pulmonary arteries and aorta increases in diameter (as the child and the heart grow the condition worsens, but the stenosis protects the pulmonary vasculature therefore RV failure is rare)

Tx: surgical repair is usual, though it can be complicated if the pt has pulmonary artery atresia
what is the shape of the heart in Xrays of pts with tetralogy of fallot?
the heart is enlarged and boot-shaped b/c of the right ventricular hypertrophy
describe the ventricular septal defect in tetralogy of fallot
large VSD with aortic valve forming the superior border

**causes an overriding defect of aorta and both ventricles**
what causes pulmonary obstruction in tetralogy of fallot?
due to narrowing of infundibulum, often accompanied by pulmonary artery stenosis (atresia which involves pulmonary arteries occurs but is rare; in this case a patent ductus arteriosus is necessary for survival)
what determines the direction of blood flow in tetralogy of fallot?
severity of RV outflow obstruction

mild obstruction - resembles VSD - L-R shunt - aka pink tetralogy

severe obstruction - R-L shunt - aka classic tetralogy (pt may be cyanotic at birth)
transposition of great arteries (TGA)
aorta arises from the right ventricle and pulmonary artery arises from left ventricle; the aorta is anterior and to the right of the pulmonary artery (usually behind and to the left) leading to dissociation/separation of pulmonary and aortic circulations

R-L shunt caused by abnormal formation of truncal and aortopulmonary septa

incompatible with post-natal life unless a shunt is present

RV hypertrophy occurs early b/c it functions as the systemic ventricle; LV is thin and atrophic

w/o surgery, most pts die in months
what shunts are present in pts with transposition of the great arteries that allows post-natal life?
ventricular septal defect (35% of pts) - may be a stable shunt

patent ductus arteriosus or patent foramen ovale (65% of pts) - unstable shunts, so require interventional shunt within days
what is the Tx for transposition of the great arteries?
surgery to transect and switch the great vessels

also need to fix the coronary arteries
truncus arteriosus
R-L shunt formed by failure of the embryological truncus arteriosus to separate into that aorta and the pulmonary artery

single artery receives blood from both ventricles

pt must have underlying ventricular septal defect

Sx: early cyanosis, early pulmonary HTN
tricuspid atresia
complete occlusion of the tricuspid valve because of unequal division of AV canal in embryo leads to R-L shunt

- mitral valve is large
- almost always have RV hypoplasia
- circulation occurs via ASD or PFO
- pt also has VSD

pt is cyanotic at birth
mortality is high in first wks-mos
total anomalous pulmonary venous connection (TAPVC)
no pulmonary veins directly enter the left atrium because in the embryo the common pulmonary vein fails to develop or becomes atretic causing the primitive systemic veins to remain patent

veins usually drain into the left innominate vein or coronary sinus

pt needs an ASD or PFO to get pulmonary venous blood into the left atrium

RA - hypertrophied
RV - hypertrophied
LA - hypoplastic
LV - usually normal
dilated pulmonary trunk
what are the obstructive congenital heart anomalies?
1) coarctation of aorta
2) pulmonary stenosis/atresia
3) aortic stenosis/atresia
coarctation of the aorta
congenital obstruction of the aorta

male:female ratio is 2:1
common in Turner syndrome (X0)

infantile form
- hypoplasia of arch proximal to a PDA
- symptomatic in early childhood
adult form
- ridgelike infolding of the aorta just opposite a closed ductus arteriosus (ligamentum arteriosum), distal to arch vessels
- asymptomatic until adulthood

pt may have other anomalies or the coarctation may be solitary

untreated, eventually leads to cardiomegaly, LV hypertrophy, and left CHF
what are the symptoms of aortic coarctation?
with PDA, pt is often cyanotic at birth
- needs intervention to survive neonatal period
- cyanosis of lower body

without PDA, pt is often asymptomatic until adulthood
- upper limb HTN
- low BP, weak pulses, signs of arterial insufficiency in lower limbs
- development of collateral circulation with costal notching
pulmonary stenosis/atresia
obstruction of pulmonary artery

isolated or with other anomalies
pt develops RV hypertrophy
can be mild or severe

can have post-stenotic dilation of pulmonary artery uless there is subpulmonary stenosis (when the trunk is not dilated and may be hypoplastic

if valve is atretic, there is no communication btwn RV and lung, therefore hypoplastic RV and ASD

blood enters lung through a PDA
valvular aortic stenosis/atresia
hypoplastic, thickened cusps that may be abnormal in number (2 instead of 3); isolated lesion in 80%

if severe stenosis/atresia, pt has hypoplastic LV and ascending aorta and needs PDA to allow blood into aorta and coronaries

pt may have LV endocardial fibroelastosis

hypoplastic left heart syndrome (usually fatal in first weeks)
subaortic stenosis
thickened ring or collar of dense endocardial fibrosis tissue below the level of the aortic cusps
supravalvular stenosis
inherited form caused by mutated elastin gene

wall of ascending aorta is thickened, causing luminal constriction
aortic stenosis and atresia
3 varieties:
1) valvular stenosis/atresia
2) subaortic stenosis
3) supravalvular stenosis

LV hypertrophy in response to obstruction
stenosis is usually well-tolerated unless it's very severe
ischemic heart disease (coronary heart disease)
80-90% of all CV deaths

diminished coronary perfusion relative to heart's metabolic demands

involves O2 insufficiency

>90% is due to reduction in coronary flow secondary to atherosclerotic obstruction
what factors aggravate ischemic heart disease?
- increased cardiac energy demand (hypertrophy)
- decreased blood pressure
- increased heart rate
- hypoxia/hypoxemia
what are the four basic manifestations of ischemic heart disease?
1) myocardial infarction (MI)
2) angina pectoris
3) chronic ischemic disease with heart failure
4) sudden cardiac death
stable (typical) angina pectoris
most common type

increased O2 demand outstrips ability of stenosed arteries to deliver nutrients; reduction of perfusion to a critical level, rendering the heart vulnerable to further ischemia if O2 demand is increased

plaque is stable and not disrupted

relieved by rest and/or nitroglycerin
- nitro achieves effect by dilation of peripheral vasculature
- can tx by dilating coronary arteries, but they are probably already maximally dilated
unstable (crescendo) angina pectoris
sudden change in plaque morphology induces partially occlusive platelet aggregation or thrombus and/or vasoconstriction leading to severe but transient reduction in flow

pain occurs with progressive frequency and is brought on by progressively less effort and lasts progressively longer (often occurs at rest)

harbinger of subsequent acute MI in many pts
sudden cardiac death
frequently, a disrupted plaque and partial thrombus have led to regional ischemia that induces fatal arrhythmia
what are the acute coronary syndromes?
myocardial ischemia
unstable angina
sudden cardiac death

**frequently initiated by unpredictable and abrupt conversion of a stable plaque to an unstable lesion via erosion, ulceration, fissuring, rupture or hemorrhage**
**usually thrombosis is superimposed**
pathogenesis of ischemic heart disease?
1.) fixed coronary obstructions
2.) plaque change
3.) inflammation
4.) coronary thrombus
5.) vasoconstriction
fixed coronary obstructions in ischemic heart disease
>90% of IHD pts have significant coronary atherosclerosis in at least one vessel

usually lesions decrease the cross section of one of the major vessels by at least 75%
- compensatory vasodilation is no longer sufficient
- causes symptomatic ischemia on exercise

if stenosis is 90% or more, ischemia occurs at rest
where do fixed coronary artery obstructions tend to occur?
within the first few cm of left anterior descending artery and left circumflex artery

anywhere in right coronary artery
plaque change in ischemic heart disease
initiating event is usually disruption of a previously partially stenotic plaque, followed by thrombosis
- hemorrhage into atheroma can expand its volume
- plaque can rupture or fissure, exposing thrombogenic plaque contents
- fissures most often occur at junction of fibrous cap and adjacent vessel wall
- plaque can ulcerate, exposing thrombogenic subendothelium
what factors influence plaque change in ischemic heart disease?
structure/composition of plaque
adrenergic stimulation
what is the structure of disrupted atherosclerotic plaques?
disrupted lesions are usually eccentric, have a large core of debris and lipid with many macrophages, and have a thin fibrous cap
what property of the fibrous cap of an atherosclerotic plaque predisposes it to rupture?
decreased collagen
- increased degradation
- decreased synthesis
what are the most dangerous atherosclerotic lesions?
mildly to moderately stenotic lesions (<70%) b/c they don't induce angina before disruption

they tend to have a thin fibrin cap, with little inflammation
why are high-grade lesions not as risky as low-grade lesions?
- composition is less complex (more collagen is present)
- since they limit the blood flow, they cause less mechanical stress
- slow progression allows for development of collateral artery branches
- pt's heart is pre-conditioned
what is the effect of adrenergic stimulation on plaque disruption?
physical stress on the plaque in hypertension or vasospasm

stimulation on waking (peak time for MI is 6AM-noon)

emotional stress - marked increase in incidence of sudden death associated with disasters
what is the peak time for MIs to occur?
6am-noon
inflammation in ischemic heart disease
initial lesion needs interaction btwn endothelial cells & wbcs, leading to accumulation of T cells and macrophages in arterial wall

late plaque destabilization and rupture involve secretion of metalloproteinases

inflammatory markers for atherosclerosis

ultra-sensitive C-reactive protein
ultra-sensitive C-reactive protein
>3mg/L indicates a high risk for CV disease

1-3mg/L indicates moderate risk for CV disease

<1mg/L indicates low risk for CV disease
coronary thrombus
total occlusion by a thrombus associated with disrupted plaque causes acute transmural MI

incomplete occlusion causes unstable angina, subendocardial infarcts or sudden death

thrombosis activates growth-related signals in smooth muscle, which can contribute to growth of plaque
vasoconstriction in ischemic heart disease
decreases lumen size and can increase mechanical forces leading to plaque rupture

stimulated by:
- adrenergic agonists
- platelet contents
- impaired secretion of endothelial relaxing factors
- inflammatory mediators
angina pectoris
symptoms complex of paroxysmal, usually recurrent attacks of substernal/precordial chest discomfort/pain caused by transient (15sec-15min) myocardial ischemia that falls short of inducing cell necrosis

three patterns:
1) stable/typical
2) prinzmetal/variant
3) unstable/crescendo
prinzmetal (variant) angina
uncommon

occurs at rest with no relation to activity, HR, or BP

caused by coronary artery spasm

usually relieved by vasodilators or calcium channel blockers
what type of angina pectoris is also known as preinfarction angina?
unstable (crescendo) angina
what is the leading cause of death in the US?
myocardial infarction (MI)

about 1.5 million MIs/yr
- 1/3 of these pts die
what are the types of myocardial infarction?
1) transmural
2) subendocardial (non-transmural)
transmural MI
more common than subendocardial MI

full thickness in distribution of a single coronary vessel

plaque change + complete, occlusive thrombosis
subendocardial MI
infarction is limited to inner 1/3-1/2 of cardiac wall, but can extend beyond the territory of a single vessel, affecting the areas that have poorest perfusion

usually caused by diffuse stenosing atherosclerosis and flow reduction, not by plaque disruption or thrombosis

severe global hypotension can cause circumferential subendocardial infarcts

also occurs after lytic therapy - save some muscle that would otherwise be damaged in a plaque rupture
incidence and risk factors for myocardial infarction
same risk factors for atherosclerosis

frequency increases with age
- 10% in pts <40yo
- 45% in pts <65yo

women are usually protected during reproductive years, but after menopause their risk increases rapidly (IHD is overwhelming COD in elderly women)
coronary artery occlusion
caused by sudden plaque change

exposure of subendothelial collagen or plaque content induces platelet adhesion, aggregation, and activation

stimulation of vasospasm by platelet aggregation

activation of extrinsic path of coagulation cascade

coronary artery can completely occlude in minutes

10% of transmural MI are not thrombotic (vasospasm, emboli, vasculitis, amyloidosis, hematologic disorders)
what platelet aggregators are released in response to sudden plaque change?
TxA2
serotonin
platelet factor 3
platelet factor 4

these factors stimulate vasospasm
myocardial response to coronary artery occlusion
outcome is dependent on severity and duration of flow deprivation

cessation of aerobic glycolysis within seconds and loss of contractility in 1-2 minutes

severe ischemia for 20-30 minutes causes irreversible damage
- permanent damage if perfusion severely reduced for 2-4 hrs
- rationale for window before irreversible changes in thrombolytic therapy

in humans, necrosis progresses over 6 hrs, 12 if there are collaterals
what parts of the heart are commonly affected by MIs?
- all transmural MIs involve at least a part of the LV
- 15-30% of those affecting posterior wall and posterior septum extend into RV
- isolated RV infarction is only 1-3%

LAD is affected in 40-50% of thrombi
RCA is affected in 30-40% of thrombi
LCX is affected in 15-20% of thrombi

less frequent in the left main coronary, diagonal branches of LAD, and marginal branches of LCX
morphology of MIs
transmurals involve nearly the entire perfusion zone of the affected vessel, with a rim of preserved subendocardial tissue, supplied by blood in the heart cavities

infarcts can extend in next days-weeks - see older infarcts at the center, with more recent changes at the periphery
gross morphology of MI
<12 hrs, no gross changes unless the tissue is marinated in triphenyltetrazolium chloride (dehydrogenases are depleted in damaged area, so it does not pick up dye)

12-24 hrs: red-blue appearance due to stagnated blood

progressive delineation: muscle becomes yellow-tan and soft

10-14 days: peripheral hyperemic zone of vascular granulation tissue

eventually involutes to fibrous scar
what is seen in infarcted tissue microscopically 4-12 hrs after infarction?
long & thin wavy fibers at periphery

vacuolization or myocytolysis in peripheral reversible ischemic fibers, especially viable subendothelium

beginning stages of coagulative necrosis
what is seen in infarcted tissue microscopically 1 day after infarction?
definite coagulative necrosis
pyknosis
hypereosinophilic muscle fibers
edema
scattered neutrophils
what is seen in infarcted tissue microscopically 2-3 days after infarction?
acute inflammation peaks
what is seen in infarcted tissue microscopically 5-10 days after infarction?
macrophages remove necrotic myocytes
what is seen in infarcted tissue microscopically 2-4 weeks after infarction?
prominent granulation tissue forms
what is seen in infarcted tissue microscopically 6 wks after infarction?
well-advanced scarring (fibroblast proliferation causes collagen deposition)
therapeutic interventions for acute MI
idea is to rescue ischemic but not necrotic tissue to limit the size of the infarct

benefit depends on rapidity of occlusion relief

3-4 hours after onset of symptoms is the critical time

1) thrombolysis
2) percutaneous transluminal coronary angioplasty (PTCA)
3) coronary arterial bypass graft (CABG)
thrombolysis for treatment of MI
streptokinase/tPA dissolves thrombus via activation of the fibrinolytic system

affects thrombus, but not the underlying plaque
percutaneous transluminal coronary angioplasty (PTCA)
Tx for acute MI

can eliminate/disrupt thrombus and relieve some of the underlying plaque obstruction

plaque ruptures at the weakest point and oftern hemorrhages into adjacent wall

media dissects and stretches with obstruction relief, which creates an unstable plaque
why is reperfused myocardium hemorrhagic?
injured vasculature is leaky
what are contraction bands?
intensely eosinophilic transverse bands composed of contracted sarcomeres in critically damaged myocytes
reperfusion injury
cell damage to a small amount of cells after infarcted tissue has been reperfused with blood

free radicals from wbcs can cause apoptosis and endothelial swelling at the capillary level
what is stunned myocardium?
difficulty of temporarily infarcted cells to recover after reperfusion of ischemic myocardium

may result in reversible heart failure that benefits from temporary cardiac assistance
what is cardiac preconditioning?
repetitive short-lived severe ischemia (repetitive angina or silent ischemia) protecting myocardium from greater subsequent ischemic insult
coronary artery bypass graft (CABG)
usually not Tx for acute situations, unless there is a complication of angioplasty

most often is an "elective" procedure
symptoms of MI
chest pain, radiating down left arm
rapid, weak pulse
diaphoresis
dyspnea

10-15% are silent (picked up by changes in EKG)
when do most MI deaths occur?
1/2 occur within the first hour, often b/c the pt never reaches a hospital

if pts get to hospital, death rate has decreased from 30% to between 7-13% since the 60s
what cardiac markers are typically used to test for MI?
marker - rise - peak - normalize

CK-MB - 2-4hrs - 24hrs - 72hrs

troponin - 2-4hrs - 48hrs - 7-10days
why are there cardiac markers that indicate MIs?
intracellular molecules (creatine kinase and troponins) leak out of fatally injured cells via damaged cell membranes
creatine kinase (MI diagnosis)
old cardiac marker, but still used
3 isoenzymes from 2 dimers (M&B)
CK-MM: skeletal muscle and heart
CK-BB: brain, lung
CK-MB: mainly heart

CK-MB rises 2-4 hrs after MI, peaks at 24hrs, and normalizes at 72 hours

myocardial damage is likely when total CK>190U/L, CK-MB>24U/L, CK-MB>6% of total
troponins (MI diagnosis)
not normally detectable in the blood
appear 2-4 hrs after MI, peak at 48hrs, normalize at 7-10 days

cardiac and skeletal muscle troponin I and T have differences in amino acid sequences, so assays (esp. for T) can be made specific for the cardiac form

since it has a longer t1/2 than CK, it is useful if CK is normal
what is the effect of reperfusion on CK and Tn levels?
peak of both accelerates (will be less than 24/48 hrs respectively)
consequences of MI
in-hospital death at 10%
complications occur in 75%
- contractile dysfunction of LV
- arrhythmias
- myocardial rupture
- pericarditis
- infarct extension/expansion
- thrombus
- ventricular aneurysm
- papillary muscle dysfunction
- late heart failure

as a rule, the larger the infarct, the more likely there will be complications
on what factors is long-term prognosis dependent?
quality of residual LV function

extent of vascular obstruction in vessels perfusing viable tissue

mortality in the first year is 30% (including those that die before reaching ER)
3-4% mortality for subsequent years
contractile dysfunction of LV after MI
can result in varying degrees of LV failure, hypotension, pulmonary congestion & edema

cardiogenic shock occurs in 10-15%, associated with large infarcts (>40% of LV)
- 70% mortality
- 2/3 of in-hospital deaths
what is the cause of 2/3 of in-hospital deaths related to MI?
cardiogenic shock due to contractile dysfunction of LV

associated with large infarcts that involve >40% of the LV
arrhythmias as a consequence of MI
common

causes most sudden death

results from conduction disturbances or myocardial irritability

parts of the AV conduction system are in an inferoseptal location
myocardial rupture as a consequence of MI
weakening of the necrotic, inflamed tissue

most common location is the free LV wall with hemopericardium and cardiac tamponade (generally btwn 3-7 days after MI)

IV septal rupture creates L-R shunt

papillary muscle is least common site (causes acute, severe mitral regurgitation)
when does pericarditis occur as a consequence of MI?
day 2 or 3
ventricular aneurysm as a consequence of MI
late complication from anteroseptal infarct

heals with a thin scar that bulges during systole
why does an MI cause papillary muscle dysfunction?
only causes papillary muscle dysfunction if they are in the affected area

first causes ischemia and then fibrosis
chronic ischemic heart disease
progressive heart failure as a result of ischemic myocardial damage

usually pt has a previous MI or bypass surgery in hx
- post-infarction decompensation due to exhaustion of compensatory hypertrophy of viable tissue

occasionally no history of MI, but severe obstructive CAD
morphology of chronic ischemic heart disease
heart is heavy with LV hypertrophy and dilation

moderate to severe stenosing atherosclerosis

often scars of old infarcts

hypertrophy of remaining viable fibers

may have thrombi and/or patchy endocardial fibrous thickening

subendocardial vacuolization and fibrosis
clinical features of chronic ischemic heart disease
insidious onset of CHF in pts with past MIs or angina

Dx of exclusion of other causes of heart failure
sudden cardiac death
unexpected cardiac death early after onset of symptoms or in absence of symptoms

most caused by acute MI
- in younger pts, look for other causes

death is usually caused by arrhythmia
pathogenesis of sudden cardiac death
some are hereditary

often caused by primary electrical abnormalities
- channelopathies (most important)
- long QT syndrome (prototype)
what are channelopathies?
AD inheritance of mutations in genes needed for normal ion channel fcn

either genes coding for ion channels or accessory proteins needed for functioning of the channels

most important cause of arrhythmias that lead to death in pts with sudden cardiac death
morphology of sudden cardiac death
80-90% have coronary stenosis, usually severe (75-90% occlusion)

1/2 have plaque disruption
1/4 have acute MI
pts commonly have old MIs

similar to severe chronic ischemia
how can a physician improve the prognosis of pts that are susceptible to sudden cardiac death?
implanting a pacemaker or automatic cardioverter defibrillator
what are the minimum criteria for dx of systemic (left-sided) hypertensive heart disease?
LV hypertrophy, usually concentric, in absence of other CV pathology

Hx or pathological evidence of elevated BP
what is the minimum BP that is required to produce LV hypertrophy?
no minimum

even mild elevations, if prolonged, can induce LV hypertrophy

it is an adaptive response to pressure overload
gross morphology of compensated systemic (left-sided) hypertensive heart disease
circumferential LV hypertrophy without dilation

wt increase is disproportionate to cardiac size

LV>2cm and wt may exceed 500gm

eventually LV gets stiff, impairs diastolic filling, and causes subsequent left atrial enlargement
microscopic morphology of compensated systemic (left-sided) hypertensive heart disease
increase in myocyte diameter

cell and nuclear enlargement

intersitial fibrosis
clinical features of compensated systemic (left-sided) hypertensive heart disease
- may be asymptomatic
- EKG or echo evidence of LV hypertrophy
- atrial fibrillation
- BP control can prevent/cause regression of hypertrophy
pulmonary (right-sided) hypertensive heart disease (cor pulmonale)
RV hypertrophy and dilation
potential heart failure secondary to pulmonary HTN (cor pulmonale)

caused by disorders of the lung or pulmonary vasculature; by definition, excludes RV hypertrophy and dilation caused by congenital heart disease or caused by left-sided heart disease

can be acute (after massive PE) or chronic (secondary to prolonged overload b/c of obstruction of pulmonary vasculature)
morphology of acute pulmonary (right-sided) hypertensive heart disease (cor pulmonale)
caused by massive PE

marked dilation of right ventricle without hypertrophy (no time)
normal crescentic shape of RV changes to dilated ovoid
morphology of chronic pulmonary (right-sided) hypertensive heart disease (cor pulmonale)
secondary to prolonged overload b/c of obstruction of pulmonary vasculature

- wall thickens up to 1cm or more (may resemble thickness of LV)
- thickened muscle bundles in outflow tract or thickened muscle connecting septum to anterior RV papillary muscle

if severe, can compress LV or cause tricuspid regurgitation

loss of normal fatty component of RV
stenosis
failure of a valve to open completely, with impedance of forward blood flow
incompetence
failure of a valve to close completely, with reversal of flow
insufficiency
failure of a valve to close completely, with reversal of flow
regurgitation
failure of a valve to close completely, with reversal of flow
functional regurgitation
valve becomes incompetent due to ventricular dilation, causing papillary muscles to be pulled down and outward and preventing co-aptation of otherwise normal valve leaflets

can also be caused by dilation of aortic or pulmonary annulus
how quickly do valvular diseases present?
can be rapid, if a cusp is destroyed by an infection, but more often results gradually over years
what is the most frequent valvular disease?
acquired stenosis of mitral or aortic valves (2/3)
what are the mechanisms that cause valvular insufficiency?
disease of valve cusps

damage to supporting structures (annulus, papillary muscles, ventricular free wall)

can be acute or chronic
what are the most common chronic valve diseases?
1) mitral stenosis from rheumatic heart disease
2) mitral insufficiency from mitral valve prolapse (myxomatous degeneration)
3) aortic stenosis from calcification of normal or congenitally bicuspid valve
4) aortic insufficiency from dilation of ascending aorta (HTN or aging)
valve degeneration caused by calcification
dystrophic calcification process without significant lipid deposition or cell proliferation
1) wear & tear with dystrophic calcification
2) chronic injury secondary to hyperlipidemia, HTN, or inflammation

valves have osteoblast-like cells making bone matrix proteins and promoting calcium deposition
calcific aortic stenosis
aortic stenosis is the most frequent valve abnormality (can be congenital or acquired)

acquired - calcification induced by wear/tear of congenitally bicuspid valve (presents in 50s-60s) or calcification of normal valves with aging (presents in 70s-80s)
what is senile calcific aortic stenosis?
dystrophic calcification of normal aortic valves that occurs with aging

presents in 70s-80s
morphology of calcific aortic stenosis
heaped up calcifications within cusps protrude into sinus of Valsalva, preventing opening of cusps

distortion primarily seen at base; free cusp edge is not involved
- no fusion of commissures until very late (distinguish from rheumatic valvular disease)

mitral valve is usually normal but can have extension of aortic calcification onto anterior leaflet and/or have annular calcification
clinical course of calcific aortic stenosis
narrowing causes inc. in pressure gradient across stenotic valve (LV pressure may reach 200mmHg)

concentric LV hypertrophy that causes LV to be prone to ischemia

Sx: angina and syncope, with eventual decompensation and CHF

once symptomatic, 50% die in 5 yrs w/o intervention; if pt has CHF, 50% die in 2 yrs
calcification of congenital bicuspid aortic valve
aortic valve is normally tricuspid (bicuspid occurs in 1% of the population)

causes 50% of aortic stenosis in adults

one cusp is usually larger with a raphe from incomplete embryologic separation OR can be acquired from fusion of commissure in rheumatic disease

raphe is the major site of calcification
valve may become incompetent
predisposing factor for infective endocarditis
mitral annular calcification
calcification in the ring of the mitral valve

irregular, hard, occasionally ulcerated nodules 2-5mm behind the leaflets

usually doesn't affect function, but if nodules ulcerate a thrombus can form and embolize (also provides a site for infective endocarditis)

common in women>60yo
myxomatous mitral valve
elevated LV pressure
myxomatous degeneration of mitral valve
aka mitral valve prolapse

floppy valve balloons back into the LA during systole

most common valve disease in the west (present in 3% of adults, usually young women)
what is the most common valve disease in the west?
myxomatous degeneration of mitral valve (aka mitral valve prolapse)
what is the morphology of mitral valve prolapse?
- intercordal ballooning
- leaflets are enlaged, thick and rubbery
- tendinous cords are elongated and thin (can rupture)
- annular dilation (rare in other causes of mitral insufficiency)
- attenuation of fibrosa layer of valve with thickening of spongiosa layer with deposition of myxomatous material
what are the secondary valve changes in mitral valve prolapse?
- fibrous thickening of the leaflets
- thickening of LV endocardial surface where valve hits
- thickening of LA endocardium from the prolapse back into atrium
- thrombi form on atrial surface of leaflet
- calcification at the base of the posterior leaflet
pathogenesis of mitral valve prolapse
developmental anomaly of connective tissue

common in Marfan syndrome and in some other herditary CT disorders
clinical features of mitral valve prolapse
usually asymptomatic; picked up on physical exam as a midsystolic click

3% develop complications:
- infective endocarditis
- mitral insufficiency
- stroke/systemic infarct from thromboembolism
- arrhythmia
rheumatic fever
acute immunologically mediated multisystem disease, occuring a few weeks after group A strep throat

acute rheumatic carditis, which complicates the active phase of rheumatic fever, may progress to chronic valve deformities
how frequent is rheumatic fever?
occurs in about 3% of cases of strep pharyngitis

pts who do get it are prone to reactivation of disease with subsequent throat infections
what major findings are common in rheumatic fever?
1) migratory polyarthritis of large joints
2) carditis
3) subcutaneous nodules
4) erythema marginatum of skin
5) sydenham chorea (involuntary purposeless rapid movements of extremities)
Dx of rheumatic heart/valve disease by Jones criteria
evidence of preceding group A strep infection

two major findings
OR
one major and two minor findings
**minor manifestations are nonspecific sx's like fever, arthralgia, acute phase reactants**
pathogenesis of rheumatic heart/valve disease
antibodies form against M proteins of S. pyogenes cross-react with heart antigens

CD4 cells specific for S. pyogenes peptides also react against heart proteins and produce cytokines that activate macrophages
what are aschoff bodies?
foci of swollen eosinophilic collagen surrounded by lymphocytes, some plasma cells and plump macrophages

pathognomic for rheumatic fever
(found in the endo-, myo-, and pericardium in acute disease)
what are anitschkow cells?
macrophages with abundant cytoplasm and with a central nucleus having chromatin in a central, thin, wavy ribbon

aka caterpillar cell

pathognomic for rheumatic fever
acute rheumatic fever
aschoff bodies
anitschkow cells in endo-, myo-, and pericardium in acute disease

pericarditis with fibrinous or serofibrinous exudate (bread & butter exudate) that resolves w/o sequelae

myocarditis especially in interstitial perivascular tissue

endocarditis or valve involvement
- fibrinoid necrosis w/in cusps or along tendinous cords
- 1-2mm vegetations along lines of closure
- subendocardial thickened lesions in LA (MacCallum plaques)
what are MacCallum plaques?
subendocardial thickened lesions in left atrium

seen in acute rheumatic fever
chronic rheumatic heart disease
- deforming fibrosis, particularly of the valve leaflets
- mitral valve always deformed, but involvement of other valves may be more important clinically
- mitral leaflet thickening (commissure fusion; short, thick, fused tendinous cords; fibrous bridging across commissure and calcification)
what is fish mouth (buttonhole) stenosis?
fibrous bridging across commissure and calcification of mitral leaflets

seen in chronic rheumatic heart disease
microscopic morphology of chronic rheumatic heart disease
diffuse fibrosis
often see neovascularization
Aschoff bodies replaced by scar
what is the most frequent cause of mitral stenosis?
chronic rheumatic heart disease

causes 99% of cases
what is the prevalence of valve involvement in chronic rheumatic heart disease?
mitral only in 65-70% of pts
mitral/aortic in 25% of pts
can involve tricuspid valve; pulmonary valve involvement is rare
what is the pathological course of chronic rheumatic heart disease?
with mitral valve stenosis, left atrium dilates and may contain thrombi

eventually lung changes and RV hypertrophy develop
clinical course of rheumatic fever/heart disease
starts 10d-6wks after strep pharyngitis

usually occurs in children 5-15 years old, but 20% of first attacks are in adults

culture negative but antibodies to strep enzymes in serum (streptolysin O and DNAse B)

arthritis is more common in adults than children (fever plus one large joint after another is painful and swollen for days)

- may develop arrhythmias, esp in mitral stenosis
- thromboembolic complications
- infective endocarditis
describe carditis in rheumatic fever
friction rubs, weak heart sounds, tachycardia, arrhythmias

1% of pts die from acute fulminant rheumatic fever

myocarditis may cause cardiac dilation to point of mitral valve insufficiency or heart failure

if attacks are recurrent, carditis gets worse
when does rheumatic valve disease present?
decades after the initial attack of rheumatic fever
infective endocarditis
colonization or invasion of valves or endocardium by an organism

bulky, friable vegetations made up of organisms (mostly bacterial) and thrombotic debris

often causes destruction of underlying tissue
acute endocarditis
destructive infection by a virulent organism, frequently of a previously normal valve

50% mortality in days-weeks, even with treatment

usually requires surgery
usually caused by S. aureus
subacute endocarditis
destructive infection caused by organisms of lower virulence (commonly S. viridans) that often involves previously abnormal valves

insidious onset

untreated, it can last wks to mos, but most recover with antibiotics
what valve abnormalities are predisposing factors for infective endocarditis
rheumatic heart disease
floppy mitral valve
degenerative
artificial valves
what host factors are predisposing factors for infective endocarditis?
immunosuppression/deficiency
neutropenia
diabetes
EtOH
IV drug abuse
what organisms commonly cause infective endocarditis on abnormal valves?
native bacteria (Strep viridans 50-60% of pts)
what organisms commonly cause infective endocarditis in normal or deformed valves?
Staph aureus (10-20%)
- esp. in IV drug users
what kind of organisms cause infective endocarditis in prosthetic valves?
coagulase-negative Staph (e.g. Staph epidermidis)
what conditions predispose pts to seeding of blood by microbes?
- obvious infection elsewhere
- dental/surgical work with transient bacteremia
- unrecognized infection
- IV drug abuse
morphology of infective endocarditis
- fibrin, inflammatory cells, organisms
- fungal vegetations tend to be larger than bacterial vegetations
- aortic and mitral valves are the most common sites (right side may be involved in drug users)
- vegetations can be single or multiple; can involve one or more valves
- can erode into adjacent myocardium, producing ring abscess, and eroding cusp
- systemic emboli often produce septic infarcts
- subacute endocarditis usually causes less valvular destruction
- often granulation tissue at base of vegetation
- eventual fibrosis, calcification, chronic inflammation
clinical course of infective endocarditis
fever
- rapidly developing in acute endocarditis
- chills and weakness
- may be slight or absent in elderly with subacute disease
- accompanying mild fatigue, flu-like symptoms, wt loss

murmurs
- 90% of left-sided lesions
- can be mistaken for abnormal valve murmur

ring abscess and septic emboli in acute endocarditis

rare - microemboli in the retina, subungual hemorrhage, petechiae
nonbacterial thrombotic endocarditis (marantic vegetations)
- sterile, no organisms
- loosely attached masses of fibrin, platelets, other blood elements on valve leaflets
- usually on normal valves
- no inflammation
- can be found on either side of heart
- 1-5mm, single or multiple lesions located on line of closure or cusps
- don't cause damage to valve, but can embolize
- often seen in debilitated pts (e.g. CA pts)
pathogenesis of nonbacterial thrombotic endocarditis
pt often has concomitant PE or venous thrombosis (hypercoaguable state)

often associated with mucin-producing adenocarcinomas (mucin has a procoagulant effect)

also associated with other malignancies/hypercoagulable states, and with endocardial trauma (i.e. heart catheter)
libman-sacks endocarditis
SLE endocarditis
occasional occurrence
- sterile granular vegetations on mitral, aortic, tricuspid valves (can cause regurgitation)
- single or multiple, 1-4mm lesions frequently on the undersurface of AV valves (can be scattered on valves, cords, and endocardium)
- fine, granular eosinophilic material; may have hematoxylin bodies
- often intense fibrinoid necrosis type valvulitis adjacent to vegetation
- can result in fibrosis and valve deformity
carcinoid heart disease
1/2 ot pts with carcinoid syndrome have lesions on right endocardium and valves (mostly on RV)

plaque-like endocardial fibrous thickenings of cardiac chambers, right-sided valves, and occasionally IVC and pulmonary artery
morphology of carcinoid heart disease
plaque-like endocardial fibrous thickenings of cardiac chambers, right-sided valves, and occasionally IVC and pulmonary artery

fibrous intimal thickenings of smooth muscle and sparse collagen

mucopolysaccharide matrix that expands endocardium

underlying structures are intact
pathogenesis of carcinoid heart disease
there is a relationship btwn the levels of serotonin and severity of lesions

confined to right heart, since lungs can inactivate serotonin and bradykinin

pts treated with 5-HT analogues for migraine have similar (rare) left-sided lesions (also occurs with fen-phen, with pulmonary carcinoid, and with patent foramen ovale)
clinical features of carcinoid heart disease
tricuspid insufficiency > pulmonary insufficiency (if there is pulmonary insufficiency, there there is always tricuspid insufficiency as well)

may also get right-sided stenoses
complications of artificial valves
- about 60% develop serious complications in 10yrs
- thrombotic complications are the major ones (can obstruct valve or embolize)
- pts on long-term anticoagulation, so they can have bleeding problems
- infective endocarditis, often with ring abscess
- structural deterioration of biological prostheses
- hemolysis, mechanical obstruction, overgrowth by fibrous tissue