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Cardiovascular Pathology

What is the most common primary tumor of the heart?
--atrial myxoma (rare, pedunculated tumor that can occlude valves, cause murmurs)
--congenital, assoc w/ Carney's syndrome

More common than the myxoma is a metastasis to the heart from what malignancy?
--melanoma

What percentage of people with heart attacks die before they get to the hospital?
--50%

How many MI patients then die in the hospital?
--10%

How many more die in the first year after the MI?
--another 10%
--"feel more secure after a year"

Name three cell types that are involved in the development of atherosclerosis.
--EC's, SMC's, PLT's, Leukocytes

Name the most widely accepted theory as to a mechanism of action for atherosclerosis.
--response to injury (EC's initiate process when injured)

What are some factors that contribute to endothelial injury?
--HTN, hyperglycemia-->glycosylation, hyperhomocystinemia, shear forces, high LDL-->deposition, infx, toxins esp cig smoke-->oxidation

Macrophages that eat more oxidized LDL than they ever wanted to turn into what?
--"foam cells"

What's the first visible lesion of atherosclerosis?
--fatty streak = an accumulation of serum lipoproteins in the intima of vessel wall
--visible in aorta and coronary arteries of most US individuals by age 20
--next visible lesion: fatty plaque

What causes atherogenesis at important sites in the coronary arteries, major branches of the thoracic and abdominal aorta, and the large vessels of the lower extremities?
--increased shear stress and turbulence at branches/curves in vessels

What is CAD, coronary artery disease?
--reduction of blood flow to cardiac muscle due to atherosclerosis of coronary arteries

What's the #1 CAD risk factor that is in our control?
--cigarette smoking

Which lipoprotein has been linked to elevated risk of MI?
--lipoprotein a (elevations are dangerous)

What foods help us bring down homocysteine levels?
--onions, garlic

What's the best blood test for acute MI today?
--troponin

Which populations under age 45 are highest risk for MI's? (4)
--cocaine/amphetamine/ephedrine users (sympathomimetic drugs)
--insulin-dependent diabetics
--pts with hypercholesterolemia
--positive family hx for early coronary dz

How do the sympathomimetic drugs mentioned above increase myocardial demand?
--they increase afterload resistance and produce inotropic effects (increase the force of contraction)-->increased workload for heart muscle
--also increase risk of vasospasm of coronary arteries

MONA is an acronym for treatment of a suspected MI. What does MONA stand for?
--morphine (angiolytic and decrease anxiety)
--oxygen (increase blood gas load)
--nitrates (nitroglycerine to vasodilate)
--aspirin (decrease platelet aggregation and reduce thrombus formation)

What are the three types of angina pectoris?
--stable = occurs with exertion, relieved w/ rest or nitro
--variant = Prinzmetal, dt vasospasm, occurs at rest
--unstable = pain at rest w/o variant hx, cardiac emergency, mb prodrome of MI

What are the four presentations of IHD, ischemic heart disease?
1) MI
2) angina
3) chronic IHD with heart failure
4) sudden cardiac death

During an MI, how long does it take ATP production (in infarcted tissue) to be halved?
--10 minutes
--decreased ATP-->membrane channel disruption (Na/K ATPase not working)-->increase in cell membrane permeability-->myocardial cells swell-->more permeability increase-->Ca2+ flows into cardiac muscle-->activation of degradative enzymes (lipases, proteases, nucleases)-->cell fx disrupted-->irreversible cell death 15-20 minus from onset of injury

Re-perfusion during what time frame may resurrect the myocardium?
--1-6 hours
--how does this match up with death in 15-20 minutes?? most cells must not die.

What is the histologic progression of MI tissues after the event? (4 stages)
--1 day: coagulative necrosis, wavy fibers and widened edematous spaces
--3-4 days: dense leukocytic infiltrate
--7-10 days: necrotic myocytes phagocytized, fibrin deposition begins
--2 months: dense collagenous scar (blue) with residual cardiac muscle cells

What are the GROSS changes to myocardium post MI? (7 stages)
-- < 4 hours may see no change
--4-12 hours: pale, bluish, edematous
--12-24 hours: darker hemorrhage may appear deep blue/purple
--1-3 days: tannish-yellow infarcted areas
--3-7 days: red hyperemic border around tan-yellow-->coagulation necrosis
--2-8 weeks: grey-white scar formation
--2-3 months: completed scar formation

END OF QUIZ, NOTES FROM HERE DOWN

ATHEROEMBOLISM
--ETIO: usu iatrogenic: lower extremity & hip surgery, cardiac & aortic surgery, angiography
--S/Sx: digital necrosis, GI bleed, MI, retinal ischemia, cerebral infarct, renal failure
--RISK factors: tobacco, obesity, cardiac arrhythmias, immobilization, estrogens (OCPs or HRT)

MI
--S/Sx: chest pain @ anterior precordium, tightness, squeezing, weight/pressure on chest
--S/Sx: pain in jaw, neck, arms, back, epigastrium, usu L side arm/jaw
--S/Sx: dyspnea or SOB is most common presentation in women, elderly, diabetics
--S/Sx: nausea with inferior or posterior wall ischemia
--S/Sx: diaphoresis, anxiety, lightheadedness, syncope, cough/wheezing, abdominal pain
--Signs: hyper or hypotension, hyper dt anxiety or hypo dt large R ventricle infarct
--Signs: acute valve dysfx-->dysrhythmias
--2 types:
--1) transmural (ddt acute coronary thrombosis, on EKG: Q pt deepened, ST goes up, then down)
--2) subendocardial (coronary aa. narrow but patent, occlusion, time limit on high demand, anemia, may not show on EKG)
--LABS: elevated WBC, LDH, cardiac enzymes incl: troponin & creatine phosphokinase (MB band)
--COMPLIC: 3/4 of pts have 1+ complications following an acute MI, often: L ventric infarct-->cardiogenic shock (10-15% of pts, 70% mort rate, 2/3 of in-hospital deaths), arrythmias incl: sinus bradycardia, heart blocks, tachcardia, ventricular premature contractions or tachycardia, ventricular fibrillation. V fib is the most common cause of heart arrest and sudden death.
--COMPLIC: also heart may rupture: free wall rupture most common and usu fatal, septum or papillary muscle may also rupture, pap m rupt-->acute onset mitral regurg mb delayed after MI
--COMPLIC: hypotension, CHF, hypoxemia, VSD, accute MR, pericarditis, repeat MI
--most common complication is pericarditis, Dressler syndrome

CHF
--S/Sx: 1st sign is usu tachycardia
--obvious exception is CHF dt bradyarrhythmias or complete heart block
--S/Sx: SOB worse when lying down or exerted, waking breathless at night
--Sx: sleeping propped on pillows, coughing, swelling, rapid weight gain, fatigue
--decreased contractile properties of heart: coronary atherosclerosis, arterial HTN, IHD and MI, inflam and degenerative muscle dz
--primary or secondary, L or R, acute or chronic, compensated vs de-, low vs high output
--primary: CAD, valve disorder, cardiomyopathy
--mb precipitated by cessation of cardiac drug esp a diuretic
--mb aggravated by dysrhythmias or tachycardia
--other precipitators: viral and bact infx, envir, emot, fever, anemia, hypoxia, resp/metabolic acidosis, electrolyte imbalance (low Ca2+), physical stress that incr O2 demand
--300,000 Americans die per year with this problem
--affects over 2 million/year
--heart can't pump enough to meet metabolic needs of body
--compensated or decompensated, acute or chronic
--PE: JVD, S3 sound, rales in lung
--Frank Starling curve: muscle force of contraction increases as muscle stretch during relaxation increases (to optimal preload), up to a point when muscle is overstretched and fails
--L side failure affects lungs first
--R side failure affects periphery first
--usually L first then R, presenting together clinically
--with fluid buildup in periphery, afterload increases so output decreases
--cardiac muscle enlarges to compensate for increased load, but bulk lowers preload capacity because ventricles won't stretch, so preload is decreased, stroke volume decreases and so does cardiac output

LCHF
--pulmonary congestion
--incr L vent end-diastolic pressure
--incr L atrial pressure
--ETIO: usu L vent infarct, HTN and/or mitral valve dz
--pure L sided heart failure usudt pulmonary venous congestion

RCHF
--ineffective R ventricular contraction
--isolated R side mb acute dt infarct, pulmonary embolus
--most common cause of R CFH is L CHF
--COR PULMONALE is heart failure dt pulmonary dz
--such as: emphysema, chronic bronchitis, pulm embolus, pulm HTN
--pure R sided usu assoc with systemic venous congestion

ACUTE CHF
--sympathetic nervous sys and renin-angiotensin system maintain flow pressure to vital organs
--increase myocardial contractility and selective peripheral vasoconstriction
--salt and fluid retention
--blood pressure maintenance by incr catecholamines-->periph vasoconstrict keeps blood @ core
--renin-angiotensin-aldosterone-->renal arteriolar constriction-->decr GFR-->incr resorption of Na-->fluid retention

CHRONIC CHF
--myocardial cells die from energy starvation
--cytotoxic mechanisms-->necrosis
--acceleration of apoptosis
--necrosis of myocytes-->fibroblast prolif-->replace muscle with collagen/scar
--HEART FAILURE CELLS = macrophages full of hemosiderin in alveoli dt LCHR & chronic pulm edema
--fluid retention enhanced by decreased hepatic metabolism of aldosterone dt venous congestion
--all leads to ventricular hypertrophy

HIGH OUTPUT CHF
--ETIO: sustained tachyarrhythmia, A fib, pregnancy, anemia
--ateriovenous fistulas, berberi
--hyperthyroid, cocaine, methamphetamine
--Paget's: abn bone growth dt increasted osteoblast activity, bone is vascular and needs big supply, is warm with vascularity
--pt has warm extremities
--peripheral vasodilation

LOW OUTPUT CHF
--peripheral vasoconstriction and cool extremities
--after weakening dt MI or IHD, dilation or hypertrophy, endocarditis, myocarditis, IHD, HTN, valvular and pericardial dz
--late CHF

HYPERTENSION
--affects up to 25% of Americans, increases with age
--African-Americans have 2x more than whites
--stage 1 = 140-50's/90's
--stage 2 = 160-70's/100-109
--stage 3 = over 180/over 110
--usu Asx until late-->MI, stroke, renal failure
--ETIO: 90% of so idiopathic, primary, essential
--ETIO: some dt chronic renal failure or steonsis of renal arteries
--HTN is leading cause of IHD, PVD, stroke, ventricular hypertrophy, CHF, renal failure
--labil, benign, or accelerated
--labile means elevations are inconsistent, ie dt stress catecholamines from seeing doc
--labile also with pheochromocytoma but usu dramatic events: paroxysmal HA, sweat, palpations, HTN and orthostatis hypotension
--benign is slow developing, not really benign
--S/Sx: headaches, retinal hemorrhage, papilledema, decreased LOC, seizure, renal failure

ANEURYSM
--ballooning" of vessel wall
--usu in aorta and circle of Willis
--listen for bruit in abdomen

AORTIC DISSECTION
--usu blood thru medial tissue of aorta and can affect any part of the aorta
--excruciating pain not relieved by morphine
--Tx: lower BP
--life threatening
--incr risk with Marfans

MARFAN'S SYNDROME
--genetic disorder of connective tissue
--collagen abn
--tall with long digits and extremities: arm span exceeds height
--S/Sx: lens dislocation

CARDIOMYOPATHY
--dilated (90%), hypertrophic or restrictive
--dilated, all 4 chambers, idiopathic, usudt chronic alcoholism-->low thiamine, may also be dt viral myocarditis-->autoimmune
--HCM = hypertrophic cardiomyopathy, genetic dz dt sarcomere abn, characterized by thick walls, abn diastolic filling, and 1/3 of cases have intermittent ventricular outflow obstruction, interstitial fibrosis
--classic pattern in hypertrophic is disproportionate thickening of the ventricular septum!!!
--restrictive: myocardium infiltrated with abn tissue, amyloidosis or hemochromatosis

INFECTIOUS ENDOCARDITIS
--invasion of heart valves or muscle by microbes
--forms vegetations = mass of infx thrombotic debris (PLT's & fibrin & bact) on/around affected valve
--veges may destroy valve/tissue
--veges may "infect" prosthetic valves/pacemakers
--veges may embolize
--veges are friable
--orgs involved: bact, fung, Chlamydia, Rickettsiae: bact most common
--portals of invasion: teeth, parynx, GU, skin, pulm infx, IV use
--acute vs sub-acute
--acute: virulent org-->death for 50% even with tx
--sub-acute: usu on valve already damaged, less virulent org USU alpha hemolytic STREP VIRDANS, most pts recover, Strep v usu on native valves..
--acute S/Sx: fever (dramatic onset), new murmurs, emboli, abscesses beneath leaflets
--sub-acute S/Sx: fever except in elders, emboli, petechiae in mouth under tongue, everywhere, finger nail beds, retina (Roth's spots), finger pads
--RISK: artificial valve (usu STAPH EPIDERMITIS), immunocompromise, IV user (STAPH AUREUS), alcoholic (ANAEROBES & ORAL BUGS), indwelling catheter (GRAM NEG IE E COLI), vascular graft
--infecting org not found 5-20% of cases-->? sterile endocarditis? inflam only? SLE.
--endocarditis of SLE is LIBMAN-SACKS endocarditis, vegetations spread flat
--MARANTIC endocarditis = dt hypercoagulable state, Trousseau's syndrome, paraneoplastic syndrome assoc w/ malignancy

ENDOCARDITIS MATCHING ORGS:
--native valves, subacute === Strep viridans (alpha hemolytic)
--prostetic valves === Staph epidermitis
--alcoholics === anaerobes and oral cavity bugs
--IV drug abusers === staph aureus
--cytoscopy, prostatectomy, catheter === gram neg such as E. Coli
--colon cancer === Strep bovis (if this bug is cultured-->indication for colonoscopy)

STREP --> RHEUMATIC FEVER --> RHEUMATIC HEART DISEASE
--#1 cause of rheumatic fever: pharyngitis with group a hemolytic strep
--alpha hemolytic strep-->rheumatic in .3-3%
--acute, immunologically mediated multi-system inflam dz a few weeks after strep pharyngitis
--mbdt anti-strep M protein ab's that cross-react with cardiac myosin
--may progress to chronic RHD
--RHD used to be leading cause of death in age 5-20, now mainly affects people who got it some 40-50 years ago (uncommon among children)
--still prevalent in Africa and parts of Asia, millions die worldwide
--DX strep w/ throat culture, rapid strep antigen test, or elevated/rising antibody titer
--group A strep --> toxins streptolysin S and O, O gives high Ab titers
--ASCHOFF BODIES in rheumatic fever = foci among abnormally enlarged heart muscle cells: islands of collagen and lymphocytes & occasional plasma cells, PATHOGNOMIC for carditis dt RHD
--mitral stenosis most common, "fish mouth"
--erythema martinatum == rash
--Sx: dyspnea, exercise intolerance, rapid heart rate out of proportion to fever
--COMPLIC: most common: chronic valvular deformities esp mitral-->stenosis and insuff develop much later, 2-10 years
--COMPLIC: 2nd most common: carditis (in 50% of cases) w/ new murmur and tachycardia
--Sx (noncardiac): polyarthritis/arthalgias, chorea (jerky mvts), erythema marginatum, subcu nodules, abdominal pain, pneumonia

MYOCARDITIS
--most often viral, most commonly Coxsackie B virus, w/ lymphocytic infiltrates
--inflam mbdt autoimmune (RHD, SLE, RA) or from drugs, or dt transplant rejection
--some other infx agents in myocarditis: borrelia b, CMV, HIV, meningococcus, R. typhi, toxoplasmosis, trichinosis, trypanosoma cruzi (Chagas dz)

VALVES
How many cusps does the aortic semilunar valve normally have?
--three
--sometimes congenitally has two and is at greater risk of stenosis

MITRAL ANNULAR CALCIFICATION MAY --> MITRAL STENOSIS
--degenerative calcific deposits in annulus (fibrous ring) as nodules behind leaflets
--doesn't affect valve fx
--when it does affect fx it's called stenosis

MVP, MITRAL VALVE PROLAPSE
--myxomatous degeneration common
--leaflets flop into L atrium during systole
--affects 3% or more of adults in US
--more women than men, age 20-40
--most ASx or mid-systolic click
--if there's regurg hear late systolic or holosystolic murmur
--may lead to serious complications in 3-4%
--usu revealed by echocardiography
--a few pts have chest pain, dyspnea, fatigue
--COMPLIC: IE, mitral insufficiency, stroke or other systemic infarct dt embolism of leaflet thrombi, arrhythmias, sudden death

PERICARDITIS
--most common complication of MI, see DRESSLER syndrome below
--inflam of pericardium
--five types: serous, fibrinous (bread & butter), hemorrhagic, purulent, caseous
--ETIO: idiopathic, infx, inflam, autoimmune, drugs, trauma, tumors
--serous: uremia, mb viral or autoimmune, minimal fluid and less inflam-->resolves
--serous: mbdt post mi (dressler's sydrome), surgery, trauma, uremia, RF, SLE
--serous: may hear friction rub, looks like bread and butter
--hemorrhagic: dt TB, tumor, bact, poor coag, trauma, looks rough/red
--purulent: usudt infx, embolus, septicemia, iatrogenic, fluid contains pus & fibrin, resolution may incl scarring-->restrictive pericarditis

DRESSLER SYNDROME
--percardiotomy??? pericarditis
--7% of MI pts get it
--fibrinous pericarditis
--occurs weeks-months post MI and subsides in a few days (2-10 weeks)
--post surgical patients get it too
--Sx: low fever, chest pain (usu pleuritic), pericardial effusion or rub,
--LABS: increased ESR
--Tx: NSAIDS or corticosteroids

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