• Coronary

Artery Disease
o Rx: HTN, obesity, smoking, diabetes à are modifiers
o Rx: age, gender, familial present
§ Estrogen is cardio-protective
o Stable angina
§ Chest pain on exertion and relieved on rest and nitroglycerin
o Unstable
§ At rest and exertion; relieved by nitrates b/c NO is a
vasodilator
o Prinzmetal
§ Idiopathic coronary vasospasms
§ Only angina with ST segment elevation other two have
depression
§ More common in middle aged women
§ Wakes you up from rest and relived by nitrates
§ Only angina w/o atherosclerosis JUST vasospasms
• MI
o Transmural MI (STEMI = ST elevation MI)
§ Most common cause is thrombus of LAD
o Subendocardial (NSTEMI ST elevation MI)
§ Inner one third
§ Caused by hypovolemic shock or hypotension
o Pain not relieved by enzymes
o Sub sternal chest pain radiating to the jaw and leg on left arm;
diaphoresis, dyspnea, nausea,
o T wave inversion = ischemia
o Diabetics (peripheral neuropathy), women (higher
• Blood supply to heart
o LAD
§ Anterior wall and anterior 2/3 of the septum
o RCA
§ Nodes (conduction problems), posterior wall and anterior 1/3
of wall
o Left circumflex artery
o LAD (V1-V4), RCA (2,3, avF), Left circumflex (1, V5, V6, AvL)
• MI Enzymes
o Troponin I is best enzyme
§ Peaks at 48 hrs
§ Fades 7-10 days
o CK-MB
§ Peaks at 24 hrs
§ Fades 72 hours
o Both come out at 2-4 hours
• Timing of MI
o 0-30 min à no change
 o 30 mins-4hrs à wavy fibers
o 4-12 hrs à early coag necrosis
o 12-24 hrs à contraction band necrosis
§ Transverse lines b/c no ATP to relax and you have Ca2+ due to
reperfusion and that causes contraction
o 1-3 days à neutrophils infiltration
o 3-7 days à macrophages à chew up necrotic debris and make
myocardium very soft so most of the ruptures happen 7-10 days
o 10-14 days à granulation tissue: type III collagen, angiogenesis,
fibroblast
§ Angiogenesis due to FGF (fibroblast growth factor) and VEGF
• Lots of blood vessels
o 2-8 weeks à cicatrization
§ Increased cellularity and collagen
o >2 months à scar made of type I collagen
• Cx of MI/ACS
o Most common cause of dead arrhythmias
o Cardiogenic shock (systolic dysfunction) and
o Cardiac Tamponade
§ Beck’s triad = muffled heart sounds, JVD, low BP
§ Caused by free wall rupture resulting in hemopericardium
(blood in pericardial cavity)
§ Diastolic problem can’t fill
o IV septum rupture
§ L à R shunt b/c high pressure on left side and all the blood
shoots back to RV and get pul edema à productive cough,
congestion,
§ Parasternal boarder holosystolic / pansystolic murmer = VSD
murmur
o Papillary muscle rupture
§ Can be on left or right
§ If on left get mitral regulation
• Pansystolic murmur
• Loudest at apex
o Ruptures happen 3-10/7-10 days b/c the macrophages are coming in
and eating the necrotic debris
o Pericarditis
§ Chest pain worse when you are laying flat and relieved when
leaning forward
§ Friction rub heard on auscultation à visceral and parietal
surfaces rubbing against each other
§ ST elevation in all the leads
§ Acute fibrosis
• 1-3 days after MI
• Neutrophils à will have an exudate
 § Autoimmune pericarditis
• This happens after 2 weeks
• Dressler’s
• This has same pathogenesis as RF
o Caused by GAS pharyngitis
o Aneurysm of LV (ballooning of the wall)
§ Only happens when have a fibrous scar
§ Has to be >2 months à myocardium is weak can’t handle
hemodynamic stress
• Stasis leads to mural thrombus
o If it embolizes then first to leg then brain
o This is a systemic thromboembolism
o Dry gangrene in the leg or a CVA/stroke in the
brain
• Can’t contract so systolic problem
• Rheumatic fever (RF)
o Follow GAS pharyngitis infection
o More common in children in developing countries b/c don’t have
access to antibiotic therapy
o Ab directed the M protein of the organism but the Ab cross react w/
protein in the heart that resembles the M protein = molecular mimicry
(lol the bacteria are smarter than us)
o Type II hypersensitivity
o JONES (these are the 5 major symptoms of RF)
§ Joints
• Migratory poly arthritis affecting large joints (hips and
knees)
§ O (Heart)
• Involves all three layers
• Endocardium
o Affects the valves
o Mitral, aortic, tricuspid
o Get verrucae = sterile vegetations
§ Wart like
§ No organisms b/c these occur 2 weeks
after infection
§ Only see fibrinoid necrosis
o Can cause regurgitation
o Valvulitis aka endocarditis
• Myocardium
o See Aschoff bodies
§ Perivascular
§ Made up of Anitschkow cells (activated
macrophages = Epithelioid histiocytes), T
 cells, plasma cells; anitschkow cells come
together and form giant cells
§ Anitschkow cells have a caterpillar like
appearance on longitudinal section
§ Anitschkow cells have owl eye
appearance on transverse section
• CMV also has an owl eye à intra-
nuclear inclusion (don’t forget
that CMV also has an intra-
cytoplasmic inclusion as well)
• Pericardium
o See fibrin
§ Fibrinous bread and butter
o All antibody mediated damage
o Pain worse when leaning back relieved on
leaning forward
o Pericarditis!!!!
§ Dressler syndrome is also antibody
mediated form of pericarditis à so this
would over 2 weeks following an MI
§ Subcutaneous Nodules
§ Erythema marginatum
• Maculopapular rashes found on trunk
§ Sydenham's chorea
§ Minor symptoms of RF
• Fever
• Arthralgia (joint pain)
• Elevated ESR and CRP
o Non specific marker of acute inflammation
o Increased ESR—sedimentation b/c of rouleaux
formation
• Prolongation of PR interval
o Equivalent to first degree AV block
o Investigations for RF
§ Anti-DNAase B titers and ASO titers
o If it becomes chronic will see fibrosis of cardiac valves à Rheumatic
heart disease (RHD)
§ Mitral first then aortic and eventually tricuspid (order of
valves affected = MAT)
• Fish mouth orifice of mitral valve aka button hole (look
at the picture in pathoma y’all)
§ RF is acute (VERRUCAE on valves) in Rheumatic heart disease
see FIBROSIS b/c it is a CHRONIC condition
 • Verrucae = warty vegetations that average only a few
millimeters and form along the line of valve closure
over areas of endocardial inflammation.
• In RHD will see shortening and thickening of chordae
tendineae; also see angiogenesis à neovascularization
o Mitral valve stenosis
§ Most common cause worldwide is RF
o Rheumatic heart disease (RHD)
§ LA gets enlarged and compresses three mediastinal structures
• Esophagus get dysphagia
• Recurrent laryngeal get hoarseness
• Trachea get dyspnea
§ RHD Cx: LHF leading to pul edema and pul HTN then RHF =
CHF
• B/c of stasis get mural thrombus (can cause embolic
ischemic stroke) and cardiac arrhythmias
o Infective endocarditis from strep viridans
§ Which is part of normal flora and will
cause a subacute endocarditis on an
already damaged valve
§ Dentist is common cause of bacteremia
• Investigation = do a echo cardiogram
§ Most common causes of mitral stenosis
• Diastolic murmur sfter opening snap
• LA dilation
• HIGH YIELD à HOW TO TELL THE DIFFERENCE BETWEEN AORTIC
STENOSIS IS OLD PEOPLE AND IN AORTIC VALVE INVOLVEMENT IN RHD
o Dystrophic calcification for old peeps shows up 70 years from wear
and tear à aortic stenosis
o In RHD get fusion of commissures valve leaflets b/c of fibrosis
§ In old people no fibrosis and there is no fusion
o Congenital bicuspid aortic valve
§ Aortic stenosis will present at age 40
§ Turner syndrome (45X) can predispose you to bicuspid aortic
valve)
• Turner Syndrome can also predispose you to
coarctation of aorta (will see rib notching)
o Aortic stenosis Sx; syncope, dyspnea, angina
o Crescendo decrescendo murmur = ejection systolic
§ Radiates to the carotids
o Echocardiogram
§ Will see LV hypertrophy
• Most common cause of LVH is HTN
o Cx: LHF which leads to pul edema
§ Less than 2 weeks see frothy sputum and transudate
 § After 2 weeks will see hemosiderin laden macrophages = heart
failure cells
• These cells will stain Prussian blue b/c Fe
§ Arrhythmia and mural thrombus
§ Systemic thromboembolism
§ If go to dentist get infective endocarditis b/c strep viridans
§ Ca2+ causing hemolytic anemia
o Will see same cx as RHD
§ But no fusion of valves b/c no fibrosis
• Mitral valve prolapse = myxomatous degeneration
o Main predisposing factor is Marfan Syndrome à mutation of fibrin-1
on chromosome 15
§ Other CV problems aortic dissection, lens problems, berry
aneurysm
o Bulbus spongionsum layer of mitral valve
§ Accumulation of GAGs/ground
substance/mucopolysac/myxoid substances
o Chordae tendineae are thin and elongated = TIME BOMB à chordae
tendineae will rupture à mitral valve regurgitation into the LA à
DEATH naturally
o Midsystolic click which is b/c of the ballooning of mitral valve
leaflets in to the LA during systole
o Most of the pts are asymptomatic until the chordae tendineae rupture
à changes to pansystolic murmur loudest at the apex and now they
have regurgitation into the lung so they get pul edema leading to RHF
à mural thrombus, cardiac arrhythmias, systemic cardiac
thromboembolism, OF ALL VALVE PROBLEMS THIS IS THE MOST
COMMON TO LEAD TO INFECTIVE ENDOCARDITITIS (s. virdians)
§ Loudest at apex and radiates to axilla
o Most common in women aged 20-40
§ If pt with mitral valve prolapse were to get pregnant à
hemodynamic pressure increases and is gonna fuck up your
valve
• Infective endocarditis
o Inflammation of cardiac valves
o Endothelial damage and get thrombus (platelets, fibrin, RBCs and
bacteria stic b/c of fibronectin)
§ Esp in damaged valve b/c of turbulence
o Acute
§ Bacterial colonies w/ fibrin, platelets, RBCs
§ No neutrophils b/c valves are avascular
§ IVDU
• Tricuspid affected
• S. aureus or pseudomonas
o Subacute
 § Macrophages, fibroblasts, lymphocytes
o Sx: fever, chills, murmur
§ Fever due to: TNF-alpha/IL-1/IL6/PGE2/thromboxane
§ Murmur
§ Subacute will see a low grade fever b/c caused by a low
virulence organism
• Chronic
• Splenomegaly
• Finger clubbing
• Anemia of chronic disease
o Peripheral emboli b/c of vegetations à seen in acute and sub
§ Splinter hemorrhages found under nails, Osler’s nodes (painful
nodules at tips fingers and toes), Janeway lesions on palms and
soles, roth spots (retinal hemorrhage)
o Acute vs sub-abcute
§ Acute is seen in IVDU
• Staph aureus is part of your normal flora
o Most common cause à affects tricuspid
• Pseudomonas can also cause
• Can affect healthy or deformed native
§ Subacute à has to be on a damaged or prosthetic valve
• If it’s a prosthetic valve
o Think staph epidermidis à found on skin
o Coag necrosis
• Strep viridans is part of the normal flora of mouth
o Think this if pt had recent dental work or oral
cancer
• Think sterp bovis if pt has colorectal cancer
§ If it’s a culture negative endocarditis think HACEK
• Haemophilus species
• Aggregatibacter species
• Cardiobacterium hominis
• Eikenella corrodens
• Kingella species
§ HACEK organisms are typically oropharyngeal commensals
• Culture negative refers to an inability to produce a
colony on regular agar plates; this is because these
bacteria are fastidious (requiring a specific nutrient
o Investigation
§ Multiple blood cultures, echo cardiogram to see vegetations
§ Acute has bigger, bulkier vegetations
o Cx: HF b/c of regurg, septic emboli which can lead to à infarcts b/c
occlusion and abscess b/c the bacteria travels with the vegetation;
mycotic aneurysm, glomerulonephritis (IC mediated) in subacute, ring
 abscess = perivalvular abscess it is around the valve, heart valves,
arrhythmia b/c affecting the myocardium
• Q fever on valve = coxiella burnetii à can settle on valve
• Metallic valve and pig valve (bio prosthetic)
o Metallic can shear red cells à hemolytic anemia and jaundice
§ Microangiopathic hemolytic anemia
o Pig valve can’t lol not metal
• Viral myocarditis
o Caused by
§ Parvo virus B19
§ Coxsackie B more common than A (also causes hand foot and
mouth disease in children) aerosol droplets
§ Can cause pericarditis
• Most common cause
• B more common cause
§ CMV
§ Enterovirus
o Immune system causes more damage than the org
§ CD8+ CTL
o Worst case scenario get arrhythmias and heart failure
o Best investivation for virus is PCR
o Most common outcome is complete resolution
o Can lead to DCM, arrhythmias
§ DCM = dilation of both ventricles à systolic problem can’t
contract properly
• Sterile IE vegetation
o Lebinmen sacks in SLE à on both sides of the valve
o Verruca in RF
o Mirrantic nonbacteraial thrombotic from adeno carcinoma of lung
• HIV myocarditis
o Candida and CMV
o Fungal mixed immune response
• Trypanosoma cruzi (protozoan parasite) that causes Chagas diseaseà can
cause myocardiatis
o Megaesophagus (achalasia), toxic megacolon (loss of auerbach’ plexus
lead to perforation peritonitis), and huge DCM
• Corynebacterium diphtheriae à if exotoxin gets into blood it can cause
myocarditis a
o Don’t scrape the pseudo membrane
• RF can cause myocarditis
o But it does all three layers at same time
o Only one where you see aschoff bodies in myocardium