Cardiovascular Pathology

Cardiovascular
pathology
CONGENITAL HEART DISEASES
Cyanotic = right-to-left shunt.
Acyanotic = left-to-right shunt.
CYANOTIC CONGENITAL HEART
DISEASES
Early cyanosisblue babies.
Often diagnosed prenatally or become
evident immediately after birth.
Usually require urgent surgical treatment
and/or maintenance of a PDA.
cyanosis
CYANOTIC CONGENITAL HEART
DISEASES
The 5 Ts:
1. Truncus arteriosus (1 vessel)
2. Transposition (2 switched vessels)
3. Tricuspid atresia (3 = Tri)
4. Tetralogy of Fallot (4 = Tetra)
5. TAPVR (5 letters in the name)
+ Ebstein anomaly
Tetralogy of Fallot
Most common cause of early childhood
cyanosis.
Caused by anterosuperior displacement of the

infundibular septum
Tetralogy of Fallot
Tetralogy of Fallot
Pulmonary infundibular stenosis (most
important determinant for prognosis).
Overriding aorta
Right ventricular hypertrophy (RVH)
boot-shaped heart on CXR .
VSD ( usually large and does not affect the
blood flow )
Tetralogy of Fallot
Tetralogy of Fallot
Pulmonary stenosis forces right-to-left flow
across VSD tet spells (often
caused by crying, fever, and exercise due to
exacerbation of RV outflow obstruction by
causing subvalvular spasm).
Tetralogy of Fallot
Squatting: SVR, right-to-left shunt, improves
cyanosis.
Tetralogy of Fallot
Treatment: early surgical correction.
PERSISTENT TRUNCUS
ARTERIOSUS
Truncus arteriosus fails to divide into
pulmonary trunk and aorta due to lack of
aorticopulmonary septum formation.
Most patients have accompanying VSD.

PERSISTENT TRUNCUS
ARTERIOSUS
D-transposition of
great vessels
D = dextro .
Aorta leaves RV (anterior) and pulmonary
trunk leaves LV (posterior) separation of
systemic and pulmonary circulations.
Not compatible with life unless a shunt is
present to allow mixing of blood (eg, VSD,
PDA, or patent foramen ovale).
Due to failure of the aorticopulmonary
septum to spiral.
D-TRANSPOSITION OF
GREAT VESSELS
Without surgical intervention, most infants die
within the first few months of life.
D-TRANSPOSITION OF
GREAT VESSELS
Associated with maternal DM.
What if associated with PDA ? Reversed
Differential cyanosis. ( BONUS ).
TRICUSPID ATRESIA
Absence of tricuspid valve and hypoplastic RV;
requires both ASD and VSD for viability.
TOTAL ANOMALOUS PULMONARY
VENOUS RETURN
Pulmonary veins drain into right heart
circulation (SVC, coronary sinus, etc);
associated with ASD and sometimes PDA to
allow for right-to-left shunting to maintain CO.
EBSTEIN ANOMALY
Characterized by displacement of tricuspid
valve leaflets downward into RV, artificially
atrializing the ventricle.
Associated with tricuspid regurgitation and
right HF.
caused by lithium exposure in utero.
EBSTEIN ANOMALY
LEFT-TO-RIGHT SHUNTS
Late cyanosis why ? (2 to Eisenmenger
syndrome)blue kids.
Frequency: VSD > ASD > PDA.

VENTRICULAR SEPTAL EFECT
VSD
Most common congenital cardiac defect.
Asymptomatic at birth ( HIGH PULMONARY
VASCULAR RESISTENCE) , may manifest weeks
later or remain asymptomatic throughout life
depending on the size of the defect.
Most self resolve; larger lesions may lead to LV
overload and HF
INCREASE O2 saturation in RV and pulmonary
artery.
VSD
Associated with FETAL ALCOHOL SYNDROME.
Murmur ? Severity ?
ATRIAL SEPTAL DEFECT
Defect in interatrial septum ;
loud S1; wide,fixed split S2.
Ostium secundum defects most common and
usually occur as isolated findings;
ostium primum defects rarer yet usually occur
with other cardiac anomalies ( associated with
Down )
Symptoms range from none to HF
Distinct from patent foramen ovale in that septa
are missing tissue rather than unfused.
ASD
INCREASE O2 saturation in RA, RV, and
pulmonary artery.
ASD
PATENT DUCTUS ARTERIOSUS
In fetal period, shunt is right to left (normal).
In neonatal period, DECREASE INpulmonary
vascular resistance shunt becomes left to
right progressive RVH and/or LVH and HF.
PDA
Associated with a continuous, machine-like
murmur.
Patency is maintained by PGE synthesis and
low O2 tension.
Uncorrected PDA can eventually result in late
cyanosis in the lower extremities (differential
cyanosis).
PDA
PDA
PDA
RF : rubella , prematurity.
PDA is normal in utero and normally closes
only after birth.
EISENMENGER SYNDROME
Uncorrected left-to-right shunt (VSD, ASD,
PDA) increase
pulmonary blood flow
pathologic remodeling of vasculature
pulmonary arterial hypertension RVH.
RVH occurs to compensate shunt becomes Right
to left.
Causes late cyanosis, clubbing , and
polycythemia.
Age of onset varies.
OTHER ANOMALIES : COARCTATION OF
AORTA .
Aortic narrowing near insertion of ductus arteriosus
(juxtaductal).
Associated with bicuspid aortic valve, other heart
defects, and Turner syndrome.
Hypertension in upper extremities and weak,delayed
pulse in lower extremities (brachial-femoral delay).
With age, intercostal arteries enlarge due to collateral
circulation; arteries erode ribs notched appearance on
CXR.
Complications include HF, risk of cerebral hemorrhage
(berry aneurysms), aortic rupture, and possible
endocarditis.
COARCTATION OF AORTA
Preductal V.S Postductal.
Treatment :
Surgery.
HTN
persistent systolic BP 140 mm Hg and/or
diastolic BP 90 mm Hg.
RF: age, obesity, diabetes, physical inactivity,
excess salt intake, excess alcohol intake, family
history;African American > Caucasian > Asian.
HTN
90% of hypertension is 1 (essential) and
related to
INCREASE in CO or INCREASE in
TPR.
remaining 10% mostly 2 to
renal/renovascular disease OR
hyperaldosteronism.
OTHER CAUSES ?!!
HTN
renal/renovascular disease :
1. fibromuscular dysplasia [string of beads
appearance ] RENIN-ANGIOTRNSIN .
Kidney size ?
2. Atherosclerosis.
AGE !!
HTN
HTN
Hypertensive urgencysevere ( 180/ 120 mm
Hg) hypertension without acute end-organ
damage.
Hypertensive emergencysevere hypertension
with evidence of acute end-organ damage (eg,
encephalopathy, stroke, retinal hemorrhages and
exudates, papilledema, MI, HF, aortic dissection,
kidney injury, microangiopathic hemolytic
anemia, eclampsia).
HTN
Complications :
CAD, LVH, HF, AF; aortic dissection, aortic
aneurysm; stroke; chronic kidney disease
(hypertensive nephropathy) ; retinopathy.
HTN
TREATMENT :
Diuretics , ACEI , ARBs, BB, CCB.
HYPERLIPIDEMIA
LDL < 130.
HDL > 40 males, > 50 females
TRIGLYCERIDE < 200.
HYPERLIPIDEMIA
XANTHOMA :
Composed of lipid-laden histeocytes .
HYPERLIPIDEMIA
On eyelids >>> xanthalesma.
HYPERLIPIDEMIA
Corneal arcus (arcus senilis).
Age ?
ARTERIOLOSCLEROSIS
Hardening of arteries, with arterial wall
thickening and loss of elasticity.
ARTERIOLOSCLEROSIS
1. Arteriolosclerosis:
Affects small arteries and arterioles
Two types:
hyaline (thickening of vessel walls in essential
hypertension or diabetes mellitus (non-enzymetic
glycosylation) )
Consequences ? Kidney ischemia >>
glomerulosclerosis and shrunken kidneys >> CKD
ARTERIOLOSCLEROSIS
hyperplastic (onion skinning in severe
hypertension , with proliferation of smooth
muscle cells).
Consequences ? ARF >>> FLEA-BITTEN
APPEARANCE (PIN-POINT HMG)
ARTERIOLOSCLEROSIS
ARTERIOLOSCLEROSIS
2. M nckeberg sclerosis(medial calcific
sclerosis)
Affects medium-sized arteries
Calcification of internal elastic lamina and
media of arteries >>>vascular stiffening
without obstruction.
Pipestem appearance on x-ray . Does not
obstruct blood flow; intima not involved.
ARTERIOLOSCLEROSIS
ARTERIOLOSCLEROSIS
3. ATHEROSCLEROSIS :
Disease of elastic arteries and large- and
medium-sized muscular arteries;
a form of arteriosclerosis caused by buildup of
cholesterol plaques >>> THICK INTIMA.
ARTERIOLOSCLEROSIS
Abdominal aorta > coronary artery > popliteal
artery > carotid artery.
ARTERIOLOSCLEROSIS
RF:
Modifiable: smoking, hypertension,
hyperlipidemia (LDL), diabetes.
Nonmodifiable: age, sex (in men and
postmenopausal women), family history.
ARTERIOLOSCLEROSIS
PATHGOGENSIS :
Inflammation is important in pathogenesis:
endothelial cell dysfunction >>> macrophage
and LDL accumulation >>>foam cell formation
>>> fatty streaks* >>>> smooth muscle cell
migration (involves PDGF ( FROM PLATTLETS )
and FGF), proliferation, and extracellular
matrix deposition >>>fibrous plaque >>>
complex atheromas .
ARTERIOLOSCLEROSIS
PRESENTATION : SITE !!
Angina, claudication, but can be asymptomatic.
ARTERIOLOSCLEROSIS
COMPLICATION :
Aneurysms, ischemia, infarcts, peripheral
vascular disease, thrombus, emboli.
AORTIC ANEURYSM
Localized pathologic dilatation of the aorta.
AORTIC ANEURYSM
AORTIC ANEURYSM
Sx :
May cause abdominal and/or back pain
which is a sign of leaking, dissection, or
imminent rupture.
AORTIC ANEURYSM
1. Abdominal Aortic Aneurysm (AAA)
Associated with atherosclerosis.
Risk factors include history of tobacco use, age,
male sex, family history.
May present as palpable pulsatile abdominal
mass
Mostly INFRARENAL .
SIZE 5 cm ??!
Screening ??!
AORTIC ANEURYSM
1. Thoracic aortic aneurysm:
Associated with cystic medial degeneration.
Risk factors include hypertension, bicuspid
aortic valve, connective tissue disease (eg,
Marfan syndrome).
Also historically associated with 3syphilis
(obliterative endarteritis of the vasa vasorum).
AORTIC ANEURYSM
Mycotic aneurysm :
Due to septic emboli
Inflamatory aneurysm :
Associated with vasculitis .
AORTIC ANEURYSM
Treatment :
SURGERY when indicated.
Aortic dissection
Longitudinal intimal tear forming a false
lumen.
Aortic dissection
Associated with hypertension, bicuspid aortic
valve, inherited connective tissue disorders
(eg, Marfan syndrome).
present with tearing chest pain, of sudden

onset, radiating to the back +/ markedly
unequal BP in arms.
Aortic dissection
CXR shows mediastinal widening.
Definitive Dx : CT angio , MRI , TEE.
Aortic dissection
Two types:
Stanford type A (proximal): involves Ascending aorta.
May extend to aortic arch or descending
aorta.
May result in acute aortic regurgitation or cardiac
tamponade.
Treatment: surgery.
Stanford type B (distal): involves descending aorta
and/or aortic arch. No ascending aorta involvement.
Treat medically with -blockers, then vasodilators.
ISCHEMIC HEART DISEASE
Angina :
Chest pain due to ischemic myocardium 2 to
coronary artery narrowing or spasm;
NO Myocyte necrosis.
Stable Angina : < 20 mins
usually 2 to atherosclerosis; >70%.
Sx: exertional chest pain in classic distribution.
ECG : ST depression (subendocardial ischemia)
resolving with rest or nitroglycerin.
Biomarkers ??
Treatment ? BB , ASPIRIN , STATIN.
Variant (Prinzmetal) angina :
occurs at rest 2 to coronary artery spasm; more
at night hours.
ECG : transient ST elevation .
Known triggers include tobacco, cocaine, and
triptans, but trigger is often unknown.
Treat with Ca2+ channel blockers, nitrates, and
smoking cessation (if applicable).
BB?
Ergonovine test :
Stimulate alpha receptors.
Small dose causes chest pain and and ST
elevation .
Very sensetive.
Unstable angina :
thrombosis ( why ?) with incomplete coronary
artery occlusion or obstruction of small arteries ?.
increase in frequency or intensity of chest pain or
any chest pain at rest, increase dose , post MI,
new onset angina up to 6 weeks.
ECG : +/ ST depression and/or T-wave inversion .
no cardiac biomarker elevation (unlike NSTEMI);
TTT : same as NSTEMI.
Coronary steal syndrome:
Distal to coronary stenosis, vessels are maximally
dilated at baseline.
Administration of vasodilators (eg, dipyridamole
[PDE INHIBITOR], regadenoson [ ADENOSINE
AGONIST]) dilates normal vessels and shunts
blood toward well-perfused areas decreases
flow and ischemia in poststenotic region.
Principle behind pharmacologic stress tests.
Sudden cardiac death:
Death from cardiac causes within 1 hour of onset
of symptoms.
most commonly due to a lethal arrhythmia (eg,
VF).
Associated with CAD (up to 70% of cases),
cardiomyopathy (hypertrophic,dilated), and
hereditary ion channelopathies (eg, long QT
syndrome, Brugada syndrome).
Prevent with implantable cardioverter-
defibrillator (ICD).
Chronic ischemic heart disease:
Progressive onset of HF over many years due
to chronic ischemic myocardial damage.
Hypernation : decrease metabolic activity in
response to low blood flow.
Myocardia stunning : removal of stenosis
blood flow normalization return of function
after week\ months.
Myocardial infarction :
Most often acute thrombosis due to rupture
of coronary artery atherosclerotic plaque.
cardiac biomarkers (CK-MB, troponins) are
diagnostic WHY ? Bx ?
ECG : STEMI v.s NSTEMI
Commonly occluded coronary arteries: LAD >
RCA > circumflex.
Symptoms: diaphoresis, nausea, vomiting,
severe retrosternal pain, pain in left arm
and/or jaw,shortness of breath, fatigue.
ATYPICAL PRESENTAIONS ??
ST-segment elevation MI (STEMI):
Transmural infarcts
Full thickness of myocardial wall involved
ST elevation on ECG, Q waves
NonST-segment elevation MI (NSTEMI):
Subendocardial infarcts
Subendocardium (inner 13) especially
vulnerable to ischemia ( why ? )
ST depression on ECG
Diagnosis of myocardial infarction:
In the first 6 hours, ECG is the gold standard.
Biomarkers .
ECG changes can include ST elevation (STEMI,
transmural infarct), ST depression (NSTEMI,
subendocardial infarct), hyperacute (peaked) T
waves 1ST SIGN, T-wave inversion, new left
bundle branch block, and pathologic Q waves
or poor R wave progression (evolving or old
transmural infarct).
Cardiac troponin I rises after 4 hours (peaks at
24 hr) and is elevatedfor 710 days; more
specific than other protein markers.
CK-MB rises after 612 hours (peaks at 1624
hr) and is predominantly found in myocardium
but can also be released from skeletal muscle ,
Useful in diagnosing reinfarction following
acute MI because levels return to normal after
48 hours.
Large MIs lead to greater elevations in
troponin I and CK-MB.
ECG localization of STEMI :
Evolution of MI :
024 hr:
Early coagulative necrosis,release of necrotic cell
contents into blood; edema,hemorrhage, wavy
fibers.
Neutrophils appear.
Reperfusion injury:
associated with generation
of free radicals increasing biomarkers .
leads to hypercontraction of myofibrils through
free calcium influx.
COMPLICATIONS : Ventricular arrhythmia, HF,
cardiogenic shock.
MCC of deathin hospital : cardiogenic shock

MCC of death pre-hospitalization : Arrythmia.
13 days:
Extensive coagulative necrosis.
Tissue surrounding infarct shows acute
inflammation with neutrophils.
Complication : Postinfarction fibrinous

pericarditis , only with transmural MI .
314 days:
Macrophages, then granulationtissue at margins.
Complicaions :
Free wall rupture tamponade;
papillary muscle rupturemitral regurgitation;
interventricular septal rupture
due to macrophage-mediated structural
degradation.
LV pseudoaneurysm (risk of rupture).
2 weeks to several months:
Contracted scar complete.
Complications :
Dressler syndrome,
HF,
arrhythmias,
true ventricular aneurysm (risk of mural
thrombus).
COMPLICATIONS OF MI:
Cardiac arrhythmia:
Occurs within the first few days after MI.
Important cause of death before reaching the
hospital and within the first 24 hours post-MI.
Postinfarction fibrinous pericarditis
Occurs 13 days after MI ( only transmural )
Friction rub.
Ttt : aspirin.
Papillary muscle rupture:
Occurs 27 days after MI.
Posteromedial papillary muscle rupture
risk due to single blood supply from posterior
descending artery.
Can result in severe mitral regurgitation.
Treatment: surgery.
Papillary muscle rupture:
Interventricular septal rupture:
Macrophage-mediated degradation
VSD.
Ventricular pseudoaneurysm formation:
Contained free wall rupture ;
low CO, risk of arrhythmia, embolus from
mural thrombus.
Ventricular pseudoaneurysm formation:
Ventricular free wall rupture:
Free wall rupture may lead tocardiac
tamponade.
True ventricular aneurysm:
Occurs 2 weeks to several months after MI.
Outward bulge with contraction
dyskinesia),associated with fibrosis.
Dressler syndrome
Occurs several weeks after MI.
Autoimmune phenomenon resulting in
fibrinous pericarditis ( diffused ).
Pericardial antigens get exposed to immune
system.
LV failure and pulmonary edema
Can occur 2 to LV infarction, VSD, free wall
rupture, papillary muscle rupture with mitral
regurgitation.
Acute coronary syndrome treatments:
Unstable angina/NSTEMIAnticoagulation (eg,
heparin), antiplatelet therapy (eg, aspirin+ ADP
receptor inhibitors (eg, clopidogrel), -blockers,
ACE inhibitors, statins. Symptom control with
nitroglycerin and morphine.
STEMIIn addition to above, reperfusion therapy
most important (percutaneous coronary
intervention preferred over fibrinolysis).
HEART FAILURE
Clinical syndrome of cardiac pump dysfunction
congestion and low perfusion.
Symptoms: include dyspnea, orthopnea,
fatigue;
signs: include rales, jugular venous distention
(JVD), pitting edema.
HEART FAILURE
Systolic dysfunctionreduced EF, increased
EDV; due to decrease contractility often 2 to
ischemia/MI or dilated cardiomyopathy.
Diastolic dysfunctionpreserved EF, normal

or decreased EDV; decresed compliance often
2 to myocardial hypertrophy.
HEART FAILURE
Right HF most often results from left HF.
Cor pulmonale refers to isolated right HF due
to pulmonary cause ( causes ? Low o2 ?).
HEART FAILURE
Left heart failure :
Orthopnea: Shortness of breath when supine,
increasedvenous return from redistribution of blood
(immediate gravity effect) exacerbates pulmonary
vascular congestion.
Paroxysmal nocturnal dyspnea: Breathless awakening
from sleep: venous return from redistribution of
blood, reabsorption of peripheral edema, etc.
Pulmonary edema:increased pulmonary venous
pressure pulmonary venous distention and
transudation of fluid. Presence of hemosiderin-laden
macrophages (HF cells) in lungs . Dye ??
HEART FAILURE
Pulsus alternans :
Alternating weak and strong pulses .
Always indicates LV failure and carries poor
prognosis .
HEART FAILURE
HEART FAILURE
Right heart failure :
Hepatomegaly (nutmeg liver): increase d
central venous pressure increased
resistance to portal flow. Rarely, leads to
cardiac cirrhosis.
Painful hepatomegally
HEART FAILURE
Jugular venous distention due to increase
venous pressure.
HEART FAILURE
Peripheral edema due to increasevenous
pressure fluid transudation.
HEART FAILURE
HEART FAILURE
Cardiac remodeling due to :
neurohormonal stimulation : renin-angio,
sympathetic (catecholeamines), aldosterone.
hemodynamic stress : increased afterload
and preload .
HEART FAILURE
ACE inhibitors or angiotensin II receptor
blockers, -blockers (except in acute
decompensated HF),and
spironolactone decrese mortality.
Thiazide or loop diuretics are used mainly for
symptomatic relief. Digoxin also .
Hydralazine with nitrate therapy improves
both symptoms and mortality in select
patients.
CARDIOMYOPATHY
Myocardial diseases that result in cardiac
dysfunction.
CARDIOMYOPATHY
Types :
Dilated ( M.C )
Hypertrophic.
Restrictive \ infiltrative.
CARDIOMYOPATHY
Dilated cardiomyopathy :
Eccentric hypertrophy.
All chambers are dilated biventricular H.F.
Increased complience Systolic dysfunction.
CARDIOMYOPATHY
Often idiopathic or familial.
Other etiologies:
include chronic Alcohol abuse
wet Beriberi
Coxsackie B viral myocarditis ( lymphocytic infiltrate)
chronic Cocaine use,
Chagas disease ( trypanosoma cruzi )
Doxorubicin toxicity
hemochromatosis, sarcoidosis,
peripartum cardiomyopathy.
CARDIOMYOPATHY
Findings:
HF
S3
systolic regurgitant murmur
dilated heart on echocardiogram
balloon appearance of heart on CXR.
Arrythmias ?
CARDIOMYOPATHY
Treatment :
Na+ restriction
ACE inhibitors
-blockers
diuretics
digoxin,
ICD
heart transplant.
CARDIOMYOPATHY
Takutsobo : broken heart syndrome
Sudden , temporary weakening of the
myocardium ballooning of the apex
acute heart failure.
Triggered by emotional stress ( death , divorce
) catecholamine rush .
Post menopausal women.
CARDIOMYOPATHY
Takutsobo
CARDIOMYOPATHY
Hypertrophic cardiomyopathy:
Concentric hypertrophy.
Marked ventricular hypertrophy , often septal
predominance low complience Diastolic
dysfunction ensues.
CARDIOMYOPATHY
Biopsy :
Myofibrillar disarray and fibrosis.
CARDIOMYOPATHY
6070% of cases are familial, autosomal
dominant (commonly a -myosin heavy-chain
mutation).
Can be associated with Friedreich ataxia.
CARDIOMYOPATHY
Presentation :
Causes syncope during exercise and may lead

to sudden death in young athletes due to
ventricular arrhythmia.
CARDIOMYOPATHY
Obstructive hypertrophic cardiomyopathy
(subset) HOCM
asymmetric septal hypertrophy and systolic
anterior motion of mitral valveoutflow
obstruction dyspnea, possible syncope.
CARDIOMYOPATHY
Findings:
S4.
systolic murmur ?
May see mitral regurgitation due to impaired
mitral valve closure.
CARDIOMYOPATHY
Treatment:
cessation of high-intensity athletics.
use of -blocker or non-dihydropyridine Ca2+
channel blockers (eg, verapamil).
ICD if patient is high risk.
CARDIOMYOPATHY
Diastolic dysfunction ensues and somehow
systolic .
Low complience .
S3?
CARDIOMYOPATHY
Major causes include :
Sarcoidosis.
amyloidosis ( thick myocardium with low-voltage ECG)
postradiation fibrosis
endocardial fibroelastosis (thick fibroelastic tissue in
endocardium of young children).
L ffler syndrome (endomyocardial fibrosis with a
prominent eosinophilic infiltrate)
Hemochromatosis (although dilated cardiomyopathy is
more common).
SHOCK
Inadequate organ perfusion and delivery of
nutrients necessary for normal tissue and
cellular function.
Initially may be reversible but life-threatening
if not treated promptly.
SHOCK
BACTERIAL ENDOCARDITIS
Infection of the endocardium of the heart ..
Mostly valves .
Fever (most common symptom)
New murmur
Immunologic phenomena (Roth spots [round
white spots on retina surrounded by
hemorrhage],Osler nodes [tender raised lesions
on finger or toe pads])
Systemic emboli ( Janeway lesions [small,painless,
erythematous lesions on palm or sole] ,
glomerulonephritis , mycotic aneurysm, splinter
hemorrhages on nail bed)
septic arterial or pulmonary emboli
Roth spots
Osler nodes
Janeway lesions
splinter hemorrhages
Acute
S aureus (high virulence [adhesion molecules]).
Large vegetations on previously normal valves.
Rapid onset.
IV drug users .
Tricuspid valve endocarditis is associated with S
aureus, Pseudomonas, and Candida in IV DRUG
ABUSES.
S ubacute mc
viridans streptococci (low virulence) mcc
Smaller vegetations on congenitally abnormal or
diseased valves less likely to damage the valve.
Sequela of dental procedures
Gradual onset.
Mechanism ?
Mitral valve is most frequently involved.
S bovis (gallolyticus) is present in colon cancer.
A patient presented to you with s bovis
endocarditis endoscopy.
S epidermidis on prosthetic valves.
Endocarditis may also be nonbacterial
(marantic/thrombotic) 2 to malignancy (
adenocarcinoma), hypercoagulable state, or
lupus( libman-sachs endocarditis both sides
of the valve ).
Dx : DUKE criteria.
Major : valvular lesion on TEE AND +ve blood
culture.
Minor : .
Culture most likely Coxiella burnetii,
Bartonella spp., HACEK (Haemophilus,
Aggregatibacter (formerly Actinobacillus),
Cardiobacterium, Eikenella, Kingella)
RHEUMATIC FEVER
A consequence of pharyngeal infection with
group A -hemolytic streptococci.
Immune mediated (type II hypersensitivity);
not a direct effect of bacteria. Antibodies to M
protein cross-react with self antigens
(molecular mimicry).
+ve antistreptolysin O (ASO) titers.
RHEUMATIC FEVER
Presentaion : migratory polyarthritis ,
arthralgia, carditis (endocarditis , myoraditis,
pericarditis), subutaneous nodules, erythema
marginatum, sydenham chorea, fever.
RHEUMATIC FEVER
Late sequelae include rheumatic heart
disease .
affects heart valvesmitral > aortic >>
tricuspid (high-pressure valves affected
most).
Mitral + aortic stenosis at the same time = RF
RHEUMATIC FEVER
Early lesion is mitral valve regurgitation =
damage.
late lesion is mitral stenosis = recurrent
damage leads to fibrosis.
Fibrosis of mitral = thick cusps and cordae
temdenae.
Fibrosis of aortic valve = fish mouth
appearance
RHEUMATIC FEVER
Dianosis : JONES criteria .
RHEUMATIC FEVER
Bx : Associated with Aschoff bodies
(granuloma with giant cells), Anitschkow cells
(enlarged macrophages with ovoid, wavy, rod-
like nucleus).
RHEUMATIC FEVER
Treatment/prophylaxis: penicillin.
ACUTE PERICARDITIS
Inflammation of the pericardium
presents with sharp pain, aggravated by
inspiration, and relieved by sitting up and
leaning forward.
Presents with friction rub.
ECG changes include widespread St-segment
elevation and/or PR depression (very specific)
ACUTE PERICARDITIS
ACUTE PERICARDITIS
Often complicated by pericardial effusion \
tamponade.
ACUTE PERICARDITIS
ACUTE PERICARDITIS
Causes include idiopathic (most common;
presumed viral), confirmed infection (eg,
Coxsackievirus), neoplasia, autoimmune (eg,
SLE, rheumatoid arthritis), uremia,
cardiovascular (acute STEMI or Dressler
syndrome), radiation therapy.
Constrictive pericarditis
Calcification and Thickening of the
pericardium due to recurrent acute
pericarditis.
Presents with S&S of rt. Heart failure .
Exam: pericardial knock.
Prominent x and y.
Constrictive pericarditis
CARDIAC TAMPONADE
Compression of the heart by fluid (eg, blood,
effusionsin pericardial space) decreased
CO.
Equilibration of diastolic pressures in all 4
chambers absent Y wave.
CARDIAC TAMPONADE
Findings: Beck triad (hypotension, distended
neck veins, distant heart sounds), increased
HR, pulsus paradoxus.
Pulsus paradoxusin amplitude of systolic BP
by > 10 mm Hg during inspiration.
Seen incardiac tamponade, asthma,
obstructive sleep apnea, pericarditis, croup.
CARDIAC TAMPONADE
Dx: ECHO.
Late diastolic collapse of the rt.atrium
sound.
CARDIAC TAMPONADE
ECG shows low-voltage QRS and electrical
alternans (due to swinging movement of
heart in large effusion).
CARDIAC TAMPONADE
Tension pneumothorax presents with
hypotension, distended neck veins.
So how to differentiate ?
SYPHILITIC HEART DISEASE
3 syphilis disrupts the vasa vasorum of the
aorta with consequent atrophy of vessel wall
and dilatation of aorta and valve ring.
May see calcification of aortic root and
ascending aortic arch. Leads to tree bark
appearance of aorta.
SYPHILITIC HEART DISEASE
CARDIAC TUMORS
Most common heart tumor is a metastasis.
Most common 1ry tumors :
Myxomas: adults.
Rhabdomyomas: children.
CARDIAC TUMORS
Myxomas:
Benign.
Most common 1 cardiac tumor in adults .
90% occur in the atria (mostly left atrium).
are usually described as a ball valve
obstruction in the left atrium (associated with
multiple syncopal episodes) platypnea
May hear early diastolic tumor plop sound.
CARDIAC TUMORS
Dx: echo
CARDIAC TUMORS
CARDIAC TUMORS
Myxoma produce high amount of VEGF and IL-
6.
VEGF : ANGIOGENESIS
IL-6: CONSTITUTIONAL SYMPTOMS.
CARDIAC TUMORS
Most frequent 1 cardiac tumor in children
(associated with tuberous sclerosis).
Hamartomatous tumor.
Kussmaul sign
INCREAS in JVP on inspiration instead of a
normal DECREASE .
Inspiration negative intrathoracic pressure
not transmitted to heart impaired filling of
right ventricle blood backs up into venae
cavae elevated JVD.
Kussmaul sign
May be seen with constrictive pericarditis,
restrictive cardiomyopathies, right atrial or
ventricular tumors.

Cardiovascular Pathology

Hochgeladen von

Dokumentinformationen

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Cardiovascular Pathology

Hochgeladen von

Copyright:

Verfügbare Formate

Cardiovascular

Caused by anterosuperior displacement of the

Most patients have accompanying VSD.

Frequency: VSD > ASD > PDA.

present with tearing chest pain, of sudden

MCC of deathin hospital : cardiogenic shock

Complication : Postinfarction fibrinous

Diastolic dysfunctionpreserved EF, normal

Causes syncope during exercise and may lead

Das könnte Ihnen auch gefallen